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Regulation and pharmacological targeting of RAD51 in cancer
Regulation of homologous recombination (HR) is central for cancer prevention. However, too little HR can increase cancer incidence, whereas too much HR can drive cancer resistance to therapy. Importantly, therapeutics targeting HR deficiency have demonstrated a profound efficacy in the clinic improv...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7520849/ https://www.ncbi.nlm.nih.gov/pubmed/33015624 http://dx.doi.org/10.1093/narcan/zcaa024 |
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author | Grundy, McKenzie K Buckanovich, Ronald J Bernstein, Kara A |
author_facet | Grundy, McKenzie K Buckanovich, Ronald J Bernstein, Kara A |
author_sort | Grundy, McKenzie K |
collection | PubMed |
description | Regulation of homologous recombination (HR) is central for cancer prevention. However, too little HR can increase cancer incidence, whereas too much HR can drive cancer resistance to therapy. Importantly, therapeutics targeting HR deficiency have demonstrated a profound efficacy in the clinic improving patient outcomes, particularly for breast and ovarian cancer. RAD51 is central to DNA damage repair in the HR pathway. As such, understanding the function and regulation of RAD51 is essential for cancer biology. This review will focus on the role of RAD51 in cancer and beyond and how modulation of its function can be exploited as a cancer therapeutic. |
format | Online Article Text |
id | pubmed-7520849 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-75208492020-10-01 Regulation and pharmacological targeting of RAD51 in cancer Grundy, McKenzie K Buckanovich, Ronald J Bernstein, Kara A NAR Cancer Critical Reviews and Perspectives Regulation of homologous recombination (HR) is central for cancer prevention. However, too little HR can increase cancer incidence, whereas too much HR can drive cancer resistance to therapy. Importantly, therapeutics targeting HR deficiency have demonstrated a profound efficacy in the clinic improving patient outcomes, particularly for breast and ovarian cancer. RAD51 is central to DNA damage repair in the HR pathway. As such, understanding the function and regulation of RAD51 is essential for cancer biology. This review will focus on the role of RAD51 in cancer and beyond and how modulation of its function can be exploited as a cancer therapeutic. Oxford University Press 2020-09-25 /pmc/articles/PMC7520849/ /pubmed/33015624 http://dx.doi.org/10.1093/narcan/zcaa024 Text en © The Author(s) 2020. Published by Oxford University Press on behalf of NAR Cancer. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Critical Reviews and Perspectives Grundy, McKenzie K Buckanovich, Ronald J Bernstein, Kara A Regulation and pharmacological targeting of RAD51 in cancer |
title | Regulation and pharmacological targeting of RAD51 in cancer |
title_full | Regulation and pharmacological targeting of RAD51 in cancer |
title_fullStr | Regulation and pharmacological targeting of RAD51 in cancer |
title_full_unstemmed | Regulation and pharmacological targeting of RAD51 in cancer |
title_short | Regulation and pharmacological targeting of RAD51 in cancer |
title_sort | regulation and pharmacological targeting of rad51 in cancer |
topic | Critical Reviews and Perspectives |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7520849/ https://www.ncbi.nlm.nih.gov/pubmed/33015624 http://dx.doi.org/10.1093/narcan/zcaa024 |
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