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Homologous Recombination and Its Role in Carcinogenesis

Cancer develops when cells no longer follow their normal pattern of controlled growth. In the absence or disregard of such regulation, resulting from changes in their genetic makeup, these errant cells acquire a growth advantage, expanding into precancerous clones. Over the last decade, many studies...

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Detalles Bibliográficos
Autores principales: Bishop, Alexander J. R., Schiestl, Robert H.
Formato: Texto
Lenguaje:English
Publicado: 2002
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC153790/
https://www.ncbi.nlm.nih.gov/pubmed/12488587
http://dx.doi.org/10.1155/S1110724302204052
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author Bishop, Alexander J. R.
Schiestl, Robert H.
author_facet Bishop, Alexander J. R.
Schiestl, Robert H.
author_sort Bishop, Alexander J. R.
collection PubMed
description Cancer develops when cells no longer follow their normal pattern of controlled growth. In the absence or disregard of such regulation, resulting from changes in their genetic makeup, these errant cells acquire a growth advantage, expanding into precancerous clones. Over the last decade, many studies have revealed the relevance of genomic mutation in this process, be it by misreplication, environmental damage, or a deficiency in repairing endogenous and exogenous damage. Here, we discuss homologous recombination as another mechanism that can result in a loss of heterozygosity or genetic rearrangements. Some of these genetic alterations may play a primary role in carcinogenesis, but they are more likely to be involved in secondary and subsequent steps of carcinogenesis by which recessive oncogenic mutations are revealed. Patients, whose cells display an increased frequency of recombination, also have an elevated frequency of cancer, further supporting the link between recombination and carcinogenesis.
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spelling pubmed-1537902003-06-02 Homologous Recombination and Its Role in Carcinogenesis Bishop, Alexander J. R. Schiestl, Robert H. J Biomed Biotechnol Review Article Cancer develops when cells no longer follow their normal pattern of controlled growth. In the absence or disregard of such regulation, resulting from changes in their genetic makeup, these errant cells acquire a growth advantage, expanding into precancerous clones. Over the last decade, many studies have revealed the relevance of genomic mutation in this process, be it by misreplication, environmental damage, or a deficiency in repairing endogenous and exogenous damage. Here, we discuss homologous recombination as another mechanism that can result in a loss of heterozygosity or genetic rearrangements. Some of these genetic alterations may play a primary role in carcinogenesis, but they are more likely to be involved in secondary and subsequent steps of carcinogenesis by which recessive oncogenic mutations are revealed. Patients, whose cells display an increased frequency of recombination, also have an elevated frequency of cancer, further supporting the link between recombination and carcinogenesis. 2002 /pmc/articles/PMC153790/ /pubmed/12488587 http://dx.doi.org/10.1155/S1110724302204052 Text en Copyright © 2002, Hindawi Publishing Corporation
spellingShingle Review Article
Bishop, Alexander J. R.
Schiestl, Robert H.
Homologous Recombination and Its Role in Carcinogenesis
title Homologous Recombination and Its Role in Carcinogenesis
title_full Homologous Recombination and Its Role in Carcinogenesis
title_fullStr Homologous Recombination and Its Role in Carcinogenesis
title_full_unstemmed Homologous Recombination and Its Role in Carcinogenesis
title_short Homologous Recombination and Its Role in Carcinogenesis
title_sort homologous recombination and its role in carcinogenesis
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC153790/
https://www.ncbi.nlm.nih.gov/pubmed/12488587
http://dx.doi.org/10.1155/S1110724302204052
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