KIT as a therapeutic target in neuroendocrine prostate cancer

Arun A Azad; Louise Kostos; Neeraj Agarwal

doi:10.1016/j.ccell.2022.10.010

KIT as a therapeutic target in neuroendocrine prostate cancer

Cancer Cell. 2022 Nov 14;40(11):1266-1268. doi: 10.1016/j.ccell.2022.10.010. Epub 2022 Nov 3.

Authors

Arun A Azad¹, Louise Kostos¹, Neeraj Agarwal²

Affiliations

¹ Department of Medical Oncology, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia; Sir Peter MacCallum Department of Oncology, University of Melbourne, Melbourne, VIC, Australia.
² Huntsman Cancer Institute, University of Utah, Salt Lake City, UT, USA. Electronic address: neeraj.agarwal@hci.utah.edu.

PMID: 36332623
DOI: 10.1016/j.ccell.2022.10.010

Abstract

Understanding lineage plasticity in prostate cancer cells is crucial to overcoming disease progression and therapeutic resistance. In this issue of Cancer Cell, Han et al. demonstrate that Foxa2 promotes luminal-to-neuroendocrine differentiation and that it also upregulates Kit expression in neuroendocrine cells. KIT signaling inhibition represents a promising therapeutic strategy in neuroendocrine prostate cancer.

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MeSH terms

Carcinoma, Neuroendocrine* / drug therapy
Carcinoma, Neuroendocrine* / genetics
Cell Line, Tumor
Humans
Male
Prostatic Neoplasms* / drug therapy
Prostatic Neoplasms* / genetics
Prostatic Neoplasms* / metabolism
Signal Transduction