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Lisa D Berman-Booty and Karen E Knudsen

Introduction Prostate cancer is the second most common cancer in men worldwide ( Ferlay et al . 2010 ). With >90% of prostate cancers initially diagnosed as acinar adenocarcinomas ( Fine 2012 , Humphrey 2012 ), neuroendocrine carcinomas of the

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Alastair Davies, Amina Zoubeidi, and Luke A Selth

et al . 2018 , Ku et al . 2019 ). Clinically, this lineage reprogramming has been associated with loss of luminal epithelial identity and the ensuing transition from a typical prostate adenocarcinoma to an aggressive neuroendocrine prostate cancer

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Ta-Chun Yuan, Suresh Veeramani, and Ming-Fong Lin

therapy. Table 1 Comparison of normal neuroendocrine (NE) and NE-like prostate cancer (PCa) cells in prostate NSE, neuron-specific enolase; CgA, chromogranin A; CgB, chromogranin B; PTHrP, parathyroid hormone-related protein; NT

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Martin K Bakht, Iulian Derecichei, Yinan Li, Rosa-Maria Ferraiuolo, Mark Dunning, So Won Oh, Abdulkadir Hussein, Hyewon Youn, Keith F Stringer, Chang Wook Jeong, Gi Jeong Cheon, Cheol Kwak, Keon Wook Kang, Alastair D Lamb, Yuzhuo Wang, Xuesen Dong, and Lisa A Porter

Introduction The main treatment protocol for patients suffering from castration-resistant prostate cancer (CRPC) is androgen receptor pathway inhibition (ARPI). Selection pressure and lineage plasticity of ARPI can lead to neuroendocrine (NE

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Rosalinda M Savoy and Paramita M Ghosh

been interested in the study of NED in prostate cancer ( Tawadros et al . 2005 ) and has now shown that MIF activates proliferation and survival through the stimulation of Akt and ERK pathways. Neuroendocrine (NE) cells are a component of the normal

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S Humez, M Monet, G Legrand, G Lepage, P Delcourt, and N Prevarskaya

. References Abrahamsson PA 1999 Neuroendocrine cells in tumor growth of the prostate. Endocrine Related Cancer 6 503 –519. Aumuller G , Leonhardt M, Janssen M, Konrad L, Bjartell A & Abrahamsson PA 1999

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Thomas Tawadros, Florian Alonso, Patrice Jichlinski, Noel Clarke, Thierry Calandra, Jacques-Antoine Haefliger, and Thierry Roger

Shabsigh A Hayek O Dorai T Buttyan R 1999 Transdifferentiation of prostate cancer cells to a neuroendocrine cell phenotype in vitro and in vivo . Journal of Urology 162 1800 – 1805 . ( doi:10.1016/S0022-5347(05)68241-9 ). Calandra T

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L Lemonnier, R Lazarenko, Y Shuba, S Thebault, M Roudbaraki, G Lepage, N Prevarskaya, and R Skryma

work was supported by grants from INSERM, La Ligue Nationale Contre le Cancer, l’ARC (France) and INTAS-99-01248. References Abrahamsson PA 1999 Neuroendocrine cells in tumour growth of the prostate. Endocrine

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Himisha Beltran and Francesca Demichelis

Lineage plasticity and histologic transformation to small cell neuroendocrine prostate cancer (NEPC) is an increasingly recognized mechanism of treatment resistance in advanced prostate cancer. This is associated with aggressive clinical features and poor prognosis. Recent work has identified genomic, epigenomic, and transcriptome changes that distinguish NEPC from prostate adenocarcinoma, pointing to new mechanisms and therapeutic targets. Treatment-related NEPC arises clonally from prostate adenocarcinoma during the course of disease progression, retaining early genomic events and acquiring new molecular features that lead to tumor proliferation independent of androgen receptor activity, and ultimately demonstrating a lineage switch from a luminal prostate cancer phenotype to a small cell neuroendocrine carcinoma. Identifying the subset of prostate tumors most vulnerable to lineage plasticity and developing strategies for earlier detection and intervention for patients with NEPC may ultimately improve prognosis. Clinical trials focused on drug targeting of the lineage plasticity process and/or NEPC will require careful patient selection. Here, we review emerging targets and discuss biomarker considerations that may be informative for the design of future clinical studies.

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Marianne E Pavel and Christine Sers

EGFR mutant (T790M) non-small cell lung cancer ( Barton et al . 2010 ), whereas in most neuroendocrine tumors, neither high level EGFR expression nor mutations have been observed ( Kidd et al. 2013 ). In a preliminary analysis of a phase II study of