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)

Adenomatosis coli is recently regarded as a systemic disease with a predisposition to multiple tumor formation. We report siblings of familial adenomatosis coli with gastric cancers. Case 1 was a 58 year-old elder brother. His diagnosis was familial adenomatosis coli accompanied with colon cancer and simultaneous early gastric cancer. Total colectomy and partial gastrectomy were carried out on Mar. 13, 1984 at our hospital. Numerous polyps over the whole colon and an ulcerative tumor in the hepatic flexure were found in the resected colon. Histologically tubular adenocarcinoma were demonstrated in the ulcerative tumor, and all other polyps were adenomas. In the resected gastric specimen, there were two shallow, depressed lesions on the each anterior and posterior wall of the antrum. Histologically both of them were adenocarcinoma confined within the mucosa. Postoperative course was satisfactory and he is quite healthy 2 and a half years after surgery. Case 2 was a 56 year-old younger brother. He received a partial gastrectomy for advanced gastric cancer at another hospital on May 20, 1982. In one and a half year from the surgery, a large lung tumor (probably metastasis of the gastric cancer) was found and he received chemotherapy. He also received radiation therapy in June, 1984 and during this admission barium enema study was performed. It revealed numerous polyps over the whole colon. No cancerous lesions were found. He died of lung tumor on Dec. 8, 1985. The similar siblings were first reported by Kokaji et al. in 1984, and our cases seem to be the second ones.
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PMID:[Siblings of familial adenomatosis coli with gastric cancer--case report]. 282 86

Ulcerative colitis and Crohn's disease (together known as Inflammatory Bowel Disease or IBD) are both associated with increased risk for colorectal cancer. Although it is conventional to emphasise differences between IBD-associated and sporadic colon cancer, such as a lower rate of Adenomatosis Polyposis Coli mutations and earlier p53 mutations, IBD-associated cancer has a similar dysplasia-cancer sequence to sporadic colon cancer, similar frequencies of major chromosomal abnormalities and of microsatellite instability and similar glycosylation changes. This suggests that IBD-associated colon cancer and sporadic colon cancer might have similar pathogenic mechanisms. Because the normal colon is arguably in a continual state of low-grade inflammation in response to its microbial flora, it is reasonable to suggest that both IBD-associated and sporadic colon cancer may be the consequence of bacteria-induced inflammation. We have speculated that the glycosylation changes might result in recruitment to the mucosa of bacterial and dietary lectins that might otherwise pass harmlessly though the gut lumen. These could then lead to increased inflammation and/or proliferation and thence to ulceration or cancer. The glycosylation changes include increased expression of onco-fetal carbohydrates, such as the galactose-terminated Thomsen-Friedenreich antigen (Gal beta1,3GalNAc alpha-), increased sialylation of terminal structures and reduced sulphation. These changes cannot readily be explained by alterations in glycosyltransferase activity but similar changes can be induced in vitro by alkalinisation of the Golgi lumen. Consequences of these changes may be relevant not only for cell-surface glycoconjugates but also for intracellular glycoconjugates.
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PMID:Altered glycosylation in inflammatory bowel disease: a possible role in cancer development. 1282 Jul 18