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
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
Sarah B Bateni, Natalie G Coburn, Calvin Law, Simron Singh, Sten Myrehaug, Angela Assal, and Julie Hallet
There is an increased risk of second primary cancers (SPCs) after neuroendocrine tumor (NET) diagnosis. The clinical significance of SPCs in this population is unknown. The purpose of this study was to evaluate the association between SPCs after NET diagnosis and survival. We performed a population-based, retrospective cohort study of NET patients (gastrointestinal, pancreatic, or lung primary) from 2000-2016 using the Surveillance, Epidemiology, and End Results (SEER) database. Cox regression models assessed the association between SPCs and NET-specific (NET-SS), cancer-specific (CSS), and overall survival (OS). Of 58,553 NET patients, 7.9% experienced a SPC. SPCs were associated with worse OS (HR 2.14, 95%CI 1.94-2.36) and CSS (HR 2.31, 95%CI 2.06-2.59) with no difference in NET-SS (HR 1.04, 95%CI 0.87-1.23). Stratified analyses by histologic grade showed similar results for well and moderately differentiated NETs, but no difference in OS or CSS for poorly differentiated NETs (p>0.05). In stratified analyses by NET site, SPCs were associated with worse OS (HR 3.41, 95%CI 3.01-3.87) and CSS (HR 4.96, 95%CI 4.28-5.74) in gastrointestinal NETs and worse OS (HR 1.25, 95%CI 1.03-1.52) with no difference in CSS (HR 1.08, 95%CI 0.85-1.36) in lung NETs. SPCs were not associated with a difference in OS or CSS in pancreatic NETs (p>0.05). In conclusion, SPCs after NETs were associated with inferior OS and CSS compared to no SPC, but were not associated with NET-SS. These data highlight the need for long-term follow-up in NETs to include detection of SPCs to ensure early diagnosis and timely management.
