Homologous Recombination Deficiency Unrelated to Platinum and PARP Inhibitor Response in Cell Line Libraries

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Location: Deutsche Nationalbibliothek Frankfurt am Main

Extent: 1 Online-Ressource.

Language: Englisch

Bibliographic citation: Homologous Recombination Deficiency Unrelated to Platinum and PARP Inhibitor Response in Cell Line Libraries ; volume:11 ; number:1 ; day:6 ; month:2 ; year:2024 ; pages:1-8 ; date:12.2024
Scientific data ; 11, Heft 1 (6.2.2024), 1-8, 12.2024

Creator: Takamatsu, Shiro
Murakami, Kosuke
Matsumura, Noriomi

Contributor: SpringerLink (Online service)

DOI: 10.1038/s41597-024-03018-4

URN: urn:nbn:de:101:1-2024041511024644270247

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

Last update: 14.08.2025, 10:53 AM CEST

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Takamatsu, Shiro
Murakami, Kosuke
Matsumura, Noriomi
SpringerLink (Online service)

Other Objects (12)

PLK1 overexpression suppresses homologous recombination and confers cellular sensitivity to PARP inhibition

Prediction of homologous recombination deficiency identifies colorectal tumors sensitive to PARP inhibition

The deubiquitylating enzyme USP15 regulates homologous recombination repair and cancer cell response to PARP inhibitors

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

PALB2 or BARD1 loss confers homologous recombination deficiency and PARP inhibitor sensitivity in prostate cancer

Tumors defective in homologous recombination rely on oxidative metabolism: relevance to treatments with PARP inhibitors

BRCA loss of function including BRCA1 DNA-methylation, but not BRCA-unrelated homologous recombination deficiency, is associated with platinum hypersensitivity in high-grade ovarian cancer

Loss of NFBD1/MDC1 disrupts homologous recombination repair and sensitizes nasopharyngeal carcinoma cells to PARP inhibitors

Correlation of homologous recombination deficiency induced mutational signatures with sensitivity to PARP inhibitors and cytotoxic agents

Structural basis of homologous recombination

Suppression of Homologous Recombination by insulin-like growth factor-1 inhibition sensitizes cancer cells to PARP inhibitors

Evaluation of different methods to assess homologous recombination status and sensitivity to PARP inhibitors in ovarian cancer

PLK1 overexpression suppresses homologous recombination and confers cellular sensitivity to PARP inhibition

Prediction of homologous recombination deficiency identifies colorectal tumors sensitive to PARP inhibition

The deubiquitylating enzyme USP15 regulates homologous recombination repair and cancer cell response to PARP inhibitors

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

PALB2 or BARD1 loss confers homologous recombination deficiency and PARP inhibitor sensitivity in prostate cancer

Tumors defective in homologous recombination rely on oxidative metabolism: relevance to treatments with PARP inhibitors

BRCA loss of function including BRCA1 DNA-methylation, but not BRCA-unrelated homologous recombination deficiency, is associated with platinum hypersensitivity in high-grade ovarian cancer

Loss of NFBD1/MDC1 disrupts homologous recombination repair and sensitizes nasopharyngeal carcinoma cells to PARP inhibitors

Correlation of homologous recombination deficiency induced mutational signatures with sensitivity to PARP inhibitors and cytotoxic agents

Structural basis of homologous recombination

Suppression of Homologous Recombination by insulin-like growth factor-1 inhibition sensitizes cancer cells to PARP inhibitors

Evaluation of different methods to assess homologous recombination status and sensitivity to PARP inhibitors in ovarian cancer

PLK1 overexpression suppresses homologous recombination and confers cellular sensitivity to PARP inhibition

Prediction of homologous recombination deficiency identifies colorectal tumors sensitive to PARP inhibition

The deubiquitylating enzyme USP15 regulates homologous recombination repair and cancer cell response to PARP inhibitors

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

PALB2 or BARD1 loss confers homologous recombination deficiency and PARP inhibitor sensitivity in prostate cancer

Tumors defective in homologous recombination rely on oxidative metabolism: relevance to treatments with PARP inhibitors

BRCA loss of function including BRCA1 DNA-methylation, but not BRCA-unrelated homologous recombination deficiency, is associated with platinum hypersensitivity in high-grade ovarian cancer

Loss of NFBD1/MDC1 disrupts homologous recombination repair and sensitizes nasopharyngeal carcinoma cells to PARP inhibitors

Correlation of homologous recombination deficiency induced mutational signatures with sensitivity to PARP inhibitors and cytotoxic agents

Structural basis of homologous recombination

Suppression of Homologous Recombination by insulin-like growth factor-1 inhibition sensitizes cancer cells to PARP inhibitors

Evaluation of different methods to assess homologous recombination status and sensitivity to PARP inhibitors in ovarian cancer

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Homologous Recombination Deficiency Unrelated to Platinum and PARP Inhibitor Response in Cell Line Libraries

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Other Objects (12)

PLK1 overexpression suppresses homologous recombination and confers cellular sensitivity to PARP inhibition

Prediction of homologous recombination deficiency identifies colorectal tumors sensitive to PARP inhibition

The deubiquitylating enzyme USP15 regulates homologous recombination repair and cancer cell response to PARP inhibitors

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

PALB2 or BARD1 loss confers homologous recombination deficiency and PARP inhibitor sensitivity in prostate cancer

Tumors defective in homologous recombination rely on oxidative metabolism: relevance to treatments with PARP inhibitors

BRCA loss of function including BRCA1 DNA-methylation, but not BRCA-unrelated homologous recombination deficiency, is associated with platinum hypersensitivity in high-grade ovarian cancer

Loss of NFBD1/MDC1 disrupts homologous recombination repair and sensitizes nasopharyngeal carcinoma cells to PARP inhibitors

Correlation of homologous recombination deficiency induced mutational signatures with sensitivity to PARP inhibitors and cytotoxic agents

Structural basis of homologous recombination

Suppression of Homologous Recombination by insulin-like growth factor-1 inhibition sensitizes cancer cells to PARP inhibitors

Evaluation of different methods to assess homologous recombination status and sensitivity to PARP inhibitors in ovarian cancer

PLK1 overexpression suppresses homologous recombination and confers cellular sensitivity to PARP inhibition

Prediction of homologous recombination deficiency identifies colorectal tumors sensitive to PARP inhibition

The deubiquitylating enzyme USP15 regulates homologous recombination repair and cancer cell response to PARP inhibitors

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

PALB2 or BARD1 loss confers homologous recombination deficiency and PARP inhibitor sensitivity in prostate cancer

Tumors defective in homologous recombination rely on oxidative metabolism: relevance to treatments with PARP inhibitors

BRCA loss of function including BRCA1 DNA-methylation, but not BRCA-unrelated homologous recombination deficiency, is associated with platinum hypersensitivity in high-grade ovarian cancer

Loss of NFBD1/MDC1 disrupts homologous recombination repair and sensitizes nasopharyngeal carcinoma cells to PARP inhibitors

Correlation of homologous recombination deficiency induced mutational signatures with sensitivity to PARP inhibitors and cytotoxic agents

Structural basis of homologous recombination

Suppression of Homologous Recombination by insulin-like growth factor-1 inhibition sensitizes cancer cells to PARP inhibitors

Evaluation of different methods to assess homologous recombination status and sensitivity to PARP inhibitors in ovarian cancer

PLK1 overexpression suppresses homologous recombination and confers cellular sensitivity to PARP inhibition

Prediction of homologous recombination deficiency identifies colorectal tumors sensitive to PARP inhibition

The deubiquitylating enzyme USP15 regulates homologous recombination repair and cancer cell response to PARP inhibitors

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

PALB2 or BARD1 loss confers homologous recombination deficiency and PARP inhibitor sensitivity in prostate cancer

Tumors defective in homologous recombination rely on oxidative metabolism: relevance to treatments with PARP inhibitors

BRCA loss of function including BRCA1 DNA-methylation, but not BRCA-unrelated homologous recombination deficiency, is associated with platinum hypersensitivity in high-grade ovarian cancer

Loss of NFBD1/MDC1 disrupts homologous recombination repair and sensitizes nasopharyngeal carcinoma cells to PARP inhibitors

Correlation of homologous recombination deficiency induced mutational signatures with sensitivity to PARP inhibitors and cytotoxic agents

Structural basis of homologous recombination

Suppression of Homologous Recombination by insulin-like growth factor-1 inhibition sensitizes cancer cells to PARP inhibitors

Evaluation of different methods to assess homologous recombination status and sensitivity to PARP inhibitors in ovarian cancer

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