Nascent prostate cancer heterogeneity drives evolution and resistance to intense hormonal therapy

Author:

Wilkinson ScottORCID,Ye HuihuiORCID,Karzai FatimaORCID,Harmon Stephanie A.ORCID,Terrigino Nicholas T.ORCID,VanderWeele David J.ORCID,Bright John R.ORCID,Atway RayannORCID,Trostel Shana Y.ORCID,Carrabba Nicole V.ORCID,Whitlock Nichelle C.ORCID,Walker Stephanie M.ORCID,Lis Rosina T.ORCID,Sater Houssein A.ORCID,Capaldo Brian J.ORCID,Madan Ravi A.ORCID,Gulley James L.ORCID,Chun Guinevere,Merino Maria J.ORCID,Pinto Peter A.,Salles Daniela C.ORCID,Kaur Harsimar B.,Lotan Tamara L.ORCID,Venzon David J.ORCID,Choyke Peter L.ORCID,Turkbey BarisORCID,Dahut William L.ORCID,Sowalsky Adam G.ORCID

Abstract

ABSTRACTLocalized prostate cancer is distinctively characterized by intratumoral heterogeneity, and tumors with more complex evolutionary paths display more aggressive characteristics. In clinical trials of intense neoadjuvant androgen deprivation therapy (inADT), patients with complete or near-complete responses experience durable remissions. However, the molecular characteristics distinguishing exceptional responders and nonresponders at baseline have not been established. Here, we present the integrated histologic and genomic analysis of pre-treatment baseline tissue from our recent Phase 2 clinical study of inADT. Multiregion sampling demonstrated that patients with incomplete and nonresponding tumors demonstrate greater tumor diversity as estimated by phylogenetic tree reconstruction from DNA sequencing and automated analysis of immunohistochemical stains. Development of a four-factor binary model to predict poor response correlated with increased genomic diversity in our 37-patient cohort and a validation cohort of 188 Gleason score 8-10 prostate cancers. Together, these findings demonstrate that even in the primary setting, more highly evolved tumors have increased fitness to resist therapy.

Publisher

Cold Spring Harbor Laboratory

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