PARP inhibition — not all gene mutations are created equal

Jun Luo; Emmanuel S. Antonarakis

doi:10.1038/s41585-018-0129-3

PARP inhibition — not all gene mutations are created equal

Jun Luo, Emmanuel S. Antonarakis

Research output: Contribution to journal › Article › peer-review

19 Scopus citations

Abstract

Preliminary results from TRITON2 demonstrate efficacy of the poly(ADP-ribose) polymerase (PARP) inhibitor rucaparib in ~50% of patients with metastatic castration-resistant prostate cancer and inactivation of BRCA1/BRCA2. However, those with ATM and CDK12 mutations do not seem to benefit. An improved homologous recombination deficiency test must be developed and alternative treatments defined for these subsets of patients.

Original language	English (US)
Pages (from-to)	4-6
Number of pages	3
Journal	Nature Reviews Urology
Volume	16
Issue number	1
DOIs	https://doi.org/10.1038/s41585-018-0129-3
State	Published - Jan 1 2019
Externally published	Yes

Bibliographical note

Funding Information:
This work was partially supported by NIH Cancer Center Support Grant P30 CA006973, the Department of Defense (DOD) grant W81XWH-16-PCRP-CCRSA, NIH grant R01 CA185297, and US Department of Defense Prostate Cancer Research Program grant W81XWH-15-2-0050, and the Patrick C. Walsh Research Fund.

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© 2018, Springer Nature Limited.

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abstract = "Preliminary results from TRITON2 demonstrate efficacy of the poly(ADP-ribose) polymerase (PARP) inhibitor rucaparib in \textasciitilde{}50\% of patients with metastatic castration-resistant prostate cancer and inactivation of BRCA1/BRCA2. However, those with ATM and CDK12 mutations do not seem to benefit. An improved homologous recombination deficiency test must be developed and alternative treatments defined for these subsets of patients.",

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AU - Antonarakis, Emmanuel S.

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N2 - Preliminary results from TRITON2 demonstrate efficacy of the poly(ADP-ribose) polymerase (PARP) inhibitor rucaparib in ~50% of patients with metastatic castration-resistant prostate cancer and inactivation of BRCA1/BRCA2. However, those with ATM and CDK12 mutations do not seem to benefit. An improved homologous recombination deficiency test must be developed and alternative treatments defined for these subsets of patients.

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PARP inhibition — not all gene mutations are created equal

Abstract

Bibliographical note

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