| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 5690748 | Gynecologic Oncology | 2016 | 10 Pages |
Abstract
Mutations in HR genes are neither necessary nor sufficient to predict response to niraparib. Assessment of repair status through multiple complementary assays is needed to guide PARP inhibitor therapy, design future clinical trials and identify ovarian cancer patients most likely to benefit from PARP inhibition.
Keywords
HGSOCCDKPBSFBSBRCASCIDPARPPDXXenograftsTP53BRCA1/2Patient-derived xenograftDNA repairtumor protein p53intraperitonealOvarian cancerHigh-grade serous ovarian carcinomaheat-inactivated fetal bovine serumPARP inhibitorsSCID, Severe combined immunodeficiencyHomologous recombinationpADPrPoly(ADP-ribose) polymerasecyclin-dependent kinase
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Authors
Mariam M. AlHilli, Marc A. Becker, S. John Weroha, Karen S. Flatten, Rachel M. Hurley, Maria I. Harrell, Ann L. Oberg, Matt J. Maurer, Kieran M. Hawthorne, Xiaonan Hou, Sean C. Harrington, Sarah McKinstry, X. Wei Meng, Keith M. Wilcoxen,