Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Colonic Neoplasms”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 649 records · Page 36Linked to original sources
PubMed2006

Hyperplastic polyposis coli syndrome and colorectal carcinoma.

BACKGROUND: Patients with hyperplastic polyposis coli syndrome (HPCS) have a propensity to develop colorectal carcinoma (CRC). PATIENTS AND METHODS: Details were retrieved from the files of patients attending our hospital between 1988 and 2004 who fulfilled the World Health Organization criteria for HPCS. RESULTS: Over a period of 16 years, 10 cases of HPCS were identified at our hospital (0.625 cases/year or one case every 1.6 years). A mean of 40.3 hyperplastic polyps per patient were found (range 6-159). Other colorectal lesions were found as follows: two patients each had one mixed polyp; there were 15 serrated adenomas in eight patients; and there were 30 tubular, tubulovillous, or villous adenomas in eight patients. Among the 10 patients with HPCS, seven developed a CRC. Of the four villous adenomas, three were associated with a CRC, but only one of the 15 serrated adenomas was associated with a CRC. The pathway of cancer evolution in HPCS patients remains unresolved. CONCLUSIONS: Similarly to our results, a review of the literature indicates a high incidence of CRCs in HPCS patients. These patients are at a high risk of developing a CRC and should therefore receive regular colonoscopic surveillance.

Adenoma↗
PubMed1986

Complications and pitfalls of laser therapy.

228 patients have been studied in retrospect, in an attempt to delineate the limits and pitfalls of laser treatment of benign (n = 104) and malignant (n = 124) tumors. Benign colorectal adenomas (n = 78) were divided into 3 groups according to the size of the lesion. The occurrence of complications, the persistence and recurrence rate paralleled the size of the tumor. No relationship as to the number of sessions, the interval between them or the mean and/or total amount of energy was found. The prolonged time span of treatment in larger lesions was related to the formation of large ulcers and edema. Poor accessibility and difficult positioning of the laser beam interfered with adequacy of laser treatment. In familial polyposis (n = 26) laser photocoagulation appeared a highly effective, safe and easy procedure. In esophageal cancer (n = 16), gastric (n = 13) and colorectal malignancies (n = 95) laser therapy was very efficaceous in the palliation of bleeding and/or obstruction. Unfavorable anatomy and difficult accessibility were the main drawbacks. Problems in the assessment of pathology and submucosal extension impeded effective treatment of early cancer. Generally speaking, the presence of a whitish appearance, fibrosis of bloody tissue pointed toward a less favorable response, but much more has to be learned about the interaction between laser light and tissue properties.

Adenocarcinoma↗
PubMed2000

Genetic reconstruction of individual colorectal tumor histories.

It is difficult to observe human tumor progression as precursor lesions are systematically removed. Alternatives to direct observations, commonly used to reveal the hidden past of species and populations, are sequence comparisons or molecular clocks. Noncoding microsatellite (MS) loci were employed as molecular tumor clocks in 13 human mutator phenotype (MSI(+)) colorectal tumors. Quantitative analysis revealed that specific patterns of somatic MS mutations accumulate with division after loss of mismatch repair (MMR). Tumors had unique patterns of MS mutation, and, therefore, based on this model, each tumor had its own unique history. Loss of MMR occurred very early relative to terminal clonal expansion, with an estimated average of 2,300 divisions since loss of MMR and 280 divisions since expansion. Contrary to the classical adenoma-cancer sequence, MSI(+) adenomas were nearly as old as cancers (2,000 versus 2,400 divisions since loss of MMR). Negative clinical examinations preceded six tumors, independently documenting an absence of visible precursors during early MSI(+) adenoma or cancer progression. These findings further extend a window beyond visible progression since loss of MMR appears to start a genetic phase involving clone sizes or phenotypes below a threshold of clinical detection. This previously occult prologue before visible neoplasia is longer and therefore likely more important than generally appreciated.

Adenocarcinoma↗
PubMed1997

Eicosanoids: role in gastrointestinal inflammation and cancer.

This paper contains a brief review of the metabolism and physiological actions of eicosanoids, with a discussion of the potential clinical implications of disturbances in eicosanoid metabolism, particularly in NSAID-induced upper gastrointestinal damage and inflammatory bowel disease. There follows a summary of current evidence for the role of eicosanoids in the pathogenesis of colorectal neoplasia.

Animals↗
PubMed1990

Low diacylglycerol values in colonic adenomas and colorectal cancer.

The biochemical events that make colonic epithelial cells proceed along the adenoma-carcinoma sequence are not well understood. The phosphoinositol signal transduction pathway is involved in the regulation of cell growth and differentiation. To determine its role in colonic neoplasias we performed mass measurements of its second messenger sn-1,2-diacylglycerol in biopsy specimens from normal mucosa and neoplasias of the colon. Normal colonic mucosa was also investigated in patients without colonic abnormalities (n = 10). Compared with pooled diacylglycerol values from five colonic sites (100%), values in patients with a normal colon were highest in the ascending colon (120 (5)%, p less than 0.05) and lowest in the rectum (81 (5)%, p less than 0.01). Absolute diacylglycerol values in patients with normal colons (2.62 (0.16) nmol/mg protein) were not significantly different from those found in the normal mucosa of patients with colorectal neoplasias (2.45 (0.17) nmol/mg protein). Both colonic adenomas (n = 15) and colorectal carcinomas (n = 14) showed significantly decreased diacylglycerol values compared with the adjacent normal mucosa of each patient (72 (4)%, p less than 0.001, and 71 (4)%, p less than 0.001 respectively). The appreciable decrease in mass diacylglycerol values clearly distinguishes adenomas and carcinomas of the colon from the surrounding normal mucosa. This finding suggests that profound metabolic changes of the phosphoinositol signal transduction pathway occur early in the adenoma-carcinoma sequence and may be important in colonic carcinogenesis.

Adenocarcinoma↗
PubMed1987

Correlation of nuclear ploidy with histology in adenomatous polyps of colon.

Histological sections of adenomatous polyps of the colon showing carcinoma were studied by video image analysis. Nuclear DNA content and morphology were measured in regions identified as either dysplasia, carcinoma confined to the mucosa, or carcinoma invading the muscularis mucosa. Where carcinoma was present, areas of dysplasia in the same polyp were found to have similar distributions of nuclear DNA content and size, supporting the notion that adenomatous polyps becomes cancer. The method can be used to detect those regions in sections of adenomatous polyps with the most severe nuclear abnormality.

Adenocarcinoma↗
PubMed1999

Pathology report in colon cancer: what is prognostically important?

Surgical resection is the primary treatment modality for colorectal cancer, and the most powerful tool for assessing prognosis following surgery is pathologic analysis of the resection specimen. Although the parameters that determine the pathologic stage are the strongest predictors of postoperative outcome, a number of additional pathologic features have prognostic significance that is independent of stage. These include: histologic grade; small vessel (lymphatic or venular) invasion; extramural venous invasion; perineural invasion; tumor border configuration; host lymphoid response to tumor, and the status of surgical margins. For specimens in which the radial (circumferential) margin is applicable, surgical clearance around the tumor is also of import. It is self-evident that, compared to data derived from additional assays, prognostic information that can be derived directly from standard histologic sections of a tumor is of the greatest cost-benefit to the patient. In the current era of cost containment, it is essential that surgical pathologists evaluate and report the pathologic features that are of prognostic and/or predictive significance in every case of colorectal cancer and, in turn, that the import of these be understood by the treating physicians.

Adenocarcinoma↗
PubMed1999

A bile acid-induced apoptosis assay for colon cancer risk and associated quality control studies.

Bile acids are important in the etiology of colorectal cancer. Bile acids induce apoptosis in colonic goblet cells at concentrations comparable to those found in fecal water after high-fat meals. Preliminary evidence indicated that cells of the normal-appearing (nontumorous) portion of the colon epithelium of colon cancer patients are more resistant to bile salt-induced apoptosis than are cells from normal individuals. In the present study, 68 patients were examined, and biopsies were taken at 20 cm from the anal verge, cecum, and descending colon. The patients included 17 individuals with a history of colorectal cancer, 37 individuals with adenomas, and 14 individuals who were neoplasia free. The mean bile salt-induced apoptotic index among normal individuals was 57.6 +/- 3.47 (SE), which differed significantly (P < 0.05) from the mean value of 36.41 +/- 3.12 in individuals with a history of colon cancer. The correlation between independent observers was 0.89 (P < 0.001), indicating good interobserver reliability. Components of variance comparing interindividual versus intraindividual sources of variation suggested that site-to-site variability, both between regions of the colon and for adjacent biopsies, was larger than the interpatient variability for individuals with a history of neoplasia. Therefore, there was "patchiness" of the susceptibility of regions of the colon to bile acid-induced apoptosis in individuals with a history of neoplasia (a patchy field effect). There was no obvious correlation of low-apoptotic index regions with regions in which previous neoplasias had been found and removed. On the other hand, for normal, i.e., neoplasia-free, individuals, there was relatively less intraindividual variation compared to interindividual variation. Our assay shows an association between resistance to bile acid-induced apoptosis, measured at 20 cm from the anal verge, and colon cancer risk. Thus, this assay may prove useful as a biomarker of colon cancer risk.

Adenoma↗
PubMedDate not supplied

Change in telomerase activity during human colorectal carcinogenesis.

Telomerase activities in endoscopically resected colorectal adenomas, surgically resected colorectal cancers and adjacent normal colonic mucosa were examined semiquantitatively by a polymerase chain reaction-based telomeric repeat amplification protocol (TRAP) assay. All normal mucosa (n = 15) presented weak telomerase activity (mean +/- SE: 0.99 +/- 0.00). When the value of 1.00 was arbitrary given to the mean activity of normal mucosa, the telomerase activity in the adenomas (n = 14) was up-regulated (2.01 +/- 0.22) relative to the normal mucosa. The telomerase activity in the high-grade atypia (severe atypia and carcinoma in situ) (2.58 +/- 0.34) was significantly higher than that in the low-grade (mild and moderate) atypia (1.59 +/- 0.18) (P < 0.05), and the adenomas 10 mm or more in diameter presented significantly higher telomerase activity (2.56 +/- 0.09) than compared to the smaller ones (1.44 +/- 0.17) (p < 0.05). Carcinomas (n = 20), showed a telomerase activity that varied from 0.97 to 16.93, which was than the greater mean telomerase activity (6.96 +/- 1.25) noted in the adenomas. The telomerase activity in the carcinomas tended to be higher in the larger (> or = 4 cm), histologically less-differentiated (moderately differentiated), late-stage (Dukes C + D), and nodal metastatic tumors, suggestive of unfavorable prognosis. These results suggests that the weak telomerase activity in normal colonic mucosa is gradually activated during the course of colorectal carcinogenesis.

Adenoma↗
PubMedDate not supplied

Non-polypoid colorectal neoplasias: a multicentric study.

A total of 781 non-polypoid colorectal neoplasias harvested at 4 main Hospitals in Tokyo, Japan (n = 420) and at 4 different time-intervals at the Karolinska Hospital, Stockholm, Sweden (n = 361) were reviewed. By applying strict histologic definitions, the lesions were classified into adenomas with low grade dysplasia (LGD), with high grade dysplasia (HGD), intramucosal carcinomas (IMC) or submucosal carcinomas (SMC). Of the non-polypoid neoplastic lesions reviewed in Sweden, 82.8% (n = 299) had LGD. In Japanese patients only 42.6% (n = 179) had LGD (p < or = 0.001). On the other hand, as many as 42.4% (n = 178) of the non-polypoid lesions in Japanese patients had HGD, but only 14.1% (n = 51) of those in Swedish patients (p < or = 0.001). Whereas 15.0% (n = 63) of the non-polypoid neoplasias seen in Japan were IMC or SMC, only 3.0% (n = 11) of those seen in Sweden were IMC or SMC (p < or = 0.001). The cause(s) for these differences remains unclear. In Japan, however, a marked increased incidence of colonic cancer has been recorded in later years. Whether the "catching up phenomenon" by the Japanese with western colonic cancer incidence includes increased histologic aggressiveness of non-polypoid neoplastic polyps--as found in this survey--remains to be elucidated.

Adenoma↗
PubMedDate not supplied

[Mutation in the MSH2 gene in Muir-Torre syndrome].

BACKGROUND: The Muir-Torre syndrome is an autosomal dominant hereditary condition predisposing to cancer. It is characterized by skin tumors associated with adenocarcinoma of the colon or other neoplasias observed in the context of hereditary non-polyposis colorectal cancer (HNPCC). The Muir-Torre syndrome is also characterized by the frequent presence of multiple colonic polyps and the relatively moderate aggressivity of the tumors. CASE REPORT: We studied a family with Muir-Torre syndrome. We sequenced the exons of the hMSH2 gene in this family and identified heterozygous germinal mutation by G insert at position 2427 (2427insG). This mutation changes the lecture phase producing a premature codon stop. DISCUSSION: Our study confirms the predominant responsibility of the hMSH2 gene in Tuir-Torre syndrome. This clinical case and data reported in the literature demonstrate the importance of searching for a history of non-polyposis colorectal cancer in patients and relatives and the unstable genome characteristic of these tumors found in sebaceous tumors or keratoacanthomas. Sequencing the hMSH2 gene should be a priority when clinical features, history and laboratory tests suggest Muir-Torre syndrome.

Adenocarcinoma↗
PubMedDate not supplied

Telomerase activity and p53 gene mutation in familial polyposis coli.

BACKGROUND: Familial adenomatous polyposis (FAP) is a dominantly inherited disorder and it is difficult to know when polyps change to carcinoma. In this study, we retrospectively evaluated whether telomerase activity and p53 gene mutations are useful parameters for detecting malignant changes in polyps in patients with FAP. MATERIALS AND METHODS: Twenty-one tissue samples (carcinoma: 5, large polyp: 8, and small polyp: 8) were obtained from 8 patients with FAP. Colorectal carcinomas were detected in 5 patients. As a control, 68 colorectal carcinomas and 11 adenomatous polyps with synchronous colorectal carcinoma from 68 patients and 8 polyps from 8 patients without colorectal carcinoma were obtained. The telomeric repeat amplification protocol (TRAP) assay was used for the detection of telomerase activity. In 21 samples from FAP patients, mutations of exon 5 to 8 in the p53 gene were analyzed by the polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) method. RESULTS: In 5 patients with FAP who had carcinomas in their colon and rectum, all the samples (carcinomas, large polyps and small polyps) showed telomerase activity. In contrast, in the 3 patients with FAP who had no carcinomas, telomerase activity was not detected in either the large or small polyps. Telomerase activity was detected in 51 out of 68 control colorectal carcinomas (75%) and in 6 out of 19 adenomas (32%). The p53 gene mutation was detected in only 2 carcinomas from 2 patients with FAP and was not detected in any large and small polyps. CONCLUSION: These findings suggest that telomerase is activated before the occurrence of the p53 gene mutation. In FAP, genetic changes associated with the development of colonic adenoma into carcinoma might activate telomerase and such genetic changes might occur in whole polyps of the colon and rectum.

Adenomatous Polyposis Coli↗