BRCA1 CpG island hypermethylation predicts sensitivity to poly(adenosine diphosphate)-ribose polymerase inhibitorsBRCA1 CpG island hypermethylation predicts sensitivity to poly(adenosine diphosphate)-ribose polymerase inhibitors
Recently, Fong et al reported the antitumor activity of the poly(adenosine diphosphate)-ribose polymerase (PARP) inhibitor olaparib (AZD2281; KU-0059436) in patients with BRCA1/BRCA2 germline mutated ovarian cancer. Female BRCA1 and BRCA2 mutation carriers have a significantly elevated lifetime risk...
| Autores: | , , , , , , , |
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| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2010 |
| País: | España |
| Institución: | Universidad de Barcelona |
| Repositorio: | Dipòsit Digital de la UB |
| OAI Identifier: | oai:diposit.ub.edu:2445/198525 |
| Acceso en línea: | https://hdl.handle.net/2445/198525 |
| Access Level: | acceso abierto |
| Palabra clave: | Proteïnes supressores de tumors ADN Malalties de l'ovari Genètica Tumor suppressor protein DNA Ovary diseases Genetics |
| Sumario: | Recently, Fong et al reported the antitumor activity of the poly(adenosine diphosphate)-ribose polymerase (PARP) inhibitor olaparib (AZD2281; KU-0059436) in patients with BRCA1/BRCA2 germline mutated ovarian cancer. Female BRCA1 and BRCA2 mutation carriers have a significantly elevated lifetime risk of breast and ovarian cancer. BRCA1 and BRCA2 proteins play major roles in DNA double-strand break repair through homologous recombination, and inhibition of DNA single-strand break repair leads to the accumulation of double-strand breaks. These potentially lethal events in homologous recombination-deficient cells could be exploited for therapeutic purposes. The PARP-1 protein is essential for single-strand break repair, and inhibition of PARP leads to persistence of DNA lesions normally repaired by homologous recombination. |
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