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

We describe 2 extended kindreds supposedly manifesting familial multiple adenomatous polyposis coli (FPC), but which show marked heterogeneity in the phenotypic expression of colorectal adenomatous polyps. In one family, 2 individuals had diffuse polyposis at very early ages (7 and 10 years), while 6 others (aged 23 to 72 years) had solitary polyps only. Of the patients with solitary polyps, 2 had associated colonic malignancies (ages 26 and 35), while another had a prophylactic colectomy performed at age 46. In the second family, 5 of the 11 patients with evidence of polyps showed the classical presentation of FPC, while the remainder showed marked phenotypic variation. The marked variability in frequency and location of colon polyps points to the need to reassess our traditional criteria for diagnosis of FPC. The high risk of early onset colon cancer in patients from these families who have the most minimal manifestation, namely isolated polyps, recommends more careful scrutiny of supposedly unaffected members of all FPC kindreds.
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PMID:Familial polyposis coli: heterogeneous polyp expression in 2 kindreds. 3 39

Inhibition of leukocyte migration in agarose-agar was used as a probe for tumor-associated antigen in 3-M KCl solubilized extracts of gastric, colon, and lung cancers from humans. Twelve of 40 (30%) leukocyte preparations from gastric cancer patients, 10 of 21 (48%) from colon cancer patients, and 7 of 14 (50%) from lung cancer patients were inhibited by their respective histologically homologus cancer extract. However, among 75 preparations from various cancer patients, leukocytes from only 2 gastric cancer patients were inhibited by paired normal gastric tissue extracts. Only 2 of 68 preparations from normal individuals and none of 67 preparations from patients with nonmalignant diseases, such as gastric peptic ulcer, gastritis, colon polyposis, colitis, pulmonary tuberculosis, chronic bronchitis, and sarcoidosis, were inhibited by cancer extracts. These findings suggest the presence in KCl extracts of gastric cancer of presumed tumor-associated antigen(s) that is antigenically distinct from that of either colon or lung cancer.
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PMID:Inhibition of human leukocyte migration in agar by 3-M potassium chloride extracts of stomach, colon, and lung cancers. 28 34

Several pre-malignant diseases are known to have a genetic etiology. This study focuses attention upon precancerous disorders wherein the mode of inheritance is either well established or wherein it remains unclear even though familial aggregation of the particular diseases have been amply documented. These conditions will be discussed as useful models for systematic investigations of the host etiologic component in carcinogenesis. Our survey of hereditary precancerous syndromes includes multiple polyposis of the coli, the multiple mucosal neuroma syndrome, the Cancer Family Syndrome, Sipple's syndrome, Von Recklinghausen's neurofibromatosus, the multiple nevoid basal cell carcinoma syndrome, tuberous sclerosis, familial cutaneous malignant melanoma, and carcinoma of the breast. We have emphasized the heterogeneous character of many forms of familial cancer. Familial breast cancer associations clearly show such heterogeneity, as do colon cancer syndromes. Certain of these precancerous states are characterized by phenotypes which are clinically apparent, polyposis coli being the classic example. Others, such as Sipple's syndrome are amenable to routine screening for biochemical markers. The bulk of putative genetic cancer-predisposing problems require further basic investigation of modes of inheritance. Cancer control may be enhanced through communication of useful genetic and diagnostic information to primary care physicians. Referral of cancer clusters of possible genetic etiology from clinicians to human geneticists facilitates the necessary basic research.
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PMID:Familial cancer syndromes: a survey. 40 22

Familial polyposis is a genetically-transmitted disease characterized by multiple adenomatous colorectal polyps and a high risk for development of adenocarcinoma. Familial polyposis and Gardner's syndrome should be differentiated from other penetically-linked polyposis syndromes lacking a predisposition for cancer. Total colectomy and ileorectal anastomosis, aggressive follow-up and intensive surveillance of non-polyp bearing relatives can reduce the risk of developing cancer. From an epidemiologic point of veiw, polyposis is a valuable model for the study of the interaction of genetic and environmental factors in the genesis of colon cancer.
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PMID:Familial polyposis. 83 40

Of six children with carcinoma of the colon, none had ulcerative colitis or a family history of carcinoma of the colon or colonic polyposis. In 75 cases traced in the literature, a common early symptom of carcinoma of the colon in children is acute, crampy abdominal pain. At laparotomy for suspected appendictis, the possibility of the acute pain being due to carcinoma of the colon should be borne in mind. Otherwise the symptoms of carcinoma of the colon in children do not differ substantially from those in adults. The prognosis is unfavorable; in only 2.5% of the cases on record did the children survive 5 yr after the operation.
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PMID:Carcinoma of the colon in children: a report of six new cases and a review of the literature. 100 8

Relatives of patients with multiple polyposis are among those at high risk for development of neoplasms in the colon. Examination of 4 siblings, 3 men and 1 woman, of a patient with multiple polyposis was conducted for the possible presence of colonic polyps. All patients were over 40 years of age and received barium enemas for the radiological detection of excrescences. Proctoscopic examinations were also carried out during which time a biopsy and colonic wash were obtained. Polyps were absent on films as well as on endoscopy, and colonic cytologies of all 4 subjects were within normal limits. However, isotopic incorporation studies revealed the presence of an abnormal labeling pattern in some crypts of the biopsy incubated with TdR-3H of 1 family member. Along with normal crypts with label in the lower two-thirds of the colonic crypts, some were seen to have cells labeled at the surface, a proliferative lesion thought to precede the apperarance of a polyp. Among the surface cells removed by the colonic wash, some were found to be isotopically labeled, that is, engaged in DNA synthesis. Thus, a defect in the regulation of colonic epithelial cell replication was found, suggesting the need for close surveillance in the interest of early colon cancer detection.
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PMID:The detection of aberrant DNA synthesis in a member of a high-risk cancer family. 116 21

This report describes the evaluation of a chemical test for T-antigen in rectal mucus as a screening test for colon cancer. The test, called the Mucus Strip Test, detects the disaccharide residue sialic acid-free beta-D-Gal(1-->3)-D-GalNAc or T-antigen, which accumulates in mucus from malignant cells and colonic mucosa adjacent to cancer but not in normal mucosa. Participants were an unselected case series of 660 persons undergoing colonoscopy, excluding those with ulcerative colitis, polyposis, Crohn's disease, or nonspecific inflammatory bowel disease. In the first study (n = 608) rectal mucus was collected after preparation of the bowel for colonoscopy; in the second study (n = 52) a modified protocol was used to collect mucus approximately 2 weeks before colonoscopy and again following preparation for the procedure. Mucus Strip Test results were compared to the diagnosis received after colonoscopy, which was classified as cancer, adenomatous polyp(s), and others (normal). Analyses were also stratified by previous history of large intestinal disease, classified as previous cancer; previous diagnosis of adenomatous polyp(s); or others. In the first study, T-antigen was detected in approximately 30% of mucus samples, and test results were independent of both diagnosis at colonoscopy and previous medical history. In the second study, T-antigen was detected in 85% of samples collected before and 96% of samples collected after preparation for colonoscopy, but test results were again independent of diagnosis and medical history.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of a test for abnormal rectal mucus for early detection of colon cancer. 130 75

We have studied three patients, one with extensive polyposis of the colon, who have constitutional interstitial deletions of the long arm of chromosome 5. High-resolution banding studies indicated that the deletion in the patient with polyposis spans the region 5q21-q22, which includes APC, a gene involved in familial adenomatous polyposis and sporadic colon cancer. Molecular analysis with probes for sequences flanking APC confirmed this conclusion. The deletions in the other two patients, who are too young to have developed polyposis, had breakpoints within this region, precluding the use of cytogenetic analysis alone in making definitive predictions about their risks. Molecular studies resolved the uncertainty; in situ and quantitative Southern hybridizations of four probes for polymorphic segments revealed that one of the patients has a deletion of MCC, a gene which is approximately 150 kb proximal to APC, and two flanking markers. He is at increased risk for polyposis, while the other patient is not. The physical descriptions of these patients, in conjunction with cases in the literature, begin to allow delineation of two distinct 5q-syndromes. These studies also provide precise physical mapping data for D5S71, D5S81, D5S84, and MCC on 5q.
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PMID:Phenotypic, cytogenetic, and molecular studies of three patients with constitutional deletions of chromosome 5 in the region of the gene for familial adenomatous polyposis. 832 66

Adenomatous polyps are an intermediate in the pathway to colon carcinoma. An inherited disorder, familial adenomatous polyposis coli (APC), is characterized by hundreds to thousands of adenomatous polyps. A previously reported family had colon cancer associated with a low average but highly heterogenous number of colonic polyps, this phenotype mapped to the APC locus on 5q. Four new families have been ascertained in which the phenotypic pattern was different from classical polyposis but similar to that of the "prototype" kindred reported earlier. By multilocus linkage analysis, the gene responsible for the disease phenotype was mapped, with a high level of confidence, to the APC locus in two of the four families with the attenuated or variant form of polyposis (AAPC); the results for the two remaining kindreds were inconclusive. A combined maximum LOD score of approximately 7.6 at a recombination fraction of 0 was obtained when the results were summed over the four pedigrees with markers closest to the APC locus. The establishment of genetic linkage in such families may point to the APC locus as having a more significant role in inherited predispositions to colorectal cancer than was previously thought.
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PMID:Linkage of a variant or attenuated form of adenomatous polyposis coli to the adenomatous polyposis coli (APC) locus. 131 15

Described in Switzerland in the early '60, the major features of hereditary non-polyposis colon cancer syndrome (HNPCCS) were established 20 years ago by H. T. Lynch. HNPCCS accounts for at least 60% of the colon cancer etiology. Cancer family syndrome is defined by the presence of extracolonic primary tumors in addition to colon cancer. Both syndromes are transmitted by an autosomic dominant pattern. None of the known biomarkers are specific and/or sensitive enough to rely on their predictive values of patient's risks. A typical Swiss family was investigated on the basis of the cancer-prone family history. 21% of the family members observed over 5 generations presented one or more (30% of the cases) colo-rectal neoplasms at the age of 50. 55% of the tumors were right sided. Histologically, half of the tumors were mucinous. 30% of metachronous cancer appeared within 10 years. Polyps (1-3) and flat adenomas were associated to the lesion in 57%. Extra-colonic tumors appeared in 18% of family members and in half of the colon cancer patients. The sites of these tumors were the urinary tract, ovary, small bowel, breast and stomach. Two fibroblast strains of affected individuals were established. No increased tetraploidy was noted. Preliminary results suggest that this two strains are rather sensitive to ionising radiation. Often neglected, family history of colon cancer remains the major diagnostic and decision-making tool of a such syndrome. It will necessitate special treatment of affected subjects and early screening of the relatives.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hereditary colorectal cancer: observations of a family study]. 133 Sep 93


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