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)

Seventy-seven patients with polyposis coli operated on at The Mount Sinai Hospital in the last 40 years were studied. Forty-two patients had a subtotal colectomy. Sixteen were found to have colon cancer at the time of operation, and a second rectal cancer developed in 50 percent of the survivors within 1 to 13 years after subtotal colectomy. Rectal cancer subsequently developed in only 3 of 23 patients without colon cancer. Thirty-five patients had total proctocolectomy or total colectomy with mucosal proctectomy and ileoanal anastomosis. Recurrent adenomatous polyps developed in two patients after mucosal proctectomy. A villous adenoma with carcinoma in situ of the ileum developed in one patient 30 years after total proctocolectomy and ileostomy. Another patient died from a periampullary carcinoma 24 years after subtotal colectomy. It seems that as the life expectancy of patients with polyposis improves, the incidence of small bowel and duodenal cancers may be expected to increase.
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PMID:Results of surgical treatment for familial polyposis coli. 375 76

Of 226 consecutive papillary carcinoma patients, 14 indicated that at least one other relative was similarly affected. Pathology confirmation was obtained in 8 of the 14 families. Of the eight families with documented familial papillary carcinoma, one had five members, another had four members, and yet another had three members affected. The remaining families had two members affected. In those families with two or more persons with confirmed papillary carcinomas of the thyroid, 20 first- and second-degree relatives were examined. Of those, one had a previously unidentified papillary carcinoma and 6 had a benign thyroid disease (4 primary hypothyroidism and 2 simple goiters). High-resolution chromosome studies of four patients from four different families were normal, and there was no increase in chromosome breakage in a fifth patient from yet another family. Autosomal dominant inheritance is possible. Although there was no family history of lipomas, osteomas, or intestinal polyposis to suggest Gardner syndrome, four parents of our familial papillary carcinoma patients had colon cancer. In addition, three other relatives died of unidentified intra-abdominal cancer. The apparently high frequency of colon cancer and other abdominal cancer in relatives was an additional concern. Based on our observations, three clinical recommendations can be made: obtain a family history of all patients with papillary carcinoma of the thyroid, since between 3.5 to 6.2% will have another affected relative; when two or more persons in a family have papillary carcinoma of the thyroid, all first- and second-degree relatives should have a neck palpation by an experienced examiner; and families with two or more persons with papillary carcinoma should be observed for possible colon cancer.
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PMID:Familial papillary carcinoma of the thyroid. 378 26

We hypothesize that: hereditary nonpolyposis colorectal cancer (HNPCC) accounts for a significant proportion of the colon cancer burden; the premalignant colonic mucosa in HNPCC patients may be comparable in many respects to the premalignant polyps in its hereditary multiple adenomatous polyposis counterpart; and finally, study of HNPCC colonic mucosa may harbor important clues for elucidation of the multistep process of carcinogenesis, including relationships between activated oncogenes, genetics, and environmental perturbations.
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PMID:Hereditary nonpolyposis colorectal cancer (Lynch syndromes I and II): a common genotype linked to oncogenes? 406 33

Adenomatous polyps lead directly to carcinoma of the colon in patients with one of the familial syndromes of intestinal polyposis. Elective colectomy is prophylactic and life-saving. A subgroup of patients will develop periampullary carcinoma, again arising from the presence of adenomatous polyps. Such a case is presented. These polyps should be surgically excised to ensure adequate pathologic examination. Yearly upper endoscopic examination is an essential element of management. Either the presence of carcinoma in situ or the recurrence of these polyps following excision is confirmation of behavior with a high propensity for the development of invasive cancer and requires aggressive treatment.
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PMID:Intestinal polyposis and periampullary carcinoma--changing concepts. 407 94

In a kindred of 46 individuals of an Indian Sikh family with no history of consanguinity, 8 suffered from site specific colon (caecum) cancer (not associated with polyposis). The clinical features in the affected kindred were indicative of a "cancer family syndrome". The study of the family depicted an autosomal dominant transmission pattern of site specific colon cancer, with probably 100% penetrance in the affected individuals. A low percentage of mitotic index (MI) was observed in the two probands who were available for the study. No structural or numerical chromosomal aberrations were observed in either case. It is probable that the gene responsible in this family could have begun by mutation at the germ cell level in the 1st generation and remained in a heterozygous condition in the affected individuals.
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PMID:Genetics of site specific colon cancer: a family study. 608 33

Among about 20.000 patients who had a gastroscopy in a period of 6 years, 92 had gastric mucosal polyposis, diagnosed by endoscopy and histology, an incidence of 0.46%. Eight patients with an age average of 38 years had familial gastrointestinal adenomatosis, in six of them the criteria of Gardner's disease were fulfilled. The remaining 84 patients had an average age of 62 years. In patients with more than ten polyps the sex ratio (female to male) was 3.9:1. In 56 patients without familial gastrointestinal adenomatosis, coloscopy and(or) proctosigmoidoscopy was performed. In 18 there were polyps in the colon, in three an invasive carcinoma in an adenoma. In three further patients extensive carcinoma of the colon (in two with stenosis) was found. These observations suggest that patients with gastric mucosal polyposis have a higher incidence of colon polyps and carcinoma.
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PMID:[Gastric mucosal polyps--an irrelevant finding? Studies on the incidence and clinical significance]. 614 21

Patients with sporadic or hereditary colon cancer (cancer family syndrome) demonstrate in vitro defects of cellular immunity characterized by decreased lymphocyte responsiveness in mixed leukocyte culture, which can frequently be attributed to the influence of suppressor macrophages. Healthy relatives of affected patients with hereditary colon cancer can show the same defects of cellular immunity. Affected members with polyposis coli or healthy relatives do not show these defects, whereas individuals with Gardner's syndrome can. These defects of cellular immunity may be an important etiologic component of, or marker for, the cancer family syndrome. These defects could also serve to differentiate the colonic polyposis syndromes.
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PMID:Suppressor cells in healthy relatives of patients with hereditary colon cancer. 644 42

A child with a malignant undifferentiated adrenal medullary tumor of neural crest origin, removed at six months of age, was treated with chemotherapy and is alive without evidence of cancer after seven years. He developed osteomas of the skull, a thyroglossal cyst and has had one episode of gastrointestinal bleeding. A three-generation history of multiple colonic polyposis and colon cancer, osteomas, recurrent pancreatitis, and Wilms' tumor was elicited. One of three females in this family, with direct lineage from polyposis afflicted fathers, exhibited Gardner's Syndrome and Wilms' tumor. The constellation of tumors afflicting this family may represent an underlying defect of excessive cell proliferation affecting mesenchymal and neuroblastic tissue. These may be extracolonic conditions associated with Gardner's Syndrome.
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PMID:Pre-Gardner's syndrome, thyroglossal cysts and undifferentiated tumor of neural crest origin. 648 28

Familial polyposis is a systemic defect of growth regulation. Extracolonic expressions are common and serious, about equal in risk to carcinoma of the large intestine. Periodic surveillance of the upper gastrointestinal tract is particularly important. More intensive surveillance of the large intestine may lead to better results in patients with polyposis who have carcinoma of the large intestine develop.
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PMID:The spectrum of polyposis. 650 38

Two cancer-prone families are reported. In the first one four first-degree relatives over three generations presented a colonic carcinoma, three of them at a proximal anatomic site. For grandmother and father these occurred at ages of 43 and 54 years, respectively, for the son and the daughter at ages of 26 and 22. The grandmother underwent a palliative ileotransversostomy, surgery typically associated with a bad prognosis, but she survived for forty years that initial neoplasm and had an hysterectomy with oophorectomy at age of 63 for endometrial malignancy; she deceased at age of 83 a few days after surgical treatment of tumoral small bowel obstruction: pathological evaluation disclosed a fourth cancer on first duodenum. The second kindred shows over three generations 11 cancer-affected individuals, three of them with double primary cancer: breast and sigmoid, breast and endometrium, colon and Hodgkin disease. This pedigree includes 8 colorectal neoplasms occurring at 47 years of mean age. These findings are consistent with the cancer-family syndrome and hereditary non-polyposis colon cancer described by Henry Lynch upon four criteria: high frequency of adenocarcinoma, excess of multiple primary malignancies, synchronous or metachronous, early age of onset of cancer and autosomal dominant inheritance. Moreover the hereditary colon cancer is usually localised to the proximal colon, not associated to polyposis coli and allows a prolonged survival. Up to day such families are only identified by pedigree data. The identification of a cancer-prone family calls for an active follow-up of relatives putatively at risk starting at the age of 15 to 20.
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PMID:[Familial cancer of the colon without polyposis and the familial cancer syndrome. Apropos of 2 cases over 3 generations]. 666 87


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