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

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

Carbohydrate antigen 19.9 (CA19.9) is used as a tumor marker for clinical and research purposes assuming that it is abundantly produced by gastrointestinal cancer cells due to a cancer-associated aberrant glycosylation favoring its synthesis. Recent data has instead suggested a different picture, where immunodetection on tissue sections matches biochemical and molecular data. In addition to CA19.9, structurally related carbohydrate antigens Lewis a and Lewis b are, in fact, undetectable in colon cancer, due to the down-regulation of a galactosyltransferase necessary for their synthesis. In the pancreas, no differential expression of CA19.9 or cognate glycosyltransferases occurs in cancer. Ductal cells only express such Lewis antigens in a pattern affected by the relative levels of each glycosyltransferase, which are genetically and epigenetically determined. The elevation of circulating antigens seems to depend on the obstruction of neoplastic ducts and loss of polarity occurring in malignant ductal cells. Circulating Lewis a and Lewis b are indeed promising candidates for monitoring pancreatic cancer patients that are negative for CA19.9, but not for improving the low diagnostic performance of such an antigen. Insufficient biological data are available for gastric and bile duct cancer. Studying each patient in a personalized manner determining all Lewis antigens in the surgical specimens and in the blood, together with the status of the tissue-specific glycosylation machinery, promises fruitful advances in translational research and clinical practice.
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PMID:Complementary Use of Carbohydrate Antigens Lewis a, Lewis b, and Sialyl-Lewis a (CA19.9 Epitope) in Gastrointestinal Cancers: Biological Rationale Towards A Personalized Clinical Application. 3252 16