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Molecular Subtypes of Prostate Cancer

Molecular Subtypes of Prostate Cancer Purpose of Review This review will examine the taxonomy of PCa subclasses across disease states, explore the relationship among specific alterations, and highlight current clinical relevance. Recent Findings Prostate cancer (PCa) is driven by multiple genomic alterations, with distinct patterns and clinical implications. Alterations occurring early in the timeline of the disease define core subtypes of localized, treatment-naive PCa. With time, an increase in number and severity of genomic alterations adds molecular complexity and is associated with progression to metastasis. These later events are not random and are influenced by the underlying subclasses. Summary All the subclasses of localized disease initially respond to androgen deprivation therapy (ADT), but with progression to castrate-resistant PCa (CRPC), mechanisms of resistance against ADT shift the molecular landscape. In CRPC, resistance mechanisms largely define the biology and sub-classification of these cancers, while clinical relevance and opportunities for precision therapy are still being defined. . . . . . . . . . Keywords Androgen receptor Androgen deprivation therapy Genomics SPOP CHD1 ETS ERG SPINK1 PTEN . . . . . . . . . . . TP53 NEPC CRPC HG-PIN FOXA1 Rearrangements Prognosis Metastasis Clonal Subclonal TMPRSS2 . . . . Taxonomy PARP IDH1 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Current Oncology Reports Springer Journals

Molecular Subtypes of Prostate Cancer

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Publisher
Springer Journals
Copyright
Copyright © 2018 by Springer Science+Business Media, LLC, part of Springer Nature
Subject
Medicine & Public Health; Oncology
ISSN
1523-3790
eISSN
1534-6269
DOI
10.1007/s11912-018-0707-9
Publisher site
See Article on Publisher Site

Abstract

Purpose of Review This review will examine the taxonomy of PCa subclasses across disease states, explore the relationship among specific alterations, and highlight current clinical relevance. Recent Findings Prostate cancer (PCa) is driven by multiple genomic alterations, with distinct patterns and clinical implications. Alterations occurring early in the timeline of the disease define core subtypes of localized, treatment-naive PCa. With time, an increase in number and severity of genomic alterations adds molecular complexity and is associated with progression to metastasis. These later events are not random and are influenced by the underlying subclasses. Summary All the subclasses of localized disease initially respond to androgen deprivation therapy (ADT), but with progression to castrate-resistant PCa (CRPC), mechanisms of resistance against ADT shift the molecular landscape. In CRPC, resistance mechanisms largely define the biology and sub-classification of these cancers, while clinical relevance and opportunities for precision therapy are still being defined. . . . . . . . . . Keywords Androgen receptor Androgen deprivation therapy Genomics SPOP CHD1 ETS ERG SPINK1 PTEN . . . . . . . . . . . TP53 NEPC CRPC HG-PIN FOXA1 Rearrangements Prognosis Metastasis Clonal Subclonal TMPRSS2 . . . . Taxonomy PARP IDH1

Journal

Current Oncology Reports – Springer Journals

Published: Jun 1, 2018

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