Cellular Origin of Androgen Receptor Pathway-Independent Prostate Cancer and Implications for Therapy

Research output: Contribution to journalShort survey

Abstract

In this issue of Cancer Cell, Bluemn et al. report that ∼20% of metastatic castration-resistant prostate cancers express neither AR nor neuroendocrine genes and show AR pathway-independent growth, driven instead by a FGFR/MAPK/ID1 signaling cascade. These results provide a strong rationale for co-targeting AR bypass pathways with initial AR antagonism. In this issue of Cancer Cell, Bluemn et al. report that ∼20% of metastatic castration-resistant prostate cancers express neither AR nor neuroendocrine genes and show AR pathway-independent growth, driven instead by a FGFR/MAPK/ID1 signaling cascade. These results provide a strong rationale for co-targeting AR bypass pathways with initial AR antagonism.

Original languageEnglish (US)
Pages (from-to)399-401
Number of pages3
JournalCancer Cell
Volume32
Issue number4
DOIs
StatePublished - Oct 9 2017

ASJC Scopus subject areas

  • Oncology
  • Cell Biology
  • Cancer Research

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