Subscribe Now Subscribe Today
Review Article

Incidence, Epidemiology and Prevention of Cancer and Management of Cancer Patients-an Overview

Mahpara Safdar and Alam Khan
Facebook Twitter Digg Reddit Linkedin StumbleUpon E-mail

Cancer is characterized by the malignant cellular growth that tends to spread. It is the second leading cause of death after heart disease. Cancer incidence varies with regions and populations around the world. The incidence of various types of cancer ranges from rare of gallbladder to 12% of most common cancer of lung. In men, the minimum incidence of cancer is that of gallbladder (4.4%) an the maximum is the incidence of lung cancer (18.6%). In women, the minimum incidence of cancer is that of endometrium (3.44%) and the maximum is that of breast cancer (18.18%). Dietary prevention of cancer is also a long term process and it may take 10 to 60 years to have an impact, the time scale depending, to some extent on the type of cancer. The epidemiological data suggest that the major causative factor for the incidence of cancer is environment. The environmental factors causing cancer include diet, radiation, chemicals and tobacco. The diet plays a major role in the development and prevention of cancer. Consumption of more meat, fatty foods of animal origin and salted foods increase the incidence of cancer. Method of preparation like grilling and barbecuing of meat also increase the incidence of cancer. Intake of foods of plant origin reduce the chance of cancer incidence.

Related Articles in ASCI
Search in Google Scholar
View Citation
Report Citation

  How to cite this article:

Mahpara Safdar and Alam Khan, 2003. Incidence, Epidemiology and Prevention of Cancer and Management of Cancer Patients-an Overview. Journal of Medical Sciences, 3: 429-456.

DOI: 10.3923/jms.2003.429.456



Cancer is a human disease and is defined as malignant tumor or a disease which is characterized by excess of cells beyond the number needed for normal function of the body. Cancer may grow slowly or rapidly. Many tumors grow into nearby organs or tissue, or spread to other parts of the body. This process is called metastasis. Metastasis usually occurs through the blood stream or lymph vessels. Benign tumors are made up of cells that are not cancerous; they usually do not grow and spread in the same way as malignant tumors. The benign tumors are not dangerous.

A combination of genetic, environmental and lifestyle factors are involved in turning a normal cell into an abnormal cell and an abnormal cell into cancer. In most cases, the cancer process starts when the genetic material responsible for cell division inside a cell becomes faulty. This may occur by chance or because a cancer causing substance called carcinogen has been introduced into, or produced by, the body.

Potential carcinogens are present in the air, food and water and enter the human body through breathing, eating and drinking. Other carcinogens are found in tobacco, industrial compounds and in the form of viruses. The human bodies are designed to deal with carcinogens either by eliminating the carcinogens before they do any harm to the body or repairing any damage done by them. Sometimes, the body's defenses fail and a carcinogen becomes activated inside a body cell and damages the genetic material of the cell permanently. Once the damage occurs, the cell can no longer function properly. The cell then may grow and multiply abnormally and as it divides, the flawed genetic material may be passed on. In full fledge cancer, the abnormal cells must reproduce to such an extent that they start to occupy the space of normal cells or threaten the function of healthy cells or organs.

Cancer may develop in any part of the body and is named after the name of that body part where it is developed. The most common types of cancer are mouth and pharynx, nasopharynx, Larynx, esophagus, lungs, stomach, colon and rectum, breast, ovary, endometrium, cervix, prostrate, pancreas, gall bladder, liver, bone marrow, intestine, thyroid, kidney, bladder, skin and uterine cancer etc. The rates of cancer incidence vary with factors such as age, sex, economical condition, migration and urbanization etc.

Between 30 and 40% of cancer cases throughout the world are preventable by feasible dietary means. Of course death cannot be prevented, so the main task for dietary prevention of cancer is, first, to reduce the occurrence of premature cancers greatly and, second, to seek to avert many of the cancers that are deferred to, or destined for, old age. Information about the effect of various diet constituents including energy and related factors, carbohydrates, fat and cholesterol, protein, vitamins (especially Vitamins A, C, D and E), vegetables and fruits, meat, poultry, fish and eggs, milk and dairy products, coffee, tea and other drinks, cereals (grains), pulses (legumes) and minerals are beneficial both for the patients and diet care professionals. The specific mechanism by which individual constituents of diet affect the cancer process are not fully understood and no doubt many remain to be identified. However, existing knowledge gives key insights into the cancer process, which, in turn, can lead to make better dietary guide lines for prevention of cancer. The nutritional needs of cancer patients changes during the course of the disease and with different treatments so the nutritional care for cancer patients must be individualized and readjusted to meet the specific changing nutritional needs and dietary/eating peculiarities.

This review paper is to provide recent information to the researchers of the field and medical professionals and guide lines to the diet planners in hospitals. The review will help in educating the cancer patients.

Incidence of cancer
There is marked variation in the incidence of and mortality from, many cancers in different regions and populations around the world, but certain general patterns can be identified. With few exceptions, the economically developing countries of Africa, Latin America and Asia have relatively high rates of cancers of the upper aero digestive tract (mouth and pharynx, larynx and esophagus) and of the stomach, liver and cervix. In contrast, the economically developed countries of Europe, North America and Australia have relatively high rates of cancers of the colon and rectum and of the hormone-related cancers of the female breast, the endometrium and the prostate. This pattern has now also emerged in urban areas of developing countries. Lung cancer, mainly caused by use of tobacco, is now the most common cancer throughout the world (WCRF, 1997).

Cancer rates may change dramatically. For example, in most populations in the developed world, stomach cancer has been declining rapidly in recent decades, whereas rates of cancers of the colon, breast and prostate have been rising. Further variations in cancer patterns are seen in studies of migrants. Also, patterns of cancer are now changing rapidly within the economically developing world as populations age and become increasingly industrialized and urbanized. Such variations with time, migration and urbanization indicate that cancer rates are strongly influenced by environmental factors, including diets (WCRF, 1997).

It has been estimated that 10 million new cases and over 7 million deaths from cancer occurred in 1996 (WHO, 1997). Cancer is second to heart disease as a cause of death in westernized countries. In Britain, it accounts for 23% of all deaths and the risk of it increases with age. Rate of stomach cancer in men and women are declining and rate of skin and bladder cancer are increasing. In women, the rates of incidence of breast and lung cancers are increasing. In men rates for cancer of the prostate, colon and esophagus are increasing (Thomas, 1994). Approximately 150 diseases caused by abnormal cells that develop and divide uncontrollably. The high risk countries for incidence of cancer are North America, Europe, Australia while low risk countries are Central and South America, Asia and Africa. The incidence of various types of cancer has been reported by the World Health Organization (WHO, 1997) as under.

Gastro-intestinal cancer
The incidence of mouth and pharyngeal cancer is relatively high in the developing world, notably in India and elsewhere in Asia and is more common in men. This cancer is the fifth most common incident cancer. Nasopharyngeal carcinoma is a rare cancer in most parts of the world. The age standardized incidence rate for either sex is generally less than 1 per 100,000 population. Cancer of the larynx is the fourteenth most common cancer in the world. Approximately 60% of the global incidence of laryngeal cancer is found in developing countries. Men account for 85% of the worldwide incidence of laryngeal cancer. Cancer of the esophagus is the eighth most common cancer in the world. Esophageal cancer incidence is higher among males than females.

Cancer of the stomach is the second most common cancer .in the world and is decreasing throughout the world. Stomach cancer rates are 50% lower in women than in men (Aoki et al, 1992, Parkin et al, 1992, WHO, 1997). Incidence rates of colorectal cancer have generally increased. Cancer of colon and rectum is the forth most common cancer in the world. Central and South America, Asia and Africa are areas of low risk. In both men and women, incidence of colon cancer occurs at a similar rate. However, cancer of the rectum is more common in men than women, with a 20-50% higher incidence (WHO, 1997).

Lung cancer
Lung cancer have increased throughout the world with sharp increase for women almost everywhere. Cancer of the lung is the most common cancer in the world. In 1996, an estimated 1,320,000 new cases were diagnosed worldwide, accounting for 12.8% of all new cancers (WHO, 1997). Rates of lung cancer are highest in North America and Europe and lowest in Africa, Asia and South America (Parkin et al., 1992).

Liver cancer
Cancer of the liver is the sixth most common cancer in the world. In 1996, an estimated 540,000 new cases were diagnosed worldwide, accounting for 5.2% of all new cancers. In the developing world, liver cancer is very common, accounting for more than 80% of the global cases. China alone accounts for 55% of the worldwide incidence. Incidence among men is over twice that among women. Infection with hepatitis B virus is the predominant cause of liver cancer, with more than 80% of cases being the result of infection with this virus. (WHO, 1997).

Breast cancer
The incidence of breast cancer have also increased overall. It is low in developing countries and high in developed countries. Cancer of the breast is the third most common cancer in the world. In 1996, there were an estimated 910,00 new cases diagnosed worldwide, accounting for 9% of all new cancers. Over 50% of breast cancer incidence (494,000 cases) occurred in the developed world in 1996. The lowest rates are reported in Africa and Asia. However, breast cancer is increasing in many countries, particularly in areas which have previously had low rates, although at least part of the increase is due to early detection of cases by screening (WHO, 1997; Doll et al., 1994).

Glands cancer
Cancer of the pancreas is the thirteenth most common cancer in the world. Men have approximately a one third greater age adjusted incidence rate than women (Parkin et al., 1993). Most gallbladder cancers arise in the epithelium and are classified as carcinomas. The incidence of this cancer is low compared with other sites, even among those populations who are at highest risk and accounts for about 1% of all cancer deaths. In high risk populations, incidence in women is approximately double that of men but, in other populations, the rates are similar for men and women (Parkin et al., 1992). Cancer of the prostate is the ninth most common cancer in the world. The rate of this male hormone related cancer is generally low in developing world and high in the developed world. In 1996, there were an estimated 400,000 new cases diagnosed worldwide, accounting for 3.9% of all new cancers (WHO, 1997). Thyroid cancers are relatively rare, representing fewer than 2% of all recorded neoplasm’s worldwide (Goodman et al., 1988; Omran and Ahmed, 1993 and WHO, 1997). In patients with a history of non melanoma skin cancer, a low fat diet reduces the actinic keratosis (Black et al., 1994).

Ovarian, endometrial and cervical cancers
Cancer of the ovary is the fifteenth most common cancer in the world. Cancer of the endometrium is the sixteenth most common cancer in the world. Africa and Asia have the lowest incidence of endometrial cancer. Cancer of the cervix is the seventh most common cancer in the world. The highest incidence rates are seen in parts of Sub-Saharan Africa, South East Asia and Latin America. Developing countries account for 80% cases of the cervical cancer (WHO, 1997).

Kidney and bladder cancers
Cancer of the kidney is the seventeenth most common cancer in the world. Worldwide, there is at least a ten fold difference in the incidence of renal cancer. The rates are lowest in Asia and South America (Parkin et al., 1992). Cancer of the bladder is the eleventh most common cancer in the world. Incident of bladder cancer is two to five times higher in men than in women (Parkin et al., 1992; Silverman et al., 1992). In 1996, approximately 75% of cases were male (WHO, 1997). In tropical and subtropical countries, where schistosoma haematobium is endemic, bladder cancer is the most common cancer in men and second only to breast cancer in women, accounting for about 30% of all cancers (Badawi et al., 1995). The predominant histological type of bladder cancer is transitional epithelial cell carcinoma (Silverman et al, 1992). However, squamous cell carcinoma is the major type in areas where urinary schistosoma infestation is prevalent (Badawi et al., 1995).

The rates of incidence of the various types of cancer are shown in the decreasing order in Table 1.

Salam et al. (1992) conducted two studies in Peshawar and one study in D.I. Khan on the incidence of various types of cancer. They showed strong correlation among the frequency of various malignant tumors in Peshawar and D. I .Khan. Their data is presented in Tables 5 and 6.

Epidemiology of cancer
Knowledge of the causes of human cancer comes primarily from epidemiological studies which compare population groups or categories of individuals who share some common characteristics.

Table 1: Incidence of various types of cancer in decreasing order
Image for - Incidence, Epidemiology and Prevention of Cancer and Management of Cancer Patients-an Overview
Source: WHO (1997).The incidence of cancer in various regions and population of the world are summarized in Table 2.

Table 2: Incidence of cancer in the different regions or population of the world
Image for - Incidence, Epidemiology and Prevention of Cancer and Management of Cancer Patients-an Overview
Image for - Incidence, Epidemiology and Prevention of Cancer and Management of Cancer Patients-an Overview
Source: WHO (1997). The world wide incidence and mortality rates from different types of cancers in men and women are shown in Tables 3 and 4.

The principal causes of most cancers are environmental in origin and diet may be a major environmental factor (NAS, 1982). One estimate of the proportion of all cancers attributable to diet ranges from 10-70%, with an overall average of 35%. This compares with 25-40% from tobacco and 2-8% from occupational exposure. Food additives contribute less than 1%, but virtually this is no risk.

Table 3: Estimated number of new cases and deaths from cancer worldwide in 1996 (men)
Image for - Incidence, Epidemiology and Prevention of Cancer and Management of Cancer Patients-an Overview
Source: WHO (1997).

Table 4: Estimated number of new cases and deaths from cancer worldwide 1996 (women)
Image for - Incidence, Epidemiology and Prevention of Cancer and Management of Cancer Patients-an Overview
Source: WHO (1997).

Table 5: Five commonest tumors in males in Peshawar and D.I.Khan
Image for - Incidence, Epidemiology and Prevention of Cancer and Management of Cancer Patients-an Overview

Table 6: Five commonest tumors in females
Image for - Incidence, Epidemiology and Prevention of Cancer and Management of Cancer Patients-an Overview

Table 7: Dietary factors implicated in the promotion of/or protection against cancer
Image for - Incidence, Epidemiology and Prevention of Cancer and Management of Cancer Patients-an Overview

Some food additives may protect from cancer (Doll and Peto, 1981). The international correlation between the meat intake and the incidence of colon cancer has been measured as 0.85 for men and 0.89 for women (Armstrong and Doll, 1975). Major changes in the rates of a disease within a population over time provide evidence that non genetic factors play an important role in that disease. In Japan, for example, the rates of colon cancer has risen dramatically since 1950 (Aoki et al., 1992).

Role of diet in cancer
Cancer development is thought to be a several stage process of initiation, followed by promotion. The initiation step is brought about by carcinogens which are widespread in the environment and which cause changes in the DNA of cells. Before malignancy develops, another stage, promotion is necessary. In general, diet is thought to be particularly important in the promotion of cancer and in protection against the effects of carcinogens, rather than as a carrier of carcinogens themselves. It is to be expected that the causes of cancers in different organs of the body would be different, but the way in which diet is thought to be involved is often uncertain. In addition, several sites have a dietary constituent in common. Those that have been implicated in either promotion of or protection against cancer are shown in Table 7 (NRC. 1982).

Changes in diet could prevent upto half of all cases of breast cancer, three out of four cases of stomach cancer and three out of four cases of colon and rectal cancer (WCRF, 1994). Epidemiological evidence suggests that a diet rich in fruits and vegetables may reduce the risk of various forms of cancer, most likely contributable to their vitamins and minerals content. Recent intervention studies from population of Linxian, China have indicated that vitamins and minerals supplementation, specifically beta carotene, vitamin E and selenium, may play a role in the reduction of cancer risk (Mobarhan, 1994).

Effect of milk and milk products on cancer
Diets high in milk and dairy products possibly increase the risk of prostate and renal cancer (Armstrong and Doll, 1975; Role et al., 1986; Maclure and Willett, 1990).

Effect of egg on cancer
Diets high in eggs may increase the risk of pancreatic cancer, but is, as yet, insufficient (Zheng et al., 1993). Consumption of eggs possibly increases risk of colorectal cancer (Hiramatsue et al., 1983). Diets high in eggs may increase the risk of ovarian cancer but is not proven yet (Snowdon, 1985).

Effect of meat and meat products on cancer
Eating more than 80 g (3 ounces) of red meat, that is beef, lamb, or the products made from these meats, probably increase the risk of cancers of the colon and rectum and may also increase the risk of developing cancers of the pancreas and kidney, as well as prostate and breast cancer. Red and processed meat is a major source of animal fat which possibly increases the risk of cancers of the lung, colon and rectum, breast, edometrium and prostate. Red meat should contribute less than one tenth or 10% of the total calorie intake. Three ounces or less is roughly equivalent to 2-3 slices of beef or lamb. White meat is the better choice if meat has to be eaten. Salted fish increases the risk of nasopharyngeal cancer, especially when eaten frequently in early childhood (HO, 1971; Huang et al., 1978). Diets high in cured meats may increase the risk of stomach cancer, but yet to be investigated more (Boeing et al., 1991). Diets high in meat and fish that has been grilled (broiled) and barbecued possibly increase the risk of stomach cancer (Hansson et al., 1993). Diets high in meat possibly increase the risk of pancreatic cancer, perhaps particularly at the higher levels and with certain preparation methods commonly used in Western societies (Zheng et al., 1993). Diets high in cured or smoked meat or fish may increase the risk of pancreatic cancer, but is, as yet, insufficient (Anderson et al., 1996). Red meat probably increases the risk and processed meat possibly increases risk of colorectal cancer (Steinmetz and Potter, 1993; Gerhardsson de Verdier et al., 1991). Diets high in meat possibly increase the risk of breast cancer (Toniolo et al., 1994); Diets high in fish may decrease the risk of breast cancer; (Rose et al., 1994) and ovarian cancer (Mori et al., 1988). High meat diets possibly increases the risk of prostate cancer and renal cancer. Diets high in animal protein may increase the risk of breast cancer, but is, as yet insufficient (Armstrong and Doll, 1975).

Effect of cereals on cancer
Carbohydrates provide about half the calories in our diets. In nature, foods rich in starches and non-starch polysaccharides such as wholegrain bread and cereals, pulses and tubers (potatoes), contain valuable amounts of vitamins, minerals and dietary fibre - all of which are important for good health and for preventing cancer. The starch in foods is thought to protect against cancers of the colon and rectum. Processing can destroy nutrients and other food components that are important in fighting cancer. That is why wholegrain bread and brown rice are generally better than their white counterparts. A diet containing a large amount of refined sugar may increase the risk of cancers of the colon and rectum. There is no evidence that the naturally occurring sugars found in whole fruits affect cancer risk so, grapes, bananas, peaches and strawberries should be preferred than foods made with refined sugar like cakes, pastries, biscuits and chocolate. Diets high in cereals possibly increase the risk of esophageal cancer. However, any relationship between cereal consumption and esophageal cancer is probably not with cereals as such, but with diets that are deficient in a number of protective micro nutrients or contaminated with mycotoxins or both (Thurnham et al., 1985). Deits high in starch possibly increase the risk of stomach caner. It is likely that this applies to starch in refined form (Ramon et al., 1993b; Hansson et al., 1993). Diets high in extrinsic (refined) sugars possibly increase risk of colorectal cancer. The evidence is strongest for sucrose (Luceri et al., 1996a).

Effect of fiber on cancer
Diets high in fiber may decrease the risk of stomach cancer, but not yet proven ((Hansson et al., 1993). Diets high in NSP/dietary fiber possibly decrease the risk of pancreatic cancer (Howe and Bruch, 1996). Diets high in fiber possibly decrease the risk of colorectal cancer (Ma et al., 1996). NSP/dietary fiber possibly decreases the risk of breast cancer (Cohen et al., 1991). The importance of dietary habits for colorectal cancers and adenomas was studied in Denmark. It was concluded that the intake of crude dietary fibers is associated with reduce risk of cancer as well as adenomas (Olsen et al., 1994).

Effect of fruits and vegetables on cancer
Eating 400-800 g (15-30 ounces), of vegetables and fruits daily could decrease the cancer risk upto 20%. Eating plenty of vegetables and fruits protects against many cancers, particularly those of the mouth, pharynx, esophagus, lung, stomach, colon and rectum. Vegetable and Fruits also reduce the risk of those cancers that affect the larynx, pancreas, breast and bladder. It possibly lower the risk of cancers of the liver, ovary, endometrium, cervix, prostate, thyroid and kidney too. The protective effects of vegetables and fruits is due to complex interactions between vitamins, minerals, fibre and plant chemicals. Diets high in vegetables and fruits decrease the risk of cancer of the mouth and pharynx, esophageal and lung cancer (Gridley et al., 1992; Zheng et al., 1992; De Stefani et al., 1990; Steinmetz and Potter, 1991 and McPhillips et al., 1994). Also diets high in vegetables and fruits decrease the risk of lung cancer is convincing (McPhillips et al., 1994). Diets high in vegetables and fruits, collectively and separately decrease the risk of stomach cancer. Raw vegetables, alliums vegetables and citrus fruits are particularly abundant and consistent for a protective effect. Any evidence not consistent with a protective effect relates almost entirely to salted and pickled vegetables. (Fontham et al., 1986; Kneller et al., 1992 and Kato et al., 1990).

There is substantial evidence from epidemiological studies that diets high in vegetables and fruits probably decrease the risk of pancreatic cancer (Stemmetz and Potter, 1991). Diets high in vegetables and fruits probably decrease the risk of breast and bladder cancer (Ingram et al., 1992 and Bruemmer et al., 1996); and possibly decrease the risk of ovarian, Endometrial and thyroid cancer (Role et al., 1986; Levi et al., 1993 and Franceschi et al., 1989). A population based case control study was conducted in Maxico City during 1989-1990 to evaluate the relation between chili pepper consumption and gastric cancer risk. Results indicated that chilli pepper consumers were at high risk for gastric cancer compared with non consumers (Lopez- Carrilo et al., 1994).

Effect of carotenoid and vitamins on cancer
High dietary carotenoids intake possibly decreases the risk of esophageal, stomach, colorectal, breast, cervical and lung cancers (Hu et al., 1994; Singh and Gaby, 1992; Zaridze et al., 1993; Jan et al., 1994; Harris et al., 1986 and Steinmetz et al., 1993). The evidence suggests that high dietary carotenoids may decrease the risk of ovarian, endometrial and balder cancer but is yet to be proved (Engle et al., 1991; Vecchia et al., 1986; Moon and Mehta, 1986 and Vena et al., 1992). High dietary retinol intake possibly has no relationship with the risk of stomach cancer (Haenszel et al., 1985). High dietary vitamin E intake possibly decreases the risk of lung and cervical cancer (Mayne et al., 1994; Knekt, 1988). Evidence on diets high in vitamin E and the risk of colorectal cancer is relatively null but higher pre diagnostic blood levels are associated with a lower risk of subsequent cancer. The evidence suggests that higher dietary vitamin E may reduce the risk of colorectal cancer, but is, as yet, insufficient (Longnecker et al., 1992). Vitamin E and A were negatively associated with adenoma occurrence (Olsen et al., 1994). Vitamin D and higher intakes of both folate and methionine may reduce the risk of colorectal cancer but is at present insufficient (Lointier et al., 1987; Giovannucci et al., 1993). High dietary vitamin C intake possibly decrease the risk of cancer of the mouth and pharynx (Rossing et al., 1989; Gridley et al., 1990; Ramaswamy et al., 1996; Zheng et al., 1992). Also, high dietary vitamin C intake possibly decreases the risk of esophageal, lung, stomach, pancreatic and cervical cancer (Chen et al., 1992; Steminmetz et al., 1993; Singh and Gaby, 1992; Zhang et al., 1994; Appel et al., 1991 and Van Enwyk et al., 1992). High dietary vitamin C intake may reduce the risk of colorectal cancer, but the evidence is, at present, insufficient (Dion et al., 1982). High dietary vitamin C may decrease the risk of breast cancer (Jain et al., 1994) and bladder cancer but yet to be proven (Steinmetz and Potter, 1991).

Effect of minerals on cancer
Epidemiological and experimental data and plausible biological pathways, amount to evidence that diets high in salted foods probably increase the risk of stomach cancer (Kneller et al., 1992). Daily consumption of salt should be limited to less than 6 grams (or 0.2 g of sodium)- that is roughly equivalent to only a teaspoon of salt a day - from all sources. Evidence suggests that iron intake may increase the risk of colorectal caner but is, as yet, insufficient (Nelson et al., 1994) and also iron overload with diverse aetiologies may increase the risk of primary liver cancer. However this is to be proven yet (Hann et al., 1992). High dietary selenium intake possibly decrease the risk of lung and stomach cancer (El-Bayoumy et al, 1993; Sivam et al., 1997) and may decrease the risk of stomach, liver and thyroid cancer, but is, as yet, insufficient (Kobayashi et al., 1986; Han, 1993 and Knizhnikov et al., 1993). Diets deficient in iodine or with an excessive intake of iodine probably increase the risk of thyroid cancer (Wigren et al., 1992; Kanno et al., 1992). The chlorinated drinking water may increase the risk of bladder cancer though not proven yet (Zierler et al., 1986).

Effect of fat on cancer
High fat diets increase the number of tumors initiated by a variety of chemical carcinogens in virtually all animal models of breast, bowel, pancreas and prostate cancer provided that the diets fed supply sufficient of the essential n-6 poly-unsaturated, linoleic acid, for which there is a tumor requirement of approximately 10% total energy. Lowering the total amount and kind of fat is important for reducing cancer risk. Saturated fat possibly increase the risk of developing cancers of the lung, colon, rectum, breast, prostate and endometrium. Healthy eating involves reducing all fat consumption to less than a third or 30% of one’s total calorie intake. It is best to avoid fats of animal origin, hydrogenated oils, palm and coconut oils. Diets high in total fat possibly increase the risk of lung, colorectal, breast and prostate cancers. Effect of fat is minor compared to that of cigarette smoking (Knekt et al., 1991b; Alavanja et al., 1993; Guillem and Weinstein, 1990; WCRF, Expert Pannel, 1994; Armstrong and Doll, 1975; Rose et al., 1986). As a whole diets high in total fat may increase the risk of ovarian and endometrial cancer but is, as yet, insufficient (Armstrong and Doll, 1975; Rose et al., 1986). Diet high in total fat or consumption of fried foods may increase the risk of bladder cancer, but is, as yet, insufficient (Bruemmer et al., 1996; Wakabayashi et al., 1992).

Effect of cholesterol on cancer
The evidence relating cholesterol to cancer risk is conflicting. In a report of 1500 individuals in Scotland for example, there was a strong negative association in men between serum cholesterol and lung cancer but there was not such association in the few patients who developed colon cancer, nor in women who developed breast cancer (Isles et al., 1990). A number of studies have reported that a low serum cholesterol is associated with increased risk of cancer. But some of these studies were small and the increased risk was usually shown for lung cancer which is primarily related to cigarette smoking. The evidence regarding dietary cholesterol and lung cancer is somewhat mixed. One of four cohort studies and three of five case control studies have shown moderate to strong increases in risk with higher intakes and no studies have shown a statistically significant decrease in risk. Diets high in cholesterol possibly increase the risk of lung and pancreatic cancer (McMichael et al., 1984; Howe et al., 1992). Diets high in cholesterol may increase the risk of endometrial caner but is, as yet, insufficient (Goodman et al., 1994).

Effect of tea on cancer
High consumption of coffee and black tea probably has no relationship with the risk of stomach cancer (Hansson et al., 1993; Heilbrum et al., 1986 and IARC, 1991). However, high consumption of green tea possibly decreases the risk of stomach cancer (Yamane et al., 1995). Coffee may decrease the risk of colorectal cancer, but not yet proven (Jacobsen and Thelle, 1987). Also, high consumption of coffee possibly increase the risk of bladder cancer at high levels of intake, but is probably not associated with risk at consumption below 5 cups per day (Avanzo et al., 1992).

Effect of alcohol on cancer
Drinking alcohol regularly increases the risk of cancers of the mouth, pharynx, larynx, esophagus and primary cancer of the liver. Furthermore, the risk is even greater for people who drink and smoke. Drinking alcohol probably also increases the risk of developing cancers of the colon, rectum and breast. High alcohol consumption, irrespective of the type of beverage, increases the risk of laryngeal and mouth & pharynx cancer (Hedberg et al., 1994; Keller and Terris, 1965). High alcohol consumption also increases the risk of oesophageal cancer (Blot, 1992; Yamada et al., 1992). High alcohol intake possibly increases the risk of cancer of the gastric cardia (Vaughan et al., 1995) and also increases the risk of lung cancer but any impact of alcohol consumption is minor compared with that of cigarette smoking (Potter et al., 1982).

Heavy and persistent drinking of alcohol, leading to cirrhosis and alcoholic hepatitis which increase the risk of primary liver cancer (Austin, 1991) but has no relationship with the risk of pancreatic cancer (Lowenfels et al., 1993). High alcohol consumption probably increases the risk of breast cancer (Longnecker, 1994) and cancers of colon and rectum. The effect generally seems to be related to total ethanol intake, irrespective of the type of drink (Garro and Lieber, 1990). The association between alcohol and colon and rectal neoplasms were examined in the Iowa Women's Health Study (USA). Results showed that alcohol intake was inversely associated with distal colon neoplasm, however, no association was observed with proximate colon neoplasm (Gapsture et al., 1994).

Effect of obesity on cancer
Animal studies which suggest an effect of fat in the promotion of cancer can largely be explained by the fact that over feeding had a definite and marked effect on the progression of cancers of the large bowel, breast and probably pancreas. However, a marked energy restriction of approximately 20% is needed to overcome the effect of fat in animal studies. There is no evidence that this level of energy restriction alters cancer risk in humans. Risks of mortality from, or development of, post menopausal breast cancer and cancer of the endometrium are probably increased with increasing obesity, but may be decreased in pre-menopausal breast cancer (Willett et al., 1987). Diets high in energy possibly increase the risk of pancreatic, gallbladder and colon cancer (Pariza, 1987; Zatonski et al., 1992; Giovannucci et al., 1995). High energy intake may increase the risk of prostate cancer, but is, as yet, insufficient (Rohan et al., 1995). Higher body mass and adult weight gain probably increases the risk of breast cancer after menopause (Pike, 1990; Radimer et al., 1993).

Effect of additives, contaminants and residues on cancer
Contamination of foods with chemicals and other substances is the major problem in Pakistan. Chemical residues may be found on vegetables and fruits. Dietary residues of DDT or its metabolites may increase the risk of breast cancer, but more information is needed (Wolff et al., 1995). Aflatoxin contamination of food probably increases the risk of primary liver cancer (Scorsone et al., 1992).

Effect of nitrate and n-nitroso compounds on cancer
Nitrate and nitrite are present naturally in food, the level developing on fertilizer use (both organic and inorganic). The major sources are vegetables, which supply 70-90% of the total and water which supplies 5-20%. Less than 3% of the total is supplied by added nitrate and nitrite used to preserve foods such as ham, bacon and corned beef. Added nitrate is metabolized in the body to nitrite which is also produced in the body by white blood cells in response to infection and inflammation. Under certain conditions, nitrite can combine with nitrogen-containing substances to form N-nitroso compounds, most of which are known to be potent carcinogens. There is however, no consistent epidemiological evidence to suggest that individuals consuming more nitrate or nitrite are at greater risk than those consuming less, rather the reverse. In Britain, mortality from stomach cancer is lowest in areas where exposure to nitrate is highest, for example in East Anglia (Forman et al., 1985).

A case control study on diet and gastric cancer was carried out in Spain, in 1988 and 1989. Cases and controls were selected from 15 hospitals. An increased risk of gastric cancer was observed for high consumption of exogenous nitrosamines. An inverse association with the risk of gastric cancer was seen for high intake of fibre, vitamin C, folate, carotene and nitrates. High consumption of vitamin C seemed to neutralize the increased risk related to simultaneous consumption of nitrosamines. For histologic type, no meaningful differences in the effect of most of the nutrients were found between intestinal and diffuse cancers. The findings are consistent with previously reported results about the protective effect of fruit and vegetables and the increased risk associated with foods that are important sources of nitrites and preformed nitrosamines (Gonzalaz et al., 1994). Ecological evidence supported by experimental data suggests that exogenous dietary N nitrosamine exposure and endogenous N nitrosamine formation possibly increases the risk of oesophageal cancer (Lu et al., 1991).

Effect of food preparation and pattern of eating on cancer
The risk of cancer is also associated with the method of food preparation. Overcooked, barbecued, grilled or fried meat and fish may increase the risk of stomach cancer due to carcinogens produced on the surface of food by direct flame. Nitrites and nitrous compounds formed or added to food during smoking and curing process can be transformed into carcinogens, therefore, such food should be eaten occasionally. Frequent eating possibly increases the risk of colorectal cancer (Verdier and Longnecker, 1992).

Effect of temperature on cancer
Cooking meat at high temperatures possibly increases the risk of colorectal cancer (Robert Thomson et al., 1996) and esophageal cancer (De Stefani et al., 1990). Refrigeration decreases the risk of stomach cancer is convincing (Joossens and Kesteloot, 1996).

Effect of exercise on cancer
Three cohort studies of lung cancer have shown moderately decreased risk with higher levels of physical activity, after taking into account potential confounding by smoking habits, where as one case control study reported a weekly increased risk. Physical activity possibly decreases the risk of lung, colon and postmenopausal breast caner (Thompson, 1992; Brownson et al., 1991 and Simon, 1984).

Effect of smoking on cancer
Smokers are at a higher risk of lung, as well as other cancers and other diseases, against which antioxidants may have a protective effect. Moreover, smokers tend to consume diets relatively low in antioxidants. Smoking is associated with the consumption of diets including relatively fewer vegetables and fruits (McPhillips et al., 1994). For these reasons, it could be argued that smokers should consume relatively high quantities of antioxidant nutrients, in the form of supplements and that the more cigarettes smoked and the longer the duration of the habit, the higher the dose required. There are a number of arguments against any such policy. First, smoking is the overwhelming cause of lung cancer and any protective effect of antioxidants or other dietary factors is certain to be modest by comparison. Second, it would be unfortunate if smokers were encouraged to believe that they might continue their smoking habit safely if they were to take supplements.

Prevention of cancer
Cancer can be prevented if proper eating habits and life style are adopted. Proper storage and preparation of food help in prevention of cancer. Control of additives and insecticidal residues in foods help in reduction of cancer incidence. Methods of preparation of foods also reduce the occurrence of cancer. The World Cancer Research Fund (WCRF) has developed 14 diet and health recommendations for prevention of cancer (WCRF, 1997). These recommendations must be adopted to reduce the chances of incidence of cancer. These recommendations are as under.

Food supply and eating
Choose predominantly plant-based diets rich in a variety of vegetables and fruits, pulses (legumes) and minimally processed starchy staple foods.

Maintaining body weight
Avoid being underweight or overweight and limit weight gain during adulthood to less than 5 kg (11 pounds).

Maintaining physical activity
If occupational activity is low or moderate, take an hour's brisk walk or similar exercise daily and also exercise vigorously for a total of at least one hour in a week.

Vegetables and fruits
Eat 400-800 g (15-30 ounces) or five or more portions a day of a variety of vegetables and fruits, all year round.

Other plant foods
Eat 600-800 g (20-30 ounces) or more than seven portions a day of a variety of cereals (grains), pulses (legumes), roots, tubers. Proper minimally processed foods. Limit consumption of refined sugar.

Alcoholic drinks
Alcohol consumption is not recommended. If consumed at all, limit alcoholic drinks to less than two drinks a day for men and one for women.

If eaten at all, limit intake of red meat to no more than 80 grams (3 ounces) daily. It is preferable to choose fish, poultry or meat from non-domesticated animals in place of red meat.

Total fats and oils
Limit consumption of fatty foods, particularly those of animal origin. Choose modest amounts of appropriate vegetable oils.

Salt and salting
Limit consumption of salted foods and use of cooking and table salt. Use herbs and spices to season foods.

Do not eat food which, as a result of prolonged storage at ambient temperatures, is liable to fungal contamination.

Use refrigeration and other appropriate methods to preserve perishable food as purchased and at home.

Additives and residues
When levels of additives, contaminants and other residues are properly regulated, their presence in food and drink is not known to be harmful. However, unregulated or improper use can be a health hazard and this applies particularly in economically developing countries.

Do not eat charred food. Consume the following only occasionally: meat and fish grilled (broiled) in direct flame; cured and smoked meat.

Dietary supplements
For those who follow the recommendations presented here, dietary supplements are probably unnecessary and possibly unhelpful, for reducing cancer risk.

Nutritional management of cancer patients
Theologides (1987) has beautifully summarized the nutrition management of cancer patients. It is reproduced here with little modification

General principles
Because there usually are some nutritional problems from the time of the original diagnosis of a visceral cancer, the nutritional management should be coordinated with the overall therapeutic plan from the beginning. The specific nutritional recommendation will depend on the nutritional state of the patient, the type of cancer, the anticipated therapy and the prognosis. After the development of cancer, the nutritional needs may be higher than they were when the person was healthy. If a minimum of 30 to 35 kcal/kg with 1.0 g of protein/kg body weight was adequate for a person to maintain weight when afebrile with normal metabolic rate and limited activity, then after the development of cancer he or she may need more calories, protein, vitamins and minerals to maintain a nutrition and energy balance. With progression of the disease and with various therapies, the need for specific nutrients, minerals and vitamins may change.

When curative surgery is anticipated, a short period of nutritional rehabilitation, replenishment of deficiencies and correction of water, electrolyte and acid base imbalances may be advisable. Following curative surgery, the management should be directed toward restoring the patient's nutritional health to the pre-illness level with increased protein and calorie intake, adequate carbohydrates, fat, vitamins and minerals, along with exercise and other physical therapy when needed. Adverse nutritional implications from complications or after effects of surgery should be prevented when possible or managed.

In an effort to maintain their weight, patients receiving radiotherapy should be prevented from resorting to a deficient and imbalanced diet because of anorexia and nausea. After curative radiotherapy, a nutritional rehabilitation, if needed, can be achieved with a gradual increase of food intake of a balanced, easily digestible and absorbable diet.

The major nutritional problems appear in patients with recurrent, un-resectable, radioresistant, or disseminated cancer who are treated with aggressive chemotherapy. If the gastrointestinal tract is functioning properly in the patient with advanced cancer who is receiving chemotherapy, gastrointestinal feeding is preferable to parenteral nutrition. This enteral feeding can be accomplished through oral alimentation or through a nasogastric, esophagogastric, gastric, or jejunal feeding tube.

For oral feeding, the value of common food is modified in texture and consistency, blenderized and liquefied. The importance of frequent small feedings of food high in caloric and nutritional value is emphasized. Because it is digested faster, a diet of low fat content should be implemented. A regimen of nibbling rather than of widely spaced large meals is very important, especially in the presence of early satiety.

For tube feeding, either the common family food, blenderized and liquefied, or commercial preparations can be used. A very thin, pliable nasogastric tube should be inserted; this can be tolerated well, sometimes for weeks. The risk of a properly performed feeding gastrostomy is minimal, while a jejunostomy, although technically more difficult, has the advantage that it obviates the problem of gastric reflux. The percutaneous insertion of a gastric feeding tube is gaining popularity. Because a bolus might cause diarrhea and, occasionally manifestations of a dumping syndrome, the feeding should be given slowly through the tube. For the passage of thicker preparations through a thin tube, a mechanical pump is more dependable than gravity flow to drip feed. In patients receiving hyperosmolar and high protein feedings, the water balance should be evaluated and corrected daily. Without sufficient water, the kidneys may be unable to clear metabolic products, resulting in hyperosmolar loading. If there is no glucose in the urine, a specific gravity higher than 1.02 should alert one to give the patient more water.

After chemotherapeutic control of the cancer, the restoration of wasted tissues is a slow process, but correction of vitamin and mineral deficiencies can often be accomplished rapidly. With reactivation of the disease, a new constellation of nutritional challenges appears and a revised nutritional approach may be needed.

Elemental diets
The commercially available elemental or defined diets contain mixtures of pure amino acids or protein hydrolysate, simple carbohydrates, small quantities of essential fatty acids and other triglyceride, minerals and vitamins. The powder or concentrated forms can be diluted in water, soft drinks, or milk. For patients with lactase deficiency, the formulas containing milk products and milk as a diluents should be avoided. The elemental diets have properties that are potentially useful in the nutritional support of the cancer patient. They can be nutritionally balanced and complete dietary formulations. They have a high nutritional value, relatively flexible composition and complete water solubility. They are easily digestible and readily absorbable. Elemental diets also may have several undesirable effects and potential complications. In most cases these are described on the package by the manufacturer. Fortunately major complications are uncommon.

In the nutritional management of the patient with advanced cancer, the elemental diet can be used either as a sole source of nutritional support or as a nutritional supplement between meals. Because it is bulk-free and is absorbed directly across a relatively short segment of the small intestine, the main indications for its use are malfunction of the gastrointestinal tract, short bowel and intestinal fistulas. Such a diet may protect the patient from losing weight due to mal absorption resulting from radiotherapy or chemotherapy induced enteritis. As a supplement between meals, elemental diets can provide additional calories and nutrients to the anorectic, cachectic cancer patient. Three packages or cans of elemental diet taken between meals may increase caloric intake by at least 900 Kcal/day.

Slow sipping is important to prevent bloating, nausea and hyperosmolar diarrhea. Because of the un-palatability of elemental diets and the flavor fatigue, it is very difficult to convince patients to continue using them for more than a few days. Only the appreciation of their importance in contributing calories and nutrients can assure patients' acceptance and cooperation for longer periods.

When the elemental diet is given as the sole source of total nutritional support, it is very difficult to voluntarily consume the required volume orally. In such cases a small, pliable nasogastric tube should be inserted to secure total control of the caloric and fluid intake. This hypertonic elemental diet should be given through a tube at a constant rate for a 24 hour period rather than intermittent boluses. A pump with a controllable speed for continuous administration is preferable to the unpredictable gravity dripping from a plastic bag reservoir. Because most elemental diets are hyperosmolar, tube feeding should begin with diluted solutions in small volumes per hour, then increase in concentration and volume gradually so as to reach the required caloric and fluid intake in 5 to 6 days. Because there may be some fluid retention during the administration of the elemental diet, occasional monitoring of the patients' fluid and electrolyte balance and urine specific gravity is imperative. Patients on nasogastric tube feeding have a potential risk of aspiration, which should be guarded against. When the reasons and indications for elemental diet alimentation are no longer present, the patient should return gradually to oral feeding with common food.

Total parenteral nutrition
Total parental nutrition (TPN) plays an important role in the nutritional management of selected patients with advanced cancer. It can provide all the nutritional requirements for prolonged periods during and after the administration of effective chemotherapy, which is very toxic to the gastrointestinal tract. The technique involves insertion of a catheter into a central vein (usually subclavian) and infusion of concentrated nutrient preparations in quantities and composition individualized for the patient. With this approach nutrition may be improved and maintained in a malnourished, debilitated cancer patient. This assures a better tolerance of the effective anti neoplastic therapy in certain malignant neoplastic diseases. TPN should not be used merely to prolong survival of patients who are at the end stage of their disease.

The patients selected for TPN should have a cancer that is potentially controllable with surgery or radiotherapy and responsive to available chemotherapy. They should also be unable to meet their nutritional requirements through enteral feeding because they are unable to ingest adequate food or because their gastrointestinal tracts are incapable of adequately digesting and absorbing nutrients. Patients who meet the above criteria and weight 5 kg or more below the ideal body weight and who have a serum albumin concentration of less than 3 g/100 ml are candidates for TPN.

The goal should be to provide adequate nutrition before and during treatment and to maintain and increase the body weight aiming toward a better tolerance of the effective treatment and a faster recovery. It is hoped that with tumor regression and recovery from the adverse effect of chemotherapy and radiotherapy, appetite will return, the gastrointestinal tract will function properly and the weight that was gained will be maintained with oral intake.

TPN usually requires a team of a physician, nurse, pharmacist and dietitian to prepare the nutritional fluids, insert the central catheter, guarantee sterility and supervise safe administration. Close clinical observation and biochemical monitoring are imperative to prevent or correct various metabolic complications that may occur with TPN and meticulous care is needed to keep the incidence of catheter-related infections very low.

A 10% fat emulsion (intra-lipid) given intravenously in a peripheral vein concomitantly with glucose and free amino acid solutions represents another approach to short-term parenteral alimentation. It can be used also in cancer patients who have an inadequate or imbalanced oral food intake to provide essential fatty acids, triglyceride, amino acids, lipids and glucose. This combination of free amino acids, lipids, glucose, electrolytes, other minerals and vitamins is a simple approach to parenteral nutrition through a peripheral vein and it is useful for short term nutritional maintenance. There are potential local and systemic complications: the intra-lipid cannot be mixed with other intravenous (IV) fluids and no electrolyte solutions or drugs can be added to the preparation. Administration of Intralipid and amino acids with sugar should be through a separate IV needle or through a shared needle or catheter with a Y-connector at the needle bulb or catheter end.

It is hoped that with the improved surgical techniques, more aggressive radiotherapy, more effective chemotherapy and prevention and control of complications of the disease and of the treatment, a greater number of patients with cancer may live longer. Maintenance of a good nutritional state may improve the quality of life. In selected patients who are markedly malnourished, cannot maintain adequate protein and calorie intake and have a malignancy that is potentially responsive to aggressive chemotherapy, the parenteral nutrition might make the inference between life and death. For the cancers in which chemotherapy is not very effective, concomitant enteral or parenteral hyper alimentation is of questionable benefit.


1:  Alavanja, M.C., C.C. Brown, C. Swanson and R.C. Brownson, 1993. Sturated fat intake and lung cancer risk among non smoking women in Missouri. JNCI, 85: 1906-1916.
CrossRef  |  Direct Link  |  

2:  Anderson, R.E., J.D. Potter and T.M. Mack, 1996. Pancreatic Cancer. In: Cancrs Epidemiology and Prevention, Schottenfeld, D. and Fraumeni, JF. Jr. (Eds.). Oxford Unitersity Press, New York

3:  Aoki, K., M. Kurihara, N. Hayakawa and S. Suzuki, 1992. Death Rates for Malignants Neoplasms for Selected Sites by Sex and Five Year Age Group in 33 Countires, 1953-57 to 1983-87. University of Nagoya Coop Press, Nagoya

4:  Appel, M.J., G. Roverts and R.A. Woutersen, 1991. Inhibitory effects of micronutrients on pancreatic carcinogenesis in agasexne treatd rats. Carcinogenesis, 12: 2157-2161.
Direct Link  |  

5:  Armstrong, B. and R. Doll, 1975. Environmental factors and cancer incidence and mortality in different countries, with special reference to dietary practices. Int. J. Cancer, 15: 617-631.
CrossRef  |  PubMed  |  Direct Link  |  

6:  Austin, H., 1991. The Role of Tobacco use and Alcohol Consumption. In: The Etiology of Hepatocellular Carcinoma in Etiology, Pathology and Treatment of Hepatocelluar Earcinoma in North America, Tabor, E. (Ed.). Am. Di Bisceglie and RH Purcell Gulf Publishing Co., Houston, TX, pp: 57-75

7:  Badawi, A.F., M.H. Mostafa, A. Probert and P.J. OConnor, 1995. Role of schistosomiasis in human bladder cancer: evidence of association, actiological factors and basic mechanisms of earcinogenesis. Eur. J. Cancer Prev., 4: 45-59.
Direct Link  |  

8:  Black, H.S., J.A. Herd, L.H. Goldberg and J.E. Wolf et al., 1994. Effect of low-fat diet on the incidence of actinic keratosis. N. Engl. J. Med., 330: 1272-1275.
Direct Link  |  

9:  Blot, W.J., 1992. Alcohol and cancer. Cancer Res., 52: 2119-2123.
Direct Link  |  

10:  Boeing, H.F., R. Beyme, M. Berger and V. Berndt et al., 1991. Case control study on stomach cancer in Germany. Int. J. Cancer, 47: 858-864.
PubMed  |  

11:  Boeing, H., W. Jedrychowski, J. Wahrendorf, T. Popiela, B. Tobiasz-Adamezyk and A. Kulig, 1991. Dietary risk factors in intestinal and diffuse types of stomach cancer: a multicenter case control study in Poland. Cancer Causes Control, 2: 227-233.
PubMed  |  

12:  Bostick, R.M., J.D. Potter, L.H. Kushi, T.A. Sellers and K.A. Steinmetz et al., 1994. Sugar, meat and fat intake and non-dietary risk factors for colon cancer incidence in Iowa women (US). Cancer Causes Control, 5: 38-52.
CrossRef  |  

13:  Breslow, N.E. and N. Day, 1980. Statistical Methods in Cancer Epidemiology. International Agency for Research on Cancer, IARC Scientific Publications No. 32. Lyon, France

14:  Brownson, R.B., J.C. Chang, J.R. Davis and C.A. Smith, 1991. Physical activity on the job and lung cancer in missouri. Am. J. Publ. Health, 81: 639-642.
Direct Link  |  

15:  Bruemmer, B., E. White, T.L. Vaughan and C.L. Cheney, 1996. Nutrient intake in relation to bladder cancer among middle aged men and women. Am. J. Epidemiol., 144: 485-495.
Direct Link  |  

16:  Butle, M.A., M. Iwasaki, F.P. Guengerich and F.F. Kadlubar, 1989. Human cyrochrome P-450 PA (P-450IAZ), the phenacetin O. Decthylase, is primarily responsible for the hepatic 3 demethylation of caffeine and N oxidation of carcinogenic arylamines. Proc. Natl. Acad. Soci. USA., 86: 7696-7700.

17:  Chen, J., C. Geissler, B. Parpia, J. Li and T.C. Campbell, 1992. Antioscidant status and cancer mortality in China. Int. J. Epidemiol., 22: 625-635.
Direct Link  |  

18:  Cohen, L.A., M.E. Kendall, E. Zang, C. Meschter and D.P. Rose, 1991. Modulation of N-nitros methylurca induced mannary tumorpromotion bydietary fiber and fat. J. Natl. Cancer Inst., 83: 496-501.

19:  D'Avanzo, B., C. La Vecchia, S. Franceschi, E. Negri, R. Talamini and I. Buttino, 1992. Coffee consumption and bladder caner risk. Eur. J. Cancer, 28: 1480-1484.
Direct Link  |  

20:  De Stefani, E., N. Manoz, J. Esteve, A. Vassallo, C.G. Victora and S. Teuchmann, 1990. Mate drinking, alcohol, tobacco, diet and oesophageal cancer in Uruguay. Cancer Res., 5: 426-431.
PubMed  |  

21:  Dion, P.W., E.B. Bright See, C.C. Smith, R. Furrer and W.R. Bruce, 1982. The effect of dietry ascorbic acid in alpha tocopherol on fecal mutagenicity. Mutat. Res., 102: 27-37.
PubMed  |  

22:  Doll, R. and R. Peto, 1981. The causes of cancer quantitative estimates of avoidable risks of cancer in the United States today. J. Natl. Cancer Inst., 66: 1192-1308.
PubMed  |  

23:  Doll, R., J.F. Jr. Fraumeni, C.S. Muir, 1994. Trends in Cancer Incidence and Mortality Cold. Spring Harbor Laboratory Press, USA

24:  El-Bayoumy, K., P. Updhyaya, D.H. Desai, S. Amin and S.S. Hecht, 1993. Inhibition of 4 (methylnitrosamino) 1-(3-pyridyl) 1- butanon e tumorigenicity in mouse lung by the synthetic organoselenium compound, 1,4-phemylenebis (methylene). Selenocyanate Carcinogenesis, 14: 1111-1113.

25:  Engle, A., J.E. Muscat and R.E. Harris, 1991. Nutritional risk factors and ovarian cancer. Nutr. Cancer, 15: 239-247.
PubMed  |  

26:  Fontham, E., D. Zavala, P. Correa, E. Rodriquez, F. Hunter, W. Haenszel and S.R. Tannenbaum, 1986. Diet and chronic atrophic gastritis: A case control study. J. Natl. Cancer Inst., 76: 621-627.

27:  Franceschi, S., A. Fassina, R. Talamini, A. Mazzolini and S. Vianello et al., 1989. Risk factors for thyorid cancer in northern Italy. Int. J. Eidemiol, 18: 578-584.

28:  Gapstur, S.M., J.D. Potter and A.R. Folsom, 1994. Alcohol consumption and colon and rectal cancer in postmenopausal women. Int. J. Epidemiol., 23: 50-57.
Direct Link  |  

29:  De Gerhardsson, V.M. and M.P. Longnecker, 1992. Eating frequency a neglected risk factor for colon cancer?. Cancer Causes Controls, 3: 77-81.
PubMed  |  

30:  De Gerhardsson, V.M., U. Hagman, R.K. Peters, G. Steineck and E. Overvik, 1991. Meat, cooking methods aid colorectal cancer: a case referent study in stockholm. Int. J. Cancer, 49: 520-525.
PubMed  |  

31:  Giovannucci, E., A. Ascherio, E.B. Rimon, G.A. Colditz, M.J. Stamfer and W.C. Willett, 1995. Physical activity, obesity and risk for colon cancer and adenoma in men. Ann. Int. Med., 122: 327-334.
CrossRef  |  PubMed  |  Direct Link  |  

32:  Giovannucci, E., M.J. Stampfer, G.A. Coldiz, E.B. Rimm and D. Trichopoulos et al., 1993. Folate, methionine, and alcohol intake and risk of colorectal adenoma. J. Natl. Cancer Inst., 85: 875-884.
PubMed  |  

33:  Gonzalez, C.A., E. Riboli, J. Badosa, E. Batiste and T. Cardona et al., 1994. Nutritional factors and gastric cancer in Spain. Am. J. Epidemiol., 139: 466-473.
PubMed  |  

34:  Goodman, M.T., A.M.Y. Nomura, L.N. Kolonel and J.H. Hankin, 1994. Case control study of the effect of diet, body size on the risk of endomaterial cancer. Proceedings of the International Cancer Congress Rao RS, (ICCRRS'94), New Dehli, India: Monduzzi Editore, pp: 2325-2328

35:  Gridley, G., J.K. McLaughlin, G. Block, W.J. Blot, M. Gluch and J.F. Jr. Fraumeni, 1992. Vitamin supplement use and reduced risk of oral and pharyngeal cancer. Am. J. Epidemiol., 135: 1083-1092.
Direct Link  |  

36:  Gridley, G., J.K. McLaughlin, G. Block, W.J. Blot and D.M. Winn et al., 1990. Diet and oral and pyaryngeal cancer among blacks. Nutr. Cancer, 14: 219-225.
Direct Link  |  

37:  Guillem, J.G. and I.B. Weinstein, 1990. Teh Role of Protein Kinase C in Colon Neoplasia in Familial. Alam R Lis, New York, pp: 352-332

38:  Haenszel, W., P. Correa, A. Lopez, C. Cuello and G. Zarama et al., 1985. Serum mironutrients levels in relation to gstric pathology. Int. J. Cancer, 36: 43-48.

39:  Han, J., 1993. Highlights of the cancer chemoprevention studies in china prev. Medicine, 22: 712-722.
PubMed  |  

40:  Hann, H.W.L., M.W. Stahlhut, R. Rubin and W.C. Maddroy, 1992. Antitumer effect of defeoxamine on human hepatocellular carcinoma growing in athymic nude mice cancer. Cancer, 70: 2051-2056.

41:  Hansson, L.E., O. Nyren, R. Bergstrom, A. Wolk, A. Lindgren, J. Baron and H.O. Adami, 1993. Diet and risk of gastric cancer a population based case control study in Sweden. Int. J. Cancer, 55: 181-189.
Direct Link  |  

42:  Harris, R., D. Forman and R. Doll, 1986. Cancer of the cervix uteri and vitamin AB. J. Caner, 53: 653-659.

43:  Hedberg, K., T.L. Vaughan, E. White and D.B. Thomas, 1994. Alcoholism and cancer of the larynx: A case control study in western Washington (United States). Cancer Causes Control, 5: 3-8.

44:  Heilbrun, L.K., A. Nomura and G.N. Stmmermann, 1986. Black tea consumption and cancer risk: A prospective study. Br. J. Cancer, 64: 677-683.
PubMed  |  

45:  Howe, G.R. and J.D. Bruch, 1996. Nutrition and pancreatic cancer. Cancer Cause Control, 7: 69-82.
CrossRef  |  

46:  Howe, G.R., P. Ghadirian, H.B.B. De Mesquita, W.A. Zatonski and P.A. Baghurst et al., 1992. A collaborative case control study of nutrient intake and pancreatic cancer within the SARCH program. Int. J. Cancer, 51: 365-372.
Direct Link  |  

47:  Hu, J., W. Nyren, A. Wolk, R. Bergstrom and J. Yuen et al., 1994. Risk factors for oesophageal cancer in northeast China. Int. J. Cancer, 57: 38-46.
PubMed  |  

48:  Huang, D.P., J.H.C. Ho, D. Saw and T.B. Teoh, 1978. Carcinoma of the Paranasel Regions in Rats Fed Cantonese Salted Fish. In: asophasyngeal Careinoma: Etiology and Control, De, G. and Y. Lto (Eds.). International Agency for Research on Cancer, IARC Science Publication, Lyon, pp: 315-328

49:  IARC, 1988. Monographs on the Evaluation of Carcinogenic Risks to Humans Alcohol Drinking. International Agency for Cancerr Research, Lyon

50:  IARC, 1991. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Human, Coffee, Tea, Mate, Methylxanthines and Methylglyoxa. Vol. 51. International Agency for Reserch on Cancer Lyon

51:  Ingram, D.M., A. Roberts and E.M. Nottage, 1992. Host factors and breast cancer growth characteristics. Eur. J. Cancer, 28: 1153-1161.
PubMed  |  

52:  Isles, C.G., J.H. Hole, C.R. Gillis, V.M. Hawthorne and A.F. Lever, 1990. Plasma cholesterol, CHD and cancer in the renfrew and paisley survey. Br. Med. J., 298: 920-924.
Direct Link  |  

53:  Jacobsen, BK. and D.S. Thelle, 1987. Coffee cholesterol and colon cancer: Is these a link?. Br. Med. J., 294: 4-5.
Direct Link  |  

54:  Jain, M., A.B. Miller and T. To, 1994. Premorbid diet and the prognosis of women with breast cancer. J. Natl. Cancer Inst., 86: 1390-1397.
CrossRef  |  

55:  Kanno, J., H. Onodera, K. Furuta, A. Maekawa, T. Kasuga and Y. Hayashi, 1992. Tumor peonioting effects of both iodne deficiency and iodine excers in the rt thyroid. Toxical Path, 20: 227-235.
CrossRef  |  Direct Link  |  

56:  Kato, I., S. Tomimaga, Y. Ito, S. Kobayashi and Y. Yoshii et al., 1990. A comparitive case control analysisof stomach cancer and atrophic gastricts. Cancer Res., 50: 6559-6564.

57:  Keller, A.Z. and M. Terris, 1965. The association of alcohol and tobacco with cancer of the mouth and pharynx. Am. J. Publ. Hlth., 55: 1578-1585.

58:  Knekt, P., 1988. Serum vtimain E level and risk of female cancers. Int. J. Epidemiol, 17: 281-286.

59:  Knekt, P., R. Jarvinen, R. Seppanen, A. Rissanen and A. Aromaa et al., 1991. Dietary antioxidants and the risk of lung cancer. Am. J. Epidemiol., 134: 471-479.
Direct Link  |  

60:  Kneller, R.W., W.D. Guo, A.W. Hsing, J.S. Chen and W.J. Blot et al., 1992. Risk fctors for stomach cancer in sixtyfive Chinese countries. Cancer Epidemiol Biomalk Prev., 1: 113-118.
Direct Link  |  

61:  Knizhnikov, V.A., V.A. Komleva and N.K. Shandala, 1993. Study of the anticarcinogenic characteristics of the trace element, selenium, sanitary hygienic experiment. Gigiena Sanitariia, 7: 54-57.
Direct Link  |  

62:  Kobayashi, M., M. Kogta and M. Yamamua, 1986. Inhibitory effect of dietary selenium on carcinogenesis in ra glandular stomach induced by N-methyl-N-nitro N-nitrosoguanidine. Cancer Res., 46: 2266-2270.

63:  Kono, S.I., M. Keda, S. Tokudome, M. Nischizume and M. Kuratsune, 1986. Alcohol and mortality: A cohort sutyd of male Japanese Physicians. Int. J. Epidemiol., 15: 527-532.
Direct Link  |  

64:  La Vecchia, C., A. Decarli, M. Fasoli and A. Gentile, 1986. Nutrition, diet in the etiology of endometerial. Cancer, 57: 1248-1253.
PubMed  |  

65:  Levi, F., S. Franceschi, E. Negri and C. La Vecchia, 1993. Dietary factors, the risk of endometrial. Cancer, 71: 3575-3581.
Direct Link  |  

66:  Lointier, R., M.J. Wargovich and S. Saez, 1987. The role of vitamin D3 in the proliferation of a human colon cancer cell line in vitro, Anticancer Res., 7: 817-822.
Direct Link  |  

67:  Longnecker, M.P., 1994. Alcoholic beverage consumption in relation to risk of breast cancer: meta analysis and review cancer. Causes Cancer Control, 5: 73-82.
PubMed  |  

68:  Longnecker, M.P., J.M. Martin, P. Moreno, A.M.Y. Knekt and S.E. Nomura et al., 1992. Serum alpha tocopherol concontration in relation to subsequent colorectal cancer: Pooled data from five cohorts. JNCI, 84: 430-453.

69:  Lopez-Carrillo, L., M. Hernandez-Avila and R. Dubrow, 1994. Chili pepper consumption and gastric cancer in Mexico: a case-control study. Am. J. Epidemiol., 139: 263-271.

70:  Lowenfels, A.B., P. Maisonneuve and G. Cavallni, 1993. Pancreatitis and the risk of pancreatic cancer. N. Engl. J. Med., 328: 1433-1437.

71:  Lu, S.H., S.Z. Chui, W.X. Yang, X.N. Hu, L.P. Guo and F.M. Li, 1991. Relevance of nitrosamines to oesophageal cancer in China. IARC Sci., 105: 11-17.

72:  Luceri, C., G. Caderni, L. Lancioni, S. Aiolli and P. Dolara et al., 1996. Effects of repated boluses of sucxose on proliferation. Nutr. Cancer, 25: 187-196.
PubMed  |  

73:  Ma, Q., M. Hoper, I. Halliday and B.J. Rowlands, 1996. Diet and experimental colorectal cancer. Nutr. Res., 16: 413-426.
CrossRef  |  

74:  Maclure, M. and W. Willett, 1990. A case control study of diet and risk of renal ademocarcinoma. Epidemiology, 1: 430-440.

75:  Mayne, S.T., D.T. Janerich and P. Greenwald, 1994. Dietary Beta carotene and lung cancer risk in US nonsmokders. JNCI, 86: 33-38.

76:  McMicheal, A.J., O.M. Jensen, D.M. Karkin and D.G. Zardize, 1984. Dietary and endogenous cholesterol and human cancer. Epidemiol. Rev., 6: 192-216.

77:  McPhillips, J.B., C.G. Eaton, K.M. Gans, C.A. Derby, T.M. Lasater, J.L. McKenney and R.A. Garleton, 1994. Dietary differences in smokers and nonsmokers from two southeastern New England Communities. J. Am. Diet Assoc., 94: 287-292.

78:  Mobarhan, S., 1994. Micronutrient supplementation trials and the reduction of cancer and cerebrovascular incidence and mortality. Nutr. Rev., 52: 102-105.

79:  Moon, R.C. and R.G. Mehta, 1986. Anticarcinogenic effecs of retinoids in animals. Adv. Exp. Med. Biol., 206: 339-411.

80:  Mori, M., I. Harabuchi, H. Miyake, J.T. Casagr, B.E. Henderson and R.K. Ross, 1988. Reproductive, genetic and dietary risk factors for ovarian cancer Am. J. Epidemiol., 128: 771-777.
Direct Link  |  

81:  Naseer, F., F. Ahmad, S. Zai and A.K. Afridi, 1992. Incidence of breast cancer in the North Western Region of Pakistan. J. Med. Sci., 2: 11-12.

82:  NRC, 1982. Diet Nutrition and Cancer. National Academic Press, Washington DC.

83:  Nelson, R.L., F.G. Davis, E. Sutter, L.H. Sobin, J.W. Kikenhall and P. Bowen, 1994. Body iron stores and risk of colonic neoplasia. J. Nat. Cancer Insti., 86: 455-460.
PubMed  |  

84:  Olsen, J., O. Kronborg, J. Lynggaard and M. Ewertz, 1994. Dietary risk factors for cancer and adenomas of the large intestine: A case-control study within a screening trial in Denmark. Eur. J. Cancer, 30: 53-60.
PubMed  |  

85:  Pariza, M.W., 1987. Dietary fat, calorie restriction, ad libitum feeding and cancer risk. Nutr. Rev., 45: 1-7.

86:  Parkin, D.M., C.S. Muir, S.L. Whelan, Y.T. Gao, J. Ferlay and J. Powell, 1992. Cancer Incidence in Five Fontinents. VI IARC Science Publicaton No. 120, Lyon

87:  Parkin, D.M., P. Pisani and J. Ferlay, 1993. Estimates of the worldwide incidence of eighteen major cancers in 1985. Int. J. Cancer, 54: 594-606.
PubMed  |  Direct Link  |  

88:  Pike, M.C., 1990. Reducing cancer risk in women through life style mediated changes in hasmone levels cancer. Detect. Prev., 14: 595-607.

89:  Potter, J.D., A.J. McMicheal and J.M. Hartshorne, 1982. Alcohol and beer consumption in relation to cancers of bowel and lung: an extended correlation analysis. J. Chronic Dis., 35: 833-842.
PubMed  |  

90:  Radimer, K., V. Siskind, C. Bain and F. Schofield, 1993. Relation between anthropometric indicators and risk of breast cancer among Austrialian women. Am. J Epidemiol., 138: 77-89.
Direct Link  |  

91:  Ramaswamy, G., V.R. Rao, S.V. Kumaraswany and N. Anatha, 1996. Serum vitamins status in oral leucoplakias a preliminary study oral oncol. Eur. J. Cancer, 32: 120-122.
CrossRef  |  

92:  Ramon, J.M., L. Serra, C. Cerdo and J. Oromi, 1993. Dietary factors and fastric cancer risk: A case control study in Spain. Cancer, 71: 1731-1735.
PubMed  |  

93:  Ramon, J.M., L. Serra, C. Cerdo and J. Oromi, 1993. Nutrient intake and gastric cancer risk: A case control study in Spain Int. Epidemiol., 22: 983-988.
Direct Link  |  

94:  Rohan, T.E., G.R. Howe, J.D. Burch and M. Jain, 1995. Dietary factors and risk of prostate cancer: A case control study in Ontario Canada. Cancr Causes Control, 6: 145-154.
PubMed  |  

95:  Rose, D.P., A.P. Boyar and E.L. Wynder, 1986. International comparison of mortality rates for cancer of breast, ovary, prostate and colon and per capita food consumption. Cancer, 58: 2263-2271.
PubMed  |  

96:  Rose, D.P., R. Rayburn, M.A. Hatala and J.M. Connoly, 1994. Effects of dietary fish oil on fatty acids and eicosanoids in metastasizing human breast cancer cells. Nutr. Cancer, 22: 131-141.
PubMed  |  

97:  Schrauzer, G.N., D.A. White and C.J. Schneider, 1977. Cancer mortality correlation studies-III: Statistical association with dietary selenium intakes. Bioinorg Chem., 7: 23-31.

98:  Scorsone, K.A., Y.Z. Zhou, J.S. Butel and B.L. Slagle, 1992. p 53 mutations cluster at codon 249 in hepatitis-B virus positive hepatocellular carcinmas from China. Cancer Res., 52: 1635-1638.
Direct Link  |  

99:  Sherman, B., R. Wallace, J. Bean and L. Schlabaugh, 1981. Relationship of body weight to menacheal and menopausal age: iimplecations for breast cancer risk. Clin Endocional Metab., 52: 488-493.
PubMed  |  

100:  Silverman, D.T., P. Hartge, A.S. Morrison and S.S. Devesa, 1992. Epidemiology of bladder cancer. Hematol. Onool. Clin. North Am., 6: 1-30.

101:  Simon, H.B., 1984. The immunology of exercise, A bief review. JAMA, 252: 2735-2738.

102:  Singh, V.N. and S.K. Gaby, 1991. Premalignant lesions: Role of antioxidant vitamins and beta-carotene in risk reduction and prevention of malignant transformation. Am. J. Clin. Nutr., 53: 386S-390S.

103:  Sivam, GP., J.W. Lampe, B. Ulness, S.R. Swanzy and J.D. Potter, 1997. Helicobacter pylori in vitrosusceptibility to galic (Allium sativum) extract. Nutr. Cancer, 27: 118-121.

104:  Snowdon, D.A., 1985. Diet and ovarian cancer. J. Am. Med. Assoc., 254: 356-357.

105:  Steinmetz, K.A., J.D. Potter and A.R. Folsom, 1993. Vegetables, fruit and lung cancer in the lowa Wommen's Health study. Cancer Res., 53: 536-543.

106:  Tavani, A., E. Negri, S. Francheschi and C. La Cecchia, 1994. Risk fectors for oesophageal cancer in life long nonsmokers. Cancer Epidemiol. Biomarkers Prevention, 3: 387-392.
Direct Link  |  

107:  Theologides, A., 1987. Nutrition in Cancer. In: Quick Reference to Clinical Nutrition, Seymour, L. (Ed.). J.B. Lippincott Company, Philadelphia, pp: 290-294

108:  Thomas, B., 1994. Cancer: Diet and Causation. In: Manual of Dietetic Practice, Thomas, B. (Ed.). 2nd Edn., Blackwell Science, UK, pp: 585-589

109:  Thompson, H.J., 1992. Effect of treadmill exercise intensity on hepatic glutathione content and its relevance to mannary tumorig nesis. J. Sports Med. Phys. Fitness, 32: 59-63.
PubMed  |  

110:  Thurnham, D.I., S.F. Zheng, N. Munoz, M. Crespi and A. Grassi, 1985. Comparison of riboflavin, vitamin A and zinc status in high and low risk regions for oesophageal cancer in China. Nutr. Cancer, 7: 131-143.

111:  Tonilo, P., E. Riboli, R.E. Shore and B.S. Pasternack, 1994. Consumption of meat, animal products, protein and fat and risk of breast cancer: A prespective cohort study in New York. Epidemiology, 5: 391-397.
PubMed  |  

112:  Van Eenwhk, J., F. Daivs and N. Colman, 1992. Folate, Vitamin C and cervical intracpithelial neoplasia. Cancer Epidemiol. Biomakers Prev., 1: 119-124.
Direct Link  |  

113:  Vaughan, T.L., S. Dais, A. Kristal and D.B. Thomas, 1995. Obesity, alcohol and tobacco as risk factors for cancer of the oesophagus and gastric cardia: Adenocarcinoma versces squiamous ell carcinoma. Cancer Epidemiol. Biomarkers Prev., 4: 85-92.
Direct Link  |  

114:  Vena, JE., S. Graham, J. Freudenheim, J. Marshall, M. Zielezny, M. Swanson and G. Sufrin, 1992. Diet in the epidemiology of bladder cancer in western New York. Nutr. Cancr, 18: 255-264.
PubMed  |  Direct Link  |  

115:  Wakabayashi, K., M. Nagao, H. Esumi and T. Sugimura, 1992. Food derived mutageus and careinogens. Cancer Res., 52: 2092S-2098S.
Direct Link  |  

116:  WCRF, 1994. World Cancer Research Diet and Cancers a Review of the Literature on Genetic Cellular and Physiological Mechanisms. WCRF, London

117:  Welff, M.S. and P.G. Toniolo, 1995. Environmental organochloine exposure as a potential etiologic factor in breast cancer. Environ. Health, 7: 141-145.
Direct Link  |  

118:  Welsch, C.W., 1994. Interrelationship between dietary liids and calories and experimental mammary gland tumorigenesis. Cancer, 74: 1055-1062.
CrossRef  |  Direct Link  |  

119:  WHO, 1997. World Health Organization the World Health Report Geneva WHO, London

120:  Wigren, G., T. Hatschek and O. Axelson, 1993. Determinants of papillary cancer of the thyroid. Am. J. Epidemiol., 138: 482-491.
Direct Link  |  

121:  Willet, W.C., J. Meir, M.D. Stampfer and A. Graham, 1987. Dietary fat and the risk of breast cancer. N. Eng. J. Med., 316: 22-28.
PubMed  |  Direct Link  |  

122:  Yamada, Y., R.O. Weller, P. Kleihues and B.I. Ludeke, 1992. Effects of ethanol and vaious alcoholic beverages on the formation of O6 methyl deoxyguanne from concurrently administered N. Nitrosomethylbenzylamine in rats: A dose response study. Carcinogenesis, 13: 1171-1175.
Direct Link  |  

123:  Yamane, T., T. Takahashi, K. Kuwata, K.M. Oya and Inagake et al., 1995. Inhibition of N-methyl N.Nitro N.Nitros-oguanidine induced carcinogensis by (-) epigallocatechin gallate in the rt glandular stomach. Cancer Res., 55: 2081-2084.
Direct Link  |  

124:  Zaridze, D., V. Filipchenko, V. Kustov, V. Serdyuk and S. Duffy, 1993. Deit and colorectal cancer: Results of two case control studies in Russia. Eur. J. Cancer, 29A: 112-115.
PubMed  |  

125:  Zatonski, W.A., C. La Vecchia, K. Przewozniak, P. Maisonneuve, A.B. Lowenfels and P. Boyle, 1992. Risk factors for gallbladder cancer: A Polish case control study. Int. J. Cancer, 51: 707-711.
PubMed  |  

126:  Zhand, L., W.J. Blot, W.C. Yoer, Y.S. Chang and X.Q. Liu et al., 1994. Serum micronutrients in relation to precancerous gstric lesions. Int. J. Cancer, 56: 650-654.
PubMed  |  

127:  Zheng, W., W.J. Blot and X.V. Shu, 1992. 1083-1092 Risk factors for oral and pharyngeal cancer in shanghai with emphasis on diet cancer. Epidemiol. Biomarkers Prov., 1: 441-448.

128:  Zheng, W., J.K. McLaughlin, G. Gridley, E. Bjelke and L.M. Schuman et al., 1993. A cohort study of smoking, alcohol and dietary factors for pancreatic cancer (US). Cancer Causes Control, 4: 477-482.
PubMed  |  

129:  Zheng, W., W.J. Blot and X.O. Shu, Y.T. Gao and B.T. Ji et al., 1992. Diet and other risk fectors for laryngeal cancer in Shanghai, China. Am. J. Epidemiol., 136: 178-191.
PubMed  |  

130:  Zierler, S., R.A. Danley and L. Feingold, 1986. Type of disinfectant in drinking watr and patterns of mortality in Mosaachusetts. Environ. Health Perspect, 69: 275-279.
Direct Link  |  

131:  Joossens, J.V. and H. Kesteloot, 1996. Nutriton in relation to stomach cancer and stroke mortality in press. Int. J. Epidemiol. 25: 494-504.

132:  Salam, A., G. Mustafa and A. Ali, 1992. A Survey of Malignant Tumors in D.I. Khan Division. Khyber Medical College, Peshawar

©  2021 Science Alert. All Rights Reserved