Abstract:
:Cancer cells with germline deleterious mutations of BRCA1 or BRCA2 are deficient in homologous recombination repair and therefore sensitive to PARP inhibitor treatment. However, wild-type BRCA1/2-expressing cells with defects in other DNA damage repair pathway components may also exhibit "BRCAness," which in combination with PARP inhibition can similarly induce synthetic lethality. In this issue of Cancer Research, Luo and colleagues report a novel mechanism by which BRCA1 protein degradation in response to DNA double-strand breaks is regulated by prolyl isomerase Pin1. Inactivation of Pin1 can establish BRCAness in cancer cells and thus sensitize cells to PARP inhibitor treatment.See related articles by Luo et al., p. 3033.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Cai Cdoi
10.1158/0008-5472.CAN-20-1451subject
Has Abstractpub_date
2020-07-15 00:00:00pages
2977-2978issue
14eissn
0008-5472issn
1538-7445pii
80/14/2977journal_volume
80pub_type
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