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

Colon cancer is a well known complication of ulcerative colitis. Various methods have been discussed to reduce its risk. Since the introduction of the concept epithelial dysplasia and fiberoptic colonoscopy surveillance programmes have been launched based on these methods. The incidence of colon cancer in ulcerative colitis is moderately increased but constitutes only a fraction of all colon cancers diagnosed. Among these patients colon cancer almost exclusively affects those with extensive colitis. Duration of disease in these cases usually exceeds eight to ten years. The true benefit of a cancer surveillance programme will probably never be the subject of controlled prospective studies and is therefore difficult to evaluate. The concept of dysplasia is the major instrument for selecting patients for prophylactic colectomy. Development from normal mucosa to high grades of dysplasia shows individual variations from one to several years justifying annual colonoscopies in high risk patients. Strict criteria for dysplasia and independent evaluations from several pathologists should compensate for the subjective nature of dysplasia interpretation. The need for more objective markers such as DNA-flow cytometry is clearly needed. The role of DNA flow cytometry in surveillance, however, needs to be determined. The cost benefit aspects of such surveillance programmes have to be balanced against the total resources of a gastroenterology unit.
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PMID:Ulcerative colitis and colon cancer: the role of surveillance. 250 15

Since 1977, 196 patients (177 with ulcerative colitis and 19 with familial polyposis) have undergone colectomy, mucosal proctectomy and endorectal ileal pull-through with or without an ileal reservoir (PTR) at UCLA Medical Center. Fourteen of the patients (7.1 per cent) had carcinoma of the colon or rectum at the time of operation; 12 had colitis and two, polyposis. Another 40 patients had mucosal dysplasia. Only five of the 14 patients with carcinoma were diagnosed before operation despite close surveillance by gastroenterologists. The mean duration of colitis before the diagnosis of carcinoma was made was 17 years; the mean age that the carcinoma was identified was 38 years. Eleven of the 12 patients with colitis had universal involvement. Two patients with colitis and carcinoma who underwent colectomy and PTR died a mean of 30.5 months postoperatively of metastatic disease. Twelve patients with carcinoma (ten with colitis and two with polyposis) are alive a mean of 29 months postcolectomy and PTR; two of these have received chemotherapy. The low mortality (0.4 per cent) and good clinical results after colectomy and the PTR procedure and the unexpectedly high incidence of carcinoma and mucosal dysplasia among patients referred for operation suggest that surgical treatment should be considered at an earlier stage than the current general practice, particularly in patients at high risk (mucosal dysplasia, pancolitis and duration of more than ten years).
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PMID:The endorectal ileal pullthrough procedure in patients with ulcerative colitis and familial polyposis with carcinoma. 254 48

Folate deficiency has been associated with dysplasia in human cancer models. Patients with ulcerative colitis commonly have decreased folate levels, which are partially due to sulfasalazine, a competitive inhibitor of folate absorption. To study the effect of folate supplementation on the risk of dysplasia or cancer (neoplasia) in ulcerative colitis, records from 99 patients with pancolitis for greater than 7 yr and enrolled in a surveillance program were reviewed. Thirty-five patients with neoplasia were compared with 64 patients in whom dysplasia was never found to determine the effect of folate supplementation on the rate of development of neoplasia using case-control methodology. At the time of the index colonoscopy, patients with neoplasia were older (43 +/- 11 vs. 39 +/- 12 yr) and had disease of longer duration (20 +/- 8 vs. 15 +/- 7 yr, p less than 0.05). Folate supplementation was associated with a 62% lower incidence of neoplasia compared with individuals not receiving supplementation (odds ratio, 0.38; 95% confidence interval, 0.12-1.20). There was no appreciable change in this effect when models were fit to adjust for sulfasalazine dose, duration of disease, age at symptom onset, prednisone dose, sulfa allergy, sex, race, or family history of colon cancer. The statistical power of the association between folate supplementation and neoplasia was 72%. Correction of risk factors before the development of neoplasia may prevent this serious complication. Pending a larger case-control study, folate supplementation during sulfasalazine administration is recommended to possibly prevent the complication of dysplasia or cancer in ulcerative colitis.
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PMID:Effect of folate supplementation on the incidence of dysplasia and cancer in chronic ulcerative colitis. A case-control study. 229 14

210 various colo-rectal polyps including 46 inflammatory polyps, 21 juvenile polyps, 9 hyperplastic polyps, 65 tubular adenomas, 51 familial polyps, 11 villous adenomas, 7 adenomatous polyps with focal cancer, and 14 carcinoma of the large bowel were investigated by HE,HID-AB,PAT-KOH-PAS staining in order to study the mucin changes of these lesions. N-acetylated and C7,C9 O-acetylated sialomucin were mainly obtained in those adenomas with moderate and severe dysplasia (55-64.3%) and the proportion was even higher in cases of villous adenomas, familial polyps, adenomas with focal cancer and advanced carcinoma. These mucins might be assumed as a criteria in representing malignant transformation.
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PMID:[Mucin histochemical changes in various colo-rectal polyps in relation to carcinoma of the large bowel]. 258 49

Monoclonal antibody (MAb) B72.3 reactive with the high-molecular-weight (Mr greater than 10(6) tumor-associated glycoprotein (TAG)-72 is being increasingly utilized in vivo and in vitro for a variety of purposes in colon cancer patients. Recent evidence has suggested that the TAG-72 antigen expression may be enhanced in inflammatory bowel disease, particularly ulcerative colitis (Thor et al., 1986a: Cancer Res., 46, 3118-3124). We have utilized 117 paraffin-embedded formalin-fixed colonic specimens from 56 ulcerative colitis patients which demonstrate a spectrum of epithelial abnormalities (reactive atypia, dysplasia, and carcinoma) as well as 11 inflammatory controls to evaluate TAG-72 expression. Our selected patient population all had pan-colitis and demonstrated a generally increasing incidence of dysplasia or carcinoma with duration of disease (20% at 0 to 10 years, 50% at 11 to 20 years, 59% at 21 to 30 years, and 100% at more than 31 years). TAG-72 expression was similar in the control and non-dysplastic colonic epithelia, and increased with low- or high-grade dysplasia as well as carcinomatous lesions (mean cellular reactivities 23.7%, 26.5%, 36.7%, 70% and 84.3%, respectively). Epithelium with low-grade dysplasia exhibited a focal perinuclear, superficial crypt staining (when present). High-grade dysplastic epithelium showed pancytoplasmic, pan-cryptic reactivity. Invasive disease showed cytoplasmic as well as extracellular mucin staining. Biopsies from patients with active disease showed significantly more immunoreactive cells for TAG-72 than patients with quiescent disease. For any given biopsy specimen the percentage of cells reactive did not always correlate with the degree of dysplasia. TAG-72 expression in quiescent disease generally increased with duration of disease, in contrast to active disease which showed no correlation between MAb B72.3 staining and duration of disease. The frequent expression of TAG-72 in actively inflamed colonic mucosa (ulcerative colitis and other colitides) may limit the clinical utility of this antigen for detecting colon cancer in ulcerative colitis patients by serological assay or in vivo radiolocalization techniques. The tendency for TAG-72 expression to correlate with disease duration in patients with quiescent disease and to increase with more severe degrees of dysplasia suggests that the expression of this gene product correlates with the dysplasia-to-carcinoma sequence.
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PMID:Tumor-associated glycoprotein (TAG-72) expression in ulcerative colitis. 265 25

The purpose of this experiment was to study sequential histogenesis of colonic epithelial tumours in the dimethylhydrazine (DMH) induced rat colon cancer model. Seventy outbred female Wistar rats treated with DMH (40 mg/kg, subcutaneously weekly for five weeks) were killed and autopsied in batches of 10 every five weeks from the 10th to 40th weeks from first treatment. The resulting 378 colonic lesions were assigned to benign or malignant categories using each of three standard histopathological thresholds of malignancy: alpha, the transition from dysplasia to intraepithelial carcinoma; beta, invasion through the crypt basement membrane; and gamma, invasion through the muscularis mucosae. These comprised 79 'benign' and 299 'malignant' or 273 'benign' and 141 'malignant' lesions depending on the threshold (alpha or gamma) assigned (p less than 0.001). Decreasing ratios of pre-threshold to post-threshold lesions between 15 and 40 weeks (alpha, 2.0 to 0.051; beta, 3.5 to 0.57; gamma, 8.0 to 0.87) provide some support for an 'adenoma-carcinoma' progression for each. Comparison of time-dependent prevalence curves confirms that the alpha threshold (cyto-architecture) is qualitatively different from the beta and gamma thresholds (invasion), showing that the adenoma-carcinoma and de novo hypotheses need not be mutually exclusive. The time-dependent prevalence data support de novo origin of some carcinomas, as well as at least two other modes of accrual for neoplastic lesions.
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PMID:Comparison of the significance of three histopathological thresholds of malignancy in experimental colorectal tumours. 275 8

The risk of colon cancer in patients with ulcerative colitis is related to the duration and extent of disease. Prior reports have suggested that patients with onset of disease in childhood have a high risk of cancer. These risk factors were analyzed in 99 patients in a surveillance program of annual colonoscopy to detect mucosal dysplasia. All patients had pancolitis for at least eight years. The mean age at symptom onset was 23.2 years and the mean duration of disease at entry was 17 years. An average of 4.2 tests/patient were performed, and 91% were completely followed through 1985. Cancer risk was expressed as the hazard rate or the annual probability that a patient free of cancer would develop cancer after survival to a given time period. The hazard rate for high-grade dysplasia or cancer in patients with pancolitis measured from symptom onset was 2.5% at 20 years, 4% at 25 years, 7% at 30 years, 13% at 35 years, and 20% at 40 years. Sex was not a significant predictor of cancer, but older age at symptom onset was a predictor of dysplasia and cancer. From these data, the annual hazard rate of developing high-grade dysplasia or cancer can be estimated in patients with pancolitis based on an individual's age at symptom onset and duration of disease.
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PMID:Hazard rates for dysplasia and cancer in ulcerative colitis. Results from a surveillance program. 279 5

In vitro tetraploidy (IVT) in cultures of skin fibroblasts was compared with tumor DNA ploidy, as determined by flow cytometry on paraffin-embedded material, in 99 patients with colorectal neoplasm. In 63 patients with non-heritable carcinoma we found a significant correlation between the number of aneuploid stemlines in the tumor and IVT in the fibroblast culture. Furthermore, tumor aneuploidy was significantly correlated to the size of the tetraploid subpopulation in the fibroblasts. There was no correlation between aneuploidy and Dukes's stage or the degree of differentiation. In 36 patients with adenoma no correlation between tumor aneuploidy and fibroblast IVT was demonstrated, whereas the number of tumor stemlines was significantly correlated to histopathologic stage and grade of dysplasia. IVT in cultured skin fibroblasts, which has been reported to reflect a genetic predisposition to colorectal cancer in heritable colon cancer syndromes, thus seems to be relevant also for the understanding of tumor formation and progression in the 'non-heritable' type of colorectal cancer.
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PMID:Association between tumor DNA aneuploidy and in vitro tetraploidy of skin fibroblasts in patients with colorectal neoplasms. 281 41

Patients with total long-standing mucosal ulcerative colitis are at an increased risk of developing carcinoma of the colon or rectum. Recently it has been suggested that cytological examination of the colon may play an important role in the examination of these patients. The present study was undertaken in order to determine the malignancy/severe dysplasia rate in our patients and to examine the role of cytology in comparison with mucosal biopsy in the detection of mucosal abnormality. Three patients had severe dysplasia in the absence of active inflammation (7.1%). Fifty-four patients were examined concurrently by histology and cytological brushing and at least seven specimens were obtained from each patient. Cytological examination detected active mucosal inflammation more often than histological examination at all sites in the colon. There was good agreement between the cytologists' evaluation, routine histopathological examination and endoscopic evaluation of the colorectal mucosa, although the latter tended to underestimate the degree of active inflammation. It was concluded that, since there was no real improvement in sampling by brush cytology, there may be little advantage in supplementing routine biopsy with brush cytology in patients with long-standing inflammatory bowel disease.
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PMID:Colonoscopy, mucosal biopsy and brush cytology in the assessment of patients with colorectal inflammatory bowel disease. 281 78

Type C-related human endogenous retroviral sequences have been previously discovered and characterized [Martin, M. A., Bryan, T., Rasheed, S. & Khan, A.S. (1981) Proc. Natl. Acad. Sci. USA 78, 4892-4896]. We investigated the transcriptional pattern of these sequences to determine whether and to what extent their expression is altered in colon tumors and colon cancer cell lines as compared to normal colon mucosa (NCM). Of two long terminal repeat (LTR)-specific transcripts [3.6 and 2.1 kilobases (kb)], the 3.6-kb RNA was particularly abundant in NCM but strikingly decreased in most primary colon cancers tested. In NCM we identified three envelope gene (env)-related transcripts--namely, 3.0, 1.7, and 0.6 kb. Colon tumors appeared to express higher levels of these transcripts, especially the 1.7-kb species. In one case of dysplasia and in one benign tumor, this 1.7-kb transcript was clearly increased. We also examined the pattern of transcription in colon cancer cell lines HCT and Caco2. The LTR-homologous 3.6-kb transcript, very abundant in NCM, was decreased in primary tumors and in HCT cells and virtually absent in Caco2 cells. The latter, however, appeared to produce the transcript when growing exponentially, indicating that Caco2 cultures provide an inducible system susceptible to in vitro manipulation. Both cell lines also contained higher amounts of the 1.7-kb env-related transcript. The decrease of the 3.6-kb RNA in colon tumors versus NCM may be the result of an altered pattern of differentiation, whereas the increase of the 1.7-kb RNA in tumors may represent an early marker of colon neoplasia.
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PMID:Expression of type C-related endogenous retroviral sequences in human colon tumors and colon cancer cell lines. 301 43


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