New paper below.
Nalakrats quoted some statistics 4 months ago:
"Latest statistical data from 2 studies, one said 1.2% of all Men with Prostate Cancer have this mutation. Another study indicted it was 2% of all Prostate Cancers---for those that carry the Mutated BRCA-2 Gene."
That sounds about right for familial diesease, & (to me) there doesn't seem much point in being tested unless there is a cluster of breast & prostate cancers in the family.
Lynparza (Olaparib) is a PARP inhibitor that has had some success in cases with BRCA1/2 & ATM repair gene defects
From Steve Freedland:
... we conducted "prospective whole-exome and transcriptome sequencing of bone or soft tissue tumor biopsies from a cohort of 150 mCRPC affected individuals."
"... aberrations of BRCA2, BRCA1, and ATM were observed at substantially higher frequencies (19.3% overall) compared to those in primary prostate cancers." 29 of 150 CRPC cases.
Together with the other aberrations that were discovered, it appears that there might be great value in being biopsied & tested once ADT has failed.
-Patrick
ncbi.nlm.nih.gov/pubmed/286...
Urol Oncol. 2017 Jun 13. pii: S1078-1439(17)30220-X. doi: 10.1016/j.urolonc.2017.05.010. [Epub ahead of print]
Commentary on "Integrative clinical genomics of advanced prostate cancer". Robinson D, Van Allen EM, Wu YM, Schultz N, Lonigro RJ, Mosquera JM, Montgomery B, Taplin ME, Pritchard CC, Attard G, Beltran H, Abida W, Bradley RK, Vinson J, Cao X, Vats P, Kunju LP, Hussain M, Feng FY, Tomlins SA, Cooney KA, Smith DC, Brennan C, Siddiqui J, Mehra R, Chen Y, Rathkopf DE, Morris MJ, Solomon SB, Durack JC, Reuter VE, Gopalan A, Gao J, Loda M, Lis RT, Bowden M, Balk SP, Gaviola G, Sougnez C, Gupta M, Yu EY, Mostaghel EA, Cheng HH, Mulcahy H, True LD, Plymate SR, Dvinge H, Ferraldeschi R, Flohr P, Miranda S, Zafeiriou Z, Tunariu N, Mateo J, Perez-Lopez R, Demichelis F, Robinson BD, Schiffman M, Nanus DM, Tagawa ST, Sigaras A, Eng KW, Elemento O, Sboner A, Heath EI, Scher HI, Pienta KJ, Kantoff P, de Bono JS, Rubin MA, Nelson PS, Garraway LA, Sawyers CL, Chinnaiyan AM.Cell. 21 May 2015;161(5):1215-1228.
Freedland SJ, Aronson WJ.
Abstract
Toward development of a precision medicine framework for metastatic, castration-resistant prostate cancer (mCRPC), we established a multi-institutional clinical sequencing infrastructure to conduct prospective whole-exome and transcriptome sequencing of bone or soft tissue tumor biopsies from a cohort of 150 mCRPC affected individuals. Aberrations of AR, ETS genes, TP53, and PTEN were frequent (40%-60% of cases), with TP53 and AR alterations enriched in mCRPC compared to primary prostate cancer. We identified new genomic alterations in PIK3CA/B, R-spondin, BRAF/RAF1, APC, β-catenin, and ZBTB16/PLZF. Moreover, aberrations of BRCA2, BRCA1, and ATM were observed at substantially higher frequencies (19.3% overall) compared to those in primary prostate cancers. A total of 89% of affected individuals harbored a clinically actionable aberration, including 62.7% with aberrations in AR, 65% in other cancer-related genes, and 8% with actionable pathogenic germline alterations. This cohort study provides clinically actionable information that could affect treatment decisions for these affected individuals.
Copyright © 2017 Elsevier Inc. All rights reserved.
PMID: 28623072 DOI: 10.1016/j.urolonc.2017.05.010