The spectrum of p53 mutations in colorectal adenomas differs from that in colorectal carcinomas
Background: p53 mutations are frequently observed in colorectal carcinomas but they have also been found in colorectal adenomas, although considerably less frequently. Aims: To explore p53 mutations in benign tumours, we have screened 70 colorectal adenomas for allelic loss at, and point mutations i...
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Published in | Gut Vol. 50; no. 6; pp. 834 - 839 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
London
BMJ Publishing Group Ltd and British Society of Gastroenterology
01.06.2002
BMJ BMJ Publishing Group LTD Copyright 2002 by Gut |
Subjects | |
Online Access | Get full text |
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Summary: | Background: p53 mutations are frequently observed in colorectal carcinomas but they have also been found in colorectal adenomas, although considerably less frequently. Aims: To explore p53 mutations in benign tumours, we have screened 70 colorectal adenomas for allelic loss at, and point mutations in, TP53 by analysis of selected microdissected cell populations. Results: Sixteen (22.8%) adenomas were found to have allelic loss, of which 11 (15.7%) had p53 mutations. In adenomas with mild, moderate, or severe dysplasia, mutation or allelic loss occurred in 4.8%, 16.7%, and 52.6%, respectively (p<0.001). Seven different mutations were found, all missense changes or inframe deletions: one (Thr150Arg) has not been found before while three (Gln144His, Gly245Arg, and Glu285Gln) have not been described previously in colorectal tumours. The other three mutations (Arg175Gly, ΔPro190, and Gly245Ser) have been found in colorectal carcinomas, the last commonly. Adenomas harboured a spectrum of p53 mutations which was significantly different from cancers as regards the position in the gene and a higher frequency of G→C/C→G changes. Conclusions: Combining our data on adenomas with data already published and in comparison with the spectrum of mutations in colorectal carcinomas, it is suggested that some p53 mutations have a weaker effect than others and are therefore more likely to be found in adenomas which have not progressed to carcinomas. |
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Bibliography: | href:gutjnl-50-834.pdf local:0500834 ark:/67375/NVC-GLK07W8T-4 Correspondence to: I P M Tomlinson, Molecular and Population Genetics Laboratory, Cancer Research UK, Lincoln's Inn Fields, London WC2A 3PX, UK ian.tomlinson@cancer.org.uk istex:0B91245F933C59D2B010FD8AC47617FBB5B55D44 PMID:12010886 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Cambridge University Department of Medical Genetics, Molecular Genetics Laboratory, Box 158, Addenbrooke's NHS Trust, Cambridge CB2 2QQ, UK Correspondence to: I P M Tomlinson, Molecular and Population Genetics Laboratory, Cancer Research UK, Lincoln's Inn Fields, London WC2A 3PX, UK ian.tomlinson@cancer.org.uk Present addresses: Institute of Pathology, Case Western Reserve University School of Medicine, University Hospital of Cleveland, 2085 Adelbert Road, Cleveland, OH 44106, USA |
ISSN: | 0017-5749 1468-3288 1458-3288 |
DOI: | 10.1136/gut.50.6.834 |