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dc.contributor.authorRubin, M. A.
dc.contributor.authorBristow, Robert G
dc.contributor.authorThienger, P. D.
dc.contributor.authorDive, Caroline
dc.contributor.authorImielinski, M.
dc.date.accessioned2021-01-06T11:15:31Z
dc.date.available2021-01-06T11:15:31Z
dc.date.issued2020en
dc.identifier.citationRubin MA, Bristow RG, Thienger PD, Dive C, Imielinski M. Impact of Lineage Plasticity to and from a Neuroendocrine Phenotype on Progression and Response in Prostate and Lung Cancers. Mol Cell. 2020;80(4):562-77.en
dc.identifier.pmid33217316en
dc.identifier.doi10.1016/j.molcel.2020.10.033en
dc.identifier.urihttp://hdl.handle.net/10541/623673
dc.description.abstractIntratumoral 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.en
dc.language.isoenen
dc.relation.urlhttps://dx.doi.org/10.1016/j.molcel.2020.10.033en
dc.titleImpact of lineage plasticity to and from a neuroendocrine phenotype on progression and response in prostate and lung cancersen
dc.typeArticleen
dc.contributor.departmentDepartment for BioMedical Research, University of Bern and Inselspital, 3010 Bern, Switzerland; Bern Center for Precision Medicine, University of Bern and Inselspital, 3010 Bern, Switzerland.en
dc.identifier.journalMolecular Cellen
dc.description.noteen]


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