Tousled-like kinase loss confers PARP inhibitor resistance in BRCA1-mutated cancers by impeding non-homologous end joining repair

Tousled-like kinase loss confers PARP inhibitor resistance in BRCA1-mutated cancers by impeding non-homologous end joining repair

Abstract Background Double-strand breaks (DSBs) are primarily repaired through non-homologous end joining (NHEJ) and homologous recombination (HR). Given that DSBs are highly cytotoxic, PARP inhibitors (PARPi), a prominent class of anticancer drugs, are designed to target tumors with HR deficiency (...

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Bibliographic Details
Main Authors: Min-ah Kim, Banseok Kim, Jihyeon Jeon, Jonghyun Lee, Hyeji Jang, Minjae Baek, Sang-Uk Seo, Dongkwan Shin, Anindya Dutta, Kyung Yong Lee
Format: Article
Language:English
Published: BMC 2025-01-01
Series:Molecular Medicine
Subjects:
DNA damage repair
Double-stranded breaks (DSBs)
Non-homologous end joining (NHEJ)
Homologous recombination (HR)
PARP inhibitor
Tousled-like kinase
Online Access:https://doi.org/10.1186/s10020-025-01066-z
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https://doi.org/10.1186/s10020-025-01066-z

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