Chromosome breaks and genomic instability Journal Article


Author: Jasin, M.
Article Title: Chromosome breaks and genomic instability
Abstract: Tumorigenesis is known to result from multiple genetic changes. Although endogenous and environmental insults can damage DNA, cellular mechanisms exist to repair various forms of damage or to kill those cells irreparably damaged. Hence, the accumulation of numerous genetic changes that would lead to cancer in normal cells is extremely rare. Nevertheless, disruption of a DNA repair pathway has the potential to expedite tumorigenesis by resulting in a cell that is hypermutable. Multiple pathways exist to repair the various forms of DNA damage that can cause mutagenesis. Recent studies have demonstrated a key role for homologous recombination in DNA repair, in particular in the repair chromosomal double-strand breaks. This review summarizes those studies and discusses how disruption of homologous recombination pathways can create genetic instability.
Keywords: gene mutation; mutation; review; neoplasms; animals; allele; dna damage; dna repair; cancer susceptibility; gene product; brca1 protein; brca2 protein; carcinogenesis; dna strand breakage; gene conversion; tumor suppressor gene; dna; gene rearrangement; genetic recombination; mammal; breast carcinoma; sister chromatid exchange; chromosome breakage; heterozygosity loss; chromosome aberrations; reca protein; humans; human; priority journal
Journal Title: Cancer Investigation
Volume: 18
Issue: 1
ISSN: 0735-7907
Publisher: Informa Healthcare  
Date Published: 2000-01-01
Start Page: 78
End Page: 86
Language: English
PUBMED: 10701370
PROVIDER: scopus
DOI: 10.3109/07357900009023065
DOI/URL:
Notes: Export Date: 18 November 2015 -- Source: Scopus
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  1. Maria Jasin
    249 Jasin