Impact of Lineage Plasticity to and from a Neuroendocrine Phenotype on Progression and Response in Prostate and Lung Cancers

Mark A Rubin, Robert G Bristow, Phillip D Thienger, Caroline Dive, Marcin Imielinski

Research output: Contribution to journalReview articlepeer-review

Abstract

Intratumoral heterogeneity can occur via phenotype transitions, often after chronic exposure to targeted anticancer agents. This process, termed lineage plasticity, is associated with acquired independence to an initial oncogenic driver, resulting in treatment failure. In non-small cell lung cancer (NSCLC) and prostate cancers, lineage plasticity manifests when the adenocarcinoma phenotype transforms into neuroendocrine (NE) disease. The exact molecular mechanisms involved in this NE transdifferentiation remain elusive. In small cell lung cancer (SCLC), plasticity from NE to nonNE phenotypes is driven by NOTCH signaling. Herein we review current understanding of NE lineage plasticity dynamics, exemplified by prostate cancer, NSCLC, and SCLC.

Original languageEnglish
Pages (from-to)562-577
Number of pages16
JournalMolecular Cell
Volume80
Issue number4
DOIs
Publication statusPublished - 19 Nov 2020

Keywords

  • Cell Lineage
  • Cell Plasticity
  • Disease Progression
  • Humans
  • Lung Neoplasms/pathology
  • Male
  • Neuroendocrine Tumors/pathology
  • Phenotype
  • Prostatic Neoplasms/pathology

Research Beacons, Institutes and Platforms

  • Manchester Cancer Research Centre

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