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

The flexible fibroscopic colonoscope has changed the way we approach colonic disease. The technique of safe, effective colonoscopy is discussed including the indications and contraindications for therapeutic intervention via the colonoscope. The techniques of polypectomy is described, including some tips for methodology gained by the broad experience of the author, and admonition against the possible complications which can be life-threatening. The application for polypectomy in the presence of in-situ or invasive cancer is presented. The possible future development of colonoscopic and laparoscopic techniques are presented. The article concludes with a discussion of the monumental work of the National Polyp Study documenting that patients undergoing polypectomy have a significant reduction in the incidence of colon cancer. Application of the knowledge to the general population requires the identification of at-risk populations.
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PMID:Colonoscopic polypectomy: indication, technique, and therapeutic implications. 860 11

Chemoprevention refers to the use of specific natural or synthetic chemical agents to reverse, suppress, or prevent the progression to invasive cancer. The ideal chemopreventive agent is safe and nontoxic over the long term. It should be easy to take and demonstrated to be effective in randomized trials in humans. Aspirin and NSAIDs meet many of the criteria for an ideal agent. The literature on aspirin and NSAIDs makes it clear that these agents can prevent colorectal cancer and precursor adenomas. That does not mean that we should make general recommendations for their use. First, we do not know the proper dose or duration. More important, these medications are accompanied by adverse effects that can be considerable. Indeed, the Medical Letter, an authoritative, unbiased publication on drugs and therapeutics, concluded that "for primary prevention in low-risk patients, more studies are required to establish whether the beneficial effect of aspirin is great enough to compensate for the possible increased risk of hemorrhagic stroke." These recommendations were directed at the use of these medications for prevention of myocardial infarction, but the same conclusions apply to colorectal cancer: although aspirin may prevent the disease, it may increase the risk of hemorrhagic strokes or cause other adverse effects. We must accurately balance the benefits and risks of these drugs, based on the results of ongoing randomized studies, before recommending aspirin for prevention of colorectal cancer. Is there anything that we can recommend to our patients for prevention of colorectal cancer? Based on observational epidemiologic studies, it is clear that individuals who consume a diet high in vegetables and natural fibers and low in fat have a reduced risk of colon cancer and polyps. Optimal nutrient intakes for the prevention of cancer might be more readily achieved via food fortification or supplementation, but this requires more research. Regular physical exercise and maintenance of normal body weight are also protective. Until the results of definitive studies of chemopreventive agents are available, we can recommend that our patients eat a sensible diet, exercise, and avoid obesity. Such an approach should protect them from cardiovascular disease, an even deadlier condition than colorectal cancer. In the future, we need randomized prevention trials that, for logistic reasons, may need to focus on the occurrence and progression of colorectal adenomas rather than carcinoma itself. Studies that test more than one compound at a time, using factorial designs, will be more efficient. We will need better information about duration and dose, adverse side effects, molecular mechanisms, and cellular sites of NSAID activity. Ultimately, we will need to know more about the biology and molecular biology of colorectal cancer and its precursors. That information will, perhaps, permit us to design agents to interrupt the pathway to cancer and to use intermediate markers more intelligently.
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PMID:Aspirin and other nonsteroidal anti-inflammatory agents in the prevention of colorectal cancer. 879 Nov 32

Data from the New South Wales Central Cancer Registry for the period 1972-1991 were examined to determine the risk of second primary cancers after an initial invasive cancer of the colon (ICD-9 153) or rectum (ICD-9 154). The expected numbers of cancers were obtained by assuming that subjects experienced the same cancer incidence as prevailed in the corresponding general population and by applying sex-, age-, and calendar-specific rates to the appropriate person-years at risk. The relative risk (RR) of a second primary cancer was taken to be the ratio of observed:expected numbers of second cancers. After colon cancer, there was an excess of cancers of the small intestine in both sexes (RRs of 4.5 and 4.4); prostate (RR = 1.4) and kidney (RR = 1.8) in men; and breast (RR = 1.3), body of uterus (RR = 1.9), ovary (RR = 2.8), and thyroid (RR = 2.7) in women. Lung cancer occurred less frequently in men than expected (RR = 0.7). After rectal cancer, men had increased risks of cancers of the colon (RR = 1.5) and prostate (RR = 1.3) and a reduced risk of pancreatic cancer (RR = 0.3). A reciprocal relationship of increased risk was seen between cancers of the proximal (but not the distal) colon and rectum. Shared luminal risk factors for proximal colon cancer and rectal cancer and three syndromes of hereditary predisposition to colon cancer seem to be the major contributors to second primary cancers in patients with an initial colon cancer. Sources of bias have been considered.
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PMID:Second primary cancers after cancers of the colon and rectum in New South Wales, Australia, 1972-1991. 913 57

Colorectal cancer is a significant cause of morbidity and mortality in Western populations. This cancer develops as a result of the pathologic transformation of normal colonic epithelium to an adenomatous polyp and ultimately an invasive cancer. The multistep progression requires years and possibly decades and is accompanied by a number of recently characterized genetic alterations. Mutations in two classes of genes, tumor-suppressor genes and proto-oncogenes, are thought to impart a proliferative advantage to cells and contribute to development of the malignant phenotype. Inactivating mutations of both copies (alleles) of the adenomatous polyposis coli (APC) gene--a tumor-suppressor gene on chromosome 5q--mark one of the earliest events in colorectal carcinogenesis. Germline mutation of the APC gene and subsequent somatic mutation of the second APC allele cause the inherited familial adenomatous polyposis syndrome. This syndrome is characterized by the presence of hundreds to thousands of colonic adenomatous polyps. If these polyps are left untreated, colorectal cancer develops. Mutation leading to dysregulation of the K-ras protooncogene is also thought to be an early event in colon cancer formation. Conversely, loss of heterozygosity on the long arm of chromosome 18 (18q) occurs later in the sequence of development from adenoma to carcinoma, and this mutation may predict poor prognosis. Loss of the 18q region is thought to contribute to inactivation of the DCC tumor-suppressor gene. More recent evidence suggests that other tumor-suppressor genes--DPC4 and MADR2 of the transforming growth factor beta (TGF-beta) pathway--also may be inactivated by allelic loss on chromosome 18q. In addition, mutation of the tumor-suppressor gene p53 on chromosome 17p appears to be a late phenomenon in colorectal carcinogenesis. This mutation may allow the growing tumor with multiple genetic alterations to evade cell cycle arrest and apoptosis. Neoplastic progression is probably accompanied by additional, undiscovered genetic events, which are indicated by allelic loss on chromosomes 1q, 4p, 6p, 8p, 9q, and 22q in 25% to 50% of colorectal cancers. Recently, a third class of genes, DNA repair genes, has been implicated in tumorigenesis of colorectal cancer. Study findings suggest that DNA mismatch repair deficiency, due to germline mutation of the hMSH2, hMLH1, hPMS1, or hPMS2 genes, contributes to development of hereditary nonpolyposis colorectal cancer. The majority of tumors in patients with this disease and 10% to 15% of sporadic colon cancers display microsatellite instability, also know as the replication error positive (RER+) phenotype. This molecular marker of DNA mismatch repair deficiency may predict improved patient survival. Mismatch repair deficiency is thought to lead to mutation and inactivation of the genes for type II TGF-beta receptor and insulin-like growth-factor II receptor. Individuals from families at high risk for colorectal cancer (hereditary nonpolyposis colorectal cancer or familial adenomatous polyposis) should be offered genetic counseling, predictive molecular testing, and when indicated, endoscopic surveillance at appropriate intervals. Recent studies have examined colorectal carcinogenesis in the light of other genetic processes. Telomerase activity is present in almost all cancers, including colorectal cancer, but rarely in benign lesions such as adenomatous polyps or normal tissues. Furthermore, genetic alterations that allow transformed colorectal epithelial cells to escape cell cycle arrest or apoptosis also have been recognized. In addition, hypomethylation or hypermethylation of DNA sequences may alter gene expression without nucleic acid mutation.
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PMID:Molecular biology of colorectal cancer. 943 4

Patients with ulcerative colitis have an increased risk for developing colon cancer compared to the general population. The risk is related to the extension of the disease and its duration. This risk is the same for Crohn's colitis patients of equal extension and duration. By chemoprevention we mean the use of specific natural or synthetic chemical agents to reverse, suppress or prevent progression to invasive cancer. The chemopreventive agents for colon cancer are either of natural origin (vitamins, minerals, food constituents) or synthetic chemicals (difluoromethyl ornithine) and pharmaceutical agents (aspirin, oltipraz). Apart from folate, no other agent has so far been used in vivo for the prevention of colon cancer in long-standing inflammatory bowel disease. The use of folate was, however, not primarily intended to prevent cancer but to enhance folate absorption in ulcerative colitis. From retrospective studies, within the framework of cancer surveillance programmes, it became evident that folate supplementation may play a positive role as a chemopreventive agent against colorectal cancer in patients with long-standing, extensive ulcerative colitis. There is also evidence suggesting that folate supplementation may contribute to regulation of rectal cell proliferation in ulcerative colitis patients. There is a real need for multicentre, randomized, prospective clinical studies in order to evaluate the promising role of folate in preventing colorectal cancer in patients with long-standing inflammatory bowel disease.
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PMID:Chemoprevention of colorectal cancer in inflammatory bowel disease? A potential role for folate. 978 43

The Swedish Family-Cancer Database was used to analyze relationships between parents and offspring with in situ cancers and between in situ cancers in one generation and invasive cancer in the other generation. A total of 130,000 in situ cancers and close to 400,000 invasive cancers were included from 1959 to 1994. The data on family relationships and cancers came from registered sources and should be free from bias. The offsprings' familial relative risks (FRRs) were calculated for concordant and discordant parental cancer sites. The most common male in situ site was skin (both melanoma and precancerous epithelial lesion), whereas cervix, breast, and skin were common female sites. Increased FRRs were observed for concordant sites: colon, breast, cervix, skin (melanoma), and, in males, precancerous epithelial lesions. The findings were consistent when in situ cancer-in situ cancer and in situ cancer-invasive cancer relationships were explored. FRRs were higher for in situ colon cancer and melanoma than the respective estimates in invasive cancers, and for the remaining sites, they were equal or somewhat lower. At discordant sites, increased FRRs of in situ cancers were observed for female breast and melanoma and, at many sites, implicated in tobacco and human papilloma virus carcinogenesis, together with cervix. Family histories of in situ cancers deserve clinical attention.
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PMID:Familial risks in in situ cancers from the Family-Cancer Database. 979 30

A patient with ulcerative colitis, extensive dysplasia, multifocal colon cancer, and an appendiceal cystadenoma is described. A 48-year-old man with a 26-year history of ulcerative colitis (UC) had extensive dysplasia involving nearly the entire colon and four dysplasia-associated mass lesions (DALMs). Four invasive adenocarcinomas were present. This case is the first documentation of a DALM (mucinous cystadenoma) arising in the appendix in the setting of UC. The genetic alterations present in the various lesions were analyzed. The molecular profiles of the neoplastic lesions differed. Mutations were found in p53 and ras genes, and one site showed microsatellite instability in a single genetic locus. These molecular abnormalities develop before invasive cancer develops, and may undergo clonal expansion to create large mucosal patches containing certain cells with genetic alterations. The diversity of the early changes suggests that the recurrent inflammation characteristic of long-standing UC randomly damages genes known to participate in colon carcinogenesis and that it affects multiple target genes. The findings also support a multiclonal origin of synchronous tumors because the molecular phenotypes of the preinvasive lesions differed at various sites.
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PMID:Multifocal neoplasia involving the colon and appendix in ulcerative colitis: pathological and molecular features. 983 86

We report an 89-year-old man with colon cancer that developed rapidly after an incomplete endoscopic mucosal resection (EMR), and discuss the adverse effect of this maneuver on the tumor biology. A sessile polyp, 15 mm in size, was detected at the hepatic flexure. EMR was performed immediately. Histological examination showed well differentiated adenocarcinoma with an adenomatous component invading the submucosal layer. There was vascular invasion (positive on elastica van Gieson staining) and the surgical margin was positive for cancer. A right hemicolectomy was performed. The surgical specimen showed the residual tumor, 22 mm in diameter. The relevant histopathological findings of the surgical specimen were: well differentiated adenocarcinoma, with partly mucinous carcinoma and a tubular adenomatous component, depth muscularis propria (mp), lymph node (LN) (0/9). Most of the submucosally invasive cancer was resected by the initial EMR, but the small residual tumor showed rapid growth within only 3 months after the EMR. It was assumed that the residual tumor cells had acquired more malignant characteristics after EMR. In regard to EMR we propose that: (1) except for patients who are at high risk for a major operation, EMR should be avoided for carcinoma with massive submucosal invasion, (2) colonic resection should be performed immediately when histology shows a positive surgical margin for carcinoma, and (3) patients operated after an incomplete EMR should be watched very carefully for the detection of recurrence.
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PMID:Rapid growth of residual colonic tumor after incomplete mucosal resection. 1021 29

About 13% of all colorectal cancer may be dominantly inherited. This amounts to about 300 new cases a year in Norway. Colorectal cancer can be cured by early diagnosis and treatment. Coloscopy with polypectomy may prevent infiltrating cancer. Affected families should be offered genetic evaluation, and family members subjected to regular colonoscopy. The genetic bases of five colorectal cancer syndromes, accounting for most cases of hereditary early onset colorectal cancer, have now been determined. These are familial adenomatous polyposis, colon-endometrial cancer (hereditary non-polyposis colon cancer), Cowden's syndrome, Peutz-Jegher's syndrome and juvenile polyposis. These account for at most 3% of all colorectal cancers. In this group, predictive genetic testing may be employed in families with known mutation. Demonstration of mutation carriers by predictive testing must be based on health service available to the persons at risk. With regard to prophylactic measures, experimental and epidemiological data suggest a preventive effect of aspirin and resistant starch. Empirical information on the effect of intervention is insufficient; multicentre studies are needed.
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PMID:[Hereditary colorectal cancer]. 1059 56

PURPOSE: Some studies suggest women with certain types of cancers are at increased risk for ovarian cancer. This study assessed the risk of second primary ovarian cancer among U.S. women who have cancer by anatomic site, age, race, and time since diagnosis of the first primary cancer.METHODS: We analyzed data from SEER cancer registries for women diagnosed with invasive cancer between 1973 and 1996. Person-years were accumulated from 2 months after initial cancer diagnosis to date of ovarian cancer diagnosis, death, loss to follow-up, or end of follow-up, December 31, 1996. The expected number of cases was obtained by multiplying 5-year age and calendar year interval specific ovarian cancer rates by the accumulated person-years at risk. We calculated the risk (observed [O]/expected numbers [E]) of second primary ovarian cancer by cancer site and age (<50 years, >/=50 years), race (all, white, black), and time since first cancer (0-4, 5-9, 10-14, 15-24 years). Statistical tests and 95% confidence intervals (CI) were based on the assumption of a Poisson distribution.RESULTS: A significant increased risk of ovarian cancer was found for women aged <50 years at time of diagnosis with melanoma (O/E = 3.5, 95% CI = 2.1-5.5) and cancer of the breast (O/E = 6.0, 95% CI = 4.9-7.2), cervix (O/E = 4.2, 95% CI = 2.6-6.3), corpus uteri (O/E = 11.91, 95% CI = 7.3-18.4), colon (O/E = 17.9, 95% CI = 11.1-27.3), and ovary (O/E = 4.9, 95% CI = 2.7-8.2); no increased risk was found for women aged >/=50 years. Ovarian cancer risk remained elevated following all of these first primary cancers 5-9 years after diagnosis; for women with breast and colon cancer, risk remained elevated 15-24 years after diagnosis. A significant increased risk was found for all of these cancers among white women <50 years at diagnosis; risk was increased among black women <50 years with cancer of the breast, cervix, and colon.CONCLUSIONS: We found an ovarian cancer risk higher than expected for women with certain types of cancer; however, the risk was limited to women <50 years of age.
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PMID:Second primary ovarian cancer among women with cancer. 1101 87


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