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Artigo em Inglês | WPRIM | ID: wpr-269661

RESUMO

Tumors often have DNA repair defects, suggesting additional inhibition of other DNA repair pathways in tumors may lead to synthetic lethality. Accumulating data demonstrate that DNA repair-defective tumors, in particular homologous recombination (HR), are highly sensitive to DNA-damaging agents. Thus, HR-defective tumors exhibit potential vulnerability to the synthetic lethality approach, which may lead to new therapeutic strategies. It is well known that poly (adenosine diphosphate (ADP)-ribose) polymerase (PARP) inhibitors show the synthetically lethal effect in tumors defective in BRCA1 or BRCA2 genes encoded proteins that are required for efficient HR. In this review, we summarize the strategies of targeting DNA repair pathways and other DNA metabolic functions to cause synthetic lethality in HR-defective tumor cells.


Assuntos
Animais , Humanos , Antineoplásicos , Farmacologia , Neoplasias da Mama , Genética , Reparo do DNA , Genética , Regulação Neoplásica da Expressão Gênica , Genes Letais , Genética , Genes Supressores de Tumor , Genes cdc , Mutagênese , Inibidores de Poli(ADP-Ribose) Polimerases , Proteína Rad52 de Recombinação e Reparo de DNA , Recombinação Genética , Genética
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