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)

Light-induced fluorescence endoscopy (LIFE) has been shown to differentiate between normal mucosa and dysplastic lesions, and dysplastic lesions of the colon occult to routine white-light colonoscopy may thus be visualized by LIFE. We compared the sensitivity and specificity of LIFE to routine white-light colonoscopy in patients with colonic dysplasia. In a pilot study 20 patients with colonic adenoma, inflammatory bowel disease, or with a history of colon cancer were screened for colonic dysplasia during routine colonoscopy. Forty-two sites of mucosal abnormalities regarded as suspicious for dysplasia during white-light colonoscopy were additionally examined with a prototype LIFE system. Biopsies were taken from all 42 colonic sites. The LIFE images were classified as positive or negative for dysplasia. Sensitivity and specificity were calculated by correlating positive and negative findings to the histopathological results. Histopathology detected 21 adenomas with low-grade dysplasia and one with high-grade dysplasia. All dysplastic lesions were found by routine white-light endoscopy. The specificity of conventional white-light endoscopy was 80%. Of the 22 dysplastic lesions 20 were detected by LIFE (sensitivity 91%). The specificity of LIFE was 90% (two false-positive results). LIFE combined with conventional endoscopy may thus improve the detection of colonic dysplasia.
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PMID:Detection of colonic dysplasia by light-induced fluorescence endoscopy: a pilot study. 1020 34

Pericryptal myofibroblasts (PMFs) are thought to be involved in the production of the basement membrane (BM) of the colonic epithelium. To clarify the involvement of PMFs in the formation of the BM during the growth of colon cancer, we conducted an immunohistological study of tumor specimens from 85 patients with colorectal epithelial tumor to detect the presence of PMFs. The tumor specimens were classified as adenoma with low-grade dysplasia, adenoma with high-grade dysplasia, or colon cancer. PMFs were detected in 66.6% of the specimens from patients with adenoma with low-grade dysplasia; 20% of specimens of adenoma with high-grade dysplasia; and 3.2% of specimens of colon cancer. As the degree of dysplasia of the tumor increased, the probability that PMFs existed decreased. We also tested 49 of the tumor specimens for the presence of laminin, a component of the BM, and found that in most of these 49 cases, the BM and PMFs co-existed. This provides further evidence that PMFs are involved in the production of the BM. These findings are important in gaining an understanding of the cause and growth of colorectal epithelial tumors.
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PMID:Immunohistological study to determine the presence of pericryptal myofibroblasts and basement membrane in colorectal epithelial tumors. 1021 21

There is an increased incidence of malignancies in transplant recipients. Accelerated progression from a premalignant lesion to carcinoma has been reported in transplant recipients with skin cancer and colon cancer. Whereas Barrett's esophagus is a common premalignant condition in the normal population, rapid progression to severe dysplasia or carcinoma has not been widely reported in transplant recipients. We report on a liver transplant recipient who developed rapid progression from Barrett's esophagus without dysplasia to high-grade dysplasia within 9 months after transplantation.
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PMID:Rapid progression to high-grade dysplasia in Barrett's esophagus after liver transplantation. 1038 6

In patients with chronic ulcerative colitis (CUC), polypoid dysplastic lesions (PDLs) are morphologically similar to sporadic adenomas (SAs), but may be biologically distinct from them and are managed differently. p53 mutations have been shown to occur at an earlier phase in the progression of CUC-associated neoplasia when compared with sporadic colon carcinogenesis. In contrast, APC gene mutations are common and occur at an earlier stage in the development of SA. beta catenin is a cell membrane protein that accumulates in the nucleus of colon cancer cells in response to APC gene mutations. This study was performed to test the hypothesis that CUC-associated PDLs have a different molecular profile than do CUC-associated SAs and therefore may be distinguished on this basis. Mucosal biopsy specimens of 38 benign polypoid epithelial neoplasms (17 CUC-associated PDLs and 21 CUC-associated SAs) from 33 patients with CUC and 13 SAs from patients without CUC (controls) were immunohistochemically stained for p53 and beta catenin and graded as follows: 0 = no staining, 1+ = <50% of cells positive, and 2+ = > or =50% of cells positive. The results were correlated with the clinical and histologic features and compared between the two CUC-associated polyp subgroups. Overall, six (16%) polyps were p53-positive, of which five were CUC-associated PDLs (one 1+ and four 2+) and one was a CUC-associated SA (1+) (p = 0.05). Strong (2+) p53 positivity was detected, however, in only CUC-associated PDLs (4 of 5; 80%). Nine of 32 polyps evaluated for beta catenin were positive and included 1 (8%) of 12 CUC-associated PDLs and 8 (40%) of 20 CUC-associated SAs (p = 0.06). Two of the nine beta catenin polyps were strongly positive, and both were CUC-associated SAs. Non-CUC-associated (control) SAs were positive for p53 and beta catenin in 2 (15%) of 13 and 6 (46%) of 13 cases, but none in a strong (2+) fashion. No differences were observed in p53 or beta catenin staining, between CUC-associated and non-CUC-associated SAs. Neither p53 nor beta catenin expression correlated with any clinical or pathologic features, including size and degree of dysplasia of the polyps. CUC-associated PDLs and CUC-associated SAs may have a different molecular genotype. In patients with CUC, the combination of strong p53 expression and absent or weak beta catenin expression is evidence in favor of a CUC-associated PDL in diagnostically difficult lesions. Furthermore, CUC-associated and non-CUC-associated SAs have a similar P53 and beta catenin immunophenotype and thus provide evidence that they are pathogenetically related neoplasms regardless of the presence or absence of colitis.
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PMID:P53 and beta catenin expression in chronic ulcerative colitis--associated polypoid dysplasia and sporadic adenomas: an immunohistochemical study. 1043 67

Investigate mutation of ras gene family in various stage of gastric cancer in China. PCR-RFLP, PCR-SSCP and PCR-DNA sequencing were used to detect mutation rates of H-ras, K-ras and N-ras gene. Mutation rates of H-ras at 12 codon in metaplasia, atypical hyperplasia, and progressive gastric cancer is 16.7% (6/36), 31.2% (15/48), 34.7% (25/72), respectively. In groups of superficial gastritis and normal control, no mutation were found. Mutations of H-ras 61 codon and N-ras 12 codon in various groups were the same as normal. Only 2 cases of K-ras 12 codon mutation were detected in gastric cancer by PCR-SSCP, but it was not identified by DNA sequencing. It may be of polymorphism. All H-ras 12 codon mutation were G-->T mutation. There are significant difference between groups of metaplasia, dysplasia, and gastric carcinoma comparing with group of normal control (P < 0.05, P < 0.01, P < 0.01). H-ras 12 codon mutation maybe an early event and maybe play important role in gastric carcinogenesis. Although K-ras mutation rate is high in colon cancer and leukemia it seemed to be relationship with gastric cancer. High frequency of H-ras 12 codon mutation maybe the characteristic of gastric cancer and associate with high incidence of gastric cancer in China. Three methods used in this experiment were compared that SSCP method is more sensitive than RFLP and cold SSCP is simpler and likely to be used in clinic.
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PMID:[Detection of ras gene mutation in various stages of gastric cancer by PCR/RFLP SSCP and DNA sequencing]. 1043 68

The purpose of this study was to determine whether point mutations and loss of the p53 gene take place in ulcerative colitis which is histologically negative for dysplasia. DNA was extracted from 13 frozen rectal or colon biopsies and blood samples. Ulcerative colitis was classified histologically as active (10 cases) and inactive (3 cases). Exons 5-8 were amplified by PCR, treated with exonuclease and shrimp alkaline phosphatase and sequenced by the dideoxy chain termination method with the Sequenase Version 2.0 DNA sequencing kit. PCR products of intron 6 and exon 4 were digested with MspI and AccII, respectively, for RFLP analysis. No p53 gene mutation was detected in these cases. The number of informative patients for loss of heterozygosity (LOH) at the p53 intron 6 was high, 11 out of 12 (92%), whereas no LOH was observed. LOH affecting p53 exon 4 was not detected in lesions from 5 of 12 patients (42%). In ulcerative colitis, tumor progression is similar to that in sporadic colon cancer, and other oncogenes and tumor suppressor genes are likely to be mutated before the p53 gene.
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PMID:Infrequent p53 gene alterations in ulcerative colitis. 1046 83

Patients with long-standing ulcerative colitis (UC) are at increased risk for colon cancer. These cancers are thought to arise from preexisting dysplasia in a field of abnormal cells that often exhibits aneuploidy and p53 abnormalities. Using dual color fluorescence in situ hybridization with centromere probes and locus-specific arm probes for chromosomes 8, 11, 17, and 18, we demonstrate that chromosomal instability (CIN) is present throughout the colon of UC patients with high-grade dysplasia or cancer. In rectal biopsies that were negative for dysplasia, abnormalities in chromosomal arms, especially losses, were most common, whereas centromere gains were most common in dysplasia and cancer. The frequency and type of abnormalities varied between the chromosomes examined; chromosome 8 was the least affected, and 17p loss was found to be an early and frequent event. Chromosomal arm instability showed 100% sensitivity and specificity for distinguishing control biopsies from histologically negative rectal biopsies from these UC patients, raising the possibility that a screen for CIN might detect the subset of UC patients who are at greatest risk for development of dysplasia and cancer. These results suggest that dysplasia and cancer in UC arise from a process of CIN that affects the entire colon; this may provide the mutator phenotype that predisposes to loss of tumor suppressor genes and evolution of cancer.
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PMID:Pancolonic chromosomal instability precedes dysplasia and cancer in ulcerative colitis. 1053 90

We report two cases affected by neoplasia after colectomy with ileo-rectal anastomosis (IRA) with a positive family history of colon cancer. Case 1, a 41-year-old ulcerative colitis (UC) patient, underwent IRA in 1977. In 1986, biopsies showed high-grade dysplasia. She underwent resection of the rectal stump in 1986. Submucosal invasive carcinoma was found in the surgical specimen. The immunohistological study demonstrated p53 protein overexpression in the neoplastic lesion. Her family history fulfilled the Amsterdam criteria of hereditary non-polyposis colorectal cancer (HNPCC). Case 2, a 47-year-old UC patient, underwent ascending colostomy in 1975 and the following year IRA. Endoscopic mucosal resection (EMR) for a sessile adenoma was performed in 1995 and subsequently polypectomy was performed for the residual tumor. Recurrent adenoma and dysplasia in another area were detected. The immunohistological study demonstrated p53 protein overexpression only in dysplasia. Renal cancer in the right kidney was detected. Resection of the rectal stump with ileal pouch-anal anastomosis (IAA), loop ileostomy and right nephrectomy were performed in 1998. Her mother and her mother's sister had been diagnosed with colon cancer. Only in the dysplastic lesion did we detect microsatellite instability at D5S644. Both cases with neoplasia had two relatives with colorectal carcinoma. In 33 cases with UC who had been followed up, 30 cases (96.8%) without neoplasia had no family history of colorectal carcinoma. These findings suggest that UC patients with a family history of colon cancer should be put under close surveillance. It should also be emphasized that IAA is the procedure of choice for UC patients with this particular condition.
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PMID:Ulcerative colitis patients with a family history of colorectal cancer should be subjected to close and careful surveillance. 1056 1

Ulcerative colitis(UC) is known to be associated with colon cancer. The risk factors of cancer incidence are total colitis type and over 10 years clinical course. The macroscopic appearance of cancer with UC mainly consist of type 3, 4 and dominant histological type is mucinous adenocarcinoma or poorly differentiated adenocarcinoma. Most of cancer is considered to raise from dysplasia. The dysplasia is difficult for diagnosis macroscopically, but it has characters of DNA aneuploidy and positive p53. For early diagnosis of cancer, surveillance is very important. The surveillance program is recommended to perform colonoscopy every year to UC patients with over 10 years course and take biopsies from every 10 cm of colon. If high-grade dysplasia is discovered by surveillance colonoscopy, a resection of total colon should be performed.
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PMID:[Colon cancer associated with ulcerative colitis and early diagnosis]. 1057 40

Barrett's esophagus carries a 30- to 100-fold increased risk of adenocarcinoma, which is thought to develop via a metaplasia-dysplasia-carcinoma progression. A common genetic abnormality detected in Barrett's adenocarcinoma is loss of heterozygosity (LOH) at the sites of known or putative tumor suppressor genes, of which there are at least 9 associated with esophageal adenocarcinoma. The aim of this study was to identify at which histological stage of carcinogenesis LOH at these sites occur. Microdissection of multiple paraffin-embedded tissue blocks from 17 esophagogastrectomy specimens of adenocarcinoma arising in Barrett's esophagus yielded areas of metaplasia, low-, intermediate- and high-grade dysplasia, and carcinoma. LOH analysis of microdissected tissues was performed using a double polymerase chain reaction technique with 11 microsatellite primers shown previously to have LOH in at least 30% of esophageal adenocarcinomas. Identical LOH was detected in premalignant and malignant tissues in 4 of 17 patients, and was located at 5q21-q22 (D5S346 primer), 17p11.1-p12 (TCF2 primer), 17p13.1 (TP53 primer), 18q21.1 (detected in colon cancer tumor suppressor gene [DCC] primer), and 18q23-qter (D18S70 primer). These results suggest that LOH at the sites of the DCC, adenomatous polyposis coli (APC), and TP53 tumor suppressor genes occur before the development of adenocarcinoma in Barrett's esophagus, and so merit further study as potential biomarkers of neoplastic progression in patients with Barrett's esophagus undergoing endoscopic and histological surveillance.
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PMID:LOH at the sites of the DCC, APC, and TP53 tumor suppressor genes occurs in Barrett's metaplasia and dysplasia adjacent to adenocarcinoma of the esophagus. 1066 31


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