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

The frequent coexistence of adenoma with primary carcinoma of the colon and their association with higher incidences of both synchronous and metachronous carcinomas offers only circumstantial evidence that adenomas are premalignant lesions. Detailed histopathologic investigations, however, have documented the transition from adenoma to carcinoma. Although the common, minute adenomatous polyp has a low potential of malignancy, the risk increases with size, villous architecture and degree of epithelial dysplasia. Furthermore, the association of dysplasia, which shares many adenomatous features with carcinoma in patients with chronic ulcerative colitis, and the inevitable development of adenomatous polyps followed by carcinoma of the colon and rectum in patients with familial polyposis further support this concept. Most colorectal malignant lesions, therefore, are believed to progress through the adenoma to carcinoma sequence. Moreover, histochemical investigations have demonstrated that abnormalities of DNA content, enzyme activities, CEA expression and mucin composition are shared by both adenoma and carcinoma. Thus, the malignancy potential of adenoma of the colon and rectum is reflected not only in the overt histologic transition to carcinoma, but in the disruption of the genetic and biochemical control mechanisms of cellular function as well.
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PMID:The adenoma to carcinoma sequence. 216 17

Over a period of six years a total of 407 patients with polyps of the gastrointestinal tract were examined by gastroscopy and coloscopy and the findings analysed retrospectively. Among patients with colon polyps 10.5% were found also to have polypoid gastric lesions, among those with adenoma of the colon the prevalence was 11.7%. Only 2.4% of simultaneously diagnosed gastric lesions were found to be malignant or premalignant, a figure similar to the population average. But in patients with more than ten polyps of the colon both the prevalence of polypoid gastric changes and the significance of polyps with respect to precancerous lesions were clearly increased. On the other hand, in patients with epithelial polyps and/or glandular cysts colon polyps were found in 45%, in 42% with precancerous changes (adenoma). Thus patients with epithelial gastric polyps and glandular cysts probably constitute a group with a real additional risk of colon carcinoma. Regular coloscopy will thus reveal precancerous changes (adenoma) in the colon of 42% of such patients; coloscopic polypectomy will be an effective prophylactic measure against carcinoma of the colon.
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PMID:[Are stomach polyps an indicator of colonic carcinoma and colonic polyps an indicator of stomach carcinoma?]. 282 97

It may be useful for therapeutic purposes if experimental colonic cancer can be produced in larger animals. Our protocols for experiment to produce colonic cancer in dog were as follows: Two beagle and 12 mongrel dogs were used. Endoscopic examination was done every month or every other month. 1,2-Dimethylhydrazine (DMH) was given subcutaneously in 3 mongrel dogs once a week for 25 months. The protrusion like verruca was observed macroscopically in colonic mucosa in two of them. Histologically it was like lymph follicle hyperplasia in the submucosa. N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) soaked in sponge was inserted daily into the rectum of 2 beagle and 2 mongrel dogs for about 20.4 months. A leiomyoma of the colon was detected histologically in one beagle. N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG) soaked in sponge was inserted daily into the rectum of 4 mongrel dogs for about 26.5 months. During follow up study, adenoma of the colon was detected by biopsy in one dog. ENNG suppository (containing 50 mg of ENNG) was administered through the anus in 3 mongrel dogs. Colon cancer was induced in all of three dogs. There were metastases to the liver, lung and lymph nodes in one of them. Colonic cancer was successfully induced in dogs by suppository of ENNG into the rectum. This model seems to be the most useful for producing experimental colonic cancer.
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PMID:[Production of experimental colonic cancer in dog. A comparative study of administrative methods of carcinogen]. 667 8

Colon cancer is the second most common cancer in women in the Western world and there is a trend towards an increasing risk. Colon adenoma is a potential precursor for colon cancer. Adenoma and carcinoma of the colon seem to be influenced by estrogens and progesterone/progestins. This is related to the presence of estrogen and progesterone receptors, with apparently higher concentrations in colon cancers than in adenomas. Epidemiological data and the finding of a significant reduction in colon cancer risk related to hormone replacement therapy (HRT), and in particular the length of HRT intake, indicate that progesterone/progestins have a preventive effect. This has not been shown with postmenopausal estrogen replacement therapy (ERT) alone. Furthermore, the recurrence rate of adenoma appears to be reduced, and the survival of colon cancer patients improved, with HRT; such effects have not been documented with ERT.
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PMID:Long-term use of progestogens: colon adenoma and colon carcinoma. 1794 38

Obesity and insulin resistance are associated with the risk of colon cancer. Adenomatous colonic polyps are precancerous lesions of colon cancer. We investigated whether BMI and the metabolic syndrome are associated with the presence of adenomatous colonic polyps in Korean men. Anthropometric measurements, metabolic risk factors, and colonoscopic pathologic findings were assessed in 1,898 men who underwent routine colonoscopy at the Health Promotion Center of Asan Medical Center in 2005. The modified National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP III) and International Diabetes Federation (IDF) criteria were used for the definition of the metabolic syndrome. Multiple logistic regression analysis was used to evaluate the association between BMI and the metabolic syndrome and adenomatous polyps. Compared with men in the 1st quintile of the BMI, the adjusted odds ratio (OR) and 95% confidence interval (CI) for adenomatous polyps in men in the 2nd, 3rd, 4th, and 5th quintiles of the BMI were 1.55 (1.10-2.19), 1.57 (1.10-2.24), 1.94 (1.34-2.81), and 1.99 (1.31-3.01), respectively (P for trend <0.0001). Men with triglycerides (TGs) > or = 150 mg/dl were significantly more likely to have adenomatous polyps than were men with TG <150 mg/dl (OR 1.29; 95% CI 1.03-1.62). As a function of the number of metabolic risk factors, the ORs for adenomatous polyps were 1.41 (1.03-1.93), 1.52 (1.08-2.12), 1.46 (1.01-2.12), and 1.77 (1.08-2.90) for 1, 2, 3, and > or = 4 risk factors, respectively (P for trend <0.05). Adenomatous colonic polyps were significantly associated with increased BMI levels. Subjects with even one component of the metabolic syndrome had a significantly higher risk for developing adenomatous polyps compared to those subjects without any component in Korean men.
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PMID:Association between BMI and metabolic syndrome and adenomatous colonic polyps in Korean men. 1838 94

Purpose. The association between obesity and colon neoplasia is well established but the underlying biological mechanisms are not fully understood. Rates of both obesity and colon cancer differ by race. Adipokines have been postulated as contributors to the observed association; however, few studies have examined the mediating effect of adipokines on the obesity-colon adenoma association with consideration of racial differences. Methods. We determined prediagnostic levels of adiponectin and leptin in Caucasians (217 cases and 650 controls) and African Americans (175 cases and 378 controls) participating in the Case Transdisciplinary Research on Energetics and Cancer Colon Adenoma Study. We evaluated mediating effects of adiponectin and leptin on the association of abdominal adiposity and colon adenoma separately according to race using mediational pathway analysis. Results. We observed differences in circulating adipokine concentrations by race; African Americans had higher levels of leptin and lower levels of adiponectin than Caucasians for both adenoma cases and controls (P values <0.001). Leptin and adiponectin did not mediate the waist-to-hip ratio (WHR) adenoma association in either group (all Sobel P values >0.27). Conclusions. We found no evidence that leptin or adiponectin mediates the abdominal obesity-colorectal adenoma pathway. Larger studies on how these associations vary by race, sex, and obesity are needed.
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PMID:Adipokines do not mediate the association of obesity and colorectal adenoma. 2519 77