Literature DB >> 30620391

Circulating tumor DNA alterations in patients with metastatic castration-resistant prostate cancer.

Guru Sonpavde1, Neeraj Agarwal2, Gregory Russell Pond3, Rebecca J Nagy4, Roberto H Nussenzveig2, Andrew W Hahn2, Oliver Sartor5, Theodore Stewart Gourdin6, Lakshminarayanan Nandagopal7, Elisa M Ledet5, Gurudatta Naik7, Andrew J Armstrong8, Jue Wang9, Mehmet Asim Bilen10, Shilpa Gupta11, Petros Grivas12, Sumanta K Pal13, Richard B Lanman4, AmirAli Talasaz4, Michael B Lilly6.   

Abstract

BACKGROUND: Because cell-free DNA (cfDNA) analysis facilitates the noninvasive genomic profiling of metastatic castration-resistant prostate cancer (mCRPC), the authors evaluated the association between cfDNA alterations and outcomes and evolution with therapy.
METHODS: Patients with mCRPC underwent cfDNA genomic profiling using Guardant360, which examines major cancer-associated genes. Clinical factors, therapy information, failure-free survival, and overall survival (OS) were obtained for select patients. The association between genomic alterations and outcomes was investigated.
RESULTS: Of 514 men with mCRPC, 482 (94%) had ≥1 circulating tumor DNA (ctDNA) alteration. The most common recurrent somatic mutations were in TP53 (36%), androgen receptor (AR) (22%), adenomatous polyposis coli (APC) (10%), neurofibromin 1 (NF1) (9%), epidermal growth factor receptor (EGFR), catenin beta-1 (CTNNB1), and AT-rich interactive domain-containing protein 1A (ARID1A) (6% each); and BRCA1, BRCA2, and phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) (5% each) The most common genes with increased copy numbers were AR (30%), MYC (20%), and BRAF (18%). Clinical outcomes were available for 163 patients, 46 of whom (28.8%) were untreated for mCRPC. A higher number of ctDNA alterations, AR alterations, and amplifications of MYC and BRAF were associated with worse failure-free survival and/or OS. On multivariable analysis, MYC amplification remained significantly associated with OS. Prior therapy and serial profiling demonstrated the evolution of alterations in AR and other genes.
CONCLUSIONS: ctDNA frequently was detected in this large cohort of "real-world" patients with mCRPC, and the alterations appeared to be similar to previously reported tumor tissue alterations. A higher number of alterations, and AR and MYC alterations, appear to compromise clinical outcomes, suggesting a role for immune checkpoint inhibitors and novel AR and BET inhibitors in selected patients.
© 2019 American Cancer Society.

Entities:  

Keywords:  castration resistant; circulating tumor DNA (ctDNA); failure-free survival; genomic profiling; metastatic; prostate cancer; survival

Year:  2019        PMID: 30620391     DOI: 10.1002/cncr.31959

Source DB:  PubMed          Journal:  Cancer        ISSN: 0008-543X            Impact factor:   6.860


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