Exploiting replication gaps for cancer therapy.
Exploiting replication gaps for cancer therapy.
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DOI:
10.1016/j.molcel.2022.04.023
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发表时间:
2022-07-07
期刊:
影响因子:
16
通讯作者:
Cantor, Sharon B.
中科院分区:
文献类型:
--
作者:
Cong, Ke;Cantor, Sharon B.
Defects in DNA double strand break repair are thought to render BRCA1 or BRCA2 (BRCA) mutant tumors selectively sensitive to PARP inhibitors (PARPi). Challenging this framework, BRCA and PARP1 share functions in DNA synthesis on the lagging strand. Thus, BRCA-deficiency or “BRCAness” could reflect an inherent lagging strand problem that is vulnerable to drugs such as PARPi that also target the lagging strand, a combination that generates a toxic accumulation of replication gaps.
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