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Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Palmar and plantar keratoses developed in seven patients many years after ingeston of trivalent inorganic arsenic. Six had basal cell carcinoma (superficial multicentric type in five), carcinoma "in situ" or squamous cell carcinoma of the skin. Two had systemic carcinoma--one, bilateral breast adenocarcinoma and one, carcinoma of the colon. From these observations and from the findings of a review of the literature, there seems no question that long-term arsenic ingestion can cause palmar and plantar keratoses and skin cancer, particularly basal cell carcinoma of the superficial multicentric type, usually on the torso. It is suspected but not proved to cause other cancers. Although over the last 50 years general exposure to arsenic has greatly decreased, particularly that from insecticides, this element is still found occasionally in drinking water (naturally or as a smelter byproduct), in certain foods and in cigarette smoke.
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PMID:Arsenic and cancer. 12 22

Experimental evidence indicates a relationship between cholesterol alpha-epoxide and skin cancer, and exposure of skin fibroblasts to ultraviolet radiation enduces formation of significant levels of this oxide. Colon cancer is also etiologically linked to cholesterol oxidation products. Higher than normal levels of cholestanetriol have been found in patients with colon cancer and also in those with precancerous disorders such as adenomatous polyps and ulcerative colitis. Higher than normal levels of cholesterol alpha-epoxide have been found in breast fluid aspirates of women with benign breast disease, with or without atypical hyperplasia of the epithelium, and this may be a factor in the increased incidence of breast cancer associated with hyperplasia. Similarly, the observed increased levels of cholesterol alpha and beta-epoxides in prostatic fluid of men with benign prostatic hypertrophy may be associated with subsequent development of prostate cancer. Cholesterol alpha-epoxide has been found to be mutagenic to fibroblasts in culture and to induce morphological transformation in hamster embryo cells and in mouse C3H cells. 25-Hydroxycholesterol and 20 alpha-hydroxycholesterol are potent suppressors of generation and proliferation of tumor-specific cytotoxic T lymphocytes. Although investigations into the role of cholesterol oxidation products in cancer are still in the early stages, evidence to date indicates a potentially significant role in the induction of some types of cancer.
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PMID:Cholesterol oxides and carcinogenesis. 206 46

Although a correlation has been suggested between cigarette smoking and pancreatic cancer, studies on pathological changes in the pancreas of smokers are fragmentary. In the present study we examined histopathologically 73 pancreases obtained by autopsy from 42 heavy cigarette smokers and 31 non-smoker patients. One invasive adenocarcinoma (2 cm in diameter) and three small carcinomas (2-5 mm in diameter) were found in smokers and one small carcinoma in a non-smoker patient. Although the incidence of pancreatic cancer in smokers was higher than in non-smokers, the difference was statistically not significant. Of smokers with pancreatic cancer, 2 had lung cancer, 1 skin cancer, 1 colon cancer and 1 was free of any malignancies. Ductal changes, including mucinous or squamous cell metaplasia and papillary hyperplasia, were found with equal frequencies in both groups of patients. The type and the incidence of these ductal alterations were not related to smoking but to the age. Our results do not indicate that cigarette smoking increases the incidence of pancreatic cancer, although, the limited number of the sections of the pancreas examined, as well as exclusion of other important variables, such as alcohol, diet and diabetes weaken the value of this study.
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PMID:Comparative histopathological findings in the pancreas of cigarette smokers and non-smokers. 226 10

A total of 3749 workers employed for at least three months in two Finnish glass factories (cohorts A and B) were followed up for cancer in 1953-86 through the Finnish Cancer Registry. In cohort A (1353 men, 1261 women), 106 primary cancers were diagnosed among men, and their standardised incidence ratio (SIR) for all cancers was 99. Among women the risk was low (65 cases, SIR 64). In cohort B (450 men, 685 women), the relative risk of cancer was close to unity for both men (57 cases) and women (75 cases). The risk of cancer was analysed by primary site, type of work, years since first exposure, and age at diagnosis. The only significantly increased risks were those of lung cancer among men (SIR 130, 95% CI 100-167, cohorts A and B combined), and skin cancer among glass blowers (SIR 625, 95% CI 129-1827). An increased risk of lung, stomach, and colon cancer as well as of brain tumours has been reported in previous studies. It is postulated that the excess risk of lung cancer, detected in this study, can also be accounted for by lifestyle, and not only by possible occupational exposures, because a similar excess risk of lung cancer has been found previously for all industrial workers in Finland. Although the risk of stomach cancer in this study was increased among glass blowers, it was not high in the largest groups of plain glass workers. The risks of tumours of the central nervous system and colon were not increased either.
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PMID:Cancer risk among glass factory workers: an excess of lung cancer? 227 87

The material of the Finnish Cancer Registry from 1953-79 (279,745 cancer patients, 774,518 person-yr at risk) was analyzed for the occurrence of multiple cancer. There were 5,871 new primary cancers in the series (excluding the first 12 mo from diagnosis of the first cancer). A positive association between cancers with similar etiology could be demonstrated, e.g., between cancers of the lip, larynx, and lung (smoking) and between cancers of the breast and endometrium (hormones, reproductive history). Clustering of different risk factors resulted, e.g., in an excess risk of colon cancer among female breast cancer patients (risk factors in both cancers are prevalent particularly in higher-social classes). Differences in the distribution of the risk factors resulted in risk deficits, e.g., low relative risk of lung cancer among male colon cancer patients (the prevalence of smoking was highest in the lower-social classes and the prevalence of risk factors in colon cancer was highest in the higher-social classes). The risk of leukemia was increased among patients with cancers of the breast, endometrium, and thyroid (possibly due to irradiation). There was a high relative risk of salivary gland cancer among patients with skin cancer other than melanoma or basal cell carcinoma in both sexes. The relative risk of a new primary cancer decreased with increasing age at diagnosis of the first cancer. The length of follow-up was positively associated with the relative risk of many cancers, although this finding was not as consistent as that with age.
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PMID:Multiple cancer--an epidemiologic exercise in Finland. 386 Jun 79

Certain retinoids have reproducibly prevented carcinogen-induced cancer of the skin, mammary gland, and urinary bladder of experimental animals and, in isolated experiments, have demonstrated positive activity for carcinogen-induced cancer of the esophagus, cervix, and liver. Attempts to establish activity of retinoids in prevention of lung and colon cancer have generally been unsuccessful. In the chemotherapy of established cancers, retinoids have exhibited modest activity against those that are immunogenic. The preventive activity of retinoids appears to be associated with their role in chemotherapy is consistent with general stimulation of the immune response of the host.
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PMID:Retinoids as chemopreventive and anticancer agents intact animals (review). 681 Jul 45

To quantify the risk of second primary cancers among patients with cutaneous malignant melanoma, we studied 20,354 patients in the Swedish Cancer Register during 1958-88. A second primary cancer was reported in 1605 patients, compared with an expected number of 1109.5 [standardised incidence ratio (SIR) = 1.45, 95% confidence interval (CI) = 1.38-1.52]. The highest risk was found among patients younger than 60 years. The greatest risk was seen during the first year after diagnosis (SIR = 1.91, CI = 1.69-2.14), but even after long-term follow-up--15 years or more--the risk was still significantly elevated (SIR = 1.56, CI = 1.35-1.79). The strongest association was found for a second primary malignant melanoma (men, SIR = 10.0, CI = 8.26-12.00; women, SIR = 8.66, CI = 7.22-10.30) and non-melanoma skin cancer (men, SIR = 3.58, CI = 2.85-4.44; women, SIR = 2.41, CI = 1.71-3.29). The risk of second cancers associated with tissues of neuroectodermal origin was increased, especially tumours of the nervous system (men, SIR = 1.73, CI = 1.10-2.60; women, SIR = 2.03, CI = 1.45-2.78). The SIR of second cancers involving the immune system was also increased. An excess risk of endometrial cancer was seen (SIR = 1.41, CI = 1.03-1.88), but no significant associations existed for cancers of the breast, ovary, testis or other endocrine glands. Among tumours of the digestive tract, only colon cancer in men had a significantly increased SIR (1.33, CI = 1.00-1.74).
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PMID:Second primary cancers in patients with cutaneous malignant melanoma: a population-based study in Sweden. 854 16

We analyzed cancer incidence and mortality in a cohort of 22,597 Swedish women who were prescribed replacement hormones. After 13 years of follow-up in national registries, 2,330 incident cancer cases and 848 cancer deaths were observed. Overall, our results were reassuring since incidence rate ratios (SIRs) for 16 cancer sites and mortality ratios (SMRs) for all 10 examined sites were at, or lower than, unity. However, we found that exposure to an estrogen-progestin combined brand was associated with an increasing relative risk of breast cancer with follow-up time, the SIR reaching 1.4 (95% CI 1.1-1.8) after 10 years of follow-up. The relative risk of endometrial cancer was substantially increased, with the highest SIR of 5.0 (95% CI 1.6-5.9) in women prescribed estrogens alone, whereas those given an estrogen-progestin combination showed no elevation in risk. The risk estimates for liver and biliary tract cancers and for colon cancer were reduced by about 40%, notably in women prescribed the estradiol-progestin compound. Further detailed analyses revealed no evidence of adverse or protective effects on the risk of ovarian, uterine cervical, vulvar/vaginal, rectal, pancreatic, renal, lung, thyroid and other endocrine cancers, brain tumors, malignant melanoma or other skin cancers. Hormone replacement therapy was not associated with an increase in mortality for any cancer site, at this time of follow-up. For breast and endometrial cancers, SMRs were below baseline but tended to increase with follow-up time. We conclude that hormone replacement increases the endometrial-cancer risk after unopposed estrogens and the breast-cancer risk-notably after estrogen-progestin combined therapy-and tentatively suggest that it exerts a protective effect against colon and liver cancer risks.
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PMID:Cancer incidence and mortality in women receiving estrogen and estrogen-progestin replacement therapy--long-term follow-up of a Swedish cohort. 870 4

Several epidemiological studies point to a strong correlation between nutrient composition of the diet and cancer of the colon. Phytic acid, present in grains, has been credited with reducing the risk of cancer of the colon. A number of reports are available indicating the benefits of green tea consumption in reducing the risk of stomach, lung and skin cancer, but little data are available on the effect of green tea in reducing the risk of colon cancer. Also, there are no studies on the combined effect of these compounds on colon tumorigenesis. Thus the primary objective of this investigation was to elucidate the combined effects of green tea and phytic acid on colonic preneoplastic lesions and the Phase II enzyme glutathione S-transferase. Fisher 344 male weanling rats were divided into nine groups of 15 rats each and fed the experimental diet for 13 weeks. Rats received two s.c. injections of azoxymethane in saline at 16 mg/kg body wt at 7 and 8 weeks of age. Rats received three levels (0, 1 and 2%) of phytic acid with three levels (0, 1 and 2%) of green tea within each phytic acid level in a 3 x 3 factorial experiment. Results indicate that while green tea had a marginal effect (P < 0.14), phytic acid significantly reduced the incidence of aberrant crypt foci (P < 0.008). The interaction between green tea and phytic acid was significant (P < 0.029 for distal and < 0.0168 for entire colon) and positive, pointing to a synergistic effect of green tea and phytic acid.
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PMID:Interactive suppression of aberrant crypt foci induced by azoxymethane in rat colon by phytic acid and green tea. 936 16

Alterations in mucin expression have been detected in many clinically relevant cancers and, in particular, the polymorphic epithelial mucin, encoded by the MUC1 gene, has attracted considerable attention. We investigated its expression in human breast, colon, ovarian, lung, and skin cancer cells and their metastases grown in severe combined immunodeficient (scid) mice using three different monoclonal antibodies (HMFG-1, HMFG-2, and SM3). Four of five breast cancer cell lines, three of five colon cancer cell lines, two of three small-cell carcinoma of the lung cell lines, and A 431 cells all expressed the MUC1 gene product. Neuraminidase predigestion often enhanced HMFG-1 immunoreactivity, which was more widespread and stronger than SM3 immunoreactivity. A considerable heterogeneity of MUC1 gene product expression was observed in the same tumors grown in different mice. The binding pattern between single-cell/small-cell clusters (up to 10 cells) and larger cell number aggregates varied. The results indicate that the MUC1 gene expression both in primary tumors and metastases is not tightly controlled within a particular tumor cell line. Because of this heterogeneous antigen expression in vivo, it appears impossible to target all metastatic deposits by a single monoclonal antibody directed against the MUC1 gene product. (J Histochem Cytochem 46:127-134, 1998)
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PMID:Immunohistochemical detection of the MUC1 gene product in human cancers grown in scid mice. 940 2


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