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
Search Results
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
Himisha Beltran and Francesca Demichelis
neuroendocrine carcinoma ( Beltran et al. 2011 , Bluemn et al. 2017 , Aggarwal et al. 2018 ). As new drugs enter the clinic for neuroendocrine prostate cancer, patient selection will be critical. Figure 1 Schematic of the lineage plasticity process
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
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
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
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
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
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
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