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Cancer
Cancer is the second leading cause of death in North America
(after heart and other cardiovascular diseases) with lung cancer heading the list,
followed by bowel, breast, prostate, pancreas and other malignancies.
What is cancer?
Abnormal growth of cells (clone of cells), not under the control of the body.
It kill by steeling the space and nutrition from the normal cells.
A cancer cell is a unregulated cell with damaged DNA.
How cancer occurs
1. Something damages the cell DNA Viral, Chemical, radiation - call carcinogen
(gen-Genesis, carcino cancer). We call this Initiation
2. Your immunity is damaged or blocked or overwhelmed
3. Some other agents promotes the growth of this abnormal clone of cells call
cancer/tumor/malignancy -a cancer growth factor usually referred
to as a carcinogen
but tumor promoters is more appropriate.
A promoter can cause transformed cells to proliferate and
form a tumor, but in itself it is neither mutagenic nor carcinogenic. Moreover, it must be
applied continuously to have a biological effect; if the promoting stimulus is removed,
its effects are reversible.
In Prostate Cancer one of the treatments is removal of the
testicals. Testosterone is a promoter of Prostate cancer. It doesn't cause
it. The same is true with estrogens and breast cancer.
At present several factors in the diet are seen as tumor
promoters or antipromoters. The item most clearly established as a promoter is
dietary fat.
Experimental studies show that certain dietary fats
acts as a tumor promoter or enhancer, but some evidence indicates that fat may also have a
role in cancer initiation.
Statistics
Estimated New Cases and Deaths in the United States for Major
Forms of Cancer--1992
|
Type or Cancer |
Number of
Cases |
Number of Deaths |
All
sites
Lung
Colon and rectum
Breast
Prostate
Urinary
tract
Uterus
Oral cavity and pharynx
Skin
Pancreas
Leukemia
Ovary
All other
sites |
1,130,000
168,000
156,000
181,000@
132,000
78,100
45,500@
30,300
32,000*
28,300
28,200
21,000
229,600 |
520,000
146,000
58,300
46,300
34,000
20,200
10,000
7,950
8,800**
25,000
18,200
13,000
132,250 |
@ lnvasive cancers only more than 20,000 carcinomas in situ
of the breast and 55.000
carcinomas in situ of the cervix are estimated·
* Melanoma only; more than 600,000 non- melanoma skin cancers
are estimated.
** Melanoma 6700; other skin cancers 2100.
(Boring CC, Squires TS, Tong T· Cancer statistics, 1992. CA 1992;
42:19. Based on incidence data from National Cancer lnstitute SEER
program 1986-1988 and mortality data from the National Center for
Health Statistics. All figures are rounded.)
Since 1950 the incidence of cancer in the United States
climbed about 40 percent.
Lung cancer, most of it resulting from cigarette smoking,
caused the biggest carnage. Its incidence rose 209 percent in men and 451 percent in
women. But even excluding lung cancer, the cancer rate rose 22.6 percent.
Between 1974 and 1986 the age-adjusted rates of these cancers
increased:
Breast cancer up 18.4 percent;
Brain up 22.3 percent;
Bladder up 10.3 percent;
Liver up 16.2 percent;
Thyroid up 16.7 percent;
Colon up 13.9 percent.
The list goes on.
Yet during that same time the incidence of some
cancers dropped.
Stomach cancer was down 20 percent;
Cervical cancer down 36.1 percent;
Scientists say these numbers reveal that there are indeed
powerful environmental causes of cancer.
World wide:
The most common fatal form was stomach cancer
(prevalent in Asia), but lung cancer has risen rapidly, because of the spread of cigarette
smoking in developing countries, to become the leading fatal cancer in the world
today. Also on the increase is the third-greatest killer, breast cancer,
particularly in China and Japan. The fourth on the list is colon or rectum cancer, a
disease that mainly strikes the elderly.
One of the most informative comparisons is between the
U.S. and Japan. Both countries have similar levels of industrialization and
education, high medical standards and good vital statistics.
Surprisingly, although the overall cancer rates are similar, the two countries yield
mirror images when specific types of cancer are compared. For example, cancers of
the colon, breast, and prostate are common in the U.S. but rare in Japan.
Conversely, cancer of the stomach is common in Japan but rare in the U.S. Are the
environmental factors enhancing breast, colon and prostate cancer more prevalent in the
U.S., or are factors that protect against such cancers more prevalent in Japan?
One might answer that the differences are based on genetic
differences between the two populations. That hypothesis is refuted by the data on
migration from one country to another.
They show that the worldwide geographic variation in organ-specific cancer rates can be
attributed to environmental factors rather than genetic ones. For example, within
two generations Japanese immigrants in Hawaii and California had breast-cancer rates
approaching those of the Hawaiian white population and significantly higher than those of
native Japanese. Conversely, gastric-cancer rates became significantly lower among
Japanese Hawaiians than among native Japanese. Increases in breast-cancer rates were
also found in populations emigrating from Poland, where the risk is low, to the U.S.
For example, if Japanese people (who have low rates of
breast and colon cancer but high rate so stomach cancer) move to the U.S., they acquire
typical American cancer rates - high colon and breast cancer rates, low risks of stomach
cancer.
A time-trend study that followed Japanese dietary habits and
cancer deaths found that the mean per capita fat intake, which increased from 23 g/day in
1957 through 1959 to 52 g/day in 1973, was accompanied by a doubling of the total number
of annual breast cancer deaths between 1957 and 1973.
For example, in developing countries as much as 80 percent of
total calories comes from cereals and grains, which consist of complex
carbohydrates. With industrialization and economic advance the caloric intake shifts
toward fats derived from meat and vegetable oil. The consumption of sugar (simple
carbohydrate) also increases. Such changes are taking place now in a number of
countries, including Iceland, Italy, Greece and Japan. As the changes have occurred,
rising rates of breast and colon cancer (and of prostate cancer in certain places) have
been observed. The same changes have been observed in the U.S. Since 1900, for
example, the intake of animal and vegetable fats has risen by 40 percent while the
consumption of potatoes has declined by 60 percent and of flour by 50 percent. Since
1930 the incidence rates of breast, colon and prostate cancer have gradually
increased. On the other hand, deaths from gastric cancer have fallen
dramatically. The drop has been attributed to the fact that refrigeration has
largely replaced salting, pickling and smoking in the preservation of food.
Sidney S. Mirvish of the Eppley Institute for Research
in Cancer in Omaha has shown that nitrosation reactions do not proceed in the presence of
ascorbic acid (vitamin C), which blocks the conversion of nitrates into nitrites.
Several foods consumed by populations at high risk for
gastric cancer --among them smoked fish (in Japan) and fava beans (in Colombia)-- have
been shown to yield mutagens after nitrosation. These same populations consume small
amounts of fresh fruit and vegetables and therefore take in low levels of vitamin C,
suggesting that gastric cancer may result from the formation in the stomach of
carcinogenic nitrosamines or nitrosamides from dietary nitrate in the absence of vitamin
C. In no case, however, have the hypothetical "natural' nitrosated substances
to which gastric cancer has been attributed been isolated in people or in experimental
animals.
The effects of, pickling and smoking foods have also been
explored experimentally. These methods of preservation create conditions under which
nitrates can be converted readily into reactive nitrites; these in turn have been shown to
combine with appropriate substrates (in the test tube) to form carcinogenic nitrosamines
and nitrosamides.
Preventable
A majority of the causes are know and preventable
The best estimate of the causes of cancer deaths.
| Tobacco |
35% |
| Diet |
30% |
| Infection |
10% |
|
Reproductive and sexual behavior |
7% |
|
Occupation |
4% |
|
Alcohol |
3% |
|
Geophysical
factors' |
3% |
|
Pollution |
2% |
|
Medicines and medical procedures |
1% |
|
Food
additives |
<1% |
|
Industrial
products |
<1% |
| Unknown |
4% |
Fats
Most experimental studies suggest that dietary fat acts as a
tumor promoter or enhancer, but some evidence indicates that fat may have a role in cancer
initiation.
Animal studies have also shown that the type as well as the
amount of dietary fat governs the development of mammary, colon and pancreas tumors.
High-fat diets rich in certain fatty acids promote the formation of tumors, whereas
similar diets high in other fatty acids do not.
The difference seems to be in the chemical structure of the fatty acids. High-fat
diets rich in linoleic acid (s-6 or n-6 polyunsaturated fatty acids) (found in corn,
safflower, sunflower and other common plant oils) act as promoters; similar diets rich in
oleic acid (monounsaturated fatty acid) (from olive oil) and eicosapentaenoic acid (from
fatty fishes and marine mammals) do not act as promoters.
These findings in animals may help to explain several
epidemiological enigmas, including the low rates of breast and colon cancer among the
Eskimos of Greenland. They have a diet extraordinarily high in fat (60 percent of
calories), but the fat is derived almost entirely from fish and marine mammals.
Similarly, the moderate rates of breast cancer in such countries as Greece and Spain,
where fat intake is fairly high (32 percent of calories), may be due to the fact that
olive oil is a major source of fat in Mediterranean diets.
Epidemiologic data show a relationship between the amount of
saturated fat and colon cancer.
Virus Connection
Among the viruses strongly linked with human cancers:
Virus are non living particle
of DNA with a capsule that
multiply in a cell and either destroy the cell or damage it.
1. Epstein-Barr virus, that causes the disease known as
infectious mononucleosis. This latter virus is also suspected of causing the
malignancy called Burkitt's lymphoma, prevalent in Africa, and a cancer of the nose and
throat that commonly occurs in China.
2. Papilloma viruses: Cervical cancers
3. Another human cancer related to a virus infection is a liver carcinoma that sometimes
follows a HEPATITIS-B infection.
4. Another link established between a human cancer and a virus is that between T-cell
leukemia and a form of RETROVIRUS called HTLV-l; the cancer appears to be endemic in
certain parts of Japan, the West Indies, and the southeastern United States.
5. Childhood Leukemias - Good evidence that this is a viral illness transmitted thought
the Genetic material from the parents
-Children who eat too many hot dogs may be increasing
their risk of developing childhood leukemia, a study in the medical journal
"Cancer Causes and Control", published by the Harvard School of Public Health,
says.
A 10-year study at the University of Southern California found
that children who ate more than 12 frankfurter sausages a month and whose fathers
had a history of similar consumption had 9 times the normal risk of leukemia.
The report added that while it was clear that the risk of
leukemia increased with the consumption of hot dogs, "the risks did not become
large until consumption of 12 hot dogs per month for both children and fathers.
The USC team studied 232 Los Angeles children up to the age
of 10 who had developed childhood leukemia and 232 who had not.
They studied a variety of possible causes of childhood
leukemia, including parents' occupations, environmental factors, exposure to
electro-magnetic fields, and food.
In particular, they said, they looked at a variety of
processed meats that are treated with nitrites to preserve them. The meats included
bacon, sausage, ham, salami, pastrami, lunch meat, corned beef and bologna, as well
as hot dogs.
Of all the factors studied, however, only the hot dogs
showed an increased risk of leukemia. "It was a real surprise. It just
popped out; we weren't looking for it," Peters said.
Peters and his team suggested that fathers might be
passing the leukemia genes to their children.
Remember the 3 criteria for cancer
1. Carcinogen to damage the DNA - virus in the meat damaged the Father's DNA
2. Reduced immunity - poor diet few protective foods
3. promoter - high fat diet
CURED MEAT/BROILED MEAT/CANCER IN CHILDREN
Children whose mothers consumed cured or broiled meat during
their pregnancy are at greater risk of the later development of one of several types
of cancer. Childhood brain tumors were more common in children whose mothers had
consumed one or more hot dog[s] per week during the pregnancy.
Children who consumed hamburgers once or more each week are
at increased risk of acute lymphocytic leukemia; hot dog consumption by the child also
increases the risk of brain tumors.
Earlier studies have shown a relationship between nitrite and
nitrosamine intake and cancer, ant it is felt that these substances are the cause of the
increased risk (Cancer Causes and Control 5:141-148, 1994).
LUNG CANCER/MEAT INDUSTRY
Studies from Denmark, Sweden, England and Wales have shown an increased incidence of lung
cancer in meat cutters and butchers. A study from Baltimore, Maryland, demonstrates
an unusually high incidence of lung cancer in men who worked in slaughterhouses,
chicken-slaughtering plants, meat-packing plants and the meat department of supermarkets.
This excess incidence was not related to smoking. The researchers feel that workers
may be exposed to viruses which produce lymphoma or leukemia in animals, and to papilloma viruses, which are associated with the development of cancer. (Journal of the
National Cancer
Institute 83(18)1337-1339, September 18, 1991)
The body has mechanisms to combat
the cell that develops DNA damage.
1. Each cell can repair its own DNA
2. The Immune system recognizes damaged cell and destroys them by the T Cell
system. The function of the immune system most recently discovered is the system's ability
to recognize and eliminate the abnormal (mutant) cells that frequently arise within the
body. These mutant, or cancer, cells may occur spontaneously, or they may be induced
by certain viruses (oncogenic)
viruses) or chemicals (mutagens). An immune system that is functioning properly can
usually recognize and dispose of such cancer cells by means of a process called immune
surveillance. The malfunction of this process may result in the incidence of certain types
of cancers.
.3. Enzymes detoxify carcinogens.
4. Antipromoters include dietary fiber; vitamins A, C and E; the trace
element selenium, and certain compounds in such vegetables as broccoli, cabbage and
cauliflower, which are called cruciferous vegetables because they are in the Cruciferae
family of plants.
Evidence from clinical studies and laboratory experiments suggests that some of the
vegetable compounds may act at more than one point in the carcinogenic sequence, affecting
enzymes that detoxify initiating carcinogens and also serving as antipromoters. In
addition, as demonstrated in several studies the promoting effect of dietary fat can be
modified by other dietary components, most notably fiber.
Vegetables contain a large number of substances, both
micronutrients, such as
carotenoids and ascorbate, and other phytochemicals, such as phenols,
flavonoids,
isothiocyanates, and indoles, with a variety of potent anticarcinogenic properties. The
steps from procarcinogen to cell replication or (differentiation can be broadly
considered as follows:
1.procarcinogen is activated to ultimate carcinogen (either of which may be solubilized
and excreted);
2.carcinogen passes through cell and nuclear membranes;
3.Carcinogen interacts with DNA;
4. DNA synthesis and replication (or DNA repair) occur; cell
replication with abnormal DNA and abnormal protein synthesis (or cell
redifferentiation)
result.
At almost every one of these steps, one or more known phytochemicals can alter the
likelihood of carcinogenesis.
5. Antioxidents (procarinogen are frequently oxidized carcinogen), vitamins
A, C and
E; the trace element selenium. ( oxidize a chemical reaction of adding a electron)
6. Protease inhibitors
Another class of potential dietary antipromoters has been studied in detail by Walter
Troll of the New York University School of Medicine. Found in beans and plant seeds,
they are protease inhibitors: they counteract the effects of enzymes that digest
proteins and presumably help a tumor to invade neighboring tissue.
Common types of cancer and how prevented
Lung
168,000
146,000
At least 14 studies have demonstrated a risk of lung
cancer in nonsmoking wives exposed to the secondhand smoke of their husbands.
Passive smoking has been found to increase the risk of leukemia, lymphoma, and cancer of
the breast and uterine cervix.
The risks of passive smoking extend beyond cancer. It is estimated that tobacco
smoke in the home and work place could be responsible for the deaths of 46,000 nonsmokers
annually in the United States. Most of these (32,000) are due to heart disease, making
passive smoking the third leading preventable cause of death after smoking and the
consumption of alcohol.
Colon and
rectum
156,000
58,300
With respect to colon cancer, it has been postulated that
total dietary fat influences the metabolic activity of fecal bacteria and the
concentration of sterol substrates in the large intestine. As a consequence,
tumor-promoting substances (secondary bile acids) may be produced from bile acids within
the lumen of the colon.
As suggested by some epidemiologic data, experimental studies
indicate that degree of saturation and chain length of dietary fats can influence
tumorigenesis.
Women who consumed red meat daily, compared with once a
month, had a 2.5 times greater risk for colon cancer.
The interest in defining the relation between dietary
fiber and cancer can be traced to the early 1970s, when Burkitt cited international
epidemiologic data indicating that fiber-rich diets played a protective role in cancer of
the large bowel. This study and others found that the lowest rates of colon cancer
are in African and Asian countries, where high-fiber diets are consumed, and that the
highest colon cancer rates are in western societies, where refined carbohydrates have
commonly replaced naturally occurring fiber-rich foods and where intake of fiber is
consequently low. For example, the Chinese diet contains three times more fiber than the
typical American diet, and the colon cancer incidence rate in China is approximately two
thirds lower than that of the United States. Chinese also consume about 33% less
protein, 50% as much fat, and 30% more calories based on reference body weights than do
Americans, indicating that these factors may influence colon cancer risk.
Studies comparing rural Finland and New York and Finland and
Denmark
The protective role of dietary fiber in colon cancer
can be seen when comparing populations that consume relatively comparable high levels of
fat (more than 30% of total calories), but whose diets differ with regard to fiber intake.
Studies comparing rural Finland and New York and Finland and Denmark found that Finnish
populations, with an average intake of approximately 31 g of fiber per day had a lower
risk for developing colon cancer than the other two populations, which consumed no more
than 17 g of fiber per day,5 despite a similar high intake of fat 34-37% of total.
Several mechanisms by which dietary fiber is believed to protect
against colon cancer have been suggested:
(1) by increasing fecal bulk, which, in turn, dilutes the concentrations of carcinogens in
the feces;
(2) by changing bacterial composition in the colon, which leads to deactivation of
carcinogenic metabolites by binding to carcinogens, co carcinogens, or both, or promoters
in the bowel;
(3) by inducing Structural and functional chemical changes in the gut mucosa, including
altering rates of cell proliferation;
(4) by altering bile acid metabolism;
(5) by reducing fecal pH and
(6) by accelerating the transit time of fecal material through the intestinal tracts other
carcinogens from food or other sources have less contact with colon mucosa.
The most popular current hypothesis about the link between a
high-fat diet and colon cancer is based on findings that a high fat intake results in
increased secretion of bile acids (which help to digest fat) and alters the bacterial
population in the large bowel, thereby enhancing the conversion of primary bile acids into
secondary ones. Secondary bile acids in turn are thought to be promoters of lesions
that are already present in the large bowel.
Five studies have noted a positive association with egg
consumption; four have shown an inverse association with fish or seafood consumption. (colon
cancer)
Breast
181,000@·
46,300
Experimental studies using mouse mammary tumors showed that
the amount of dietary fat consumed after, but not before, exposure to a chemical
carcinogen led to enhanced tumor genesis and to the suggestion that fat affects promotion
process of carcinogen sis rather than the initiation.
The role of fat in tumor initiation is suggested by more
recent experimental data.
A time-trend study that followed Japanese dietary habits and
cancer deaths found that the mean per capita fat intake, which increased from 23 g/day in
1957 through 1959 to 52 g/day in 1973, was accompanied by a doubling of the total number
of annual breast cancer deaths between 1957 and 1973.
Increase risk
1. Abortion
2. Early onset of menstruation
3. Late menopause
Decease risk
Pregnancies
Early Pregnancy
Some international studies suggest that high intakes of
cereals may be inversely related to breast cancer incidence. In a study of 37 countries, a
high correlation was observed between the incidence rates of colon and breast cancer in
countries with high incidence rates of these types of cancer, a weak inverse correlation
between cereal consumption and cancer incidence and a direct relation between high intakes
of fat and animal protein were found.
In a comparison of 133 breast cancer patents and 218 healthy
subjects, it was found:
Low intake of the following in the breast cancer group.
1. Cereal products
2. Beta-carotene fruits
3. Vegetables
4. All vegetable products combined
5. Energy-adjusted intake of dietary fiber
Several reports have indicated that laboratory rats fed
a diet containing starch following the intake of a chemical carcinogen showed a
significantly lower frequency of mammary tumors than rats fed a similar diet containing
dextrose (a simple sugar) in place of starch.
{Studies by}(West et al., 1980; Lyon et al., 1980; Phillips
et al., 1980; Eslstrom, 1980). Gaskill et al. (1979)...., and they find that within
the United States breast cancer mortality correlates more strongly with the consumption of
milk fat than of other types of fat.
As little a 3 drinks (Alcohol) per week increased the risk
of breast cancer.
Prostate
132,000
34,000
Several dietary studies of prostate cancer risk indicated a
small to moderate positive relation between risk and consumption of fat or high-fat foods.
A mechanism linking dietary fat to prostate cancer has
not been hypothesized; however, the endocrine system has been implicated as a mediator of
dietary influenced including fat.
Uterus
45,500·
10,000
Recent evidence has strengthened the association
between
cigarette smoking and cancer of the uterine cervix. As many as one third of the
12,000 new cases of cervical cancer in the United States each year are attributable to
cigarette smoking. Women who smoke cigarettes have four times the risk of nonsmokers for
developing cervical cancer.
Human
papilloma
Cervical
Skin
32,000*
8,800**
Sunlight combined with decreased protective foods
Pancreas
28,300
25,000
Associations between alcohol consumption and cancer vary by
site and type of alcoholic beverage. Alcohol intake is reported to be directly
associated with cancers of the oral cavity, pharynx, esophagus, and larynx where alcohol
interacts synergistically with smoking to increase risk. Primary liver rectal, pancreatic,
and breast cancer also have been linked with alcohol intake.
The protective anti-cancer effects of fruit and veggies
Low intakes of fruit and vegetables have been consistently
linked to high cancer rates in many countries around the world. Yet, less than 10 per cent
of North Americans eat the recommended 5-10 daily servings. The fruit and vegetables that
appear most protective against cancer are raw, dark green leafy vegetables (such as
spinach, kale and lettuce), cruciferous or cabbage-family types (such as brussel sprouts,
cabbage, cauliflower, broccoli), and orange forms such as carrots, squash, citrus and
other fruits. Different plant foods may protect against different cancers, for example:
* dark green vegetables may protect against lung cancer;
* cruciferous (cabbage family) vegetables and carrots appear
protective against colon cancer;
* citrus and other fruits rich in vitamin C may lower
risks of mouth, larynx, stomach and esophageal tumors.
The constituents in plant foods thought to ward off cancer
include antioxidants - such as vitamins C, E and carotenes (vitamin A precursors).
Other plant compounds such as indoles, flavones, phenols, coumarins, isothiocyanates,
sterols and limonene may also play an anti-cancer role. Together, the plant components or
phytochemicals that fight cancer have been dubbed "chemopreventive agents."
Laboratory studies also suggest an anticancer effect for
flavones, indoles and isothiocyanates (nonnutritive compounds often called secondary plant
constituents) derived from cruciferous vegetables. The compounds apparently act by
blocking the activation of hydrocarbon agents in the host. (Most carcinogens are consumed
as inactive procarcinogens and must be activated by enzymes in the liver before they can
react with the DNA of target cells.)
Overall, the epidemiological
studies of beta-carotene are
remarkably consistent in suggesting a protective effect on cancer risk. To date, more than
85 questionnaire studies of intake of fruits and vegetables rich in beta-carotene in
relation to risks for cancer have been published, including more than 15,000
cases of cancer at 16 different Sites, conducted in more than a dozen locations within the
United States and in 10 Other
" People can obtain all the necessary vitamins, minerals
and other essential nutrients from a well balanced diet. There are no scientific grounds
at present to support the anti-cancer benefits of taking vitamin or antioxidant
supplements. "Besides the risk of toxicity from vitamin mega doses, there is the added
danger," notes one University of Toronto expert, "that people who take
supplements may falsely believe they are eating well, yet fail to achieve the health
benefits of a balanced diet."
The epidemiological evidence for anticancer effects from
evidence for its dietary precursor, beta-carotene) comes almost exclusively from the
comparison of cancer patients with healthy people. There is literally no evidence
for a protective effect of other vitamins, with the exception of a possible association
between the intake of vitamins C and E and reduced rates of gastric cancer.
Conclusion
In 1982 the National Research Council, an arm of the
U.S. National Academy of Sciences, issued provisional guidelines intended to reduce
the risk of cancer related to food. The main recommendations were to lower the
intake of fat from the current U.S. average of 40 percent of total calories to 30 percent;
to eat more fiber, fruits and vegetables; to increase the consumption of complex
carbohydrates (such as the starch in flour and potatoes), and to decrease the consumption
of pickled, salted or smoked foods as well as of simple carbohydrates (such as
refined sugar).
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v257 p42(7), Cohen, Leonard A.
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government review heightens concern about hazards of the electronic age. (health effects
of electricity)" Elmer-Dewitt, Philip, Time, Dec 24, 1990 v136 n27 p67(2
4. "Plant foods, animal foods, and colon
cancer." (Research Report), Potter, J.D. Cancer Researcher Weekly, Dec 27, 1993
p18(3)
5. "The diet-cancer story. (includes related information
on dietary influences and cancer risk)", Health News, April 1994 v12 n2 p6(2)
6. The Causes of Cancer, Richard Doll and Richard Peto,
Oxford Medical Publications
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