URINE TEST

		URINE	TESTS
S.NO	TEST	SAMPLE	NORMAL VALUES	CLINICAL IMPLICATION
1	AMMONIA NITROGEN	24 HOUR	20—70 mEq/l	VALUES INCREASE IN DIABETES MELLITUS; VALUES DECREASE IN LIVER DISEASES.
2	AMYLASE	2 HOUR	35—260 SOMOGYI UNITS/HOUR	VALUES INCREASE IN PANCREATITIS AND CHOLEDOCHOLETHIASIS.
3	BILIRUBIN	RANDOM	NEGATIVE	VALUES INCREASE IN LIVER DISEASES AND OBSTRUCTIVE BILIARY DISEASE .
4	BLOOD OCCULT	RANDOM	NEGATIVE	VALUES INCREASE IN RENAL DISEASE, EXTENSIVE BRUNS, TRANSFUSION RECATIONS, AND HEMOLYTIC ANEMIA.
5	CALCIUM	RANDOM 24 HOUR AVERAGE DIET LOW Ca DIET HIGH Ca DIET	10mg/dl 100—240mg/24hour 150 mg/24hour 240—300 mg/24hour	VALUES INCREASE IN HYPERPARATHYRODISM, METASTATIC MALIGNANCIES, AND PRIMARY CANCER OF BREAST AND LUNGS , VALUES DECREASE IN HYPOPARATHYRODISM AND VITAMIN D DEFICIENCY.
6	EPITHELIAL	24HOUR	OCCASIONAL	VALUES INCREASE IN NEPHROSIS AND HEAVY METAL POISONING.
7	GRANULAR HYLAINE	24 HOUR	OCCASIONAL	VALUES INCREASE IN NEPHRITIS AND PYELONEPHRITIS.
8	RED BLOOD CELL	24 HOUR	OCCASIONAL	VALUES INCREASE IN PYLONEPHRITIS, KIDNEY STONE , AND CYSTITIS.
9	WHITE BLOOD CELL	24 HOUR	OCCASIONAL	VALUES INCREASE IN KIDNEY INFECTION.
10	CHLORIDE Cl	24HOUR	140—250 mEq/24hr	VALUES INCREASE IN ADDISON’S DISEASES, DEHYDRATION, AND STARVATION,; VALUES DECREASE IN PYLORIC OBSTRACTION, DIRRHEA, AND EMPHYSEMA.
11	COLOR	RANDOM	YELLOW, STRAW, AMBER	VARIES WITH MANY DISEASE STATES , HYDRATION AND DIET,
12	CONCENTRATION TEST	RANDOM AND AFTER RESTRICTION	Sp. Gravity; 1.025 OSMOLALITY; 850 mOsm/l	VALUES DECREASE IN RENAL DISEASE , HYPERPARATHYRODISM , AND BONE DISEASE .
13	CREATININE	24 HOUR	MALE; 1.0—2.0g/24hr FEMALE; 0.8—1.8g/24hr	VALUES INCREASE IN INFECTION , VALUES DECREASE IN MUSCULAR ATROPHY, ANEMIA, AND KIDNEY DISEASES.
14	GLUCOSE	RANDOM	NEGATIVE	VALUES INCREASE IN DIABETES MELLITUS, BRAIN INJURY, AND MYOCARDIAL INFRACTION.
15	HYDROXYCORTI COSTEROIDS	24HOUR	MALE; 5—15 mg/24 hr FEMALE; 2—13mg/24 hr	VALUES INCREASE IN CUSHING’S SYNDROME, BURNS AND INFECTIONS , VALUES DECREASE IN ADDISON’S DISEASE.
16	KETONE BODIES (acetone)	RANDOM	NEGATIVE	VALUES INCREASE IN DIABETIC ACIDOSIS , FEVER, ANOREXIA, FASTING , AND STARVATION.
17	KETOSTEROIDS ( KS )	24 HOUR	MALE; 8—25 mg/24hr FEMALE; 5—15 mg/24 hr	VALUES DECREASE IN SURGERY BURNS, INFECTIONS, ADRENOGENTIAL,SYNDROME, AND CUSHING’S SYNDROME.
18	ODOR	RANDOM	AROMATIC	ACETONELIKE IN DIABETIC KETOSIS.
19	OSMOLALITY	24HOUR	500—800 mOsm/kg water	VALUES INCREASE IN CIRRHOSIS, CONGESTIVE, HEART FAILURE, AND HIGH PROTEIN DIETS , VALUES DECREASE IN ALDOSTERONISM , DIABETES, INSIPIDUS, AND HYPOKALEMIA.
20	PH	RANDOM	4.6—8.0	VALUES INCRESE IN URINAY TRACT INFECTIONS AND SEVERE ALKALOSIS, VALUES DECREASE IN ACIDODIS , EMPHYSEMA., STARVATION, AND DEHYDRATION.
21	PHENYLPYRUVIC ACID	RANDOM	NEGATIVE	VALUES INCREASE IN PHENYLKETONURIA (PKU )
22	POTASSIUM	24HOUR	40—80 mEq/l	VALUES INCREASE IN CHRONIC RENAL FAILURE, DEHYDTATION, STARVATION , AND CUSHING’S SYNDROME, VALUES DECREASE IN DIARRHEA, MALABSORPTION SYNDROME, AND ADRENAL CORTICAL INSUFFICIENCY.
23	PROTEIN (ALBUMIN )	RANDOM	NEGATIVE	VALUES INCREASE IN NEPHRITIS, FEVER, SEVERE ANEMIAS, TRAUMA,AND HYPERTHYRODISM.
24	SPECIFIC GRAVITY	RANDOM	1.001—1.035 (normal fluid intake ) 1.001—1.035 (range )	VALUES INCREASE IN DIABETES MELLITUS AND EXCESSIVE WATER LOSS, VALUES DECREASE IN ABSENCE OF ANTIDIURETIC HORMONE ( ADH ) AND SEVERE RENAL DAMAGE.
25	UREA	RANDOM	25—35 g/24 hr	VALUES INCREASE IN RESPONSE TO INCREASE PROTEIN INTAKE, VALUES DECREASE IN IMPAIRED RENAL FUNCTION.
26	URIC ACID	24 HOUR	0.4—1.0g/24hr	VALUES INCREASE IN GOUT , LEUKEMIA , AND LIVER, DISEASE, VALUES DECREASE IN KIDNEY DISEASE.
27	UROBILINOGEN	2 HOUR	0.3—1.0 Ehrlich units	VALUES INCREASE IN ANEMIAS, HEPATITIS A , (INFECTIONS) BILIRAY DISEASE, AND CIRRHOSIS; VALUES DECREASE IN CHOLELOTHIASIS AND RENAL INSUFFICIENCY.
28	VOLUME TOTAL	24 HOUR	1000—2000 ml/24hr	VARIES WITH MANY FACTOR

CANER

Cancer

Any malignant tumor.

Cancer arises from the abnormal and uncontrolled division of cells that then invade and destroy the surrounding tissues.

Cancer is classed as an ailment of the Immune System an
Description
d Cancer cells are usually treated as Antigens by the Immune System.


Prevalence



Region/Country Annual CancerDeaths per100,000population
United Kingdom: 283
Denmark: 280
Germany: 275
Italy: 250
France: 246
United States: 242
Netherlands: 240
Norway: 237
Switzerland: 229
Sweden: 221
Ireland: 202
Canada: 196
New Zealand 190
Spain: 177
Australia: 174
Japan 100
Prevention & Treatment of Cancer

Causes of Cancer

Specific Types of Cancer:

Bladder Cancer Brain Cancer
Breast Cancer Bronchial Cancer
Burkitt's Lymphoma Cervical Cancer
Colon Cancer Duodenal Cancer
Laryngeal Cancer Leukaemia
Liver Cancer Lung Cancer
Lymphomas Mouth Cancer
Oesophageal Cancer Ovarian Cancer

Pancreatic Cancer Penis Cancer
Pharyngeal Cancer Prostate Cancer
Skin Cancer Stomach Cancer
Testicle Cancer Uterus Cancer

Vaginal Cancer

Any of the various types of malignant neoplasm derived from epithelial tissue in several sites, occurring more frequently in the skin and large intestine in both sexes, the lung and prostate gland in men, and the lung and breast in women. Carcinomas are identified histologically on the basis of invasiveness and the changes that indicate anaplasia, i.e., loss of polarity of nuclei, loss of orderly maturation of cells (especially in squamous cell type), variation in the size and shape of cells, hyperchromatism of nuclei (with clumping of chromatin), and increase in the nuclear-cytoplasmic ratio. Carcinomas may be undifferentiated, or the neoplastic tissue may resemble (to varying degree) one of the types of normal epithelium.

Cancer of the breast or axillary nodes is second only to lung cancer as a cause of cancer death among U.S. women. There were an estimated 182,000 new cases and 46,000 deaths caused by it in 1994. Breast cancer has been the subject of a major public health effort since the 1980s. Various groups, including the American Cancer Society, have campaigned for increased federal funding for breast cancer research and health insurer coverage of diagnostic mammography. A controversial statistic, publicized by the American Cancer Society, indicates that breast cancer will afflict 1 in 9 American women. However, this is a cumulative probability figure calculated on the basis of a hypothetical 100 women between the ages of 30 and 110. A more accurate representation of the statistical model is that a woman between the ages of 30 and 55 has a 1 in 40 chance of breast cancer, and only a 1 in 180 chance of dying from it. Ninety percent of those with breast cancer report no breast cancer in their families. Risk appears slightly elevated for women who have no children, or undergo their first pregnancy after age 35; who experience an early menarche or late menopause; or who have more than two first-degree relatives who have had premenopausal or bilateral breast cancers. In 1993, 10-25% of new cancers seen were preinvasive ductal carcinoma in situ; a decade earlier, such pre- invasive tumors represented just 3% of cases. The increase is attributable to mammography. It is estimated that 20–50% of ductal carcinomas in situ go on to become invasive, with a latency period of 5–10 years. Because the milk ducts are distributed throughout the breast, radical mastectomy is the recommended treatment for this type of cancer. Meanwhile, breast conservation surgery has been shown to be highly effective for more compact
tumors.

Origin
[G. karkinbma, fr. karkinos, cancer, + -oma, tumor]

acinar carcinoma
an adenocarcinoma arising from secreting cells of a racemose gland, particularly the salivary glands. Syn: acinar carcinoma, acinic cell carcinoma, acinose carcinoma, acinous carcinoma.

acinic cell carcinoma acinic cell adenocarcinoma

an adenocarcinoma arising from secreting cells of a racemose gland, particularly the salivary glands. Syn: acinar carcinoma, acinic cell carcinoma, acinose carcinoma, acinous carcinoma.

acinose carcinoma
an adenocarcinoma arising from secreting cells of a racemose gland, particularly the salivary glands. Syn: acinar carcinoma, acinic cell carcinoma, acinose carcinoma, acinous carcinoma.

adenoid cystic carcinoma
a histologic type of carcinoma characterized by large epithelial masses containing round, glandlike spaces or cysts which frequently contain mucus or collagen and are bordered by a few or many layers of epithelial cells without intervening stroma, forming a cribriform pattern like a slice of Swiss cheese; perineural invasion and hematogenous metastasis are common; occurs most commonly in salivary glands. Syn: cylindromatous carcinoma.

adenoid squamous cell carcinoma
A malignant neoplasm consisting chiefly of glandular epithelium (adenocarcinoma), usually well differentiated, with foci of metaplasia to squamous (or epidermoid) neoplastic cells. Syn: adenoid squamous cell carcinoma.

adenosquamous carcinoma
adnexal carcinom adnexal carcinoma

a carcinoma arising in, or forming structures resembling, skin appendages.

Adrenal cortical carcinomas
alveolar cell carcinoma
anaplastic carcinoma
apocrine carcinoma
basal cell carcinoma
basaloid carcinoma
basal squamous cell carcinoma
basosquamous carcinoma
bronchiolar carcinoma
bronchiolo-alveolar carcinoma
bronchogenic carcinoma
canine carcinoma 1
clear cell carcinoma of kidney
Colloid carcinoma
cylindromatous carcinoma
cystic carcinoma
duct carcinoma
embryonal carcinoma
endometrioid carcinoma
epidermoid carcinoma
epithelial myoepithelial carcinoma
fibrolamellar liver cell carcinoma
follicular carcinomas
giant cell carcinoma
giant cell carcinoma of thyroid gland
glandular carcinoma
hepatocellular carcinoma
Hürthle cell carcinoma
inflammatory carcinoma
intermediate carcinoma
intraductal carcinoma
intraepidermal carcinoma
intraepithelial carcinoma
invasive carcinoma
juvenile carcinoma
kangri burn carcinoma
large cell carcinoma
latent carcinoma
lateral aberrant thyroid carcinoma
leptomeningeal carcinoma
liver cell carcinoma
lobular carcinoma
lobular carcinoma in situ
Lucké carcinoma
medullary carcinoma
melanotic carcinoma
meningeal carcinoma
mesometanephric carcinoma
metaplastic carcinoma
metastatic carcinoma
metatypical carcinoma
microinvasive carcinoma
mucinous carcinoma
mucoepidermoid carcinoma
carcinoma myxomatodes
noninfiltrating lobular carcinoma
oat cell carcinoma
occult carcinoma
oncoplastic carcinoma
papillary carcinoma
primary carcinoma
primary neuroendocrine carcinoma of the skin
renal cell carcinoma
sarcomatoid carcinoma
scar carcinoma
scirrhous carcinoma
secondary carcinoma
secretory carcinoma
signet-ring cell carcinoma
carcinoma simplex
carcinoma in situ
small cell carcinoma
spindle cell carcinoma
squamous cell carcinoma
sweat gland carcinoma
trabecular carcinoma
transitional cell carcinoma
tubular carcinoma
V-2 carcinoma
verrucous carcinoma
villous carcinoma
Walker carcinoma
wolffian duct carcinoma
yolk sac carcinoma

Cancer - Prevention & Treatment

These Substances Inhibit, Cure or Prevent Cancer

ENDOGENOUS SUBSTANCES
Antioxidant Enzymes

Superoxide Dismutase (SOD) helps to prevent several forms of Cancer.


Enzymes

The Beta-Glucosidase enzyme is present around Cancer cells at a level 100 times greater than its presence around normal cells:

- Its purpose is to allow the Cancer-killing substances in Laetrile (Benzaldehyde and organic Cyanide) to combine forces and act synergistically to form a toxin 100 times more potent than either substance acting alone - with disastrous consequence for Cancer tissue.

Peroxidase inhibits the growth of tumour cells [scientific research - Peroxidase significantly inhibits the growth of tumour cells in-vitro].
Endogenous Proteolytic Enzymes are speculated to inhibit some forms of Cancer when produced in greater quantities than normal.



Hormones

Melatonin inhibits the growth of several forms of Cancer [scientific research - humans: Melatonin has been used as a therapy in many advanced tumours of various types that would not respond to chemotherapy drugs - 33% of these subjects exhibited significant response].

- Melatonin prevents chemically induced and genetically related Cancers.
- Melatonin promotes the release of other (as yet unnamed) Pineal Gland chemicals that work synergistically with Melatonin in the prevention of Cancer.

Supplemental synthetic Thymosin (actually a group of Thymus Hormones) effectively cures some forms of Cancer (when Cancer is attributable to Thymosin deficiency) [scientific research - humans: synthetic Thymosin is 50% effective in curing Cancers that have occurred as a result of Thymosin deficiency].

Immune System Chemicals

Interferon Alpha interferes with the growth of several types of tumors and persons afflicted with Cancer are usually found to produce insufficient quantities of endogenous Interferon Alpha.
Interferon Gamma interferes with the growth of several types of tumors and persons afflicted with Cancer are usually found to produce insufficient quantities of endogenous Interferon Gamma.

Prostaglandin

Series 1 Prostaglandins may help to prevent several forms of Cancer.

- Prostaglandin E1 halts the growth of several types of Cancer Cells [scientific research - cancer sufferers have low levels of PGE1].


Sexual Steroid Hormone Precursors

Dehydroepiandrosterone (DHEA) prevents some forms of Cancer [scientific research - protects cell cultures from the toxicity of carcinogens].
Pregnenolone may prevent some forms of Cancer (due to its role as a precursor for DHEA production) [presently under scientific investigation].

Sterols

Low Cholesterol levels increase the risk of Cancer [scientific research - humans].


EXOGENOUS CHEMICALS
Aldehydes

Benzaldehyde (a constituent of Laetrile) can shrink tumours by an average of 39% [scientific research - humans - caution: Benzaldehyde is extremely toxic to non cancer cells, however, this toxicity is avoided in the body through the Beta-Glucosidase enzyme allowing Benzaldehyde to operate only on cancer cells].

[scientific research - shrinks tumours in 55% of cancer patients].



Alkaloids

Berberines (and Berberine Sulphate) suppress some types of Cancer cells [scientific research - in vitro].



Amino Acids

Arginine blocks the formation of many forms of Cancer [scientific research - arginine blocks 24 different types of cancer in animals]. [caution: Arginine also worsens some forms of Cancer].
Alliin (a derivative of Cysteine) prevents chemically induced Cancers [scientific research].
Cysteine helps to prevent many forms of Cancer.

When Glutamine is supplemented as an adjunct to Chemotherapy, tumours decrease in size by 45%, compared to only 25% when Glutamine is not supplemented [scientific research - animals].
Glutathione protects against many forms of Cancer, similarly to Beta-Carotene.
Ornithine blocks the formation of some forms of Cancer.



Auxins

Many dietary Indoles prevent some forms of Cancer.



Bacteria

Bifidobacteria bulgaricus can suppress some tumor cells.
Streptococcus thermophilus can suppress some tumor cells.



Carbohydrates - Polysaccharides

Alginates dilute potential carcinogens in the Intestinal Tract:

- Alginates prevent the growth of some tumors and inhibit chemical carcinogenesis [scientific research - animals].

Beta 1.6 Glucan helps to prevent and treat Cancer.
Fucoidan prevents many forms of against Cancer by halting the growth of tumors and inhibiting chemical carcinogenesis [scientific research - animals].
KS-2 (a Peptidomannan found in Shiitake Mushrooms) inhibits the growth of Cancer [scientific research - animals: as little as 1 mg of KS-2 per kg of body weight produced a 100% inhibition of tumor formation in mice].

Kureha (a Peptidomannan) is very effective (although it is very expensive and presently only available in Japan) in the treatment of Cancer [scientific research - humans].
Hemicelluloses prevent some types of Cancer by facilitating the elimination of carcinogens from the Digestive Tract.
Lentinan can inhibit some forms of Cancer [scientific research - Lentinan inhibits the metastases of advanced tumors in experimental animals].

Pectin prevents some forms of Cancer by facilitating the elimination of some carcinogens from the Digestive Tract [scientific research - humans].



Carotenoids

Alpha-Carotene protects against many forms of Cancer [scientific research - Alpha-Carotene is 10 times more potent in reducing the incidence of some forms of Cancer than Beta-Carotene] [scientific research - in-vitro: when human neuroblastoma cells were exposed to Alpha-Carotene the cancerous cells returned to their normal cycle].
Beta-Carotene protects against many forms of Cancer.

Chlorophyll helps to prevent Cancer:

- Identified as one of the factors that inhibit the mutation promoting effect of carcinogens requiring metabolic activation.

Lycopene protects against many forms of Cancer.



Enzymes

Dietary Proteolytic Enzymes are speculated to inhibit some forms of Cancer.



Enzyme Inhibitors

Protease Inhibitors (PIs) suppress carcinogens within the Intestinal Tract [it has been speculated that PIs may inhibit all forms of Cancer except Stomach Cancer].

- PIs can ensure that Oncogenes remain dormant.
- PIs inhibit the detrimental actions of Collagenase.
- PIs can REVERSE the initial cancer-causing damage to cells.



Fatty Acids

10-Hydroxydecenoic Acid inhibits the development of tumours.
Alkylglycerols decrease the risk of Cancer.
Alpha-Linolenic Acid (LNA) helps to prevent Cancer by inhibiting the growth of tumours [scientific research].
Eicosapentaenoic Acid (EPA) inhibits the growth and metastasis of some forms of Cancer [scientific research - animals] [studies are often cited that contradict this claim - these studies are usually found to have used rancid, ineffective EPA].



Glycosides

Glycyrrhizin (and its derivative Glycyrrhetinic Acid) prevent the growth of some forms of Cancer and inhibit the activity of some carcinogens [scientific research - animals].
It has been proposed that Cancer occurs as a direct result of Laetrile deficiency:

- Laetrile contains 1 molecule of Benzaldehyde and 1 molecule of organic Cyanide. Both of these toxins are normally tightly bound and unavailable in the Laetrile molecule but are both released at the site of cancerous tissues by the enzyme Beta-Glucosidase where they act synergistically (by a factor of 100) to destroy Cancer cells.


Minerals

Boron has Cancer preventative properties.
Calcium may prevent pre-cancerous cells from becoming cancerous [scientific research].
Germanium protects against various forms of Cancer.
Iodine deficiency increases the risk of some forms of Cancer.

Lithium (in non-excessive amounts) may prevent some forms of Cancer.
Molybdenum helps to prevent some forms of Cancer (by protecting the body from some types of chemical carcinogens) [scientific research - animals].
Selenium protects the body from Cancer (by stimulating the anti-carcinogenic actions of Phagocytes).



Nucleic Compounds

Abnormal metabolism of Deoxyribonucleic Acid (DNA) may be implicated in Cancer.
Isoprinosine increases the potency of Interferons against Cancer [scientific research].
Ribonucleic Acid (RNA) may increase the life span of persons afflicted with Cancer [scientific research - mice with induced tumors lived significantly longer when provided with supplemental RNA].



Polyphenols

Most Polyphenols are potent anti-cancer agents.
Caffeic Acid prevents some forms of Cancer.
Catechins help to prevent many forms of Cancer.
Chlorogenic Acid prevents cell mutations involved in Cancer.
Cinnamic Acid reduces the incidence of Cancers caused by several synthetic Food Additives [scientific research - British Columbia Cancer Research Centre].

Coumarins help to prevent some forms of Cancer by blocking the reactions of carcinogens at key sites within the body.
Ellagic Acid powerfully prevents many forms of Cancer (by counteracting many synthetic and naturally occurring compounds including Polynuclear Aromatic Hydrocarbons and Benzypyrene and preventing these substances from converting normal, healthy cells into Cancer cells) [scientific research].

Epigallo-Catechin-Gallate helps to prevent some forms of Cancer (including Sarcoma tumours) [scientific research].
Ferulic Acid helps to prevent many forms of Cancer.
Gallic Acid prevents many carcinogens from inducing chromosome mutations.
Genistein inhibits the growth of Cancer cells (by preventing the growth of those Blood Vessels that feed Cancer cells).

Tannins help to prevent some forms of Cancer.



Phyto-Oestrogens

Lignans possibly help to prevent some forms of Cancer.



Proteins

MAP-30 (a dietary Protein found in unripened Bitter Melon) inhibits the progression of some forms of Cancer [scientific research - rats & in-vitro].



Quinones

Coenzyme Q10 is an adjunct in the prevention of Cancer.
Nordihydroguaiaretic Acid (NDGA) helps to prevent some forms of Cancer [scientific research].



Smart Drugs

Butylated Hydroxytoluene (BHT) inhibits the development of some forms of Cancer [It is often claimed that BHT induces Cancer - that it is a carcinogen - BHT is not a carcinogen but it does increase the carcinogenic activities of some other chemicals. It is also an anti-promoter of cancer - the current view is that its anti-promoter activities exceed its promoter activities].
Dimethyl Glycine (DMG) helps to prevent several forms of Cancer (by stimulating the Immune System) [scientific research - animals].



Sulphuric Compounds

Dithiolthiones help to prevent many forms of Cancer.
Glucosilinates block the formation of many forms of Cancer.
Isothiocyanates help to prevent Cancer.
Sulforaphane inhibits the development of Cancer cells (by enhancing the function of endogenous Enzymes that block carcinogens) [scientific research].



Vitamins

Folic Acid helps to prevent some forms of Cancer.
Vitamin A helps to prevent many forms of Cancer.

- Can prevent normal cells from mutating into cancerous ones after exposure to cancerous ones.

Vitamin B1 helps to prevent Cancer (by detoxifying various carcinogenic chemicals).
Vitamin B3 has a major role in the prevention & treatment of Cancer.
Vitamin B6 retards the growth of several forms of Cancer [scientific research - in vitro].
Vitamin C helps to prevent most forms of Cancer.

- Intravenous administration of Vitamin C prolongs life and lessens the pain of persons afflicted with Cancer.
- Cancer sufferers have low Vitamin C levels.
- Vitamin C can minimize the detrimental effects of Chemotherapy.
- Vitamin C can halt the further spread of Cancer.
- Vitamin C increases the production of Fibroplasia (a type of tissue that creates an obstacle to the further spread of Cancer).

Vitamin E suppresses the growth of many forms of Cancer.



Volatile Oils

Limonene prevents some forms of Cancer.



These Foods Prevent or Treat Various Forms of Cancer

People who adopt a Vegetarian diet have a lower incidence of most forms of Cancer.

Active Constituents
Apples help to prevent many forms of Cancer. Caffeic Acid
Chlorogenic Acid
Ellagic Acid
Barley suppresses carcinogens in the Intestinal Tract. Protease Inhibitors
Bee Pollen helps to prevent Cancer [scientific research - humans: increasesof tumor-retarding red corpuscle epifrocytes of 25-30% are often recorded with Bee Pollen supplementation].
Beetroot possibly reverses some forms of Cancer.
Bitter Melon inhibits the progression of some forms of Cancer [scientific research - rats]. MAP-30
Broccoli possesses demonstrable Cancer preventative properties [scientific research - humans]. Indole-3-Carbinol
Brussels Sprouts contain chemicals that are very potent Cancer preventative agents. Isothiocyanates
Cauliflower prevents some forms of Cancer [scientific research]. Isothiocyanates
Coffee prevents by blocking the formation of Nitrosamines. Polyphenolic Compounds
Eggplant counteracts many carcinogens. Protease Inhibitors
Enoki Mushroom protects against some forms of Cancer.
Fenugreek Seeds may protect against some forms of Cancer [scientific research - animal trials are presently underway].
Figs can shrink tumours by an average of 39% and can induce remissions in 55% of cancer patients [scientific research - humans]. Benzaldehyde
Flax Seeds and Flax Seed Oil inhibit the development of some forms of Cancer.
Fo-Ti is used in China as a treatment for Cancer.
Garlic prevents several forms of Cancer. Sulphuric Compounds
Grapefruit prevents some forms of Cancer by facilitating the elimination of some carcinogens from the Digestive Tract [scientific research - humans]. Pectin
Karawatake Mushrooms prevent many forms of Cancer. PSK
Most Legumes help to prevent Cancer by counteracting carcinogens within the Intestines. Protease Inhibitors
Lemon helps to prevent some forms of Cancer. Limonene
Maitake Mushrooms help to treat and prevent Cancer. Beta 1.6 Glucan
Miso contains anti-carcinogens that neturalize Benzypyrene.
European Mistletoe is beneficial in the treatment of some forms of Cancer [scientific research - animals; in-vitro].
Nettle (tea) is claimed to be beneficial in the treatment of Cancer [folklore] [science refutes this claim].
Onions treat some forms of Cancer [scientific research - in vitro: Onion extract can destroy tumour cells in test tubes and can arrest tumour growth when tumour cells are implanted in rats].
Parsley prevents some forms of Cancer and is claimed to decrease the carcinogenic potential of consumption of Fried Foods. Histidine
Pau D'Arco inhibits the development of some forms of Cancer [scientific research - in vitro]. Lapachol
Potatoes prevent cell mutations. Chlorogenic Acid
Radish (seeds) prevent some forms of Cancer.
Reishi Mushrooms protect against some forms of Cancer.
Rhubarb reduces the risk of some forms of Cancer [scientific research - animals].
Many types of Seeds contain enzymes that inhibit the development of various forms of Cancer [scientific research - humans: populations whose diet is rich in seeds suffer from a lower incidence of Cancer]. Enzymes
Shark Liver Oil helps to prevent Cancer. Alkylglycerols
Shiitake Mushrooms strongly inhibit the formation of Cancer [scientific research - animals: as little of 1 mg of KS-2 extract from Shiitake Mushrooms per kg of body weight produced a 100% inhibition of tumour formation in mice] [scientific research - animals: the active Lentinan in Shiitake Mushrooms can inhibit even very advanced tumours]. Benzaldehyde
KS-2
Lentinan
RNA (double stranded)
Spinach blocks the formation of several types of Cancer and prevents the formation of Nitrosamines [scientific research]. Beta-Carotene
Histidine
Strawberries block the formation of Nitrosamines. People who eat Strawberries are 3 times less likely to develop Cancer [scientific research - humans]. Ellagic Acid
Royal Jelly inhibits some tumours. 10-Hydroxydecenoic Acid
Tea (especially Green Tea) blocks the formation of Nitrosamines that are potent carcinogens/ Tannins
Polyphenols
Catechins
Tomatoes prevent many forms of Cancer. Lycopene
Turnips help to prevent some forms of Cancer. Glucosinolates
Wine (especially Red Wine) prevents many carcinogens from inducing chromosome mutations. Gallic Acid
Xloud Mushrooms contain a substance that is very effective in the treatment of Cancer. Kureha
Yoghurt has anti-tumour activity on mice [scientific research - animals].

These Herbs Prevent or Treat various forms of Cancer

Active Constituents
Astragalus increases the survival time of persons afflicted with Cancer [scientific research - humans: Astragalus doubled the survival time of Cancer sufferers].
Barberry suppresses some forms of Cancer cells. Berberine
Burdock (root) prevents the development of some forms of Cancer [scientific research].
Chaparral may protect against some forms of Cancer [folklore] [caution: it is claimed that Chaparral can also cause some forms of Cancer]. Nordihydroguaiaretic Acid (NDGA)
Cinnamon reduces the incidence of Cancer caused by several synthetic Food Additives [scientific research - British Columbia Cancer Research Centre]. Cinnamic Acid
Essiac (a mixture of Herbs, primarily Sheep Sorrel) has caused regression of the tumours involved in some forms of Cancer, and sometimes causes total elimination of Cancer. In almost every anecdotally reported case, Essiac has significantly diminished the pain and suffering of persons afflicted with Cancer [thousands of anecdotal reports].
Ginsengs are presently being investigated as a possible Cancer inhibitor - they may suppress the proliferation of Cancer cells. Ginsenosides
Goldenseal suppresses some types of Cancer cells [scientific research - in vitro]. Berberine
Berberine Sulphate
Sheep Sorrel is the active Herb in Essiac responsible for the regression of many types of Cancer.
Turmeric acts as an anti-carcinogen and neutralizes the cancer-causing compounds in Tobacco Smoke.
White Jelly Fungus protects against some forms of Cancer.


These Cells in the Body help to prevent the Development of Cancer

Immune System Cells

Fibroplasias are fibrous tissues within the body that create obstacles to the spread of Cancer.
NK Lymphocytes can kill some types of Cancer (tumour) cells [scientific research: persons who contract Cancer usually exhibit reduced levels of NK Lymphocytes].
Phagocytes can destroy many carcinogens.

T-Lymphocytes attack Cancer cells (but only when activated by Interleukin-2).



Orthodox Medical Treatment of Cancer

Electromagnetic Radiation

Various Anti-Cancer Pharmaceutical Drugs are employed in the treatment of Cancer.
Chemotherapy is commonly employed in the treatment of Cancer.
Radiation Therapy is commonly employed as a sophisticated treatment of Cancer (in an attempt to kill the malignant tissues that are involved in cancer).

Cancer - Causes

These Cells in the Body are Implicated in the Development of Cancer

Oncogenes are genes that reside in every Cell, but if mutated they incite the cell to proliferate into a tumour.
Trophoblasts are strongly implicated in Cancer in all cases except during Pregnancy when they prepare the female body for embryo growth in the Uterus.

- Trophoblasts can be detected in Cancer sufferers by testing for the presence of Chorionic Gonadotrophic Hormone that is manufactured by Trophoblasts [the only case in which Chorionic Gonadotrophic Hormone and Trophoblasts are present in people who do not have cancer is in the case of pregnant females].



These Substances Cause/Exacerbate Cancer

ENDOGENOUS SUBSTANCES
Aldehydes

Malonaldehyde can cause some forms of Cancer.



Amino Acids - Toxic Byproducts

Nitrosamines (formed within the body when Nitrates and Nitrites combine in the Stomach with Amino Acids) are extremely potent carcinogens that can cause Cancer in any part of the body.



Bile Acids

Immobile Cholic Acid is a precursor for Cancer.

- If the body's transit time is slow and Bile is permitted to stagnate in the Colon, Detrimental Bacteria convert Cholic Acid into the powerful carcinogen - Apcholic Acid [scientific research - humans].
- If the body's transit time is slow and Bile is permitted to stagnate in the Colon, Detrimental Bacteria convert Deoxycholic Acid into the extremely carcinogenic 3-methyl-cholanthrene (3-MCA) [scientific research - humans].



Blood Clotting Chemicals

Platelet Aggregating Factor (PAF) is implicated in some forms of Cancer.



Enzymes

Collagenase enzyme assists carcinogens to destroy Collagen.



Fatty Acids

Excessive serum Triglycerides levels increase the risk of Cancer.



Hormones

Trophoblasts stimulate the production of Chorionic Gonadotrophic Hormone:

- This Hormone is simply detected in the Urine and is an extremely reliable indicator of the presence of Cancer cells in the body in all cases except where Trophoblasts are assisting the preparation of the body for Pregnancy.
- The presence of this hormone in female indicates that she either has Cancer or is Pregnant.
- In males this hormone indicates with certainty the presence of malignant Cancer Cells.

Excessive manufacture of Oestrogens (especially 2-Hydroxy Oestrone) stimulates the production of Trophoblast Cells that are implicated in Cancer in all cases except in preparing the female body for Pregnancy.



EXOGENOUS SUBSTANCES
Alcohols

Excessive consumption of Alcohol (Ethanol) is implicated in many forms of Cancer.



Aldehydes

Formaldehyde is a proven carcinogen [scientific research - rats].



Alkaloids

Large quantities of Capsaicin can cause Cancer [although non-excessive consumption of Capsaicin has several health benefits].
Persons afflicted with Cancer should not consume Allantoin (due to its ability to accelerate the replication of Cells which is undesirable in Cancer sufferers).



Amino Acids

Arginine exacerbates some types of Cancer [although it also prevents some forms of Cancer].
The "D" and "DL forms of Methionine are carcinogenic (however the "L" form is not carcinogenic).
It has been theorized that Pangamic Acid may cause Cancer [however this has not yet been proven].

The Gioblastoma Multiforma and Melanoma forms of Cancer feed on Tyrosine, it is therefore prudent for persons afflicted with these forms of Cancer to avoid Tyrosine supplementation.



Carbohydrates

Fructose may be implicated in Cancer [scientific research - mice developed tumours when Fructose was injected under the Skin at a dosage of 5 grams per kg of body weight].
Excessive consumption of Simple Sugars may be implicated in Cancer - due to Simple Sugars "feeding" Cancer cells.



Electromagnetic Radiation

Excessive exposure to Gamma-Rays can cause various forms of Cancer.
Pink Fluorescent Light increases the risk of various forms of Cancer [scientific research - mice living under pink fluorescent light develop cancer more quickly than mice who live under white fluorescent light or sunlight].



Environmental Toxins

Chloroform (Chlorine vapour produced in hot showers)
Many synthetic Pesticides (including Chlordane and Heptachlor) can cause Cancer in humans.
Ingested or inhaled Polynuclear Aromatic Hydrocarbons (PAHs) are metabolically activated within the Liver to form highly carcinogenic compounds - they are strongly suspected of causing almost all forms of Cancer.

Polyvinyl Chloride (PVC) is strongly suspected of causing some forms of Cancer.



Fatty Acids

Malvalic Acid (a cyclopropenoid Fatty Acid) increases the risk of Cancer.
Sterculic Acid (a cyclopropenoid Fatty Acid) increases the risk of Cancer.
Trans-Fatty Acids increase the risk of many forms of Cancer (by altering the activities of the Liver Enzymes - Mixed Function Oxidase Cytochromes P-448/450 - that metabolize carcinogens and other toxins [scientific research].



Food Additives

Amaranth (Red Dye No. 2)
Benzopyrene is the carcinogen which is found in barbequed & smoked foods [scientific research - humans].
Cyclamates increase the risk of Cancer.
Hydrazines are carcinogenic:

- Gyromitrin (type of Hydrazine) is an extremely potent carcinogen [scientific research - animals] Damages the body's DNA (mutagen) by generating Free Radicals [scientific research - animals].

Piperine is carcinogenic if large amounts are consumed.
Saccharin has long been suspected of being carcinogenic.



Food Preservatives

Nitrites (including Sodium Nitrite) can combine with Amino Acids within the body to form Nitrosamines.



Minerals

There is a strong association between excess consumption of Iron & Cancer.
The Sodium Selenite form of Selenium (only when consumed in extremely high dosages at levels much higher than would normally be consumed) can cause Cancer and can cause mutations in Cells.
Excessive consumption of Zinc may cause the growth of tumours (by interfering with the anti-Cancer properties of Selenium).



Mycotoxins

Aflatoxin is a potent carcinogen.


Pharmaceutical Drugs



Recreational Drugs

Tobacco smoking is carcinogenic (due especially to its Polynuclear Aromatic Hydrocarbons) [scientific research - Tobacco smoke is by far the greatest source of ingestion of Polynuclear Aromatic Hydrocarbons in humans].



Terpenes

Asiaticoside is a suspected carcinogen [this has not yet been confirmed by scientific research].



Volatile Oils

Estragole is carcinogenic.
Safrole is carcinogenic if large amounts are consumed [scientific research - animals].



Other Factors that Increase the Risk of Cancer

Environmental Risks

Showering (with hot tap water) can increase the risk of Cancer (due to the formation of Chloroform
vapours when the Inorganic Chlorine that is present in tap water evaporates and is inhaled).



Food Processing Methods

Barbequing causes the production of the carcinogenic Benzopyrene [scientific research - humans].
Frying and overheating of dietary Oils causes the production of the carcinogenic Benzopyrene [scientific research - humans].
Food Irradiation increases the risk of some forms of Cancer.

Smoking (of foods) causes the production of Benzopyrene [scientific research - humans].



Free Radicals

Free Radicals are responsible for many Cancer-causing mutations to the body's endogenous Deoxyribonucleic Acid (DNA).

- Singlet Oxygen Free Radicals can induce pre-cancerous changes in cells.



Orthodox Medical Treatments

Chemotherapy can cause detrimental side-effects in Cancer patients (unless used in conjunction with Glutamine).



These Foods or Herbs Cause or Exacerbate Cancer

Excessive consumption of dietary Fats has a very strong association with the incidence of Cancer.

Active Constituents
Frequent or excessive consumption of Bacon increases the risk of Cancer. Sodium Nitrite
It is claimed that although Chaparral can prevent some forms of Cancer, it also contributes to other forms of Cancer [scientific research - animals]. Norhydroguaguaiaretic Acid (NDGA)
Chilli (in very excessive amounts) increases the risk of Cancer. Capsaicin
Frequent or excessive consumption of Corned Beef can cause Cancer. Sodium Nitrite
Excessive consumption of Gotu Kola can cause Cancer. Asiaticoside
Frequent or excessive consumption of Ham increases the risk of Cancer. Sodium Nitrite
Maize Oil can cause Cancer [scientific research - animals].
Marijuana (smoking) can cause some forms of Cancer.
Consumption of amounts greater than 140 grams of Pepper per day can cause some forms of Cancer: Safrole
Piperine
Excessive or frequent consumption of Salami can cause Cancer. Sodium Nitrite
Sassafras (especially Sassafras Oil) can cause Cancer. Safrole
Uncooked White Champignon Mushrooms increase the risk of Cancer. Agaritine


These Ailments Increase the Risk of Cancer

Digestive System

Constant Constipation increases the risk of Cancer.

Immune System

Allergies are often precursors (forerunners of Cancer).

Metabolism

People who suffer from Obesity are at greater risk of many types of Cancer.



General Symptoms of Cancer

Metabolism

Fatigue can be a symptom of Cancer.

Myths Dispelled

Bee Foods

Honey does NOT help to prevent Cancer.



Cancer - Bronchial

Description

Malignant Tumour(s) occurring in the Bronchial Tubes.


These Substances Reduce the Risk of Bronchial Cancer

Carotenoids

Beta-Carotene reduces the risk of Bronchial Cancer.

Cancer - Colon

Also known as: Bowel Cancer
Description

Tumours occurring in the Rectum and/or Colon of the Intestine.
Orthodox medicine is presently developing a vaccine against Colon Cancer.


These Substances Alleviate/Prevent Colon Cancer

ENDOGENOUS SUBSTANCES
Hormones

The body's production of Melatonin declines in Colon Cancer sufferers (due to Colon Cancer causing a decline in the production of Melatonin's precursor - Interleukin-2).



Immune System Chemicals

The body's production of Interleukin-2 declines in Colon Cancer sufferers.



EXOGENOUS SUBSTANCES
Beneficial Bacteria

Bifidobacteria bifidus slows the development of Colon Cancer.
Bifidobacteria bulgaricus slows the development of Colon Cancer.
Lactobacillus acidophilus deprives potential carcinogens in the gut of their "Energy" to become malignant.



Bioflavonoids

Quercetin is a potent inhibitor of Colon Cancer.



Carbohydrates - Polysaccharides

Cellulose counteracts carcinogens in the Colon.
Hemicelluloses counteract carcinogens in the Colon.
Lentinan extends the life span of person with Colon Cancer [scientific research - humans].
Lignin helps to protect against Colon Cancer by removing Bile Acids from the Bowel.

Pectin provides some protection against Colon Cancer.



Carotenoids

Beta-Carotene reduces the incidence of Colon Cancer.



Enzymes

Protease Inhibitors retard the growth of Colon Cancer.



Fatty Acids

Butyric Acid helps to prevent Colon Cancer (by stimulating the growth of normal cells in the Colon and retarding the growth of cancerous cells in the Colon) [scientific research - humans].



Minerals

Calcium helps to prevent Colon Cancer by forming insoluble compounds with some endogenous carcinogenic compounds such as Bile Acids.
Selenium reduces the incidence of Colon Cancer by 47%.



Phyto-Oestrogens

Lignans possibly prevent Colon Cancer.


Steroids

Beta-Sitosterol helps to prevent Colon Cancer.



Sulphuric Compounds

Diallyl Sulphide reduces the incidence of Colon Cancer by up to 75% [scientific research - animals].



Vitamins

Vitamin C speeds the passage of Stools through the Digestive Tract, preventing exposure of Carcinogens to the Colon Wall.
Colon Cancer can occur as a result of Vitamin D deficiency.



These Foods or Herbs Prevent or Retard Colon Cancer

Active Constituents
Brussels Sprouts are especially effective in retarding Colon Cancer [scientific research - humans]. Isothiocyanates
Cabbage protects against the development of Colon Cancer. Isothiocyanates
Cauliflower protects against the development of Colon Cancer. Isothiocyanates
Celery exerts a strong protective effect against Colon Cancer [scientific research].
Chives exert a strong protective effect against Colon Cancer [scientific research].
Coffee assists the prevention of Colon Cancer.
Garlic reduces the incidence of Colon Cancer by up to 75% [scientific research - animals]. Diallyl Sulphide
Rice and Rice Bran reduce the incidence of Colon cancer.
Many types of Seeds contain enzymes that inhibit the development of Colon Cancer [scientific research - humans: populations whose diet is rich in seeds suffer from a lower incidence of Colon Cancer]. Enzymes
Wheat Bran reduces the incidence of Colon cancer.


These Substances Increase the Incidence of Colon Cancer

ENDOGENOUS SUBSTANCES
Digestive Enzymes

Excessive production of Bile contributes to Colon Cancer (due to Bile Acids).



EXOGENOUS SUBSTANCES
Fatty Acids

Excessive consumption of dietary Fats increases the risk of Colon Cancer.



Proteins

Excessive consumption of dietary Protein increases the risk of Colon Cancer.



Recreational Drugs

Excessive consumption of Alcohol increases the risk of Colon Cancer.



These Ailments Increase the Risk of Colon Cancer

Digestive System

Ulcerative Colitis increases the risk of Colon Cancer.


Cancer - Brain

Description

Malignant tumour(s) present in the Brain.


These Substances Increase the Risk of Brain Cancer

Exotoxins

Polyvinyl Chloride (PVC) causes Brain Cancer.


Cancer – Breast



Description

Malignant Tumours occurring in the Breasts.


Prevalence


Region/Country Incidence per100,000 ofpopulation
North America: 91.0
Western Europe: 86.4
Northern Europe: 84.4
Australia/New Zealand: 67.4
Southern Europe: 41.4
Soviet Union: 28.0
Japan: 21.0


These Substances Enhance the Prevention or Treatment of Breast Cancer

ENDOGENOUS SUBSTANCES
Hormones

Melatonin reduces the size of Breast Cancer tumours by 50-70% [scientific research - animals - Melatonin strongly augments the effectiveness of Tamoxifen when Melatonin is used as a pre treatment prior to commencement of Tamosifen treatment] [Melatonin production declines in persons with Breast Cancer due to Breast Cancer causing a decline in the production of Interleukin-2].



Immune System Chemicals

Breast Cancer causes a decline in the body's production of Interleukin-2.



Sexual Steroid Hormone Precursors

Dehydroepiandrosterone (DHEA) protects against Breast Cancer [scientific research - animals].



EXOGENOUS SUBSTANCES
Auxins

Some dietary Indoles prevent Breast Cancer by activating protective Enzymes that deactivate Oestrogens.



Bioflavonoids - Phyto-Oestrogens

Isoflavonoids and Lignans reduce the risk of Breast Cancer by filling up the body's receptor sites for true Oestrogens, preventing the initiation of Cancer by Oestrogens [scientific research - humans].

- Genistein is particularly effective in this respect.



Carbohydrates - Polysaccharides

Lentinan increases the life span of persons who are suffering from Breast Cancer [scientific research - humans].



Carotenoids

Beta-Carotene helps to prevent Breast Cancer.
Canthaxanthin helps to prevent Breast Cancer.



Fatty Acids

Superunsaturated Fatty Acids (SUFAs) help to prevent Breast Cancer:

- Eicosapentaenoic Acid (EPA) slows the development of and significantly extends the survival time for Breast Cancer [scientific research - animals].



Indoles

Indole-3-Carbinol increases the excretion of Oestrone (2-Hydroxyestrone) - the form of Oestrogen that is believed to cause Breast Cancer when endogenous production is excessive.



Minerals

Breast Cancer can occur as a result of Iodine deficiency.
Selenium helps to prevent Breast Cancer [scientific research - supplemental Selenium reduces the risk of Breast Cancer by 47%].



Nucleic Compounds

Poly (A)/Poly (U) (a synthetic Nucleic Acid) enhances the treatment of Breast Cancer [scientific research - trials still underway but showing considerable promise].



Protease Inhibitors

Protease Inhibitors retard the progression of Breast Cancer.



Vitamins

Vitamin A helps to prevent Breast Cancer.
Vitamin C (10 grams per day) prevents and treats Breast Cancer [scientific research - vitamin c had the most consistent statistically significant inverse association with breast cancer].
Breast Cancer can occur as a result of Vitamin D deficiency.

Vitamin E prevents Breast Cancer.



These Foods or Herbs Help to Prevent Breast Cancer

Vegetarians have a lower rate of Breast Cancer.

Active Constituents
Broccoli is especially effective in treating Breast Cancer due to its ability to increase the excretion of Oestrone (2-Hydroxyestrone) which is linked to Breast Cancer. Indole-3-Carbinol
Cabbage prevents Breast Cancer.
Garlic protects against Breast Cancer [scientific research - in-vitro].
Radish (seeds applied topically to the Breast as a heated poultice) helps to treat Breast Cancer [scientific research - humans].
Red Clover helps to prevent Breast Cancer.
Rice reduces the incidence of Breast Cancer.
Schizandra may help to prevent Breast Cancer. Lignans
Many types of Seeds contain enzymes that inhibit the development of Breast Cancer [scientific research - humans: populations whose diet is rich in seeds suffer from a lower incidence of Breast Cancer]. Enzymes
Soya Beans reduce the incidence of Breast Cancer [scientific research - humans: societies with high consumption of Soya Beans - especially in the form of Fermented Soya Bean Foods - have only 25% of the incidence of Breast Cancer as the populations of Western countries; further double blind studies have confirmed the protective effects of isoflavonoids and Lignans]. Genistein
Lignans


These Substances Increase the risk of Breast Cancer

ENDOGENOUS SUBSTANCES
Female Sexual Steroid Hormones

Excessive production of Oestrone (a type of Oestrogen) has been linked closely with the incidence of Breast Cancer [scientific research].



EXOGENOUS SUBSTANCES
Carbohydrates

Excessive consumption of Sucrose increases the risk of Breast Cancer.



Fatty Acids

Excessive consumption of dietary Fats is linked to increased incidence of Breast Cancer [scientific research - observational study].
Excessive consumption of Polyunsaturated Fatty Acids is especially implicated in increased incidence of Breast Cancer.



Pharmaceutical Drugs

The Contraceptive Pill increases the risk of Breast Cancer as it depletes the body's supply of Folic Acid and increases the body's exposure to Oestrogens [scientific research - women who use the pill for at least 4 years are prone to a 40% greater risk of Breast Cancer than otherwise expected].



Recreational Drugs

Excessive consumption of Alcohol is linked to Breast Cancer.



These Ailments Increase the Risk of Breast Cancer

Musculoskeletal System

Fibrocystic Breast Disease sufferers are at greater risk of Breast Cancer.



Orthodox Medical Treatment for Breast Cancer

Pharmaceutical Drugs

Tamoxifen is utilized in the treatment of Breast Cancer due to its ability to block the receptors within the body for Oestrogens [caution: Tamoxifen is strongly implicated in Liver Cancer].



Myths Dispelled

Caffeine-Containing Beverages

Coffee has been cleared of suspicions of causing Breast Cancer.




Primary Treatment of Breast Cancer
INTRODUCTION

Cancer of the breast is the most common cancer in women with the exception of skin cancer. It is the second leading cause of cancer death after lung cancer. In 1995, there were 183,400 new cases of breast cancer, which accounted for 46,240 breast cancer deaths in the United States12. The incidence increased dramatically in the 1980s largely because of increased detection by screening mammography. Of newly diagnosed breast cancers in 1993, 75% were stage I/II, and two-thirds of all cancers were associated with negative nodes. The survival of 5 and 10 years is increasing but the overall mortality has remained constant. Between 1973 and 1987, the mortality decreased by 4.9% for women less than 65 while it increased by 10.7% for women aged 65 years and over.
The treatment of breast cancer has evolved because of the results of large, prospective, randomized clinical trials organized by the National Surgical Adjunctive Breast and Bowel Project (NSABP) in the United States and the National Cancer Institute in Milan, Italy. The majority of women with breast cancer today are eligible for breast conservation techniques and receive some form of systemic adjuvant chemotherapy.
Table of Contents
Chapter 61 Primary Treatment of Breast Cancer

RISK FACTORS

It is estimated that one in nine women in the United States who reaches the age of 85 will develop breast cancer. The etiology is unknown but is clearly multifactorial, with many exogenous and endogenous risk factors being identified
Aside from gender, age is the single most important factor in determining breast cancer risk. The probability that breast cancer will develop increases throughout a woman’s life, with most cancers occurring during the postmenopausal years. Family history is also a significant risk factor since 15% to 20% of patients with breast cancer have a family member who has had breast cancer. The magnitude of breast cancer risk is influenced by several factors.

Number and proximity of affected relatives
Menstrual status
Age at diagnosis
Presence of bilateral cancer

Many epidemiologic studies have linked early menarche, late menopause, and late age at first full-term pregnancy to breast cancer. The total duration of menstrual cycles and the number of cycles before full-term pregnancy appear to be proportional to breast cancer risk. Premalignant histology on breast biopsy may increase breast cancer risk, as is discussed in the following section. A woman with unilateral cancer is at increased risk of developing cancer in the opposite breast. Studies have not shown that the development of contralateral breast cancer impacts adversely on survival10.
TABLE 1. Breast cancer risk factors

Gender
Age
Family history
Reproductive history
Early menarche
First birth after age 30
Late menopause
Benign breast disease
Atypical hyperplasia
Lobular carcinoma in situ
Personal history
? Exogenous factors
? Dietary factors
Table of Contents
Primary Treatment of Breast Cancer
PATHOLOGY

Screening mammography, by detecting early cancers, has increased our understanding of the malignant transformation process. Most cancers arise from the ductal elements of the breast after passing, presumably, through a sequence of premalignant stages as depicted below.

Normal breast ® hyperplasia ® atypical hyperplasia ® ductal carcinoma in situ ® invasive cancer

This process can occur over a 10- to 20-year period and orderly progression through the various stages is not obligatory. Ductal carcinoma in situ (DCIS), also known as intraductal carcinoma, is cancer confined by the basement membrane of the ducts. It most commonly presents mammographically as microcalcifications. DCIS occurs in several histologic patterns with varying propensity to progress to invasive cancer. Comedo DCIS is characterized by pleomorphic cells, high-grade nuclei, and central areas of necrosis. Noncomedo DCIS occurs in several subtypes that are generally not as cytologically malignant as comedo DCIS. It may be difficult to distinguish noncomedo DCIS from atypical hyperplasia.
Invasive ductal carcinoma accounts for over 75% of all cases of breast cancer. Grossly, it appears as a gray-white, irregular, spiculated mass that is hard and gritty on cut section. It has no specific microscopic features but can be recognized histologically as an invasive adenocarcinoma involving the ductal elements.
A number of histologic variants arise from ductal epithelium. Medullary carcinoma is grossly soft and fleshy and accounts for 6% of invasive cancers. It tends to grow to a large size and is well circumscribed. Histologically, it is characterized by poorly differentiated nuclei and infiltration by lymphocytes. Medullary carcinoma has a favorable prognosis even in the presence of nodal metastases. Tubular carcinoma is a rare histologic variant in its pure form and accounts for 2% of breast cancer. It is characteristically small and is usually found on mammography. It tends to be highly differentiated and has an excellent prognosis. Mucinous or colloid carcinoma is another well-differentiated variant, which tends to form a well-circumscribed soft, gelatinous mass. Histologically, nests of tumor cells are surrounded by a mucinous matrix.
Although most cancers arise from the ductal elements, malignancies may also arise from the epithelium of the breast lobules. Lobular carcinoma in situ (LCIS) has no radiologic or physical manifestations and has traditionally not been regarded as a malignancy. It is usually an incidental finding after a biopsy of a mass or mammographic abnormality. Current evidence suggests that LCIS is a marker for an increased risk of developing cancer in either breast8.
Five to 10% of infiltrating cancers arise from the breast lobules. Once it has become invasive, lobular carcinoma has a similar prognosis to the ductal type. It tends to be extensively infiltrative without a distinct tumor mass. Histologically, the cells demonstrate a characteristic single-file pattern. The tumor does not form microcalcifications and mammographic detection may be difficult.
Table of Contents
Primary Treatment of Breast Cancer
STAGING

The American Joint Committee on Cancer (AJCC) TNM staging system is based on clinical as well as pathologic information. The classification by primary tumor (T), status of axillary lymph nodes (N), and presence of distant metastasis (M) places patients in different prognostic groups (Table 2). Stages I and II are considered early breast cancer for which surgery plays a primary role in treatment. Stage III disease is also known as locally advanced breast cancer (LABC). Despite the absence of metastatic disease, this stage has a poor prognosis and is best treated with combined-modality treatment. This stage includes inflammatory breast cancer, a clinical entity characterized by breast warmth, erythema, and edema. The orange-peel appearance of the skin results from dermal lymphatic invasion.
TABLE 2. AJCC TNM staging system of breast cancer

Primary tumor (T)
Tx Primary tumor cannot be assessed
T0 No evidence of primary tumor
Tis Carcinoma in situ or Paget’s disease of the nipple with no associated tumor
T1 Tumor 2 cm or less in greatest dimension
T2 Tumor more than 2 cm but not more than 5 cm in greatest dimension
T3 Tumor more than 5 cm in greatest dimension
T4 Tumor of any size with direct extension to chest wall or skin
Regional lymph node (N)
Nx Regional lymph node can not be assessed
N0 No regional lymph node metastasis
N1 Metastasis to ipsilateral axillary lymph nodes
N2 Metastasis to ipsilateral nodes fixed to one another or other structures
N3 Metastasis to ipsilateral internal mammary lymph node(s)
Distant metastasis (M)
Mx Presence of distant metastasis cannot be assessed
M0 No distant metastasis
M1 Distant metastasis (includes metastasis to supraclavicular lymph nodes)
Stage grouping
Stage 0 Tis N0 M0
Stage I T1 N0 M0
Stage IIA T0 N1 M0
T1 N1 M0
T2 N0 M0
Stage IIB T2 N1 M0
T3 N0 M0
Stage IIIA T0 N2 M0
T1 N2 M0
T2 N2 M0
T3 N1, N2 M0
Stage IIIB T4 Any N M0
Any T N3 M0
Stage IV Any T Any N M1
Table of Contents
Primary Treatment of Breast Cancer
LOCOREGIONAL TREATMENT

The goals of locoregional treatment are to provide optimal local control, adequate disease staging, long-term survival, and preservation or restoration of body form. Total mastectomy and axillary dissection were the standard treatment for over 50 years, based on the Halsted mechanistic theory of cancer dissemination. Halsted believed that cancer was predominantly a local disease that spread by permeation of lymphatic pathways4. He proposed the radical mastectomy to remove cancer and prevent systemic spread. Numerous prospective randomized trials have refuted this theory of tumor biology. The bloodstream is an important pathway in early tumor dissemination, and more conservative locoregional treatment combined with systemic therapy has proved to provide local disease control with prolonged survival.
Breast Conservation
Breast conservation is the treatment of choice for the majority of stage I/II breast cancers. Six prospective randomized trials of over 4,300 women have found breast-conserving treatment to result in similar survival rates to those achieved by total mastectomy1,3,5,6,9,11. Removal of the cancer with pathologically negative margins is termed a lumpectomy. The remaining breast is usually treated with 50 Gy of external beam radiation to improve local control. The NSABP B-06 trial compared total mastectomy, lumpectomy, and lumpectomy and breast irradiation in 1,843 women3. The survival was the same for all three groups but the addition of breast irradiation to lumpectomy reduced local breast recurrence from 40% to 8%. Young patients and those with extensive intraductal cancer surrounding the invasive component are at increased risk of local recurrence. Because of the propensity for ductal carcinoma to spread upward toward the nipple along the duct, a quandrantectomy has been proposed to reduce local recurrence11. Larger excisions result in slightly improved local control rates at the expense of the cosmetic result but have no impact on ultimate survival. Local recurrences are generally treated by total mastectomy
SOME USEFUL SUGGESTIONS TO AVOID BACKACHE

1: Always uses a chair with firm and stright back.

2: Avoid sitting on sofas or cushions that are very soft.

3: Transfer your weight one leg to other, if you have to stand for longer duration.

4: Avoid high heels.

5: Sleep on a stright and hard mattress.

6: Don’t lift object from the flour. By bending forward with stright legs. Instead bend your knees, keeping your back stright.

7: Avoid lifting excessive wash.

8: Walk briskly for half an hour daily

9: bathing in lukewarm water helps to relive backache.
.
There are few absolute contraindications to breast conservation (Table 3). The cosmetic outcome of lumpectomy is dependent on both treatment-related factors and patient selection, and is judged to be excellent or good by 60% to 90% of patients.
Total Mastectomy
Removal of the entire breast, nipple-areola, and skin overlying superficial tumors is still the most common local treatment of breast cancer despite the proven results of breast conservation. In continuity removal of the axillary lymph nodes is termed a modified radical mastectomy. The pectoralis major and minor muscles are usually preserved. It is the indicated treatment when a patient prefers mastectomy over other options or when breast conservation is contraindicated. Total mastectomy may also play a role in the treatment of stage III and IV breast cancer when used in conjunction with chemotherapy and radiation therapy.
Management of the Axilla
The removal of axillary lymph nodes provides pathologic staging as well as regional disease control. Lymph node involvement is the most important prognostic factor in breast cancer. The clinical examination of the axilla is inaccurate, with a quarter of clinically normal axillae harboring micrometastatic disease. Spread to a single axillary lymph node implies a reduction in long-term survival from 90% to 60% for a 1-cm cancer7.
Levels of axillary dissection refer to the relationship of the lymphatic tissue below the axillary vein to the pectoralis minor muscle: level I lateral, level II underneath, and level III medial to the muscle. Level I and II dissection removes 10 to 15 lymph nodes and is adequate staging in clinically uninvolved axillae. Skip metastasis to level III is rare without involvement of level I/II nodes. Level III dissection is indicated for clinically involved nodes but is associated with an increased risk of lymphedema.
The routine use of axillary dissection is being reevaluated because of the widespread use of systemic therapy in node-negative patients. The risk of regional recurrence is significantly increased in cases in which axillary dissection is omitted. Axillary dissection potentially can be omitted in elderly patients with very small primary lesions that are estrogen receptor (ER) positive.
Treatment of DCIS
The malignant potential of DCIS is largely unknown. If untreated some but not all will progress to invasive cancer. Local recurrence after surgical excision alone occurs in up to 30% of cases depending on tumor size and histology (comedo vs. noncomedo). One-half of recurrences will be invasive carcinomas. Radiation therapy has been shown to reduce local recurrences. The NSABP B-17 trial studied 818 women with DCIS randomly assigned to either lumpectomy alone or lumpectomy followed by breast irradiation2. With a median follow-up of 43 months, local recurrences developed in 16% treated by lumpectomy alone and 7% treated by lumpectomy plus irradiation. Studies are ongoing to define subsets of patients who can be treated by excision alone.
Table of Contents
Primary Treatment of Breast Cancer
SYSTEMIC THERAPY

Adjuvant chemotherapy and hormonal therapy are used to eliminate occult metastases responsible for later recurrences. Clinical trials have shown that adjuvant therapy can reduce the odds of cancer recurrence up to 30%. The effect on disease-free interval is generally larger than the effect on overall survival. Obviously, those at higher risk of recurrence and death will obtain a greater benefit. Commonly used chemotherapy regimens include CMF (cyclophosphamide, methotrexate, 5-fluorouracil), FAC (5-fluorouracil, doxorubicin, cyclophosphamide), and AC (doxorubicin, cyclophosphamide). Taxol has been found highly effective in metastatic disease and is currently being studied as an adjuvant agent. Tamoxifen, an estrogen antagonist, is used in the treatment of hormone-responsive tumors.
Polychemotherapy has a greater effect in premenopausal than in postmenopausal patients and tamoxifen has a greater effect in postmenopausal than in premenopausal women. The duration of chemotherapy is generally 4 to 6 months depending on the agents used. The duration of tamoxifen therapy is not firmly established but generally is 5 years after local treatment. There is evidence that the addition of tamoxifen to polychemotherapy in ER+ premenopausal women has small but significant benefit. There is inconsistent evidence that the addition of chemotherapy to tamoxifen therapy improves the overall survival in ER-positive postmenopausal patients. Postmenopausal women with ER-negative tumors are treated with chemotherapy.
Node-Negative Tumors
The risk of recurrence for node-negative breast cancer is related to tumor size and can approach 30%. Clinical trials have proved the benefit of adjuvant therapy in the majority of node-negative cancers. There is a subset of patients, however, with an extremely low risk who would not benefit from therapy. This subset includes tumors < 1 cm and certain histologic variants (tubular, medullary, mucinous) that have an excellent prognosis.
Neoadjuvant Chemotherapy
Patients with locally advanced breast cancer are extremely poor candidates for primary surgical therapy because of the prohibitive incidence of locoregional recurrence and poor long-term prognosis. Recent trials of neoadjuvant chemotherapy and hormonal therapy have shown high response rates and improved relapse-free survival. Treatment can be administered until maximal clinical response is achieved. Patients are reevaluated radiologically and pathologically. Mastectomy and chest wall irradiation together have enabled high levels of local control. For patients who achieve pathologic complete response at “lumpectomy” after induction chemotherapy, irradiation alone is an increasing option.

Cancer - Cervix

Also known as: Cervical Cancer
Description

Malignant Tumour(s) in the Cervix.


These Substances Reduce the Risk of Cervical Cancer

Carotenoids

Beta-Carotene protects the body against Cervical Cancer.
Lycopene protects the body against Cervical Cancer [scientific research - humans: females with high serum Lycopene levels have 80% less risk of developing Cervical Cancer than those with low Lycopene levels].



Vitamins

Cervical Cancer can occur as a result of Folic Acid deficiency [scientific research - low folic acid levels allow the cervix to become more susceptible to the Papilloma virus].
Vitamin A can prevent Cervical Cancer.
Vitamin B6 helps to prevent Cervical Cancer [scientific research - humans: Cervical Cancer sufferers generally have very low levels of Vitamin B6].

Vitamin C protects against Cervical Cancer:

- Cervical Cancer sufferers have 50% lower levels of Vitamin C than healthy people [scientific research - humans].



These Herbs Treat Cervical Cancer

Essiac (a mixture of various Herbs - primarily Sheep Sorrel) has been reported anecdotally as curing Cervical Cancer [anecdotal evidence: a female regarded as incurable and terminal was treated with Essiac and totally regressed to normal health].


These Substances Increase the Risk of Cervical Cancer

Recreational Drugs

Tobacco smoking increases the risk of Cervix Cancer.



Viruses

The Papilloma Virus is a direct cause of Cervix Cancer [scientific research - humans].


Cancer - Duodenum

Also known as: Duodenal Cancer
Description

Malignant Tumour(s) occurring in the Duodenum.


These Substances Increase the Risk of Duodenal Cancer

Volatile Oils

Asarone increases the risk of Duodenal Cancer [scientific research - rats].



These Herbs Increase the Risk of Duodenal Cancer

Toxic Constituents
Calamus increases the risk of Duodenal Cancer. Asarone


Cancer - Larynx

Also known as: Laryngeal Cancer
Description

Malignant tumour(s) occurring in the Larynx.


These Substances Protect Against Larynx Cancer

Carotenoids

Beta Carotene protects against Cancer of the Larynx.



Vitamins

Vitamin C protects against Cancer of the Larynx:

- People who are deficient in Vitamin C have twice the risk of contracting Laryngeal Cancer than those consuming adequate levels of Vitamin C [scientific research - humans].



These Substances Increase the Risk of Larynx Cancer

EXOGENOUS SUBSTANCES
Recreational Drugs

Alcohol increases the risk of Larynx Cancer.




Cancer - Liver

Description

Malignant tumour(s) occurring in the Liver.


These Substances Alleviate/Prevent Liver Cancer

ENDOGENOUS SUBSTANCES
Amino Acids

Glutathione may cure Liver Cancer [scientific research - Glutathione has cured Liver Cancer in animals].



EXOGENOUS SUBSTANCES
Carotenoids

Beta-Carotene reduces the risk of Liver Cancer [although Lycopene is 10 times more potent in reducing Liver Cancer risk].
Lycopene protects against Liver Cancer [scientific research - humans: Lycopene is 10 times more potent against Liver Cancer than Beta-Carotene].



These Herbs Treat Liver Cancer

Active Constituents
Ginsengs can return human Liver Cancer Cells to normal [scientific research - in vitro]. Ginsenosides


These Substances Increase the Risk of Liver Cancer

Alkaloids

Pyrrolizidine Alkaloids increase the risk of Liver Cancer [scientific research - animals].



Mycotoxins

Aflatoxin (produced by various species of detrimental Aspergillus moulds) increases the risk of Liver Cancer [scientific research - humans].



Pharmaceutical Drugs

Tamoxifen increases the risk of Liver Cancer.



Recreational Drugs

Alcohol (ethanol) increases the risk of Liver Cancer.
Polyvinyl Chloride (PVC) increases the risk of Liver Cancer.



These Herbs Increase the Risk of Liver Cancer

Toxic Constituents
Excessive oral ingestion of Comfrey can cause Liver Cancer Pyrrolizidine Alkaloids



hepatitis
Inflammation of the liver; usually from a viral infection, but sometimes from toxic agents.

Previously endemic throughout much of the developing world, viral hepatitis now ranks as a major public health problem in industrialized nations. The three most common types of viral hepatitis—A, B, and C—afflict over 500,000 people in the U.S. each year, and millions worldwide. Hepatitis B alone ranks as the ninth leading killer in the world. Hepatitis A, an RNA enterovirus, spread by contact with fecal matter or blood, most often through ingestion of contaminated food. Rarely fatal, it cannot be treated except by bed rest for 1–4 weeks, during which time no alcohol should be consumed. It may recur after 3 months. Hepatitis B is shed through blood, semen, vaginal secretions, and saliva approximately 4–6 weeks after symptoms develop; the virus may take up to 6 months to incubate, and people may also become asymptomatic carriers. Hepatitis B may heal slowly, and is a leading cause of chronic liver disease and cirrhosis. Effective vaccines exist, but it is the fastest spreading form of the disease in the U.S., with some 300,000 cases reported annually. Rates were up 80% from 1981–1986 among IV drug users and up 38% during the same period among heterosexuals; among homosexuals, previously a high-risk group, rates held stable. Hepatitis C, infecting about 150,000 Americans annually, remains in the blood for years and accounts for a large percentage of cirrhosis, liver failure, and liver cancer cases. Its main mode of transmission is through blood transfusion, and possibly sexual intercourse. Types D and E are less frequently seen in the U.S.

]

hepatitis A
chronic active hepatitis
acute parenchymatous hepatitis
anicteric hepatitis
hepatitis without jaundice.

anicteric virus hepatitis
hepatitis B
hepatitis C
cholangiolitic hepatitis
cholestatic hepatitis
chronic hepatitis
chronic interstitial hepatitis
chronic persistent hepatitis
chronic persisting hepatitis
hepatitis contagiosa canis
hepatitis D
delta hepatitis
drug-induced hepatitis
duck viral hepatitis
hepatitis E
epidemic hepatitis
equine serum hepatitis
hepatitis externa
fulminant hepatitis
giant cell hepatitis
goose viral hepatitis
halothane hepatitis
infectious hepatitis
infectious canine hepatitis
infectious necrotic hepatitis of sheep
long incubation hepatitis
lupoid hepatitis
mouse hepatitis
MS-1 hepatitis
murine hepatitis
NANB hepatitis
NANBNC hepatitis
neonatal hepatitis
non-A, non-B hepatitis
non-A, non-B, non-C hepatitis
peliosis hepatitis
persistent chronic hepatitis
plasma cell hepatitis
serum hepatitis
short incubation hepatitis
subacute hepatitis
suppurative hepatitis
transfusion hepatitis
viral hepatitis
viral hepatitis type A

a virus disease with a short incubation period (usually 15 to 50 days), caused by hepatitis A virus, a member of the family Picornaviridae, often transmitted by fecal-oral route; may be inapparent, mild, severe, or occasionally fatal and occurs sporadically or in epidemics, commonly in school-age children and young adults; necrosis of periportal liver cells with lymphocytic and plasma cell infiltration is characteristic and jaundice is a common symptom. Syn: epidemic hepatitis, hepatitis A, infectious hepatitis, MS-1 hepatitis, short incubation hepatitis, virus A hepatitis.

viral hepatitis type B
a virus disease with a long incubation period (usually 50 to 160 days), caused by hepatitis B virus, a DNA virus and member of the family Hepadnoviridae, usually transmitted by injection of infected blood or blood derivatives or by use of contaminated needles, lancets, or other instruments; clinically and pathologically similar to viral hepatitis type A, but there is no cross-protective immunity; HBsAg is found in the serum and the hepatitis delta virus occurs in some patients. Syn: hepatitis B, serum hepatitis, transfusion hepatitis, virus B hepatitis.

viral hepatitis type C

viral hepatitis type viral hepatitis type D
acute or chronic hepatitis caused by the hepatitis delta virus, a defective RNA virus requiring HBV for replication. The acute type occurs in two forms: 1) coinfection, the simultaneous occurrence of hepatitis B virus and hepatitis delta virus infections, which usually is self-limiting; 2) superinfection, the appearance of hepatitis delta virus infection in a hepatitis B virus carrier, which often leads to chronic hepatitis The chronic type appears to be more severe than other types of viral hepatitis. Syn: delta hepatitis, hepatitis D.

viral hepatitis type E viral hepatitis type E

hepatitis caused by a nonenveloped, single-stranded, positive-sense RNA virus 27–34 nm in diameter, unrelated to other hepatitis; it is the principal cause of enterically transmitted, waterborne, epidemic NANB hepatitis occurring primarily in Asia and Africa. Syn: hepatitis E.


virus hepatitis
a relatively mild hepatitis, without jaundice, due to a virus; the principal physical signs and symptoms are enlargement of the liver, lymph nodes, and often the spleen, together with headache, continuous fatigue, nausea, anorexia, sudden distaste for smoking, abdominal pains, and sometimes mild fever; labratory tests reveal evidence of hepatitis.

virus A hepatitis hepatitis A virus (HAV)

an RNA virus in the family Picornaviridae; the causative agent of viral hepatitis type A. Syn: infectious hepatitis virus.

virus B hepatitis hepatitis B virus (HBV)

a DNA virus in the family Hepadnaviridae; the causative agent of viral hepatitis type B. Syn: serum hepatitis virus.

virus C hepatitis hepatitis C virus (HCV)

a non-A, non-B RNA virus causing post-transfusion hepatitis; it appears to be a member of the family Flaviviridae.

virus hepatitis of ducks virus hepatitis of ducks

a disease of very young ducklings, caused by the duck hepatitis virus (family Hepadnoviridae) and manifested as an acute illness of several days followed by death; the principal lesions are an enlarged necrotic liver filled with ecchymotic hemorrhages.




Cancer - Lung

Description

Malignant tumour(s) occurring in the Lungs.


Prevalence of Lung Cancer


Region/Country Incidence per 100,000 ofpopulation
Males Females
Northern Europe: 98.1 29.5
Western Europe: 86.7 12.3
North America: 74.6 30.3
Southern Europe: 64.2 8.9
Australia/New Zealand: 61.6 15.9
Eastern Europe: 61.2 10.3
Soviet Union: 51.2 10.3
Japan: 31.0 11.2


These Substances Reduce the Incidence of Lung Cancer

ENDOGENOUS SUBSTANCES
Hormones

The body's production of Melatonin declines in Lung Cancer sufferers (due to Lung Cancer causing a decline in the production of one of Melatonin's precursors - Interleukin-2).



Immune System Chemicals

The body's production of Interleukin-2 declines in Lung Cancer sufferers.



Organic Acids

Optimal endogenous Uric Acid levels help to prevent Tobacco-induced Lung Cancer.



ENDOGENOUS SUBSTANCES
Carotenoids

Alpha-Carotene [scientific research - Alpha-Carotene is 10 times more effective in preventing Lung Cancer than Beta-Carotene which is also effective against Lung Cancer].
Smokers who consume high levels (approximately 6 mg per day) of Beta-Carotene have the same rate of Lung Cancer as non-smokers [scientific research - humans].



Vitamins

Folic Acid lowers the incidence of Lung Cancer [scientific research].
Vitamin A reduces the incidence of Lung Cancer.
Vitamin E protects against Lung Cancer [scientific research - humans].



These Foods or Herbs Prevent or Treat Lung Cancer

Active Constituents
Apricots help to prevent Lung Cancer. Carotenoids
Beetroot [scientific research - humans - documented case of 1 Hungarian doctor using Beetroot to totally clear Lung Cancer from a 50 year old male - after 6 weeks of treatment the tumour disappeared].
Sweet Potatoes help to prevent Lung Cancer. Carotenoids
Tomatoes help to prevent Lung Cancer: Lycopene
Wakame prevents and cures Lung Cancer [scientific research - humans].


These Substances Increase the Risk of Lung Cancer

Environmental Toxins

Polyvinyl Chloride (PVC) increases the risk of Lung Cancer.



Methylxanthines

Excessive Caffeine consumption increases the risk of Lung Cancer.



Minerals (Heavy Metals)

Long term exposure to Cadmium increases the risk of Lung Cancer [scientific research - humans].



Recreational Drugs

Tobacco Smoking increases the risk of Lung Cancer.



Sterols

Excessive consumption of dietary Cholesterol increases the risk of Lung Cancer [scientific research - humans].



These Foods Increase the Risk of Lung Cancer

Carcinogenic Constituents:
Consumption of 5 or more cups of Coffee per day increases the risk of Lung Cancer. Caffeine
Excessive consumption of Margarine increases the risk of Lung Cancer. Trans Fatty Acids


Cancer - Mouth

Description

Malignant tumour(s) occurring in the Mouth.


These Substances Reduce the Risk of Mouth Cancer

Carotenoids

Beta-Carotene can reverse pre-cancerous lesions in the Mouth.



Vitamins

Vitamin E reduces the incidence of Mouth Cancer.



These Substances Increase the Risk of Mouth Cancer

Recreational Drugs

Alcohol increases the risk of Mouth Cancer.



Cancer - Oesophagus

Also known as: Oesophageal Cancer
Description

Malignant tumour(s) occurring in the Oesophagus.


These Substances Reduce the Risk of Oesophageal Cancer

Carotenoids

Beta-Carotene helps to prevent Oesophageal Cancer.



Minerals

Oesophageal Cancer can occur as a result of Molybdenum deficiency [scientific research - humans].
Persons afflicted with Oesophageal Cancer are usually found to be deficient in Zinc.



Sulphuric Compounds

Diallyl Sulphide may provide 100% protection against Oesophageal Cancer [scientific research -animals].



Vitamins

Vitamin B2 helps to prevent Oesophageal Cancer [scientific research: Vitamin B2 reduces the number of possibly pre-cancerous Cells in the Oesophagus].



These Herbs Prevent Oesophageal Cancer

Active Constituents
Garlic may provide 100% protection against Oesophageal Cancer [scientific research - animals]. Diallyl Sulphide


These Substances Increase the Risk of Oesophageal Cancer

Alcohols

Alcohol (ethanol) increases the risk of Oesophageal Cancer.


Cancer - Ovaries

Also known as: Ovarian Cancer
Description

Malignant tumour(s) occurring in the Ovaries.


These Substances Prevent Ovarian Cancer

Minerals

Iodine may prevent Ovarian Cancer.



These Herbs Prevent Ovarian Cancer

Red Clover helps to prevent Ovarian Cancer.


These Substances Increase the Risk of Ovarian Cancer

ENDOGENOUS SUBSTANCES
Hormones

Excessive production of Oestrogens (specifically 2-Hydroxyestrone) increases the risk of Ovarian Cancer.



EXOGENOUS SUBSTANCES
Fatty Acids

Excessive consumption of Saturated Fatty Acids increases the risk of Ovarian Cancer.



These Foods Increase the Risk of Ovarian Cancer

Active Constituents
Excessive consumption of Butter increases the risk of Ovarian Cancer. Saturated Fatty Acids
Excessive consumption of Milk increases the risk of Ovarian Cancer. Saturated Fatty Acids
Excessive consumption of Meats increases the risk of Ovarian Cancer. Saturated Fatty Acids


Cancer - Pancreas

Also known as: Pancreatic Cancer
Description

Malignant tumour(s) occurring in the Pancreas.


These Substances Reduce the Risk of Pancreatic Cancer

Carotenoids

Beta Carotene reduces the risk of Pancreatic Cancer.



These Substances Increase the Risk of Pancreatic Cancer

Recreational Drugs

Excessive consumption of Alcohol (ethanol) increases the risk of Pancreatic Cancer by 100%.



These Herbs Can Cause Pancreatic Cancer

Excessive consumption of Tea increases the risk of Pancreatic Cancer.


Myths Dispelled

Caffeine-Containing Beverages

Coffee has been cleared of Pancreatic Cancer suspicions.


Cancer - Penis

Description

Malignant tumour(s) in the Penis.


These Substances Reduce the Risk of Penis Cancer

Carotenoids

Beta-Carotene reduces the risk of Penis Cancer.



Cancer - Pharynx

Also known as: Pharyngeal Cancer; Throat Cancer
Description

Malignant tumour(s) occurring within the Pharynx.


These Substances Reduce the Risk of Pharyngeal Cancer

Carotenoids

Beta-Carotene reduces the risk of Pharynx Cancer.



Vitamins

Vitamin A protects against Pharynx Cancer by strengthening the Mucous Membranes of the Pharynx (Throat).
Vitamin C helps to prevent Pharynx Cancer.



These Substances Increase the Risk of Pharyngeal Cancer

Alcohols

Alcohol (Ethanol) increases the risk of Pharynx Cancer.




Cancer - Prostate

Also known as: Prostatic Cancer
Description

Malignant tumour(s) occurring in the Prostate.


These Substances Reduce the Risk of Prostatic Cancer

ENDOGENOUS SUBSTANCES
Hormones

The body's production of Melatonin declines in Prostate Cancer sufferers (due to Prostate Cancer causing a decline in the production of Melatonin's precursor - Interleukin-2).



Immune System Chemicals

The body's production of Interleukin-2 declines in Prostate Cancer sufferers.



EXOGENOUS SUBSTANCES
Carotenoids

Beta-Carotene reduces the risk of Prostate Cancer.



Minerals

Persons afflicted with Prostatic Cancer are usually found to be deficient in Zinc.



Vitamins

Vitamin A helps to prevent Prostate Cancer by strengthening the mucous membranes of the Prostate.



These Foods Reduce the Risk of Prostatic Cancer

Active Constituents
Beetroot [scientific research - Hungary - human subject totally cleared of prostate cancer using Beetroot].
Rice reduces the incidence of Prostate Cancer.
Many types of Seeds contain enzymes that inhibit the development of Prostate Cancer [scientific research - humans: populations whose diet is rich in seeds suffer from a lower incidence of Prostate Cancer]. Enzymes
Tomatoes help to prevent Prostate Cancer.


These Substances Increase the Risk of Prostatic Cancer

ENDOGENOUS SUBSTANCES
Hormones

Excessive production of Oestrogens (specifically 2-Hydroxyestrone) in males may increase the risk of Prostatic Cancer.



EXOGENOUS SUBSTANCES
Lipids

Excessive consumption of dietary Fats increases the risk of Prostate Cancer.



Minerals - Toxic Heavy Metals

Long term exposure to Cadmium increases the risk of Prostate Cancer [scientific research - humans].



Other Factors that Increase the Risk of Prostatic Cancer

Altered Lighting

The use of Sunglasses (or other types of tinted glasses) may increase the risk of Prostatic Cancer (by blocking the absorption of the Electromagnetic Radiation in Sunlight into the Pineal Gland via the Eyes and subsequently blocking the manufacture of Melatonin) [anecdotal evidence exists of a case of total remission of Prostatic Cancer when the patient ceased using pink tinted glasses].



Myths Dispelled

Sexual Steroid Hormones

Testosterone is widely regarded by orthodox medical practitioners as "feeding" Prostate Cancer cells - this theory is now discredited and it is speculated that Testosterone may even help to prevent Prostatic Cancer.


Cancer - Skin

Description

Malignant tumour(s) affecting the Skin.


These Substances Help to Prevent Skin Cancer

Carotenoids

Alpha-Carotene helps to prevent Skin Cancer [10 times more potent against Skin Cancer than Beta-Carotene].
Beta-Carotene helps to prevent Skin Cancer.



Cosmetics & Topical Applications

Glycolic Acid (applied topically) reverses pre-cancerous growths on the Skin.
Retin-A (applied topically) reverses pre-cancerous growths on the Skin [scientific research - humans: Retin-A clears 60% of Keratoses (flat, pink, scaly bumps on the skin)].



Enzyme Inhibitors

Protease Inhibitors inhibit the development of Skin Cancer.



Minerals

Selenium prevents several forms of Skin Cancer by stimulating the anti-carcinogenic action of Phagocytes [scientific research - animals: L-Selenomethionine applied topically or orally is effective in retarding Skin Cancers initiated by excessive exposure to Ultra-Violet light].



Polyphenols & Bioflavonoids

Ellagic Acid reduces the incidence of Skin Cancer [scientific research - mice].



Vitamins

Para Aminobenzoic Acid (PABA) helps to prevent Skin Cancer.
Vitamin A helps to prevent Skin Cancer.
Vitamin B6 increases resistance to Skin Cancer (especially to Melanomas) and can cause the regression of Melanomas [scientific research - animals: supplemental Vitamin B6 increases resistance to Melanomas by 200%; scientific research - humans: subcutaneous application of Pyridoxal form of Vitamin B6 4 times per day caused regression of Melanomas by 50%].

Vitamin C helps to prevent Skin Cancer.
Vitamin E helps to prevent Skin Cancer.



These Foods or Herbs Prevent or Alleviate Skin Cancer

Active Constituents
Blackcurrants reduce the incidence of Skin Cancer [scientific research - mice]. Ellagic Acid
Chaparral is a good treatment for Skin Cancer [folklore].
Garlic helps to prevent Skin Cancer [scientific research].
Grapes reduce the incidence of Skin Cancer [scientific research - mice]. Ellagic Acid
Onions protect the body against Skin Cancer [scientific research - animals].
Propolis (consumed internally) successfully treats benign Skin Cancers [scientific research: Propolis successfully healed 65% of sufferers of benign Skin Cancers].
Raspberry reduces the incidence of Skin Cancer [scientific research - mice]. Ellagic Acid


These Substances/Factors Increase the Risk of Skin Cancer

Coumarins

Furocoumarins (Psoralens) increase the risk of Skin Cancer.



Electromagnetic Radiation

The radiation emitted from unshielded Fluorescent Lighting can cause Skin Cancer.
Microwaves increase the risk of Skin Cancer.
Excessive exposure to Sunlight can cause Skin Cancer (due to Ultra-Violet Radiation generating excessive quantities of Free Radicals).
Excessive exposure to Ultra-Violet Radiation can cause Skin Cancer.



Pharmaceutical Drugs

Continual usage of the Contraceptive Pill for more than 5 years increases the risk of Skin Cancer.



Recreational Drugs

Excessive consumption of Alcohol (Ethanol) increases the risk of the malignant Melanoma form of Skin Cancer [scientific research - females who consume 2 or more alcoholic beverages per day have a 250% greater risk of Melanoma].



These Foods Increase the Risk of Skin Cancer

Active Constituents
Margarine consumption can cause Skin Cancer: Trans Fatty Acids


Types of Skin Cancer

Basal Cell Carcinoma (BCC): Slow growing type of Skin Cancer that develops over a period of months or years. BCCs are the most common type of Skin Cancer and are 4 times more prevalent than Squamous Cell Carcinoma.
BCCs are usually firm to the touch and pink in colour.
Malignant Melanoma: The most aggressive form of Skin Cancer. Unless it is detected and treated in its early stages, it has great potential for spreading to other organs and can be fatal. Malignant Melanomas look like spilled ink and differ from moles in that they do not have even borders like normal moles.
Squamous Cell Carcinoma: Type of Skin Cancer in which the tumour has the appearance of a wart-like bump that is flesh-toned or reddish. They often first appear as a thick-scale on a skin-coloured pimple or lump. They are hard to the touch and as they enlarge they ulerate an bleed.
Solar Keratoses: Premalignant lesions of the Skin commonly known as Sun Spots. They have the potential to convert to Squamous Cell Carcinomas and are more prevalent in people over the age of 30. They appear as a small rough patch of skin that may be the colour of normal skin or may be red or yellowish.
T-Cell Lymphoma:


Melanoma

Description

Highly malignant form of Cancer (tumour) of Melanin-forming Cells (Melanocytes) - usually in the Skin.


These Substances Alleviate/Prevent Melanoma

ENDOGENOUS SUBSTANCES
Hormones

Melatonin exhibits strong potential as a therapy for Melanoma [scientific research - experiments are still proceeding].



EXOGENOUS SUBSTANCES
Glycosides - Saponins

Glycyrrhizin (and its derivative Glycyrrhetinic Acid) inhibit the progression (growth) of Melanoma [scientific research - in vitro].



Smart Drugs

Dimethyl Glycine (DMG) protects the body against Melanoma [scientific research - animals].



Vitamins

Vitamin B6 increases resistance to Melanomas and can cause the regression of Melanomas [scientific research - animals: supplemental Vitamin B6 increases resistance to Melanomas by 200%; scientific research - humans: subcutaneous application of Pyridoxal form of Vitamin B6 4 times per day caused regression of Melanomas by 50%].



These Foods Retard Malignant Melanomas

Active Constituents
Rhubarb retards the growth of malignant Melanoma [scientific research - animals: 50 mg per kg of body weight per day retards the growth of malignant melanoma by 75%]. Emodin
Rhein


These Substances Cause/Exacerbate Melanomas

Amino Acids

Melanoma sufferers should NOT consume L-Dopa as this type of tumour can feed on Phenylalanine.
Melanoma sufferers should NOT consume Phenylalanine as this type of tumour can feed on Phenylalanine.
Melanoma sufferers should NOT consume Tyrosine as this type of tumour can feed on Tyrosine.



Recreational Drugs

Excessive consumption of Alcohol (Ethanol) increases the risk of malignant Melanoma.



Cancer - Stomach

Also known as: Gastric Cancer
Description

Malignant tumor(s) occurring in the Stomach.


These Substances Reduce the Risk of Stomach Cancer

ENDOGENOUS SUBSTANCES
Digestive Enzymes

Deficiency of Hydrochloric Acid increases the risk of Stomach Cancer.

- In the absence of Hydrochloric Acid certain carcinogenic substances can be produced from normal food constituents.



Hormones

The body's production of Melatonin declines in Stomach Cancer sufferers (due to Stomach Cancer causing a decline in the production of Melatonin's precursor - Interleukin-2).



Immune System Chemicals

The body's production of Interleukin-2 declines in Stomach Cancer sufferers.



EXOGENOUS SUBSTANCES
Carbohydrates

Lentinan extends the life span of person with Stomach Cancer [scientific research - humans].



Polyphenols

Catechin reduces the risk of Stomach Cancer.



Vitamins

Vitamin A protects against Stomach Cancer by strengthening the Mucous Membranes of the Stomach.
Vitamin C reduces the risk of Stomach Cancer [scientific research - humans: 4 grams of Vitamin C per day reduces the risk of Stomach Cancer by 50%].



These Foods or Herbs Help to Prevent Stomach Cancer

Active Constituents
Capsicum (green) reduces the incidence of Stomach Cancer [scientific research].
Carrots reduce the incidence of Stomach Cancer [scientific research].
Celery reduces the incidence of Stomach Cancer [scientific research].
Cucumber reduces the incidence of Stomach Cancer [scientific research].
Garlic helps to prevent Stomach Cancer [scientific research - humans: people who eat an average of 7 cloves of garlic per day have an incidence of Stomach Cancer 10 times lower than those who don't eat garlic].
Miso helps to prevent Stomach Cancer.
Onions reduce the incidence of Stomach Cancer [scientific research].
Radish (seeds consumed as a strong tea) reduce the incidence of Stomach Cancer [scientific research - humans].
Shoyu helps to prevent Stomach Cancer.
Tea (Green) reduces the incidence of Stomach Cancer. Catechin
Tomatoes help to prevent Stomach Cancer [scientific research].


These Substances Increase the Risk of Stomach Cancer

Alcohols

Excessive consumption of Alcohol (Ethanol) increases the risk of Stomach Cancer.



Hydrazines

Agaritine causes Stomach Cancer even at very low dietary intake (due to it converting within the Stomach to a highly reactive and mutagenic metabolite of Diazonium) [scientific research - animals]:



Nitrites

Nitrosamines are a proven cause of Stomach Cancer.
Potassium Nitrite can cause Stomach Cancer by combining with toxic Amines in the Stomach and forming Nitrosamines.
Sodium Nitrite can cause Stomach Cancer by combining with toxic Amines in the Stomach and forming Nitrosamines.



These Foods/Herbs Contribute to Stomach Cancer

Active Constituents
Excessive consumption of Pickled Foods increases the risk of Stomach Cancer.
Excessive consumption of False Morel Mushrooms incrases the risk of Stomach Cancer. Agaritine
Excessive consumption of White Champignon Mushrooms increases the risk of Stomach Cancer. Agaritine


These Ailments Increase the Risk of Stomach Cancer

Digestive System

Ulcerative Colitis increases the risk of Stomach Cancer.




Cancer - Testicles

Also known as: Cancer - Testes; Testicular Cancer
Description

Malignant tumour(s) occurring in the male Testicles.


Prevalence

Testicular Cancer accounts for 1% of all cases of Cancer in males.
Testicular Cancer occurs most frequently between the ages of 20 and 49 - 75% of all cases occur during these ages.



These Substances Prevent Testicle Cancer

Vitamins

Vitamin A helps to prevent Testicular Cancer.



These Substances Can Cause Testicle Cancer

Recreational Drugs

Long term usage of Marijuana can cause Testicular Cancer.


Cancer - Uterus

Also known as: Womb Cancer
Description

Malignant tumour(s) occurring in the Uterus.


These Substance Prevent Uterus Cancer

Minerals

Iodine helps to prevent Uterus Cancer.



These Substances Increase the Risk of Cancer of the Uterus

Fatty Acids

Excessive consumption of dietary Fats increase the risk of Uterus Cancer.



These Ailments Increase the Risk of Cancer of the Uterus

Metabolism

Females who are afflicted with Obesity have an increased risk of Cancer of the Uterus.



Cancer - Vagina

Also known as: Vaginal Cancer
Description

Malignant tumour(s) occurring in the Vagina.


These Substances Reduce the Risk of Vaginal Cancer

Carotenoids

Beta-Carotene reduces the risk of Vaginal Cancer.



Cancer
.

The Center provides leadership in promoting prevention as the primary approach to cancer control. It conducts and coordinates research to identify modifiable causes of cancer and translates the findings into effective prevention strategies at the individual and community levels. Through the use of reports, publications, seminars and web sites, it makes information on cancer prevention available to the public.

Your Cancer Risk is based on the findings of the Risk Index Working Group at Harvard University. Members of the working group responsible for the content of the site are:

Graham A. Colditz, MD, DrPH
Direction of Education
Harvard Center for Cancer Prevention
Professor of Medicine
Harvard Medical School
Professor of Epidemiology
Harvard School of Public Health

Katherine Atwood, MS, ScD
Research Fellow, Department of Epidemiology
Harvard School of Public Health

Karen Emmons, PhD
Associate Professor of Health and Social Behavior
Harvard School of Public Health
Deputy Director, Center for Community-Based Research
Director of Tobacco Control
Dana-Farber Cancer Institute

Richard R. Monson, MD, SDHyg
Professor of Epidemiology
Harvard School of Public Health

Walter C. Willett, MD, DrPH
Professor of Epidemiology and Nutrition
Harvard School of Public Health
Professor of Medicine
Harvard Medical School

Dimitrios Trichopoulos, MD, Ph.D.
Vincent L. Gregory Professor of Cancer Prevention and Epidemiology
Harvard School of Public Health

David J. Hunter, MD, ScD
Director
Harvard Center for Cancer Prevention
Professor of Epidemiology and Nutrition
Harvard School of Public Health

Canyon Ranch Health Resorts provided partial funding for the development of the site.

Cancer TypeBreastProstateLungColonBladderMelanomaUterineKidneyPancreaticOvarianStomachCervical

Cancer is the general name for a large group of diseases. It occurs when cells in the body grow and divide out of control.

Our bodies are made up of millions of cells. Layers of cells form tissues. Normal cells grow, divide, and die in an orderly way. This process helps keep our bodies healthy.

Cancer cells grow and divide too quickly. The process usually starts when something damages the genetic structure (DNA) inside the cells. Instead of dying in an orderly way, cancer cells keep growing, lump together and form an extra mass of tissue. This mass is called a malignant tumor. As a malignant tumor grows, it damages nearby tissue. A malignant tumor can take a long time (up to 30 years) or a short time (2 or 3 years) to cause symptoms.

Cancer can begin in one part of the body and spread to others. This is called metastasis (me-tas-ta-ses). During metastasis, cancer cells travel through the body. In the new location, cancer cells create a new malignant tumor and grow out of control.

Not all tumors are malignant. Some are benign, which means they aren't cancerous. Benign tumors usually aren't life threatening. They can usually be removed and rarely come back.

What causes cancer?

We're not exactly sure what causes cancer. We don't always know why one person gets it and another doesn't. However, we do know a lot about the risk factors for cancer. The more we know about the risk factors, the more we can do to protect ourselves.
------------------------------------------------------------------------ Cancer TypeBreastProstateLungColonBladderMelanomaUterineKidneyPancreaticOvarianStomachCervical

Risk is a person's chance of getting a disease over a certain period of time. A person's risk factors make up a person's risk.

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Cancer TypeBreastProstateLungColonBladderMelanomaUterineKidneyPancreaticOvarianStomachCervical

A risk factor is anything that raises or lowers a person's chance of getting a disease. You can control some of them, but not all of them. Risk factors for cancer include:

A lifestyle choice, like what a person eats
An environmental exposure, like smoke from other people's cigarettes
Genetic make-up or family history
Another disease or medical problem
These things mix together with different effects on different people. Some people are more sensitive to risk factors than others. Just because you have one or even several risk factors does not mean you will definitely get cancer. And avoiding risk factors does not guarantee you will be healthy.

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Cancer TypeBreastProstateLungColonBladderMelanomaUterineKidneyPancreaticOvarianStomachCervical
At certain ages, people need regular tests to check for cancer. These tests are called screening tests. Screening tests can save your life by finding cancer early when it's most treatable. Some screening tests can even prevent cancer from developing at all.

A screening test checks for early signs of cancer in people who have no symptoms. If signs are found, the test is positive. But a positive test doesn't always mean a person has cancer. Sometimes, other tests are needed to know for sure.

Screening tests are available for:

Colon cancer
Breast cancer
Prostate cancer
Cervical cancer
Right now, other types of cancers do not have good screening tests.

Ask a doctor which screening tests are right for you. The right tests depend on your age, sex, medical history, family history, and lifestyle choices. Be sure to ask how often you need to have them.

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What is breast cancer?

Breast cancer occurs when cells in the breast grow out of control. The cells clump together and form a malignant (cancerous) tumor.
Each breast has several sections called lobes. Each lobe has smaller sections called lobules, which produce milk when a woman is breast feeding. The lobes and lobules are linked by tubes called ducts. Ducts are the tubes that carry the milk from the lobules to the nipple. The rest of the breast is mostly made up of fat.

There are two main types of breast cancer. Breast cancer that begins in the lobes and spreads to nearby tissue is called invasive lobular carcinoma. Breast cancer that begins in the ducts and spreads to nearby tissue is called invasive ductal carcinoma.

There is also a condition called carcinoma in situ, where there are abnormal cells in the breast, but they are not cancerous. Still, carcinoma in situ is a sign that breast cancer may develop at a later time. Lobular carcinoma in situ (LCIS) are abnormal cells that originate in the lobules. Ductal carcinoma in situ (DCIS) are abnormal cells that originate in the ducts.

Most breast tumors are benign, which means they are not cancerous. Benign breast tumors are not life threatening and do not spread outside the breast.

How common is breast cancer?

Breast cancer is the most common cancer among women in the US, and it's more common among older women. About 180,000 American women are diagnosed with the disease each year. Breast cancer also affects a small number of men in the US. About 1,600 American men are diagnosed with the disease each year. To compare this with other cancers, click here.

Who is at risk of getting breast cancer?

Anyone can get breast cancer (including men), but it usually strikes women over age 50. And the risk quickly goes up with age. Women who have a family history of breast cancer have a higher risk.

How do you lower your risk of breast cancer?
Cut down on the amount of alcohol you drink.
Maintain a healthy weight.
Eat more vegetables.
A drug called tamoxifen may also lower the risk of breast cancer, but only for women who are at high risk of the disease. Researchers are still studying its long-term effects.
Click here for a list of things that affect breast cancer risk.

Who should get breast cancer screening tests?

All women over the age of 20 should get screened regularly for breast cancer. But the right screening tests mainly depend on a woman's age. Use this chart to find out which tests you should get.

If you are between ages 20 and 39
Get a clinical breast exam every 1 - 3 years.

If you are between ages 40 and 49
Get a clinical breast exam every year.

Women at high risk of breast cancer may need to have regular mammograms. Talk to your doctor.

If you are age 50 or older
Get a mammogram and clinical breast exam every year.
Be sure to discuss your risk of breast cancer with a doctor. If your risk is high, you may need to have mammograms more often and at an earlier age.

Click here for more information on breast cancer screening.

What are the symptoms of breast cancer?
Breast cancer may have no symptoms in the early stages. But as the cancer grows, the symptoms may include:

A lump or mass in the breast or the under arm area
Changes in breast size, shape or color
A discharge from the nipple
A change in the feel of the skin covering the breast (the skin could become dimpled, puckered or scaly)
Some of these symptoms may be caused by other problems. Only a doctor can know for sure. If you have any of these symptoms, talk to a doctor immediately.
For more information on breast cancer, visit these web sites:

American Cancer Society
Cancer Facts Index, National Cancer Institute


Cancer TypeBreastProstateLungColonBladderMelanomaUterineKidneyPancreaticOvarianStomachCervical

What is breast cancer?

Breast cancer occurs when cells in the breast grow out of control. The cells clump together and form a malignant (cancerous) tumor.

Each breast has several sections called lobes. Each lobe has smaller sections called lobules, which produce milk when a woman is breast feeding. The lobes and lobules are linked by tubes called ducts. Ducts are the tubes that carry the milk from the lobules to the nipple. The rest of the breast is mostly made up of fat.

There are two main types of breast cancer. Breast cancer that begins in the lobes and spreads to nearby tissue is called invasive lobular carcinoma. Breast cancer that begins in the ducts and spreads to nearby tissue is called invasive ductal carcinoma.

There is also a condition called carcinoma in situ, where there are abnormal cells in the breast, but they are not cancerous. Still, carcinoma in situ is a sign that breast cancer may develop at a later time. Lobular carcinoma in situ (LCIS) are abnormal cells that originate in the lobules. Ductal carcinoma in situ (DCIS) are abnormal cells that originate in the ducts.

Most breast tumors are benign, which means they are not cancerous. Benign breast tumors are not life threatening and do not spread outside the breast.

How common is breast cancer?

Breast cancer is the most common cancer among women in the US, and it's more common among older women. About 180,000 American women are diagnosed with the disease each year. Breast cancer also affects a small number of men in the US. About 1,600 American men are diagnosed with the disease each year. To compare this with other cancers, click here.

Who is at risk of getting breast cancer?

Anyone can get breast cancer (including men), but it usually strikes women over age 50. And the risk quickly goes up with age. Women who have a family history of breast cancer have a higher risk.

How do you lower your risk of breast cancer?
Cut down on the amount of alcohol you drink.
Maintain a healthy weight.
Eat more vegetables.
A drug called tamoxifen may also lower the risk of breast cancer, but only for women who are at high risk of the disease. Researchers are still studying its long-term effects.

Click here for a list of things that affect breast cancer risk.

Who should get breast cancer screening tests?
All women over the age of 20 should get screened regularly for breast cancer. But the right screening tests mainly depend on a woman's age. Use this chart to find out which tests you should get.

If you are between ages 20 and 39
Get a clinical breast exam every 1 - 3 years.

If you are between ages 40 and 49
Get a clinical breast exam every year.

Women at high risk of breast cancer may need to have regular mammograms. Talk to your doctor.

If you are age 50 or older
Get a mammogram and clinical breast exam every year.


Be sure to discuss your risk of breast cancer with a doctor. If your risk is high, you may need to have mammograms more often and at an earlier age.

Click here for more information on breast cancer screening.

What are the symptoms of breast cancer?

Breast cancer may have no symptoms in the early stages. But as the cancer grows, the symptoms may include:

A lump or mass in the breast or the under arm area
A change in breast size, shape or color
A discharge from the nipple
A change in the feel of the skin covering the breast (the skin could become dimpled, puckered or scaly)
Some of these symptoms may be caused by other problems. Only a doctor can know for sure. If you have any of these symptoms, talk to a doctor immediately.

For more information on breast cancer, visit these web sites:
American Cancer Society
Cancer Facts Index, National Cancer Institute
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--------------------------------------------------------------------------------Your Cancer Risk is an educational web site for informational purposes only.
It does not take the place of regular medical check-ups.

© President and Fellows of Harvard College 2000



8.5.3(b) Occupational cancer

J. M. HARRINGTON


Background
Although many accounts of occupational cancer start with Percival Pott's description in 1775 of chimney sweep's scrotal cancer, there is good reason to go back further—even though the earliest accounts do not propose the link between occupation and cancer.

Agricola's account of the illnesses of Carpathian silver miners includes evidence of a rapidly progressive and fatal lung disorder. The fact that these mines contain uranium ore suggests that radon gas exposures may well have been high enough to cause lung cancer in the miners. Nevertheless, it is Pott's description of an excess risk of scrotal cancer in postpubertal chimney sweeps which first raised the possibility that chemicals—particularly polynuclear aromatic hydrocarbons—cause cancer. Confirmatory evidence from animal experiments did not arrive until 1915 and the first carcinogenic hydrocarbon was identified by Kennaway in 1924 as 1:2:5:6 dibenzanthracene (dibenz[a,h]anthracene).

Whilst the polynuclear aromatic hydrocarbons were generating interest as skin carcinogens, clinical observations of dyestuff workers were suggesting a link between bladder cancer and aromatic amines. In 1895, Rehn described three cases in a group of 45 workers in Germany involved in the preparation of fuchsin. Further reports followed from other countries and the classic studies of Case and his coworkers in the 1950s showed that 2-naphthylamine and benzidine were human carcinogens in the manufacturing industry and in the user industry (2-naphthylamine was a contaminant of the antioxidant used in tyre manufacture). Rehn's discovery added a new element to the knowledge of carcinogenesis, that is, that an organ distant from the point of first contact could bear the main force of the carcinogenic effect. In other words, the carcinogenic influence is greatest where the concentration is most prolonged and most intense.

In the same year that Rehn made his discovery, Roentgen discovered X-rays and 3 years later, the Curies isolated radium. Unfortunately, knowledge of the carcinogenic properties of ionizing radiation came from the skin and bone marrow cancers suffered by these early pioneers with confirmatory animal data following soon after. The bone sarcomata noted in laboratory animals was followed by human evidence in the 1930s among the luminous dial painters who used radium-235 and mesothorium. The inventor of the luminous paint, Dr von Sochocky, died of aplastic anaemia in 1928. Again in the 1930s, case reports were appearing of lung cancer (an unusual tumour in those days) in workers exposed to asbestos fibre. In asbestosis cases the incidence was reported as 18 per cent and reports of pleural mesothelioma followed a decade or so later.

Thus, within a century of Rehn's discovery, chemical carcinogenesis had become a well-recognized phenomenon with much of the evidence coming from occupational studies.

Diagnosis
Clinical acumen remains of paramount importance. It is the clinician who has played the major role in discovering new causes of cancer with confirmatory evidence coming from laboratory studies and epidemiological investigations. Establishing that a particular exposure causes human cancer involves all these elements and others. A schematic representation of the links between sources of evidence is shown in Fig. 1 965. To be reasonably certain that a workplace exposure causes a particular cancer, good quality epidemiological studies are essential. Further evidence from animal experiments, genotoxicity studies, and case reports add weight to the assertion but are insufficient in themselves.

Such information is collated and interpreted by various national and international agencies. The most reliable source is the Monograph Series of the International Agency for Research on Cancer (IARC) based in Lyon. To date they have published over 50 such monographs with several updating supplements. When a patient is diagnosed as having cancer, it is important that the clinician should review the occupational history to consider an occupational cause. If such a cause seems probable, enquires should be made to see if state compensation is available for that cancer and that workplace exposure.

Attribution of cancer to occupational causes
The most widely accepted estimates of the proportion of all cancers attributable to occupational exposures is 4 per cent with a range of 2 to 8 per cent for a typically industrially developed country like the United States. For that proportion of the population (20 per cent or so) in which occupationally related cancers are almost exclusively concentrated (manual workers aged 20 or over, in mining, agriculture, and industry broadly defined), perhaps as much as one cancer in every five may be attributed to workplace exposure.

In addition, it is necessary to consider other exposures which may interact with workplace exposures. These are particularly relevant when considering the relative effectiveness of removing or reducing exposure to one or more agents acting jointly. Few good studies have been completed on interaction but there is good evidence for the multiplicative effects of cigarette smoking and asbestos exposure in the genesis of lung cancer. Besides asbestos, interactions have been demonstrated to be at least additive for tobacco consumption and exposure to arsenic, nickel, and ionizing radiation. By analogy it is possible to envisage interaction between these workplace agents—as might occur in the mining industry.

Important examples of occupational exposures causing cancer
There is insufficient space in a text of this kind to describe the tens of agents or processes which have been causally linked to human cancer let alone to the hundreds of such exposures for which the evidence is somewhat more tentative. More detailed accounts may be found in the IARC Monographs or the standard texts in occupational medicine. Some important exposures are highlighted here with a summary of the causally linked processes (Table 1) 342 and agents (Table 2) 343. Ionizing radiation is dealt in Chapter 8.5.5(i) 230.

Polynuclear aromatic hydrocarbons
Polynuclear aromatic hydrocarbons are members of a large and complex group of compounds mainly generated during the incomplete combustion of carbonaceous products of which the combustion of coal and oil comprise the most important occupational exposures. Cigarette smoke, of course, contains a number of these compounds and it is thus often difficult to distinguish lifestyle from occupational factors in populations employed in these occupations. The site of action of these compounds is mainly the lung, skin, and bladder. The industries most prominently linked to such exposures are coke ovens, gas production, steel industries, aluminium refineries, and iron and steel foundries; workers exposed to soot, pitch, tar, and petroleum product exhaust fumes are also at risk.

Aromatic amines
Aromatic amines are a group of chemically similar compounds which have particular importance as dyestuffs or antioxidants or as intermediates in dye production. Some are known human bladder carcinogens, and a larger number are known animal carcinogens for which human data are limited or lacking. The more potent carcinogens are now banned and previous excess risks of bladder cancer in, for example, the dyestuffs and rubber industries have largely disappeared. Bladder cancer remains, however, a numerically important tumour and further work to delineate other potential occupational carcinogens is still required.

Metals and metalloids
The most important carcinogenic elements of this group are arsenic, chromium, and nickel. Arsenic and its compounds cause lung and skin cancer and these risks occur in the extraction of metalliferous ores (which are frequently contaminated by arsenic compounds) and in the now limited use of arsenic in pesticides and other industrial usages. Hexavalent chromium compounds, used in the pigment and plating industries, have been shown to cause lung cancer. Lung and nasal cancer is associated with the refining of nickel and the most likely causative agents are the oxidic and sulphidic nickel compounds. Other metals for which there is less clear-cut evidence of carcinogenicity include beryllium and cadmium.

Other organic compounds
Benzene is widely used both as the base compound and as an important building block in the organic chemical industry. It causes leukaemia and aplastic anaemia. Vinyl chloride monomer, which is the starting point for polyvinyl chloride, causes angiosarcoma of the liver. The most potent lung carcinogens are apparently the chloroethyl ethers, which are used in ion exchange resins. Other suspect organic compounds include acrylonitrile, diethyl sulphate, epichlorhydrin, ethylene oxide, formaldehyde, and tetrachloroethylene.

Industrial processes
Some processes are linked to specific exposures, such as polycyclic aromatic hydrocarbons in aluminium production and radon in underground mining. For others such as boot and shoe manufacture, furniture making, and painting, the specific relevant exposures have not been identified. For painting, the exposure characteristics such as construction sites may be as important as paint constituents. In the past asbestos and chromates were used in some paints but these have been removed or are being phased out. The paint manufacturing industry has not been shown to carry an excess risk of cancer.





6.2 Epidemiology of cancer

R. DOLL and R. PETO


Note: readers of this chapter may, on first examination, wish to pass over the central part, which lists separately the epidemiological features of each separate type of cancer, as the preceding and subsequent parts may be read without much reference to it.

Introduction
The epidemiology of cancer, by which is meant the study of the incidence of the disease in man under different conditions of life, has a history dating back nearly 300 years to Ramazzini's observation that cancer of the breast occurred more often in nuns than in other women and to Pott's observation, 200 years ago, that scrotal cancer in young men occurred characteristically in chimney sweeps. Both observations have been confirmed many times since, but whereas the reason for the first is still incompletely understood (except insofar as it is attributable to the avoidance of pregnancy), the second led to the realization that the combustion products of coal could cause cancer on any part of the skin with which they came into repeated contact, and became the foundation stone on which our knowledge of chemical carcinogenesis was built. One hundred years ago, lung cancer was found in the miners of Schneeberg and Jachymov (who, it has subsequently been realized, were heavily exposed to radon), and then skin cancer was found in radiologists and radiographers exposed to X-rays and in farmers and seamen exposed to ultraviolet light, bladder cancer in aniline dye workers, and buccal cancer in betel chewers. Until the interwar years, however, such observations depended for the most part on the acumen of individual physicians, surgeons, and pathologists who were struck by seeing a cluster of cases of a particular type of cancer in patients with a similar occupational or cultural background, and they provided almost all that was known about the causes of cancer. Gradually, however, the epidemiological methods that are described in Section 2 39 began to be applied to the study of cancer and other non-infectious disease. Many other causes were identified with sufficient certainty to justify preventive action and data were obtained to suggest hypotheses that would be tested in the laboratory.

Biological factors
Certain biological characteristics of cancer have constrained speculations about its causes and the mechanisms that lead to its occurrence. These include the relationships between incidence and age and sex, and the length of the ‘latent period’ between the first exposure of an individual to a carcinogenic agent and the appearance of clinical disease. These characteristics vary from one type of cancer to another and sometimes also, for a given type, between communities and at different times.

AGE
Some risk of cancer occurs at every age, but the risk of developing any particular type varies with age in many different ways. The most common relationship is a progressive increase in incidence from near zero in childhood to a high figure in old age. This type of relationship is shown by carcinomas of the skin, lung, and gastrointestinal and urinary tracts, and by myelomatosis and chronic lymphatic leukaemia. The rate of increase is rapid, being typically proportional to the fourth, fifth, or sixth power of age, so that cancers that affect only 1 or 2 persons per 1 000 000 each year at around 20 years of age may affect 1 or 2 per 1000 each year at age 80. With most of these cancers, the recorded rate of increase diminishes after about 75 years of age and the recorded incidence may stabilize, or even decrease, in the oldest age groups; but this is partly or wholly an artefact due to incomplete investigation of the terminal illnesses of old people. With the continuing development of medical services, the increasingly intensive investigation of the old, and the collection of progressively more complete data, the cancer incidence rates that are recorded in old age may be expected to increase still more, even if there is no real change in the risk of developing the disease at a given age. This pattern of a rapidly increasing incidence with age is observed for skin carcinoma due to exposure to ultraviolet light and for bronchial carcinoma both in non-smokers and in men who regularly smoke a constant number of cigarettes a day, and can, under certain circumstances, be observed in the laboratory in skin-painting experiments on mice. It is probable that it reflects the cumulative effect of processes that operate steadily throughout life, starting at around the time of birth (or, for lung cancer among habitual smokers, adolescence).

Two much less common patterns are a peak incidence early in life followed by a decline virtually to zero, or a slow rise to a second peak in old age. Retinoblastomas and nephroblastomas occur only in childhood, with peak incidences (respectively) in the first and second years of life. Teratomas and seminomas of the testis have peak incidence rates at about 20 and 30 years of age, respectively, and later almost cease to occur, while osteogenic sarcoma has a peak incidence in adolescence and then shows a slow increase with age from a lower rate in young adult life.

The remaining cancers show a bewildering variety of patterns. Carcinomas of the breast and cervix uteri of women, for example, begin to appear in adolescence and become rapidly more common up to the menopause. After the menopause the incidence of carcinoma of the breast may remain approximately constant, or may even become slightly less common for a few years, before increasing in incidence again with age, though at a slower rate. Carcinoma of the cervix continues to increase fairly steeply for a few years after the menopause, before showing a stable or declining rate. Hodgkin's disease, on the other hand, appears in childhood and then continues to occur more or less evenly throughout life with only minor peaks in young adult life and in old age, while connective tissue sarcomas become progressively more common from childhood on, but with a much slower rate of increase than is shown by the common carcinomas.

Some of these patterns, like that for retinoblastoma, are invariant, being the same everywhere and, as far as is known, at all times. Others vary from community to community, or from time to time. Cancer of the breast, for example, becomes progressively less common with increasing age after the menopause in parts of Asia, while carcinoma of the lung used to show a peak incidence at about 60 years of age in the United Kingdom, which gradually moved to older ages, and it still does show a pattern with a peak in late middle or early old age in many developing countries.

All these various patterns provide information, either about the period of activity of the stem cells from which the cancers derive, or about the times when exposure to the causative agents occurs and the duration of the exposure. Some of this variation has already helped to explain the causes of cancer, as has been the case with the shift in the peak incidence of bronchial carcinoma; but much of it still awaits elucidation.

Sex
Cancer used to be more common in women than in men in nearly all countries due to the great frequency, 70 years ago, of carcinoma of the cervix uteri and the rarity of bronchial carcinoma, and this is still the case in populations for which these conditions hold, as in parts of Latin America. Elsewhere, cancer is now more common in men. This overall male preponderance hides, however, a wide range of sex ratios for cancer of different organs. If the sites of cancer that are peculiar (or almost peculiar) to one sex are ignored, the ratio of the rates varies in Britain from a male excess of about 6 to 1 for pleural mesothelioma and carcinoma of the larynx, through many types of cancer with a small male preponderance, to carcinomas of the right side of the colon, thyroid, and gallbladder, which may be up to twice as common in women.

For many types of cancer the sex ratio is much the same in different countries and at different times. For some, however, and particularly for cancers of the mouth, oesophagus, larynx, and bronchus, the sex ratio may be extremely variable—not only between countries and at different times, but sometimes also between different ages at the same time and in the same country. The most marked variation is shown by cancer of the oesophagus, which may affect both sexes equally or be 20 times more common in men than in women. As with the various patterns of incidence with age, these different sex ratios and the variation between countries and times can provide useful clues to the causation of the particular type of cancer, not all of which have yet been successfully followed up.

Latent period
One reason why it has been difficult to recognize causes of cancer in humans is the long delay that characteristically occurs between the start of exposure to a carcinogen and the appearance of the clinical disease. This ‘latent period’, as it is commonly, but rather misleadingly, called is often a few decades, although it may be as short as 1 year or as long as 60. The exact relation between the date of exposure and the date of the appearance of different cancers is still uncertain, partly because the interval is subject to random factors, partly because few cancers are induced by a single, brief exposure, and partly because there are still very few sets of quantitative data with detailed information about the dates when exposure began and ended.

When cancer is induced by short but intensive exposure to ionizing radiation, as in Hiroshima and Nagasaki following the explosions of the atomic bombs or in patients treated by radiotherapy, the excess incidence of solid tumours rises for 15 to 20 years and then may continue to rise, level off, or decline. In the case of acute leukaemia, however, a peak incidence occurs earlier (about 5 years after exposure) and few cases appear after more than 30 years.

Short, intensive exposure to a carcinogen is, however, exceptional. The more usual situation is for exposure to a carcinogen to be prolonged for years—perhaps a decade or two in the case of occupational exposure, several decades in the case of tobacco smoking, and a lifetime in the case of ultraviolet sunlight. In this situation the incidence of cancer increases progressively with the length of exposure. In the last two cases cited, the incidence appears to vary approximately in proportion to the fourth power of the duration of exposure so that the effect after (say) 40 years is about 10 to 20 times as great as that after 20 years, and two or three hundred times as great as that after 10 years. Whether the same holds for occupational exposure is not known; but it has been shown to hold in some skin-painting experiments on mice and it may prove to be a general biological rule for many types of tumour and many carcinogens.

There is still less quantitative information about what usually happens when exposure ceases; but in the case of cigarette smoking the annual risk stabilizes and remains at approximately the same level for one or two decades before increasing again slowly. The ex-smoker, therefore, avoids the enormous progressive increase in risk suffered by the continuing smoker. Such quick benefits will, however, be conferred only by stopping exposure to agents that affect at least one of the later stages of the process that culminates in clinical cancer and cannot always be anticipated, particularly if the carcinogen persists in the body (as may happen following exposure to asbestos). For initiating agents that affect only an early stage in the process, it may be safer to assume that the risk continues to increase for some time after exposure stops, though at a slower rate.

These findings accord with the idea that the appearance of clinical cancer is the end-result of a multistage process in which different effects are exerted by initiating and promoting agents. From the point of view of the clinician the important conclusions are that cancer is more likely to occur after prolonged exposure to a carcinogen than after short exposure, that it is seldom likely to appear within 5 years after first exposure (except in the case of leukaemia and the specific cancers of childhood), that it commonly occurs several decades after first exposure, and that it may continue to occur for many years after exposure has ceased. The exact relation may differ for different carcinogens and different types of tumour. Bladder tumours, for example, began to appear within 5 years of intensive exposure to 2-naphthylamine in the dye industry, while mesotheliomas of the pleura have seldom, if ever, appeared within 10 years of exposure to asbestos, but they continue to increase in incidence for up to 50 years after first exposure, even if the exposure was relatively brief.

Preventability of cancer
Perhaps the most important result of epidemiological observation has been the realization that the common cancers occur, in large part, as a result of the way people behave and the circumstances in which they live and are, therefore, at least in principle, preventable. This does not mean that we can envisage a society in which any of the common cancers are completely eliminated (although this may prove to be possible when we understand more clearly the mechanisms by which the disease is produced). What it does mean is that we can envisage a society in which the risk of developing cancer at any particular age is greatly diminished.

The evidence that much human cancer is preventable can be summarized under four heads: differences in the incidence of a particular type of cancer between different settled communities (especially if these are obviously correlated with some quantitative characteristics of the ways those communities live); differences between migrants from a community and those who remain behind; variation with time within particular communities; and the actual identification of a large number of specific and controllable causes.

Differences in incidence between communities
Evidence of variation between communities has not been easy to establish because of differences in the provision and utilization of medical resources and changes in terminology and methods of diagnosis. Detailed clinical and pathological comparisons backed up by surveys of limited populations have, however, shown that the sort of differences now reported by good cancer registries throughout the world are for the most part real, particularly if comparisons are restricted to the limited range of ages between 35 and 64 years. This excludes the youngest ages, at which cancer is rare, and the oldest ages, at which the records of the diagnosis are least reliable.

Table 1 62 shows for selected types of cancer the range of variation recorded by cancer registries that have produced data sufficiently reliable for the purpose of international comparison (International Union Against Cancer, 1970; International Agency for Research on Cancer, 1976). Types of cancer have been included if they are common enough somewhere to have a cumulative incidence among men or women of at least 1 per cent by 75 years of age. The ranges of variation shown are for incidence rates between 35 and 64 years (see above). The range of variation is never less than sixfold and is sometimes more than a hundredfold. Despite the selection of reliable registries, some of this tabulated variation may still be an artefact, due to different standards of medical service, case registration, and population enumeration; but in many cases the true ranges will be greater. First, there are still large gaps in the cancer map of the world so that some extreme figures may have been omitted, because no accurate surveys have been practicable in the least developed areas and it is just these areas that are likely to provide the biggest contrasts (both high and low) with Western society as Chen et al. have shown in China. Secondly, the figures cited refer to cancers of whole organs and do not distinguish between different histological types or different locations within the organ. This does not matter for cancer of the oesophagus because this is nearly always squamous and the various causes thus far discovered all produce cancer in the same part of the organ (the lower two-thirds), but it does matter for many other types of cancer. It is, for example, not satisfactory to compare the aggregates of non-melanomatous skin cancers with each other, for these include such unrelated diseases as basal-cell carcinomas of the face, which affect more than half the fair-skinned population of Queensland by 75 years of age, scar epitheliomas of the leg, which develop on the site of old ulcers in Africa and account for 10 to 20 per cent of all cancers seen in some hospitals in Malawi and Rwanda Burundi, ‘dhoti’ cancers of the groin in India, and occupational cancers on the forearm due to exposure to tar and oil in industrialized countries.

The variation in incidence that is shown in Table 1 62 is not limited to the common cancers, but is also shown by many others. Burkitt's lymphoma, for example, never affects more than 1 in 1000 of the population, but it is at least 100 times as common among children in parts of Uganda as it is in Europe and North America; while Kaposi's sarcoma, which was extremely rare in most of the world until the advent of the acquired immunodeficiency syndrome (AIDS), is so common in children and young adults in parts of Central Africa that it accounted for 16 per cent of all tumours seen in one of the African hospitals surveyed by Cook and Burkitt. Some few cancers occur with approximately the same frequency in all communities; but, if any do, they are never common. Acute myeloid leukaemia at 15 to 25 years of age is one such type of cancer and nephroblastoma is another, except that it is only half as common in Japan as elsewhere.

The figures that have been cited so far all refer to the incidence of cancer in different communities defined by the area in which they live. Communities, can, however, be defined in other ways and no matter what method is used, including categorization by ethnic origin, religion, or socioeconomic status, substantial differences may be found. Jewesses, for example, have a low incidence of cervical cancer irrespective of the country in which they live, and the Mormons of Utah and the Seventh Day Adventists of California suffer fewer cancers of the respiratory, gastrointestinal, and genital systems than members of other religious groups living in the same American States.

It does not seem likely that the large differences observed between communities can be explained by genetic factors, apart from some of the differences observed in the incidence of cancer of the skin, the risk of which is much greater for whites than blacks, and possibly also some of the differences in the incidence of chronic lymphocytic leukaemia, which rarely affects people of Chinese or Japanese descent. Genetic factors, moreover, cannot explain the differences observed on migration or with the passage of time, which are discussed below, nor can they explain the correlations that are often observed between the national rates for particular types of cancer and some measures of the lifestyle of the different countries.

Changes in incidence in migrant groups
That changes in the incidence of cancer occur on migration is certain. Many groups have been studied, including Indians who went to Fiji and South Africa, Britons who went to Fiji and Australia, and Central Europeans who went to North America. Among the most reliable data are those for the black Africans whose ancestors were taken to America and the Japanese who went to Hawaii. The former experience incidence rates for internal cancers that are generally much more like those of white Americans than those of the black populations in West Africa from which most came, while the latter have experienced rates that are much more like those of the Caucasian residents in Hawaii than those of the Japanese in Japan (Table 2) 63. The ancestors of black Americans and Hawaiian Japanese will have come from many different parts of West Africa and Japan, some of which are likely to have cancer rates somewhat different from those that have been cited in Table 2 63. Nevertheless, the contrasts are so great that there can be no doubt that new factors were introduced with migration.

Changes in incidence over time
Changes in incidence with time can provide conclusive evidence of the existence of preventable factors. Such changes may, however, be difficult to be sure about, chiefly because it is difficult to compare the efficiency of case finding at different periods and partly because few incidence data have been collected for long enough, so that we have to compare mortality rates and these may be influenced by changes in treatment as well as by changes in incidence.

There are no simple rules for deciding which of the many changes in recorded cancer incidence and mortality rates are reliable indicators of real changes in incidence. Each set of data has to be assessed individually. It is relatively easy to be sure about changes in the incidence of cancer of the oesophagus as the disease can be diagnosed without complex investigations and its occurrence is nearly always recorded, at least in middle age, because it is nearly always fatal. It is much more difficult to be sure about changes in the incidence of many other types. The common basal-cell carcinomas of the skin, for example, are also easy to diagnose, but they seldom cause death and can be treated effectively outside hospital, so that they often escape registration. What appears to be a change in incidence may, therefore, be a change only in the completeness of registration. Cancers of the pancreas, liver, and brain, and myelomatosis, in contrast, are usually fatal, but may be overlooked or misdiagnosed as cancer of another type, so that an increased incidence or mortality rate may be wholly or partly due to improvements in diagnosis, in the availability of the medical services, or in the readiness of physicians to inform cancer registries of the cancers they find. Such changes are particularly likely to affect the rates recorded for people over 65 years of age, as many old people who are terminally ill used not to be intensively investigated.

Despite these difficulties, however, some changes have been so gross that there can be doubt about their reality. These include the increase in oesophageal cancer in the black population of South Africa, the increase in lung cancer throughout most of the world, the increase in mesothelioma of the pleura in males in industrialized countries, the decrease in cancer of the tongue in Britain, and the decrease in cancers of the cervix uteri and stomach throughout western Europe, North America, and Australasia. For a fuller account see Trends in the Incidence of Cancer (Doll et al., 1994).

Identification of causes
Finally, it has been possible to obtain evidence of the preventability of cancer by defining agents or circumstances that are a cause of the disease and are capable of control. The most straightforward evidence would be the demonstration by scientific experiment that an alteration led to an alteration in the incidence of the disease. Such evidence is, however, difficult to obtain and we often have to be content with the type of strong circumstantial evidence that would be sufficient to secure a conviction in a court of law. Action, based on such evidence, has in practice often been followed by the desired result—for example, a reduction in the incidence of bladder cancer in the chemical industry on stopping the manufacture and use of 2-naphthylamine and the reduction in the incidence of lung cancer that has occurred in men in England and Wales following the change in smoking habits. Cancer research workers have, therefore, accepted that the type of human evidence that has been obtained (often, but not invariably, combined with laboratory evidence that the suspected agents are carcinogenic in animals) is strong enough to conclude that a cause of human cancer has been identified and that, as a corollary, the disease can be prevented by controlling the conditions under which it is produced. Such causes, which amount altogether to about 50, are described under the specific types of cancer they are known to produce and in later sections on medicinal drugs and occupation.

Epidemiology of cancer by site of origin
In the preceding discussion, cancers arising in different anatomical sites have been treated as if they were diseases as different from each other as the different infectious diseases. They have certain obvious pathological and clinical characteristics in common, but they are in many ways aetiologically distinct, as the avoidable causes are different and there is no evidence that the prevention of any one type of cancer augments the age-specific risk of any other. It is, therefore, impossible to review the epidemiology of cancer as a whole. One must rather examine separately the epidemiology of each type. There are a few exceptions, when one agent does or may cause cancer at all or many sites (e.g. ionizing radiations, overnutrition, and deficiency of some micronutrients) but, in general, the agents responsible for the production of human cancer vary with the organ in which the tumour arises and with the tissue within it.

Not surprisingly, the large majority of all human cancers arise from the epithelial cells that line those parts of the human body that communicate, directly or indirectly, with the external environment and are subject to wear and tear. Endothelial or mesodermal cells, in contrast, although they account for most of the human body, are the source of only a small proportion of human cancers. In the account that follows, cancer always implies a carcinoma arising from epithelial tissue unless specified otherwise.

The description of each type is preceded by notes showing its importance in England and Wales. One figure gives the proportion of all cancers that arise in the site, as indicated by the national cancer register for England and Wales for 1987 (Office of Population Censuses and Surveys, 1993a) and another gives the proportion of all cancer deaths allocated to the site in the national mortality statistics for 1991 (Office of Population Censuses and Surveys, 1993b). A third gives the ratio of the age-standardized incidence rates for each sex. The way in which the incidence of the disease varies with age in each sex is shown in a series of graphs, using the data for England and Wales over the 5-year period 1983-87. The rates at ages under 25 years frequently vary irregularly due to chance variation of small numbers. (The occurrence of one case in a 5-year age group of young people over this 5-year calendar period corresponds to an annual rate of approximately 0.01/100 000.)

Major differences between Britain and other countries are commented on in the text and are described more fully in the report on Cancer Risks by Site by the International Union Against Cancer (1980) and by the International Agency for Research on Cancer (1990).

Lip
0.1 per cent of all cancers and 0.02 per cent of cancer deaths.
Sex ratio of rates 4.5 to 1. Age distribution like skin (non-melanoma)

Carcinoma of the lip was one of the first types of cancer to be related to an extrinsic cause when, more than 200 years ago, it was noted to occur characteristically in pipe smokers. Many years later it was realized that the disease could also be produced by smoking in other ways, so that it must be produced by the chemicals in smoke rather than by the non-specific effect of local heat. It is also much more common in outdoor than in indoor workers and is evidently induced by ultraviolet light in the same way as other cancers of the exposed skin. Ultraviolet light and tobacco account, between them, for the great majority of all cases in Britain, probably multiplying each other's effects. The disease is much less common than it used to be, because of the decrease in pipe smoking and outdoor work.

Oral cavity and pharynx (excluding salivary glands and nasopharynx)
1.0 per cent of all cancers and 1.1 per cent of cancer deaths.
Sex ratio of rates 2.1 to 1. Age distribution, see Fig. 1 98.

Cancers of the tongue, mouth, and pharynx (other than nasopharynx) are all related to smoking (of pipes, cigars, and cigarettes) and to the consumption of alcohol. The two factors act synergistically and cancers in these sites are extremely rare in non-smokers who do not drink alcohol.

Cancer of the tongue is much less common in Britain than it was early this century, but the reason for the sharp decline in incidence is unknown. One explanation could be the decrease in syphilis, which was commonly believed to be a predisposing factor because of the clinical association with syphilitic leucoplakia, but this hypothesis is still unproven.

Cancers that occur low in the hypopharynx are distinguished by a tendency to affect women who have suffered from iron-deficiency anaemia and dysphagia.

Cancers of the buccal cavity and pharynx (excluding nasopharynx) are particularly common in South-East and Central Asia where tobacco smoking is largely replaced by chewing tobacco, betel nut or leaf, and lime (calcium hydroxide). A close association with such chewing habits has been established by studies which have shown that the cancers tend to originate in the part of the mouth in which the quid is usually held—a characteristic that varies both between individuals and between areas. The materials chewed differ in different places and, although the disease is commonly described as ‘betel chewer's cancer’, betel is not invariably a component of the quid and the most characteristic constituent seems to be a small amount of lime and, in most cases, some form of tobacco. In parts of Asia the disease is so common that it accounts for 20 per cent of all cancers and in those populations the abandonment of chewing would be the single most effective means of reducing the total incidence of cancer—so long as the habit was not replaced by an increase in tobacco smoking. (Moreover, among habitual quid chewers, the risks are particularly elevated in those who both chew and smoke—indeed, in parts of India the majority of deaths from ‘betel chewer's cancer’ could have been avoided even if the chewing habits remained unchanged, if those affected had not also been smokers.) The incidence might also be reduced by improved nutrition, as the disease in Southern Asia tends to be associated with vitamin A deficiency.

In parts of India where women tend to smoke local cigars and cigarettes with the burning end inside the mouth to prevent them going out, the habit is associated with cancer of the palate.

Salivary glands
0.1 per cent of all cancers and 0.1 per cent of cancer deaths.
Sex ratio of rates 1.6 to 1. Age distribution like non-Hodgkin's lymphoma.

The salivary glands are not common sites for cancer anywhere. They are, however, relatively more common in the Asiatic populations of Hawaii and in Canadian Indians than elsewhere. A small proportion of cases occurs specifically in families that also have a high incidence of breast cancer. No causative factors are known and no notable changes in incidence over time have been reported.

Nasopharynx
0.1 per cent of all cancers and 0.09 per cent of cancer deaths.
Sex ratio of rates 1.3 to 1. Age distribution, see Fig. 2 99.

Cancers of the nasopharynx, unlike those in other parts of the pharynx, are not strongly related to alcohol or to tobacco. They are rare in most populations but are common in those that originated from parts of Guangdong, in southern China, where the disease is the most common type of cancer. Moderately high rates have been observed in Alaskan Eskimos and American Indians, and intermediate rates in Malaysia, Kenya, and North Africa. A weakly significant relationship with HLA type has been reported from Singapore, but the existence of a specific genetic predisposition remains to be proved. Incidence rates appear to have been decreasing among Chinese Americans.

DNA characteristic of the Epstein-Barr virus (EBV) has been detected in the nuclei of nasopharyngeal cancer cells and patients with the disease tend to have unusually high antibodies against EBV-related antigens. Among adults, sudden increases in certain EBV antigens in the blood often precede by a few years the appearance of a pathological cancer. Infection with the EBV is, however, almost universal and can be only one of several agents that act in combination to produce the disease. One such agent in Southern China occurs in the ‘salted fish’ on which children are commonly weaned. This strongly flavoured delicacy bears little relation to the salted fish eaten elsewhere, and might better be described as decomposing fish: it contains various mutagens, and it has been suggested that exposure of children to it at the same time as their first EBV infection alters the usual lifelong balance between host and virus in some hazardous way.

Oesophagus
2.2 per cent of all cancers and 3.6 per cent of cancer deaths.
Sex ratio of rates 2.0 to 1. Age distribution like gastric cancer.

Cancer of the oesophagus, like other cancers of the upper respiratory and digestive tracts, is closely related to prolonged smoking and consumption of alcohol. All types of smoking have comparable effects and, so it appears, do all alcoholic drinks, although spirits may be slightly more effective per gram of ethyl alcohol than other alcoholic drinks. Alcohol and tobacco act synergistically and, in the absence of either, the incidence of the disease in Britain would be greatly reduced. In France, where the consumption of alcohol is greater than in Britain, it would be reduced even more. A few cases originate from the scars produced by poisoning with corrosive substances and a very few in conjunction with a particular hereditary form of tylosis (presenting with keratoses of the palms and soles). The relatively small excess in men probably reflects the existence of other unknown causes in women, possibly nutritional in origin and similar to those responsible for cancers of the hypopharynx. Mortality (which, because of the high fatality rate, approaches incidence) fell progressively in the first half of the twentieth century pari passu with the fall in the consumption of alcohol, and rose again after 1950 when the trend in the consumption of alcohol reversed. Since pipe smoking affects oesophageal cancer risks at least as strongly as cigarette smoking, no large effects on male oesophageal cancer trends could be predicted from the male switch from pipes to cigarettes, although the switch by females from non-smoking to cigarettes should, other things being equal, produce a large upward trend. It appears, however, that other things are not equal and some other, possibly nutritional, cause of oesophageal cancer seems to have decreased, for any upward trends in oesophageal cancer are moderate.

In Africa and Asia the epidemiological features are quite different and present some of the most striking unsolved problems in the field of cancer epidemiology. In parts of China (particularly in North Henan but also elsewhere) and on the east coast of the Caspian Sea in Turkmenistan and Iran, oesophageal cancer is the most common type of cancer, with incidence rates in both sexes that are equal to the highest rates observed for lung cancer in men in European cities. Within China, the disease varies more than 10-fold from one county to another; alcohol and tobacco cannot account for these geographic differences, but when people within one particular Chinese county or city are compared with each other the disease is more common among those who smoke. In parts of Africa, particularly in the Transkei region of South Africa and on the east coast of Lake Victoria in Kenya, extremely high rates are also observed, sometimes equally in both sexes and sometimes only in men. In these and several other areas, as in Asia, the high incidence zones are strictly localized and the incidence falls off rapidly over distances of two or three hundred miles.

When tobacco and alcohol are used, they increase the hazard, but they are not the principal agents in these high-incidence areas. Many causes have been proposed, including molybdenum deficiency in the soil (resulting in a deficiency of the plant enzyme nitrate reductase and a build-up of nitrosamines), contamination of food and pickled vegetables by fungi (particularly by species of Fusaria) with the production of carcinogenic metabolites, an agent associated with the production of beer from maize, and the residues left behind in pipes from smoking opium (which are commonly swallowed). None, however, is supported by any impressive epidemiological data. The high incidence area in Iran, which has been intensively investigated, is characterized by extreme poverty and a restricted diet consisting chiefly of home-made bread and tea, with some sheep's milk and milk products, and very little meat, vegetables, or fruit. In this area the disease has been common for centuries. In Southern Africa, however, it seems to have become common only since the First World War. In China, where cancer of the oesophagus was the second most important neoplastic cause of death in the 1970s, large decreases in the disease are beginning to be reported.

Stomach
5.0 per cent of all cancers and 5.8 per cent of cancer deaths.
Sex ratio of rates 2.4 to 1. Age distribution, see Fig. 3 100.

Until about 1980, gastric cancer was responsible for more deaths from malignant disease worldwide than any other type. Over the last 50 years, however, the incidence has declined in Western Europe, North America, and Australasia and recently it has begun to do so in South America and Japan. High rates are now confined to China, Japan, Russia and other countries of the old Soviet Union, and Central and South America, while the lowest rates are, perhaps surprisingly, found equally in North America, Australasia, and some of the least developed parts of Africa. Irrespective of whether the incidence is high or low, the sex ratio is between 1.5 and 3 to 1.

Within Britain, cancer of the stomach is most common in North Wales and becomes progressively less common from north to south and from west to east. Over the last 70 years it has consistently been some five times more common in unskilled labourers than in members of the major professions, a gradient with socioeconomic status that has been one of the most marked for any disease. Relatively high rates have been observed in coal miners and in some chemical workers; but no specific occupational hazards have been identified and the excess in coal miners was paralleled by a similar excess in their wives. A hazard has been suspected from exposure to asbestos, but the apparent excess may be due to misdiagnosis of lung cancer and mesothelioma.

Four factors are known to predispose to the disease: blood group A constitution, gastritis associated with infection by Helicobacter pylori (sometimes leading to atrophic gastritis), a diet deficient in fruit and green and yellow vegetables, and a poor diet with large amounts of salt and salt-preserved food. Chronic infection with H. pylori is a major cause of peptic ulcer, a finding that is of considerable practical value in patients with ulcers, because the infection can generally be eliminated from the stomach by a short course of appropriate antibiotic therapy, providing long-term protection against recurrence. It is not yet known, however, whether such treatments would have any material effect on the incidence of stomach cancer. Whether smoked foods also increase the risk is less clear; if they do, they are certainly less important than the other dietary factors referred to. How these various factors influence the production of the disease is unclear. One possibility is that they encourage or discourage the formation of carcinogens in vivo, particularly perhaps the production of nitrosamines; but if they do, the intake of nitrates (which can be converted into nitrites by bacterial enzymes) is not a rate-limiting factor. Changes in all the three environmental factors could have contributed to the decline in the incidence of the disease, but it is difficult to see how they could have brought about such a large and widespread reduction in risk, and it seems probable that the better preservation of food, resulting from the extensive use of refrigeration, has played a major part.

No risk has been detected from the consumption of mutagens produced by the different methods of cooking meat and fish, nor from food additives or pesticide residues. Some food additives may, on the contrary, have served to reduce risk (by avoiding food spoilage and hence improving nutrition, by avoiding contamination by carcinogen-producing micro-organisms, or by some antioxidant or other protective effect on the gastric epithelium).

Large bowel
11.6 per cent of all cancers and 11.3 per cent of cancer deaths.
Sex ratio of rates 1.4 to 1. Age distribution, see Fig. 4 101.

Cancers of the colon and rectum ought to be considered separately, as their causes are not identical. Cancer of the colon, for example, tends to occur more often in women than in men, particularly when it occurs on the right side, while cancer of the rectum is nearly twice as common in men. The geographical distribution also differs slightly, colonic cancer varying in incidence more than rectal cancer. Separate consideration may, however, sometimes be misleading as cancers occur commonly at the rectosigmoid junction and the site of origin of these cases is not recorded consistently. Moreover, there is a growing tendency to describe both diseases merely as ‘cancers of the large bowel’, which, according to the internationally agreed rules, are classed with cancers of the colon. The two diseases will, therefore, be considered together.

Over the past few decades in the United Kingdom and United States the male rates have been approximately constant, while the female rates have decreased slightly. More recently, decreases in early middle age have begun to be seen in both sexes. In contrast, the incidence in Japan, which used to be very low, has begun to increase and the disease in Japanese migrants in Hawaii has become as common as in Caucasians. In most other parts of Asia, and in Africa and Eastern Europe, large-bowel cancer continues to be relatively uncommon (except in areas where chronic schistosomal infestation of the large intestine is common; for example, high rectal cancer rates are found in those Chinese counties where S. japonicum was, until recently, a major cause of death). Incidence rates in different countries correlate closely with the per caput consumption of fat and meat and crudely with the consumption of processed foods from which the natural fibre has been removed. Ways in which these and several other dietary constituents might influence the development of the disease are discussed later.

Within Britain there is no clear relation to socioeconomic status and no occupational hazard has been established. The association that has been reported with exposure to asbestos may be due to misdiagnosis as in the case of cancer of the stomach. Cases in childhood or early adult life occur as a complication of polyposis coli or (more rarely) Gardner's syndrome. These conditions are determined by dominant genes, which so increase the susceptibility to the disease that it almost invariably develops before middle age. Many other cases develop from adenomatous polyps and a few occur as a complication of long-standing ulcerative colitis.

Anal intercourse causing infection with type 16, type 18 or some other specific types of the human papillomavirus is a probable cause of some anal carcinomas, but patients who merely have sexually transmitted anal warts that are due to other types of human papillomavirus are not thereby placed at risk of cancer.

Liver
0.5 per cent of all cancers and 1.1 per cent of cancer deaths.
Sex ratio of rates 2.1 to 1. Age distribution, see Fig. 5 102.

Incidence rates tend to be overestimated in developed countries because the primary condition is often confused with metastases to the liver from cancer in various other organs, particularly over 65 years of age when carcinomas of the gastrointestinal and respiratory tracts are common. Changing standards of medical services make reliable assessment of trends difficult, so although the death rates attributed to liver cancer are, if anything, still decreasing in the United States, this gives no reason to suppose that there are at present any appreciable changes in liver cancer rates either in the United States or in Britain, where current rates are among the lowest anywhere. Compared with Britain and America, however, liver cancer is much more common in South-East Asia, including parts of China, and in large parts of tropical Africa it is the most common type of cancer in men.

Most cases derive from the main cells of the organ (hepatocellular carcinomas) and are attributable primarily to chronic active infection, established early in life, with the hepatitis B virus, exacerbated by some specific metabolite (e.g. aflatoxin) of particular types of fungal contamination of stored foods. Neonatal vaccination against the virus has been begun in Japan and parts of China and tropical Africa, and produces a marked decrease in the proportion of children who, at 5 years of age, are chronically infected, but it will be some years before its efficacy in the prevention of hepatocarcinoma can be seen.

In developed countries such as Britain it is uncertain whether the minute amounts of aflatoxin that are consumed could account for any of the few cases of liver cancer. A more important cause of hepatocellular carcinoma is cirrhosis, irrespective of whether it is due to hepatitis, chronic alcoholism, or haemochromatosis. Occasionally, liver cancer is produced by drugs. A few cases have occurred in young men who have taken androgenic-anabolic steroids to increase their muscular strength and a few from the use of steroid contraceptives, either by causing them to arise de novo or by complicating the development of the benign adenomas of the liver, which are themselves rare complications of the use of steroid contraceptives.

A second histological type (cholangiosarcoma) arises from the intrahepatic bile ducts, tends to occur at a somewhat later age than hepatocellular carcinoma, and, although generally less common than hepatocellular carcinoma, nevertheless accounts for an appreciable proportion of cases. In China, Thailand, and other parts of Asia it can be produced by chronic infection with liver flukes (Clonorchis sinensis or Opisthorchis viverrini).

A third histological type that is extremely uncommon everywhere has been variously described as reticuloendothelioma or angiosarcoma. It was first recognized as a complication of the use of ‘Thorotrast’ as a contrast agent in neuroradiology, a long-abandoned practice that led to chronic retention of insoluble thorium radionuclides in the marrow, spleen, and liver. In 1973 it was found to be an occupational hazard for men exposed to vinyl chloride. A few hundred cases have occurred throughout the world in men who were heavily exposed in the manufacture of vinyl chloride polymer, and it seems improbable that the minute amounts that have leached out of the plastic consumer products can have caused more than a dozen cases altogether in the general public, if indeed they have produced any. A third, and even rarer, cause is prolonged exposure to inorganic arsenic, such as used to result from the medical prescription of Fowler's solution. Despite these multiple causes only three or four cases of hepatic angiosarcoma occur each year in Britain, which is why the recognition of new causes has been so easy.

Cancer of the liver is almost uniformly fatal and it is fortunate that it should be so rare in developed countries. The fact of its rarity is intriguing, since most of the carcinogens thus far discovered in experimental animals induce, perhaps inter alia, tumours of the liver, so the lack of any high or increasing liver cancer rate in Britain and America suggests that, on average, the populations have not been substantially exposed to the sort of chemical carcinogen that is currently recognized by such studies.

Gallbladder and extrahepatic bile ducts
0.5 per cent of all cancers and 0.6 per cent of cancer deaths.
Sex ratio of rates 0.9 to 1. Age distribution like colorectal cancer.

Cancers of the gallbladder and extrahepatic bile ducts are nearly always classed together, which is unfortunate as the causes are certainly different. The former is more than twice as common in women as in men, is strongly associated with obesity, and is usually preceded by (and probably caused by) cholelithiasis. The latter is slightly more common in men and is increased in incidence by clonorchiasis and (to a less extent) by long-standing ulcerative colitis. Both types are uncommon, and their aggregate varies only slightly from one population to another. Relatively high rates are recorded among Jewesses in Israel, especially among those born in Europe and America.

The incidence of cancer of the gallbladder has fallen sharply in the United States in the last 20 years, which may be due to the decreased consumption of animal fat or, perhaps more importantly, to an increase in the rate of cholecystectomy in people who, having gallstones, are at greatest risk of cancer of the gallbladder.

Pancreas
2.7 per cent of all cancers and 4.2 per cent of cancer deaths.
Sex ratio of rates 1.5 to 1. Age distribution like stomach cancer.

Cancer of the pancreas is two to three times more common in regular cigarette smokers than in lifelong non-smokers. The mechanisms by which cigarette smoke causes pancreatic cancer are not known, but the smoke contains several thousand chemicals including minute amounts of volatile nitrosamines and some pancreatic carcinogen could well be absorbed from the alveoli and carried to the pancreas in the bloodstream. The disease is twice as common in diabetics as in the population as a whole. It should not, therefore, be surprising that the highest rate recorded is among New Zealand Maoris, who smoke heavily and are prone to obesity, hypertension, myocardial infarction, and diabetes.

Cancer of the pancreas is generally regarded as a disease of the developed world, but the diagnosis is difficult in the absence of a well-developed medical service and some of the relatively small geographical and temporal variations may be due to variation in diagnostic standards. Mortality rates in Britain and the United States have begun to decrease under 65 years of age, and this is more likely to reflect a real reduction in incidence (due perhaps to changes in diet and smoking habits) than to improvement in treatment, as the 5-year survival rate remains well under 10 per cent.

Nose and nasal sinuses
0.2 per cent of all cancers and 0.1 per cent of cancer deaths.
Sex ratio of rates 1.6 to 1. Age distribution like non-Hodgkin's lymphoma.

Surprisingly, in view of the widespread exposure of the human nose to tobacco smoke and other airborne toxins, cancers of the nasal cavity itself are extremely rare and most of the cancers in this group arise from the paranasal sinuses. Several occupational hazards have been recognized, including the refining of nickel, the manufacture of isopropyl alcohol and hardwood furniture, and some aspect of the manufacture of leather goods. It would be wrong, however, to conclude that all contact with nickel, hardwood dust, etc. creates a hazard. The hazards have been observed in special occupational situations in which exposure has been intensive and prolonged, and probably also in which specific physical and chemical conditions have occurred. The nickel-refining hazard was first observed in South Wales where the nickel carbonyl process was used, but similar hazards were subsequently observed with other processes in Canada, Norway, and the then USSR. In the Welsh refinery the workplace exposures were much heavier before the Second World War, and (despite the continued use of the nickel carbonyl process in Wales) no hazard of nasal sinus cancer has yet been observed among men first employed there since 1950. The hazard in furniture workers was first observed in High Wycombe and appears to have followed the introduction of high-speed wood-working machinery early in the twentieth century. It certainly affects some other groups but should not be assumed to affect furniture workers in general.

Most occupational and other cancers in this group are squamous carcinomas, but the hazard from hardwood dust characteristically produced adenocarcinomas. In some of the exposed groups as many as 5 per cent of the men developed the disease. This meant that the risk of adenocarcinoma was increased 1500 times (as this histological type of the disease is normally very rare) and the hazard was, in consequence, easy to confirm once suspicion had been aroused.

Chromate workers are sometimes said to experience a hazard of nasal cancer, but this is perhaps an error due to confusion with the characteristic ‘chrome ulcer’ of the nasal septum. These ulcers have not been shown to become malignant.

Larynx
0.8 per cent of all cancers and 0.6 per cent of cancer deaths.
Sex ratio of rates 5.9 to 1. Age distribution, see Fig. 6 103.

Cancers of the larynx, like cancers of the oesophagus and buccal cavity, are closely associated with tobacco smoking and with the consumption of alcohol. The two agents act synergistically and in the absence of either the disease is rare. Cancers of the glottis (like cancers of the lung) are associated particularly closely with cigarette smoking, while all types of tobacco smoking may equally cause cancers of the extrinsic larynx.

In Scandinavia the incidence has increased pari passu with the increase in cancer of the lung. A similar increase has not, however, been seen in Britain and it seems probable that some other aetiological factor, perhaps nutritional in character, has become less prevalent. That there are other causal factors is evident from the relatively high incidence rates in parts of India, Turkey, North Africa and Brazil, which cannot be accounted for by tobacco and alcohol.

The disease has also occurred as an occupational risk in the manufacture of mustard gas and possibly also from exposure to asbestos.

Lung
16.8 per cent of all cancers and 23.7 per cent of cancer deaths.
Sex ratio of rates 3.5 to 1. Age distribution, see Fig. 7 104.

Nearly all lung cancers are bronchial carcinomas and should properly be so described. The term ‘lung cancer’ is, however, in such common use that it will be used here as synonymous with bronchial carcinoma, although it actually includes a very small proportion of alveolar-cell carcinomas and other rare types of cancer with different characteristics.

Until the 1920s, lung cancer was uniformly rare (except in the Hartz mountains, see below). In the next two decades, German and then British pathologists began to comment on an apparent increase, but this tended to be dismissed as an artefact of the greatly improving methods of diagnosis and the establishment of special centres for thoracic disease, and at that time much of the increase in the incidence of the disease was indeed artefactual. Gradually, however, the increase became so pronounced, and the change in the sex ratio so marked, that it could no longer be dismissed as being wholly artefactual in males, and by the late 1940s, when the age-standardized mortality rate in men in the United Kingdom had increased 20 times, it was clear that the developed world had begun to see an epidemic of lung cancer that was comparable in severity to, though with a longer time scale than, the epidemics of infectious disease of the past. Up to the 1940s, the increase among British women was largely a diagnostic artefact, and so provides a useful indication of the quantitative extent to which such artefacts may have affected the male rates. Since 1950, however, diagnostic standards in middle age have changed very little, the increase in British men has been replaced by a decrease, while the increase among middle-aged women has continued for longer, before also reversing. As a result, the sex ratio (male rate divided by female rate) at, for example, 50 to 54 years of age, which rose from 1.8 after the First World War to 8.9 after the Second World War, was reduced to 2.2 in 1991. The male excess in the first qu first quarter of the century may have existed partly because of the effects of pipe smoking (an almost exclusively male habit in the nineteenth century).

SMOKING
Changes in treatment have had little effect on the fatality rate, which remains extremely high, and real changes in mortality can therefore be regarded as reflecting real changes in incidence. These can be almost entirely explained by the effects of smoking tobacco, particularly in the form of cigarettes, which in the early 1990s caused more than 90 per cent of all lung cancers in Britain. Evidence of the effect of smoking was first obtained in the middle of the century by comparing the smoking histories of patients with different diseases. It was found that the proportion of patients who had never smoked was much smaller if they had lung cancer than if they had some other disease, and the proportion who had smoked heavily was correspondingly greater. Further evidence was obtained by asking large numbers of apparently healthy men and women what they smoked, and then following them up to determine the causes of death of those that had died.

Interim results of a study of over 1 million people carried out by the American Cancer Society and the National Cancer Institute, which enable comparisons to be made of the mortality of both men and women are reported by Clark Heath Jr. and Michael Thun (personal communication) and are shown in Table 3 64. In both sexes, the mortality increases progressively with the amount smoked, the rates being all somewhat higher in men than in women. Similar results have been obtained in other large studies in the United Kingdom (in British doctors) in Japan, and in Sweden (in a random sample of the population). If attention is restricted to populations in which most cigarette smokers have been smoking cigarettes regularly since early adult life, lung cancer eventually becomes about 20 times more common in regular cigarette smokers than in lifelong non-smokers and up to 40 times more common in very heavy smokers. At present the differences appear to be less marked in women than in men, but this difference may be only a temporary phenomenon, arising mainly because most female smokers who are now old enough to have a high risk of cancer either did not begin smoking cigarettes so early in adult life or smoked them less intensively when they began.

No other exposures have been identified that can account for the extreme difference in lung cancer risk between regular cigarette smokers and lifelong non-smokers, and so most or all of the excess must be taken as having been caused by smoking. Further quantitative studies have found that the relative risk