TY - JOUR
T1 - Involvement of Homologous Recombination in Carcinogenesis
AU - Reliene, Ramune
AU - Bishop, Alexander J.R.
AU - Schiestl, Robert H.
N1 - Funding Information:
Supported by grants from the National Institute of Environmental Health Sciences, NIH, RO1 grant No. ES09519 (to RHS), postdoctoral research fellowship of the University of California Toxic Substances Research and Teaching Program, the Lymphoma Research Foundation Elizabeth Banks Jacobs & Byron Wade Strunk Memorial Fellowship (both to RR), and NIH/NIEHS award (K22 ES 012264) to AJRB.
PY - 2007
Y1 - 2007
N2 - DNA alterations of every type are associated with the incidence of carcinogenesis, often on the genomic scale. Although homologous recombination (HR) is an important pathway of DNA repair, evidence is accumulating that deleterious genomic rearrangements can result from HR. It therefore follows that HR events may play a causative role in carcinogenesis. HR is elevated in response to carcinogens. HR may also be increased or decreased when its upstream regulation is perturbed or components of the HR machinery itself are not fully functional. This chapter summarizes research findings that demonstrate an association between HR and carcinogenesis. Increased or decreased frequencies of HR have been found in cancer cells and cancer-prone hereditary human disorders characterized by mutations in genes playing a role in HR, such as ATM, Tp53, BRCA, BLM, and WRN genes. Another evidence linking perturbations in HR and carcinogenesis is provided by studies showing that exposure to carcinogens results in an increased frequency of HR resulting in DNA deletions in yeast, human cells, or mice.
AB - DNA alterations of every type are associated with the incidence of carcinogenesis, often on the genomic scale. Although homologous recombination (HR) is an important pathway of DNA repair, evidence is accumulating that deleterious genomic rearrangements can result from HR. It therefore follows that HR events may play a causative role in carcinogenesis. HR is elevated in response to carcinogens. HR may also be increased or decreased when its upstream regulation is perturbed or components of the HR machinery itself are not fully functional. This chapter summarizes research findings that demonstrate an association between HR and carcinogenesis. Increased or decreased frequencies of HR have been found in cancer cells and cancer-prone hereditary human disorders characterized by mutations in genes playing a role in HR, such as ATM, Tp53, BRCA, BLM, and WRN genes. Another evidence linking perturbations in HR and carcinogenesis is provided by studies showing that exposure to carcinogens results in an increased frequency of HR resulting in DNA deletions in yeast, human cells, or mice.
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U2 - 10.1016/S0065-2660(06)58003-4
DO - 10.1016/S0065-2660(06)58003-4
M3 - Review article
C2 - 17452246
AN - SCOPUS:34247164462
SN - 0065-2660
VL - 58
SP - 67
EP - 87
JO - Advances in Genetics
JF - Advances in Genetics
ER -