Schlafen 11 further sensitizes BRCA-deficient cells to PARP inhibitors through single-strand DNA gap accumulation behind replication forks

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Location: Deutsche Nationalbibliothek Frankfurt am Main

Extent: 1 Online-Ressource.

Language: Englisch

Bibliographic citation: Schlafen 11 further sensitizes BRCA-deficient cells to PARP inhibitors through single-strand DNA gap accumulation behind replication forks ; volume:43 ; number:32 ; day:3 ; month:7 ; year:2024 ; pages:2475-2489 ; date:8.2024
Oncogene ; 43, Heft 32 (3.7.2024), 2475-2489, 8.2024

Creator: Onji, Hiroshi
Tate, Sota
Sakaue, Tomohisa
Fujiwara, Kohei
Nakano, Shiho
Kawaida, Miho
Onishi, Nobuyuki
Matsumoto, Takashi
Yamagami, Wataru
Sugiyama, Takashi
Higashiyama, Shigeki
Pommier, Yves
Kobayashi, Yusuke
Murai, Junko

Contributor: SpringerLink (Online service)

DOI: 10.1038/s41388-024-03094-1

URN: urn:nbn:de:101:1-2410291009548.064642260597

Rights: Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.

Last update: 15.08.2025, 7:22 AM CEST

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Associated

Onji, Hiroshi
Tate, Sota
Sakaue, Tomohisa
Fujiwara, Kohei
Nakano, Shiho
Kawaida, Miho
Onishi, Nobuyuki
Matsumoto, Takashi
Yamagami, Wataru
Sugiyama, Takashi
Higashiyama, Shigeki
Pommier, Yves
Kobayashi, Yusuke
Murai, Junko
SpringerLink (Online service)

Other Objects (12)

Fortgeschrittenes Mammakarzinom: Therapie mit PARP-Inhibitoren und Relevanz der BRCA-Diagnostik

H2AX promotes replication fork degradation and chemosensitivity in BRCA-deficient tumours

Chlorambucil targets BRCA 1/2‐deficient tumours and counteracts PARP inhibitor resistance

MK-2206 sensitizes BRCA-deficient epithelial ovarian adenocarcinoma to cisplatin and olaparib

Biomarkers beyond BRCA: promising combinatorial treatment strategies in overcoming resistance to PARP inhibitors

VEGF pathway inhibition potentiates PARP inhibitor efficacy in ovarian cancer independent of BRCA status

Interferon restores replication fork stability and cell viability in BRCA-defective cells via ISG15

ATM depletion induces proteasomal degradation of FANCD2 and sensitizes neuroblastoma cells to PARP inhibitors

A RAD 51 assay feasible in routine tumor samples calls PARP inhibitor response beyond BRCA mutation

Nucleolytic processing of abasic sites underlies PARP inhibitor hypersensitivity in ALC1-deficient BRCA mutant cancer cells

CBL0137 impairs homologous recombination repair and sensitizes high-grade serous ovarian carcinoma to PARP inhibitors

Inhibition of PI3K-AKT-mTOR pathway sensitizes endometrial cancer cell lines to PARP inhibitors

Fortgeschrittenes Mammakarzinom: Therapie mit PARP-Inhibitoren und Relevanz der BRCA-Diagnostik

H2AX promotes replication fork degradation and chemosensitivity in BRCA-deficient tumours

Chlorambucil targets BRCA 1/2‐deficient tumours and counteracts PARP inhibitor resistance

MK-2206 sensitizes BRCA-deficient epithelial ovarian adenocarcinoma to cisplatin and olaparib

Biomarkers beyond BRCA: promising combinatorial treatment strategies in overcoming resistance to PARP inhibitors

VEGF pathway inhibition potentiates PARP inhibitor efficacy in ovarian cancer independent of BRCA status

Interferon restores replication fork stability and cell viability in BRCA-defective cells via ISG15

ATM depletion induces proteasomal degradation of FANCD2 and sensitizes neuroblastoma cells to PARP inhibitors

A RAD 51 assay feasible in routine tumor samples calls PARP inhibitor response beyond BRCA mutation

Nucleolytic processing of abasic sites underlies PARP inhibitor hypersensitivity in ALC1-deficient BRCA mutant cancer cells

CBL0137 impairs homologous recombination repair and sensitizes high-grade serous ovarian carcinoma to PARP inhibitors

Inhibition of PI3K-AKT-mTOR pathway sensitizes endometrial cancer cell lines to PARP inhibitors

Fortgeschrittenes Mammakarzinom: Therapie mit PARP-Inhibitoren und Relevanz der BRCA-Diagnostik

H2AX promotes replication fork degradation and chemosensitivity in BRCA-deficient tumours

Chlorambucil targets BRCA 1/2‐deficient tumours and counteracts PARP inhibitor resistance

MK-2206 sensitizes BRCA-deficient epithelial ovarian adenocarcinoma to cisplatin and olaparib

Biomarkers beyond BRCA: promising combinatorial treatment strategies in overcoming resistance to PARP inhibitors

VEGF pathway inhibition potentiates PARP inhibitor efficacy in ovarian cancer independent of BRCA status

Interferon restores replication fork stability and cell viability in BRCA-defective cells via ISG15

ATM depletion induces proteasomal degradation of FANCD2 and sensitizes neuroblastoma cells to PARP inhibitors

A RAD 51 assay feasible in routine tumor samples calls PARP inhibitor response beyond BRCA mutation

Nucleolytic processing of abasic sites underlies PARP inhibitor hypersensitivity in ALC1-deficient BRCA mutant cancer cells

CBL0137 impairs homologous recombination repair and sensitizes high-grade serous ovarian carcinoma to PARP inhibitors

Inhibition of PI3K-AKT-mTOR pathway sensitizes endometrial cancer cell lines to PARP inhibitors

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Schlafen 11 further sensitizes BRCA-deficient cells to PARP inhibitors through single-strand DNA gap accumulation behind replication forks

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Other Objects (12)

Fortgeschrittenes Mammakarzinom: Therapie mit PARP-Inhibitoren und Relevanz der BRCA-Diagnostik

H2AX promotes replication fork degradation and chemosensitivity in BRCA-deficient tumours

Chlorambucil targets BRCA 1/2‐deficient tumours and counteracts PARP inhibitor resistance

MK-2206 sensitizes BRCA-deficient epithelial ovarian adenocarcinoma to cisplatin and olaparib

Biomarkers beyond BRCA: promising combinatorial treatment strategies in overcoming resistance to PARP inhibitors

VEGF pathway inhibition potentiates PARP inhibitor efficacy in ovarian cancer independent of BRCA status

Interferon restores replication fork stability and cell viability in BRCA-defective cells via ISG15

ATM depletion induces proteasomal degradation of FANCD2 and sensitizes neuroblastoma cells to PARP inhibitors

A RAD 51 assay feasible in routine tumor samples calls PARP inhibitor response beyond BRCA mutation

Nucleolytic processing of abasic sites underlies PARP inhibitor hypersensitivity in ALC1-deficient BRCA mutant cancer cells

CBL0137 impairs homologous recombination repair and sensitizes high-grade serous ovarian carcinoma to PARP inhibitors

Inhibition of PI3K-AKT-mTOR pathway sensitizes endometrial cancer cell lines to PARP inhibitors

Fortgeschrittenes Mammakarzinom: Therapie mit PARP-Inhibitoren und Relevanz der BRCA-Diagnostik

H2AX promotes replication fork degradation and chemosensitivity in BRCA-deficient tumours

Chlorambucil targets BRCA 1/2‐deficient tumours and counteracts PARP inhibitor resistance

MK-2206 sensitizes BRCA-deficient epithelial ovarian adenocarcinoma to cisplatin and olaparib

Biomarkers beyond BRCA: promising combinatorial treatment strategies in overcoming resistance to PARP inhibitors

VEGF pathway inhibition potentiates PARP inhibitor efficacy in ovarian cancer independent of BRCA status

Interferon restores replication fork stability and cell viability in BRCA-defective cells via ISG15

ATM depletion induces proteasomal degradation of FANCD2 and sensitizes neuroblastoma cells to PARP inhibitors

A RAD 51 assay feasible in routine tumor samples calls PARP inhibitor response beyond BRCA mutation

Nucleolytic processing of abasic sites underlies PARP inhibitor hypersensitivity in ALC1-deficient BRCA mutant cancer cells

CBL0137 impairs homologous recombination repair and sensitizes high-grade serous ovarian carcinoma to PARP inhibitors

Inhibition of PI3K-AKT-mTOR pathway sensitizes endometrial cancer cell lines to PARP inhibitors

Fortgeschrittenes Mammakarzinom: Therapie mit PARP-Inhibitoren und Relevanz der BRCA-Diagnostik

H2AX promotes replication fork degradation and chemosensitivity in BRCA-deficient tumours

Chlorambucil targets BRCA 1/2‐deficient tumours and counteracts PARP inhibitor resistance

MK-2206 sensitizes BRCA-deficient epithelial ovarian adenocarcinoma to cisplatin and olaparib

Biomarkers beyond BRCA: promising combinatorial treatment strategies in overcoming resistance to PARP inhibitors

VEGF pathway inhibition potentiates PARP inhibitor efficacy in ovarian cancer independent of BRCA status

Interferon restores replication fork stability and cell viability in BRCA-defective cells via ISG15

ATM depletion induces proteasomal degradation of FANCD2 and sensitizes neuroblastoma cells to PARP inhibitors

A RAD 51 assay feasible in routine tumor samples calls PARP inhibitor response beyond BRCA mutation

Nucleolytic processing of abasic sites underlies PARP inhibitor hypersensitivity in ALC1-deficient BRCA mutant cancer cells

CBL0137 impairs homologous recombination repair and sensitizes high-grade serous ovarian carcinoma to PARP inhibitors

Inhibition of PI3K-AKT-mTOR pathway sensitizes endometrial cancer cell lines to PARP inhibitors

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