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Genetic analysis of multiple synchronous lesions of the colon adenoma–carcinoma sequence
The colorectal adenoma–carcinoma sequence represents a well-known paradigm for the sequential development of cancer driven by the accumulation of genomic defects. Although the colorectal adenoma–carcinoma sequence is well investigated, studies about tumours of different dignity co-existent in the sa...
Autores principales: | , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2000
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2374497/ https://www.ncbi.nlm.nih.gov/pubmed/10755401 http://dx.doi.org/10.1054/bjoc.1999.1091 |
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author | Sedivy, R Wolf, B Kalipciyan, M Steger, G G Karner-Hanusch, J Mader, R M |
author_facet | Sedivy, R Wolf, B Kalipciyan, M Steger, G G Karner-Hanusch, J Mader, R M |
author_sort | Sedivy, R |
collection | PubMed |
description | The colorectal adenoma–carcinoma sequence represents a well-known paradigm for the sequential development of cancer driven by the accumulation of genomic defects. Although the colorectal adenoma–carcinoma sequence is well investigated, studies about tumours of different dignity co-existent in the same patient are seldom. In order to address the distribution of genetic alterations in different lesions of the same patient, we coincidently investigated carcinomas, adenomas and aberrant crypt foci in patients with sporadic colon cancer. By utilizing polymerase chain reaction, single-strand conformation polymorphism, heteroduplex-analysis, restriction fragment length polymorphism, protein truncation test and sequencing techniques we looked for mutations and microsatellite instability of APC, H- ras, K- ras, p53, DCC and the DNA repair genes hMLH1/hMSH2. In accordance with the suggested adenoma–carcinoma sequence of the colon, four patients reflected the progressive accumulation of genetic defects in synchronously appearing tumours during carcinogenesis. However, two patients with non-hereditary malignomas presented different genetic instabilities in different but synchronously appearing tumours suggesting non-clonal growth under almost identical conditions of the environment. Thus, sporadically manifesting multiple lesions of the colon were not necessarily driven by similar genetic mechanisms. Premalignant lesions may transform into malignant tumours starting from different types of genetic instability, which indicates independent and simultaneous tumorigenesis within the same organ. © 2000 Cancer Research Campaign |
format | Text |
id | pubmed-2374497 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2000 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-23744972009-09-10 Genetic analysis of multiple synchronous lesions of the colon adenoma–carcinoma sequence Sedivy, R Wolf, B Kalipciyan, M Steger, G G Karner-Hanusch, J Mader, R M Br J Cancer Regular Article The colorectal adenoma–carcinoma sequence represents a well-known paradigm for the sequential development of cancer driven by the accumulation of genomic defects. Although the colorectal adenoma–carcinoma sequence is well investigated, studies about tumours of different dignity co-existent in the same patient are seldom. In order to address the distribution of genetic alterations in different lesions of the same patient, we coincidently investigated carcinomas, adenomas and aberrant crypt foci in patients with sporadic colon cancer. By utilizing polymerase chain reaction, single-strand conformation polymorphism, heteroduplex-analysis, restriction fragment length polymorphism, protein truncation test and sequencing techniques we looked for mutations and microsatellite instability of APC, H- ras, K- ras, p53, DCC and the DNA repair genes hMLH1/hMSH2. In accordance with the suggested adenoma–carcinoma sequence of the colon, four patients reflected the progressive accumulation of genetic defects in synchronously appearing tumours during carcinogenesis. However, two patients with non-hereditary malignomas presented different genetic instabilities in different but synchronously appearing tumours suggesting non-clonal growth under almost identical conditions of the environment. Thus, sporadically manifesting multiple lesions of the colon were not necessarily driven by similar genetic mechanisms. Premalignant lesions may transform into malignant tumours starting from different types of genetic instability, which indicates independent and simultaneous tumorigenesis within the same organ. © 2000 Cancer Research Campaign Nature Publishing Group 2000-04 2000-03-06 /pmc/articles/PMC2374497/ /pubmed/10755401 http://dx.doi.org/10.1054/bjoc.1999.1091 Text en Copyright © 2000 Cancer Research Campaign https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material.If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Regular Article Sedivy, R Wolf, B Kalipciyan, M Steger, G G Karner-Hanusch, J Mader, R M Genetic analysis of multiple synchronous lesions of the colon adenoma–carcinoma sequence |
title | Genetic analysis of multiple synchronous lesions of the colon adenoma–carcinoma sequence |
title_full | Genetic analysis of multiple synchronous lesions of the colon adenoma–carcinoma sequence |
title_fullStr | Genetic analysis of multiple synchronous lesions of the colon adenoma–carcinoma sequence |
title_full_unstemmed | Genetic analysis of multiple synchronous lesions of the colon adenoma–carcinoma sequence |
title_short | Genetic analysis of multiple synchronous lesions of the colon adenoma–carcinoma sequence |
title_sort | genetic analysis of multiple synchronous lesions of the colon adenoma–carcinoma sequence |
topic | Regular Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2374497/ https://www.ncbi.nlm.nih.gov/pubmed/10755401 http://dx.doi.org/10.1054/bjoc.1999.1091 |
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