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)

Promotion of carcinogenesis in rats by dietary fat depends on the amount and type of fatty acids ingested, mainly as triglycerides. A certain amount of essential fatty acid of the linoleate type (n-6) is required for promotion of mammary cancer and pancreatic cancer and probably also for colon cancer. Promotion is also enhanced by a high level of dietary fat, and this additional effect seems to be relatively independent of the type of fat. Saturated fatty acids, either medium or long chain, and cis and trans monoenoic fatty acids appear to have no specific promoting effects. Fish oils containing long-chain polyunsaturated fatty acids of the linolenate type (n-3) are inhibitory, and this may also be true for rapeseed oil high in erucic acid, a long-chain monoenoic fatty acid. The promoting action of dietary fat can be modified by other components of the diet, such as starch, sugar, and fiber. Promotion is also dependent on the length of time animals are exposed to the high-fat diet. The overall tumor yield can be decreased by reducing the level and degree of unsaturation of the dietary fat after a period of feeding a high polyunsaturated-fat diet.
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PMID:Summation: which fat/how much fat--animals. 362

Despite data favouring a role of dietary fat in colonic carcinogenesis, no study has focused on tissue n3 and n6 fatty acid (FA) status in human colon adenoma-carcinoma sequence. Thus, FA profile was measured in plasma phospholipids of patients with colorectal cancer (n = 22), sporadic adenoma (n = 27), and normal colon (n = 12) (control group). Additionally, mucosal FAs were assessed in both diseased and normal mucosa of cancer (n = 15) and adenoma (n = 21) patients, and from normal mucosa of controls (n = 8). There were no differences in FA profile of both plasma phospholipids and normal mucosa, between adenoma and control patients. There were considerable differences, however, in FAs between diseased and paired normal mucosa of adenoma patients, with increases of linoleic (p = 0.02), dihomogammalinolenic (p = 0.014), and eicosapentaenoic (p = 0.012) acids, and decreases of alpha linolenic (p = 0.001) and arachidonic (p = 0.02) acids in diseased mucosa. A stepwise reduction of eicosapentaenoic acid concentrations in diseased mucosa from benign adenoma to the most advanced colon cancer was seen (p = 0.009). Cancer patients showed lower alpha linolenate (p = 0.002) and higher dihomogammalinolenate (p = 0.003) in diseased than in paired normal mucosa. In conclusion changes in tissue n3 and n6 FA status might participate in the early phases of the human colorectal carcinogenesis.
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PMID:Changes of the mucosal n3 and n6 fatty acid status occur early in the colorectal adenoma-carcinoma sequence. 899 64