Schlafen 11 further sensitizes BRCA-deficient cells to PARP inhibitors through single-strand DNA gap accumulation behind replication forks
- Standort
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Deutsche Nationalbibliothek Frankfurt am Main
- Umfang
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1 Online-Ressource.
- Sprache
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Englisch
- Erschienen in
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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
- Urheber
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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
- Beteiligte Personen und Organisationen
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SpringerLink (Online service)
- DOI
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10.1038/s41388-024-03094-1
- URN
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urn:nbn:de:101:1-2410291009548.064642260597
- Rechteinformation
-
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Letzte Aktualisierung
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15.08.2025, 07:22 MESZ
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Beteiligte
- 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)
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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