TY - JOUR
T1 - Homologous recombination and its role in carcinogenesis
AU - Bishop, Alexander J.R.
AU - Schiestl, Robert H.
N1 - Funding Information:
Bishop Alexander J. R. 1 Schiestl Robert H. [email protected] 2 1 Department of Genetics Harvard Medical School Boston, MA 02115 USA harvard.edu 2 Department of Pathology UCLA Medical School Los Angeles, CA 90095 USA ucla.edu 2002 10 12 2002 2 2 75 85 09 01 2002 29 04 2002 29 04 2002 2002 Copyright © 2002 This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. 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. http://dx.doi.org/10.13039/100000048 American Cancer Society RPG-95-076-04-MGO http://dx.doi.org/10.13039/100000066 National Institute of Environmental Health Sciences http://dx.doi.org/10.13039/100000002 National Institutes of Health RO1 ES09519 http://dx.doi.org/10.13039/100000002 National Institutes of Health RCDA F32GM19147 http://dx.doi.org/10.13039/100000002 National Institutes of Health KO2 ES00299
PY - 2002
Y1 - 2002
N2 - 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.
AB - 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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U2 - 10.1155/S1110724302204052
DO - 10.1155/S1110724302204052
M3 - Review article
AN - SCOPUS:0347280098
SN - 1110-7243
VL - 2002
SP - 75
EP - 85
JO - Journal of Biomedicine and Biotechnology
JF - Journal of Biomedicine and Biotechnology
IS - 2
ER -