Aneuploidy Mechanisms in Human Colorectal Preneoplastic Lesions and Barrett’s Esophagus. Is There a Role for K-Ras and p53 Mutations?

The link of aneuploidy and heteroploidy in human solid tumours with early genetic events is poorly understood. The study of human preneoplastic precursor lesions, i.e., colorectal adenomas, chronic ulcerative colitis lesions, and Barrett’s esophagus, as considered in this review, appears particularl...

Full description

Saved in:
Bibliographic Details
Main Author: Walter Giaretti
Format: Article
Language:English
Published: Wiley 1997-01-01
Series:Analytical Cellular Pathology
Online Access:http://dx.doi.org/10.1155/1997/264135
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1832546558057381888
author Walter Giaretti
author_facet Walter Giaretti
author_sort Walter Giaretti
collection DOAJ
description The link of aneuploidy and heteroploidy in human solid tumours with early genetic events is poorly understood. The study of human preneoplastic precursor lesions, i.e., colorectal adenomas, chronic ulcerative colitis lesions, and Barrett’s esophagus, as considered in this review, appears particularly useful to achieve this aim. Literature data examined here on aneuploidy were obtained by image and flow cytometry, classical cytogenetics, and in situ hybridization based cytogenetics. It appears that aneuploidy is linked with specific gene mutations, i.e., of the tumour suppressor gene p53 in chronic ulcerative colitis and in Barrett’s esophagus, and of the protooncogene K‐ras in colorectal adenomas. These data and data from experiments using in vitro and mouse models, suggest that chromosome instability, tetraploidization, and asymmetrical chromosome segregation during cell division are the result of deregulated cell cycle genes with multiple functions that normally exert active checks on the cell cycle processes including apoptosis and chromosome stability.
format Article
id doaj-art-cd29ac5f20ba4bc396140be28fd0b08f
institution Kabale University
issn 0921-8912
1878-3651
language English
publishDate 1997-01-01
publisher Wiley
record_format Article
series Analytical Cellular Pathology
spelling doaj-art-cd29ac5f20ba4bc396140be28fd0b08f2025-02-03T06:48:37ZengWileyAnalytical Cellular Pathology0921-89121878-36511997-01-011529911710.1155/1997/264135Aneuploidy Mechanisms in Human Colorectal Preneoplastic Lesions and Barrett’s Esophagus. Is There a Role for K-Ras and p53 Mutations?Walter Giaretti0Laboratory of Biophysics and Cytometry, Istituto Nazionale per la Ricerca sul Cancro, Largo Rosanna Benzi 10, 16132 Genova, ItalyThe link of aneuploidy and heteroploidy in human solid tumours with early genetic events is poorly understood. The study of human preneoplastic precursor lesions, i.e., colorectal adenomas, chronic ulcerative colitis lesions, and Barrett’s esophagus, as considered in this review, appears particularly useful to achieve this aim. Literature data examined here on aneuploidy were obtained by image and flow cytometry, classical cytogenetics, and in situ hybridization based cytogenetics. It appears that aneuploidy is linked with specific gene mutations, i.e., of the tumour suppressor gene p53 in chronic ulcerative colitis and in Barrett’s esophagus, and of the protooncogene K‐ras in colorectal adenomas. These data and data from experiments using in vitro and mouse models, suggest that chromosome instability, tetraploidization, and asymmetrical chromosome segregation during cell division are the result of deregulated cell cycle genes with multiple functions that normally exert active checks on the cell cycle processes including apoptosis and chromosome stability.http://dx.doi.org/10.1155/1997/264135
spellingShingle Walter Giaretti
Aneuploidy Mechanisms in Human Colorectal Preneoplastic Lesions and Barrett’s Esophagus. Is There a Role for K-Ras and p53 Mutations?
Analytical Cellular Pathology
title Aneuploidy Mechanisms in Human Colorectal Preneoplastic Lesions and Barrett’s Esophagus. Is There a Role for K-Ras and p53 Mutations?
title_full Aneuploidy Mechanisms in Human Colorectal Preneoplastic Lesions and Barrett’s Esophagus. Is There a Role for K-Ras and p53 Mutations?
title_fullStr Aneuploidy Mechanisms in Human Colorectal Preneoplastic Lesions and Barrett’s Esophagus. Is There a Role for K-Ras and p53 Mutations?
title_full_unstemmed Aneuploidy Mechanisms in Human Colorectal Preneoplastic Lesions and Barrett’s Esophagus. Is There a Role for K-Ras and p53 Mutations?
title_short Aneuploidy Mechanisms in Human Colorectal Preneoplastic Lesions and Barrett’s Esophagus. Is There a Role for K-Ras and p53 Mutations?
title_sort aneuploidy mechanisms in human colorectal preneoplastic lesions and barrett s esophagus is there a role for k ras and p53 mutations
url http://dx.doi.org/10.1155/1997/264135
work_keys_str_mv AT waltergiaretti aneuploidymechanismsinhumancolorectalpreneoplasticlesionsandbarrettsesophagusistherearoleforkrasandp53mutations