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Article

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

Molecular medicine (Cambridge, Mass.) - 22 Jan 2025

Kim Min-Ah, Kim Banseok, Jeon Jihyeon, Lee Jonghyun, Jang Hyeji, Baek Minjae, Seo Sang-Uk, Shin Dongkwan, Dutta Anindya, Lee Kyung Yong

Abstract excerpt

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 (HRD), such as those harboring BRCA mutations. However, many tumor cells acquire resistance to PARPi, often by restoring HR...

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Identifiers

PMID: 39844055
DOI: 10.1186/s10020-025-01066-z
PMCID: PMC11753094

Genes

BRCA1
H2AX
TLK1
TLK2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

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