Journal article
Impact of Lineage Plasticity to and from a Neuroendocrine Phenotype on Progression and Response in Prostate and Lung Cancers.
- Rubin MA Department for BioMedical Research, University of Bern and Inselspital, 3010 Bern, Switzerland; Bern Center for Precision Medicine, University of Bern and Inselspital, 3010 Bern, Switzerland. Electronic address: mark.rubin@dbmr.unibe.ch.
- Bristow RG Manchester Cancer Research Centre and Cancer Research UK Manchester Institute, University of Manchester, Macclesfield SK10 4TG, UK.
- Thienger PD Department for BioMedical Research, University of Bern and Inselspital, 3010 Bern, Switzerland.
- Dive C Cancer Research UK Manchester Institute Cancer Biomarker Centre, University of Manchester, Macclesfield SK10 4TG, UK.
- Imielinski M Pathology and Laboratory Medicine and Physiology and Biophysics, Weill Cornell Medicine, New York, NY 10065, USA.
- 2020-11-20
Published in:
- Molecular cell. - 2020
English
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.
- Language
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- English
- Open access status
- closed
- Identifiers
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- DOI 10.1016/j.molcel.2020.10.033
- PMID 33217316
- Persistent URL
- https://sonar.ch/global/documents/47262
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