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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cancer is diagnosed in about 70 000 Canadians each year and is the leading cause of the loss of potential years of life before age 75 among women. Life-threatening forms of cancer will develop in at least one of every three Canadian newborns during their lifetimes if current cancer risks are not reduced. Lung and breast cancers are, respectively, the leading causes of premature death due to cancer among men and women. Compared with other countries Canada has low death rates for stomach cancer but high rates for certain smoking-related cancers (those of the lung and of the mouth and throat), leukemia and cancers of the colon, breast and lymphatic tissues. Newfoundland has the highest rates of death from stomach cancer and the lowest rates of death from prostatic cancer, whereas the western provinces have the opposite pattern. The rates of death from lung cancer among men are highest in Quebec, the province with the highest prevalence of smoking. In Canada the overall rates of death from cancer increased by 32% among men from 1951 to 1983. However, among women they declined by 12% from 1951 to 1976 and increased from 1976 to 1983, particularly among those aged 55 to 74. The rising rates of death due to lung cancer were primarily responsible for these increases. Lung cancer will likely displace breast cancer as the leading cancer killer of Canadian women by 1990. Given the relatively low survival rates for cancers caused by smoking and the lack of substantial improvement in rates for the most frequent types of cancer, preventive strategies that include effective measures to reduce tobacco consumption are urgently required.
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PMID:Cancer patterns in Canada. 394 29

The risk of developing a second primary cancer was evaluated in approximately 19,000 persons with initial cancers of the lymphatic and hematopoietic system in Connecticut between 1935 and 1982. Significant excesses for all second cancers were observed among patients with leukemia (34%), Hodgkin's disease (70%), non-Hodgkin's lymphoma (25%), and multiple myeloma (24%). In general, the risk of second cancers was greater in males than in females, even for cohorts not showing an excess of surveillance-related prostate cancer. Among patients with leukemia, significant excesses of cancers of the lung, kidney/ureter, and prostate were noted; cutaneous melanoma was elevated only in males. These excesses did not persist in the small number of long-term survivors. Possible etiologic factors included tobacco smoking for lung and kidney cancers, medical surveillance artifact for prostate cancer, and immunosuppression for malignant melanoma and lung cancer. The large number and good prognoses of patients with chronic lymphocytic leukemia strongly influenced the pattern of second cancers when all leukemias were analyzed together; no evidence was found for an increased risk of second cancer in patients with acute lymphocytic leukemia. A disproportionate number of subsequent cancers, particularly those of the kidney and ureter, were diagnosed incidentally at autopsy. Patients with Hodgkin's disease displayed significant excesses of cancers of the buccal cavity and pharynx, lung, female breast, and thyroid. The latter 3 sites remained significantly elevated in long-term survivors (10 yr or more postdiagnosis), so that radiation therapy may have contributed to their development. Among persons with non-Hodgkin's lymphoma, cancers of the stomach, lung, brain, and connective tissue occurred excessively. The first 3 sites, plus cancers of the urinary bladder, remained elevated among long-term survivors. The brain cancer excess, not previously reported, may represent misclassification of central nervous system lymphoma. The risk of gastric cancer is reminiscent of similar findings in patients with both acquired and genetically determined immunodeficiency disorders. The alkylating agent, cyclophosphamide, used extensively in the treatment of non-Hodgkin's lymphoma, is known to cause bladder cancer in man.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Second cancer following lymphatic and hematopoietic cancers in Connecticut, 1935-82. 408 98

The risk of second primary cancer was evaluated in 29,128 patients who developed tumors of the urinary tract, including benign and malignant tumors of the renal pelvis and ureter and bladder papillomas in Denmark between 1943 and 1980. Among 9,162 persons with kidney cancer, 416 developed a second primary tumor [relative risk (RR) = 1.4]. Among 19,966 persons with bladder cancer, 1,423 developed a second primary tumor against 1,239 expected (RR = 1.1). The risk of bladder cancer was increased following kidney cancer in both men (RR = 6.3) and women (RR = 10.1), and kidney cancer was increased in both men (RR = 2.9) and women (RR = 4.5) following bladder cancer. These risks were particularly pronounced for cancers occurring in the ureter and renal pelvis. Etiologic similarities are likely explanations for these observations, which also emphasize the role of host factors and the multifocal nature of urothelial tumors. A decrease in relative risks since diagnosis of the first primary cancer was seen that may partly be attributed to a lessening of the intensity of medical surveillance with time. Among long-term survivors with kidney cancer, increased risks were observed for colon and pancreatic cancers, which may be related to treatment; approximately 25% received radiotherapy. Among bladder cancer patients, increased risks of cancers of the lung and larynx occurred, probably due to tobacco smoking. A slight elevation of prostate cancer (RR = 1.3) may be attributable to medical surveillance. Unexpected findings were the significant deficits of cancers of the stomach and rectum among patients with bladder cancer and stomach cancer among those with kidney cancer.
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PMID:Second cancer following cancer of the urinary system in Denmark, 1943-80. 408 9

The risk of developing a second primary cancer was evaluated in approximately 64,000 persons diagnosed with cancer of the digestive system in Connecticut during 1935-82. Significant excesses of all second cancers combined were observed following cancer of the esophagus (58 observed vs. 33 expected), small intestine (41 vs. 24), and colon (2,268 vs. 1,714). A slight excess of multiple primaries was observed following cancer of the liver and biliary tract (47 vs. 40). The observed number of second cancers was nearly equal to the expected number for persons initially diagnosed with cancers of the stomach (251 vs. 258), rectum (952 vs. 941), and pancreas (40 vs. 40). Persons with initial cancers of the small intestine, colon, and rectum also had excess second cancers arising primarily in the colon, which suggested the influence of common etiologic factors or possibly misclassified metastases in some. Shared dietary, socioeconomic, or hormonal factors may explain the excess of uterine and ovarian cancers among patients with colon cancer and the excess of breast cancer among patients with colon and rectal cancers. Oral and respiratory cancers occurred more frequently than expected in persons with an initial esophageal cancer, which is likely due to common risk factors of cigarette smoking or alcohol intake, or both. The elevations in cancer of the prostate among males with cancers of the esophagus, small intestine, colon, rectum, liver/biliary, and pancreas are probably artifacts associated with increased medical surveillance of cancer patients. The prostate cancer excesses were limited to the first year after diagnosis of the initial cancer or decreased over time for all but cancer of the colon and small intestines. Increased medical surveillance may also contribute to the excess renal and bladder cancers seen within 5 years of diagnosis of stomach cancer. Excesses were also seen for second pancreatic cancer among small intestine and liver/biliary cancer patients and second kidney and brain cancers among those with colon cancer. The deficits of stomach and rectal cancer among persons initially diagnosed with the same tumors, respectively, were anticipated because surgical removal of the organ is the primary form of treatment. Patients with rectal cancer also had deficits of stomach and pancreatic cancers. Future research should clarify the role of diet, alcohol, metabolic and endocrine factors, and host susceptibility on the risk of second neoplasms following cancer of the digestive system.
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PMID:Second cancer following cancer of the digestive system in Connecticut, 1935-82. 408 13

There has been a general increase in the incidence of cancer of most major sites during the period 1960-69; this is true even when allowances are made for shifts in the age composition of the population. Improvements in diagnostic procedures may account for some of these increases but it is doubtful that they are solely responsible for the greater incidence recorded.A few sites stand out as being primarily responsible for the increase in the overall cancer incidence. Lung cancer is increasing in both males and females; the rate of increase, however, is much greater among females. It is generally acknowledged that women began smoking cigarettes at a later point in time and to a lesser extent. The pattern which has emerged indicates that females are experiencing a similar trend in lung cancer incidence to that of males. The increase in the incidence of female breast cancer is also noteworthy, although the forces producing this change can only be speculated upon. The high incidence of prostatic cancer among negroes and the increase in the incidence of prostatic cancer in whites are subjects which deserve further investigation, especially since the Alameda County experience is not duplicated in data from the Connecticut Tumour Registry. One of the most encouraging findings is that the incidence of stomach cancer appears to be declining.
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PMID:Cancer patterns in Alameda County, California. 464 98

Primary liver cancer incidence data from 30 populations reported in Cancer Incidence in Five Continents were analyzed. After adjustment for time trends, log incidence increases linearly with log age. Liver cancer risk increases more rapidly with age than that of colon cancer, stomach cancer, or lung cancer in non-smokers; it increases less rapidly than that of prostatic cancer or of lung cancer in smokers. Over the past 20 years, most populations have been found to have increasing age-adjusted liver cancer incidence. There is no correlation between change in rates and magnitude of rates. Male rates are higher than female rates and the ratio of the two tends to be higher in high-risk areas.
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PMID:Age and cohort effects in primary liver cancer. 632 24

The majority of human cancers have multifactorial environmental causes stemming mainly from lifestyle factors such as use of tobacco products through cigarette smoking, snuff dipping, or chewing, and specific nutritional elements and dietary practices. The mechanisms of these lifestyle factors can be analyzed in terms of specific genotoxic carcinogens, and of epigenetic agents or promoting factors. Tobacco and tobacco smoke contain not only genotoxic carcinogens but also, with a more important ultimate effect, cocarcinogens and promoters. Alcohol acts as a cocarcinogen with tobacco, possibly by modifying the metabolism of carcinogens in select organs. Genotoxic carcinogens as nutritional factors may be found in pickled, salted, and smoked foods and may be responsible for gastric cancer. Vitamins C and E and other antioxidants are effective inhibitors. Other types of genotoxic carcinogens are mutagenic chemicals found in broiled and fried foods, and these may be involved in cancer of the colon, breast, and prostate. Promoting effects derive from a high level of dietary fat, which has been linked epidemiologically and through laboratory studies to a higher risk for these cancers. Possible mechanisms by which fat exerts its effects are an increased concentration of bile acids in the stool, as related to colon cancer, and which may be countered by a high cereal fiber diet, to increase stool bulk. In relation to breast or prostate cancer, fat may exert its effect on complex hormonal balances, and also on membrane composition. These promoting effects, whether associated with tobacco smoke or nutrition, are highly dose-dependent, and provided the insult is not too far advanced, reversible. Thus, lowering the dosage, or eliminating the effect as in smoking cessation should have an appreciable effect in reducing overt disease development, and do so fairly promptly. This may apply also to a reduction of second disease in cases where a first occurrence has been successfully treated by conventional means.
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PMID:The role of genotoxic carcinogens and of promoters in carcinogenesis and in human cancer causation. 638 22

Clinical results of intraoperative radiotherapy (IOR) in carcinoma of the stomach and prostate, and malignant soft tissue tumors are reported. The 5-year survival rate was found to be increased by IOR in stages II-IV gastric cancer. From the analysis of the clinical results of prostatic cancer, a single dose of 3,500 rad was considered to be a potential curative dose for the tumor less than 3 cm in diameter. The local recurrence rate of patients with malignant soft tissue tumors who received a single dose ranging from 3,000 to 4,500 rad was 5.9 and the 5-year survival rate was 64.6%.
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PMID:[Intraoperative radiotherapy for locally advanced refractory cancer]. 641 Jan 5

In a nine-year follow-up of a southern California community of 2,852 men and women aged 60-79 years, systolic blood pressure was a significant predictor of subsequent cancer mortality in men. This effect was independent of age, antihypertensive medication, smoking, obesity, and plasma cholesterol. Trends in women were similar but not statistically significant. Compared with those still alive, higher initial systolic blood pressure levels were apparent in those who died of colon cancer, stomach cancer, and all other cancers combined except for lung and prostate cancer. Possible mechanisms for this association and the implications of the data with regard to the benefits of measures to treat high blood pressure or lower population distribution of blood pressure are discussed.
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PMID:Systolic blood pressure and cancer mortality in an elderly population. 647 25

Some evidence suggests that solvent exposures to rubber industry workers may be associated with excess cancer mortality, but most studies of rubber workers lack information about specific chemical exposures. In one large rubber and tire-manufacturing plant, however, historical documents allowed a classification of jobs based on potential exposures to all solvents that were authorized for use in the plant. A case-control analysis of a 6678 member cohort compared the solvent exposure histories of a 20% age-stratified random sample of the cohort with those of cohort members who died during 1964-1973 from stomach cancer, respiratory system cancer, prostate cancer, lymphosarcoma, or lymphatic leukemia. Of these cancers, only lymphosarcoma and lymphatic leukemia showed significant positive associations with any of the potential solvent exposures. Lymphatic leukemia was especially strongly related to carbon tetrachloride (OR = 15.3, p less than .0001) and carbon disulfide (OR = 8.9, p = .0003). Lymphosarcoma showed similar, but weaker, associations with these two solvents. Benzene, a suspected carcinogen, was not significantly associated with any of the cancers.
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PMID:Cancer mortality and solvent exposures in the rubber industry. 654 4


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