Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
 ...
PMID:Second cancer following cancer of the digestive system in Connecticut, 1935-82. 408 13

The risk of a person developing a second primary cancer was evaluated in approximately 30,000 persons who developed cancer of the respiratory system in Connecticut between 1935 and 1982. A significant 44% excess of all second cancers was observed following cancer of the lung (614 observed vs. 426 expected). The excess of second tumors was 72% following cancer of the larynx (541 vs. 314) and 34% following cancer of the nasal cavities and sinuses (43 vs. 32). For cancers of the lung and larynx, second cancers arose mainly along the respiratory tract or other sites associated with cigarette smoking (oral cavity, bladder, kidney). A threefold excess of esophageal cancer followed cancer of the larynx, which was indicative of risk factors in common (alcohol and tobacco) and possibly an effect of radiotherapy. Radiotherapy may have contributed also to the increased risk of second lung and breast cancers. A slight excess risk of leukemia after lung cancer points to a possible effect of chemotherapy given for certain histologic types. An unexpected finding was a significant 50% increased risk of colon cancer following cancer of the larynx. Significant excesses of prostate cancer are probably artifacts associated with increased medical surveillance and higher autopsy rates among cancer patients than in the general population. No deficits of any second cancers were observed. The risk of a second cancer developing did not appear to vary by sex or time since initial diagnosis, except that the risks following cancer of the nasal cavities and sinuses returned to normal levels among long-term survivors. Among persons observed for 10 or more years after their initial diagnosis of cancers of the lung or larynx, the risk of developing a second cancer remained high, i.e., on the order of 50% above expectation. Further analytic studies should clarify the role of smoking, alcohol, other life-style and host factors, and various forms of therapy on the risk of second cancers following cancer of the respiratory system.
 ...
PMID:Second cancer following cancer of the respiratory system in Connecticut, 1935-1982. 408 14

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.
 ...
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.
 ...
PMID:The role of genotoxic carcinogens and of promoters in carcinogenesis and in human cancer causation. 638 22

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.
 ...
PMID:Systolic blood pressure and cancer mortality in an elderly population. 647 25

A case-control study was conducted to investigate possible relationships between employment in the textile industry and cancers of the prostate and colon. Death certificate information on occupation and industry was obtained for 1037 male prostatic cancer cases, 820 male and female colon cases, and matched controls who died during 1970-1978 in South Carolina. Black males were the only race-sex group to show an excess risk of prostate or colon cancer among employees of the textile industry. Nonstatistically significant excesses of prostate cancer were seen in dyeing and finishing businesses and broad woven fabric mills. Overall, there was no strong evidence indicating a relationship between the textile industry and either prostate or colon cancer. It is unlikely that limitations of the data masked real risks since previously reported associations with nontextile industries were confirmed.
 ...
PMID:Death certificate case-control study of cancers of the prostate and colon and employment in the textile industry. 649 44

The incidence of gastrointestinal cancers differ greatly internationally. Blacks have higher rates than whites for esophagus, stomach, liver, and pancreatic cancer in the U.S. Differences also occur between other racial groups. Studies on migrants suggest environmental causes for these differences. Stomach cancer rates have fallen, intestine cancer is stable, pancreatic cancer rates rose, but are now falling in males. The incidence of colon, rectal, breast, corpus-uterus, ovary, and prostate cancer are positively correlated, but colon or rectal and stomach cancer are negatively correlated. Colon and rectal cancer mortality are positively and stomach cancer negatively associated with social class. Esophageal, liver, colon, and pancreatic cancer in males are higher in urban areas. Seventh Day Adventists and Mormons show a low risk of colon cancer. Internationally intake of fat is correlated with colon, rectal, and pancreatic cancer, and starch with stomach cancer.
 ...
PMID:Risk factors from geographic epidemiology for gastrointestinal cancer. 713 47

Average daily intakes of several components of fat in the diets of the five main ethnic groups in Hawaii were determined from personal interviews of 4137 subjects regarding their food consumption in a usual week. In general, fat intake was highest among Caucasians and lowest among Filipinos. Cholesterol intake did not follow the same pattern as that of the other fat components. The intake of total fat showed good correlation with the ethnic-specific incidence rates of breast cancer in Hawaii but not with colon or prostate cancer rates. There was no correlation of cholesterol intake with colon cancer incidence.
 ...
PMID:Dietary fat intake and cancer incidence among five ethnic groups in Hawaii. 726 Sep 32

The tumor suppressor gene CDKN2/p16/MTS1, located on chromosome 9p21, is frequently inactivated in many human cancers through homozygous deletion. Recently, we have reported another pathway of inactivation that involves loss of transcription associated with de novo methylation of a 5' CpG island of CDKN2/p16 in lung cancers, gliomas, and head and neck squamous cell carcinomas. We now show that this aberrant CpG island methylation also occurs frequently in cell lines of breast cancer (33%), prostate cancer (60%), renal cancer (23%), and colon cancer (92%) and is associated with loss of transcription. Primary tumors of the breast (31%) and colon (40%) also displayed de novo methylation of this CpG island. This alteration of p16 in colon cancer was particularly striking, since inactivation does not occur through homozygous deletion in this tumor type. Our data show that in tumors, de novo methylation of the 5' CpG island is a frequent mode of inactivation of CDKN2/p16 and also firmly demonstrate that CDKN2/p16 is one of the most frequently altered genes in human neoplasia.
 ...
PMID:Inactivation of the CDKN2/p16/MTS1 gene is frequently associated with aberrant DNA methylation in all common human cancers. 755 21

PSK, a protein-bound polysaccharide obtained from cultured mycelia of Coriolus versicolor in basidiomycetes, is a biological response modifier, diverse operations of which include an antitumor action. We have previously reviewed recent research which had demonstrated that in animals, PSK has a preventive effect on chemical carcinogen-induced, radiation-induced, and spontaneously developed carcinogenesis (Kobayashi et al., Cancer Epidemiol., Biomarkers & Prev., 2: 271-276, 1993). We now focus on the effects of PSK once the progression of carcinogenesis has begun, and review what is now known of the preventive action of PSK on cancer metastasis. Recent research reports that PSK suppresses pulmonary metastasis of methylcholanthrene-induced sarcomas, human prostate cancer DU145M, and lymphatic metastasis of mouse leukemia P388, and that it has prolonged the survival period in spontaneous metastasis models. PSK also suppresses the metastasis of rat hepatoma AH60C, mouse colon cancer colon 26, and mouse leukemia RL male 1 in artificial metastasis models. PSK influences the steps of cancer metastasis in a number of ways: (a) by suppression of intravasation through the inhibition of tumor invasion, adhesion and production of cell matrix-degrading enzymes; (b) by suppression of tumor cell attachment to endothelial cells through the inhibition of tumor cell-induced platelet aggregation; (c) by suppression of tumor cell migration after extravasation through the inhibition of tumor cell motility; and (d) by suppression of tumor growth after extravasation through the inhibition of angiogenesis, the modulation of cytokine production, and the augmentation of effector cell functions. In addition, PSK has suppressed the malignant progression of mouse tumor cells through superoxide trapping.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Antimetastatic effects of PSK (Krestin), a protein-bound polysaccharide obtained from basidiomycetes: an overview. 760 3


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>