Journal articles: 'Cancer de la prostate neuroendocrine'

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Berman-Booty, Lisa D., and Karen E. Knudsen. "Models of neuroendocrine prostate cancer." Endocrine-Related Cancer 22, no. 1 (October 27, 2014): R33—R49. http://dx.doi.org/10.1530/erc-14-0393.

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Prostate cancer remains the second leading cause of cancer death in men in the USA and most western countries. Prostatic acinar adenocarcinoma is the most commonly diagnosed form of prostate cancer. Small-cell neuroendocrine carcinoma is less frequently identified at the time of initial diagnosis, but this highly aggressive form of prostate cancer is increasingly observed in patients who have failed first- and second-line hormone therapy. Thus, developing and exploring models of neuroendocrine prostate cancer (NePC) are of increasing importance. This review examines the relevant xenograft tumor and genetically engineered mouse models of NePC, with the aim of addressing salient features and clinical relevance.

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Hsu, En-Chi, Meghan A. Rice, Abel Bermudez, Fernando Jose Garcia Marques, Merve Aslan, Shiqin Liu, Ali Ghoochani, et al. "Trop2 is a driver of metastatic prostate cancer with neuroendocrine phenotype via PARP1." Proceedings of the National Academy of Sciences 117, no. 4 (January 13, 2020): 2032–42. http://dx.doi.org/10.1073/pnas.1905384117.

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Resistance to androgen deprivation therapy, or castration-resistant prostate cancer (CRPC), is often accompanied by metastasis and is currently the ultimate cause of prostate cancer-associated deaths in men. Recently, secondary hormonal therapies have led to an increase of neuroendocrine prostate cancer (NEPC), a highly aggressive variant of CRPC. Here, we identify that high levels of cell surface receptor Trop2 are predictive of recurrence of localized prostate cancer. Moreover, Trop2 is significantly elevated in CRPC and NEPC, drives prostate cancer growth, and induces neuroendocrine phenotype. Overexpression of Trop2 induces tumor growth and metastasis while loss of Trop2 suppresses these abilities in vivo. Trop2-driven NEPC displays a significant up-regulation of PARP1, and PARP inhibitors significantly delay tumor growth and metastatic colonization and reverse neuroendocrine features in Trop2-driven NEPC. Our findings establish Trop2 as a driver and therapeutic target for metastatic prostate cancer with neuroendocrine phenotype and suggest that high Trop2 levels could identify cancers that are sensitive to Trop2-targeting therapies and PARP1 inhibition.

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Smith, Bryan A., Artem Sokolov, Vladislav Uzunangelov, Robert Baertsch, Yulia Newton, Kiley Graim, Colleen Mathis, Donghui Cheng, Joshua M. Stuart, and Owen N. Witte. "A basal stem cell signature identifies aggressive prostate cancer phenotypes." Proceedings of the National Academy of Sciences 112, no. 47 (October 12, 2015): E6544—E6552. http://dx.doi.org/10.1073/pnas.1518007112.

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Evidence from numerous cancers suggests that increased aggressiveness is accompanied by up-regulation of signaling pathways and acquisition of properties common to stem cells. It is unclear if different subtypes of late-stage cancer vary in stemness properties and whether or not these subtypes are transcriptionally similar to normal tissue stem cells. We report a gene signature specific for human prostate basal cells that is differentially enriched in various phenotypes of late-stage metastatic prostate cancer. We FACS-purified and transcriptionally profiled basal and luminal epithelial populations from the benign and cancerous regions of primary human prostates. High-throughput RNA sequencing showed the basal population to be defined by genes associated with stem cell signaling programs and invasiveness. Application of a 91-gene basal signature to gene expression datasets from patients with organ-confined or hormone-refractory metastatic prostate cancer revealed that metastatic small cell neuroendocrine carcinoma was molecularly more stem-like than either metastatic adenocarcinoma or organ-confined adenocarcinoma. Bioinformatic analysis of the basal cell and two human small cell gene signatures identified a set of E2F target genes common between prostate small cell neuroendocrine carcinoma and primary prostate basal cells. Taken together, our data suggest that aggressive prostate cancer shares a conserved transcriptional program with normal adult prostate basal stem cells.

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Yuan, Ta-Chun, Suresh Veeramani, and Ming-Fong Lin. "Neuroendocrine-like prostate cancer cells: neuroendocrine transdifferentiation of prostate adenocarcinoma cells." Endocrine-Related Cancer 14, no. 3 (September 2007): 531–47. http://dx.doi.org/10.1677/erc-07-0061.

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Neuroendocrine (NE) cells represent a minor cell population in the epithelial compartment of normal prostate glands and may play a role in regulating the growth and differentiation of normal prostate epithelia. In prostate tumor lesions, the population of NE-like cells, i.e., cells exhibiting NE phenotypes and expressing NE markers, is increased that correlates with tumor progression, poor prognosis, and the androgen-independent state. However, the origin of those NE-like cells in prostate cancer (PCa) lesions and the underlying molecular mechanism of enrichment remain an enigma. In this review, we focus on discussing the distinction between NE-like PCa and normal NE cells, the potential origin of NE-like PCa cells, and in vitro and in vivo studies related to the molecular mechanism of NE transdifferentiation of PCa cells. The data together suggest that PCa cells undergo a transdifferentiation process to become NE-like cells, which acquire the NE phenotype and express NE markers. Thus, we propose that those NE-like cells in PCa lesions were originated from cancerous epithelial cells, but not from normal NE cells, and should be defined as ‘NE-like PCa cells’. We further describe the biochemical properties of newly established, stable NE-like lymph node carcinoma of the prostate (LNCaP) cell lines, transdifferentiated from androgen-sensitive LNCaP cells under androgen-deprived conditions. Knowledge of understanding NE-like PCa cells will help us to explore new therapeutic strategies for treating PCa.

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Shimomura, Tatsuya, Takashi Kurauchi, Keigo Sakanaka, Takahiro Kimura, and Shin Egawa. "Clinical investigation of neuroendocrine differentiation in prostate cancer." Journal of Clinical Oncology 38, no. 6_suppl (February 20, 2020): 138. http://dx.doi.org/10.1200/jco.2020.38.6_suppl.138.

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138 Background: Neuroendocrine prostate cancer (NEPC) is a lethal disease subset with median overall survival of less than 1 year from time of detection. The treatment strategy against NEPC is not yet established and some clinical trials are ongoing now. Recently, clinical trial (RADIIANT4) showed that treatment with everolimus was associated with significant improvement in survival in patients with progressive lung or gastrointestinal neuroendocrine tumors. In this study we evaluated the neuroendocrine differentiation of prostate cancer and we tried to introduce everolimus against pathologically proven NEPC and investigated the clinical outcomes of this agent. Methods: Total of 193 prostate cancer cases were included in this study. We tested serum neuroendocrine markers, including (NSE and pro-GRP). And we evaluated positive rate of these markers. Eleven cases were pathologically proven neuroendocrine prostate cancer (NEPC) in this cohort. Seven out of eleven NEPC cases were introduced everolimus 10mg daily. We investigated the change of serum neuroendocrine markers (NSE and pro-GRP), radiologic examination and survival. Results: The positive rate of serum neuroendocrine markers (at least one of the markers increasing above normal limit) were 23.5% in hormone sensitive prostate cancer (HSPC), 59.5% in castration resistant prostate cancer (CRPC), and 100% in neuroendocrine prostate cancer (NEPC). There were significant differences in each other (HSPC vs. CRPC: p=0.0001, CRPC vs. NEPC: p=0.0109). We introduced everolimus in seven cases out of eleven NEPC cases. The median follow up period was 18 months. Neuroendocrine markers decreased in five of seven (71.4%) cases after introduction of everolimus. Median decreasing rate were 67.1% in NSE and 65.5% in pro GRP. 24M progression free survival rate was 57.1% and 24M overall survival rate was 57.1%. Conclusions: There is a possibility that the incidence of NEPC is higher than expected, and treatment against prostate adenocarcinoma accelerate neuroendocrine differentiation. Everolimus showed efficacy against NEPC. Although this study was retrospective and number of cases was limited, everolimus would be a one of the treatment options against NEPC.

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Wiesehöfer, Marc, Elena Dilara Czyrnik, Martin Spahn, Saskia Ting, Henning Reis, Jaroslaw Thomas Dankert, and Gunther Wennemuth. "Increased Expression of AKT3 in Neuroendocrine Differentiated Prostate Cancer Cells Alters the Response Towards Anti-Androgen Treatment." Cancers 13, no. 3 (February 2, 2021): 578. http://dx.doi.org/10.3390/cancers13030578.

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Patients with advanced prostate carcinoma are often treated with an androgen deprivation therapy but long-term treatment can result in a metastatic castration-resistant prostate cancer. This is a more aggressive, untreatable tumor recurrence often containing areas of neuroendocrine differentiated prostate cancer cells. Using an in vitro model of NE-like cancer cells, it could previously be shown that neuroendocrine differentiation of LNCaP cells leads to a strong deregulation of mRNA and miRNA expression. We observe elevated RNA and protein levels of AKT Serine/Threonine Kinase 3 (AKT3) in neuroendocrine-like LNCaP cells. We used prostate resections from patients with neuroendocrine prostate cancer to validate these results and detect a co-localization of neuroendocrine marker genes with AKT3. Analysis of downstream target genes FOXO3A and GSK3 strengthens the assumption AKT3 may play a role in neuroendocrine differentiation. Overexpression of AKT3 shows an increased survival rate of LNCaP cells after apoptosis induction, which in turn reflects the significance in vivo or for treatment. Furthermore, miR-17, −20b and −106b, which are decreased in neuroendocrine-like LNCaP cells, negatively regulate AKT3 biosynthesis. Our findings demonstrate AKT3 as a potential therapeutic target and diagnostic tool in advanced neuroendocrine prostate cancer and a new mRNA–miRNA interaction with a potential role in neuroendocrine differentiation of prostate cancer.

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Spetsieris, Nicholas, Myrto Boukovala, Georgios Patsakis, Ioannis Alafis, and Eleni Efstathiou. "Neuroendocrine and Aggressive-Variant Prostate Cancer." Cancers 12, no. 12 (December 16, 2020): 3792. http://dx.doi.org/10.3390/cancers12123792.

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In prostate cancer, neuroendocrine (NE) differentiation may rarely present de novo or more frequently arises following hormonal therapy in patients with castration-resistant prostate cancer (CRPC). Its distinct phenotype is characterized by an aggressive clinical course, lack of responsiveness to hormonal therapies and poor prognosis. Importantly, a subset of CRPC patients exhibits an aggressive-variant disease with very similar clinical and molecular characteristics to small-cell prostate cancer (SCPC) even though tumors do not have NE differentiation. This aggressive-variant prostate cancer (AVPC) also shares the sensitivity of SCPC to platinum-based chemotherapy albeit with short-lived clinical benefit. As optimal treatment strategies for AVPC remain elusive, currently ongoing research efforts aim to enhance our understanding of the biology of this disease entity and improve treatment outcomes for our patients. This review is an overview of our current knowledge on prostate cancer with NE differentiation and AVPC, with a focus on their clinical characteristics and management, including available as well as experimental therapeutic strategies.

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Kaarijärvi, Roosa, Heidi Kaljunen, and Kirsi Ketola. "Molecular and Functional Links between Neurodevelopmental Processes and Treatment-Induced Neuroendocrine Plasticity in Prostate Cancer Progression." Cancers 13, no. 4 (February 9, 2021): 692. http://dx.doi.org/10.3390/cancers13040692.

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Neuroendocrine plasticity and treatment-induced neuroendocrine phenotypes have recently been proposed as important resistance mechanisms underlying prostate cancer progression. Treatment-induced neuroendocrine prostate cancer (t-NEPC) is highly aggressive subtype of castration-resistant prostate cancer which develops for one fifth of patients under prolonged androgen deprivation. In recent years, understanding of molecular features and phenotypic changes in neuroendocrine plasticity has been grown. However, there are still fundamental questions to be answered in this emerging research field, for example, why and how do the prostate cancer treatment-resistant cells acquire neuron-like phenotype. The advantages of the phenotypic change and the role of tumor microenvironment in controlling cellular plasticity and in the emergence of treatment-resistant aggressive forms of prostate cancer is mostly unknown. Here, we discuss the molecular and functional links between neurodevelopmental processes and treatment-induced neuroendocrine plasticity in prostate cancer progression and treatment resistance. We provide an overview of the emergence of neurite-like cells in neuroendocrine prostate cancer cells and whether the reported t-NEPC pathways and proteins relate to neurodevelopmental processes like neurogenesis and axonogenesis during the development of treatment resistance. We also discuss emerging novel therapeutic targets modulating neuroendocrine plasticity.

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Pinto, Filipe, and Rui Manuel Reis. "Drivers of neuroendocrine prostate cancer." Translational Cancer Research 5, S3 (September 2016): S551—S553. http://dx.doi.org/10.21037/tcr.2016.09.26.

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Amorino, George P., and Sarah J. Parsons. "Neuroendocrine Cells in Prostate Cancer." Critical Reviews in Eukaryotic Gene Expression 14, no. 4 (2004): 14. http://dx.doi.org/10.1615/critreveukargeneexpr.v14.i4.40.

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Amorino, George P., and Sarah J. Parsons. "Neuroendocrine Cells in Prostate Cancer." Critical Reviews in Eukaryotic Gene Expression 14, no. 4 (2004): 287–300. http://dx.doi.org/10.1615/critreveukaryotgeneexpr.v14.i4.40.

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Shariff, Amir H., and M. Hammad Ather. "Neuroendocrine differentiation in prostate cancer." Urology 68, no. 1 (July 2006): 2–8. http://dx.doi.org/10.1016/j.urology.2006.02.002.

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Li, Zhen, Clark J. Chen, Jason K. Wang, Elaine Hsia, Wei Li, Jill Squires, Yin Sun, and Jiaoti Huang. "Neuroendocrine differentiation of prostate cancer." Asian Journal of Andrology 15, no. 3 (March 18, 2013): 328–32. http://dx.doi.org/10.1038/aja.2013.7.

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Cerovic, Snezana, Goran Brajuskovic, Vinka Maletic-Vukotic, and Sava Micic. "Neuroendocrine differentiation in prostate cancer." Vojnosanitetski pregled 61, no. 5 (2004): 513–18. http://dx.doi.org/10.2298/vsp0405513c.

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Background. In numerous recent studies attention has been focused to neuroendocrine differentiation (NED) in prostate cancer (PC). Focal NED is present in almost all PCs, but it is prominent in only 5-10% of the carcinomas. The prognostic significance of focal NED in PC is controversial, but current evidence suggests its influence on the onset and/or conversion of hormon resistant tumor phenotype. The aim of this study was to evaluate the relationship between NED status, based only on immunohistochemical use of neuroendocrine (NE) markers, with PC grade and stage, and preoperative serum levels of prostate-specific antigen (PSA). Methods. The study included the biopsy material of 73 untreated PC patients (pts.) obtained by transurethral resection (TUR) (37 pts.), and radical retropubic prostatectomy (RRP) (36 pts.). Two representative tissue samples (tipically the block containing the largest amount of neoplasm) were selected for immunohistochemical (IMM) staining. NE cells were identified using a panel of IMM markers: chromogranin A, neuron-specific enolase, and serotonin. The level of PC exocrine differentiation was detected by monoclonal antibodies against PSA. Results. Significant expression of NE cells was demonstrated in 26 (70.2%) pts. with PC after TUR. In this group, serum preoperative PSA values ranged from 0.1 to 9.6 ng/ml. The majority of pts. with NED had low differentiated PC with Gleason grade score (GGS) >7, and normal PSA values below 4 ng/ml (77%), in clinical stage D (54%). Statistically significant correlation (p<0.01) of positive NED with higher stage and grade and low PSA values was established. Among the pts. with localized PC in whom RRP was performed (n=36), significant expression of NE cells was found in 15 pts. (41.7%), 8 (53.3%) in pT2 stage, and 7 (46.7%) in pT3 stage. Significant correlation between NED with preoperative PSA values and stage of PC in pts. with RRP was not found. Conclusion. We demonstrated the significant NED in poorly differentiated PC in patients in the advanced stage of the disease. The expression of NED in organ-confined PC did not correlate with tumor stage, but it correlated with tumor grade (GGS?7).

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Wang, Jingwen, and Yang Yao. "Neuroendocrine differentiation in prostate cancer." Chinese-German Journal of Clinical Oncology 7, no. 3 (March 2008): 150–53. http://dx.doi.org/10.1007/s10330-007-0184-3.

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Kránitz, Noémi, Zsolt Szepesváry, Károly Kocsis, and Tamás Kullmann. "Neuroendocrine Cancer of the Prostate." Pathology & Oncology Research 26, no. 3 (August 14, 2019): 1447–50. http://dx.doi.org/10.1007/s12253-019-00712-2.

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Smith, D. C., J. A. Tucker, and D. L. Trump. "Hypercalcemia and neuroendocrine carcinoma of the prostate: a report of three cases and a review of the literature." Journal of Clinical Oncology 10, no. 3 (March 1992): 499–505. http://dx.doi.org/10.1200/jco.1992.10.3.499.

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PURPOSE Hypercalcemia is a rare complication of prostate cancer, and no definite association with any histologic subtype of prostatic malignancy has been documented. We have recently seen three patients who developed hypercalcemia in the setting of prostate cancer. All had neuroendocrine carcinoma of the prostate (NCPs), which prompted an exploration of the potential association of hypercalcemia with NCP. DESIGN An extensive review of literature published in the English-language was conducted to identify cases of hypercalcemia associated with prostate cancer and well-documented cases of NCP. RESULTS We found 17 reported cases of hypercalcemia clearly associated with prostate cancer and a total of 61 cases of well-documented NCP. Including our cases, 11 of the 20 reported cases of hypercalcemia associated with prostate carcinoma were in patients with neuroendocrine carcinomas. CONCLUSION Hypercalcemia in the setting of prostate cancer should prompt a search for unusual histologies.

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Wilson, Elizabeth M., Youngman Oh, Vivian Hwa, and Ron G. Rosenfeld. "Interaction of IGF-Binding Protein-Related Protein 1 with a Novel Protein, Neuroendocrine Differentiation Factor, Results in Neuroendocrine Differentiation of Prostate Cancer Cells." Journal of Clinical Endocrinology & Metabolism 86, no. 9 (September 1, 2001): 4504–11. http://dx.doi.org/10.1210/jcem.86.9.7845.

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Neuroendocrine cells have been implicated in many cancers, including small cell lung, cervical, breast, and prostate carcinomas. The increase in neuroendocrine cell number in prostate cancer has been reported to correlate with poor prognosis, progressive tumors, and androgen insensitivity. The mechanisms involved in this differentiation remain unknown. IGF-binding protein-related protein 1 is a member of the IGF-binding protein superfamily and has recently been shown to exhibit differentiation and tumor suppression activity in prostate cancer cell lines stably overexpressing IGF-binding protein-related protein 1. From a yeast two-hybrid screen, a novel IGF-binding protein-related protein 1-interacting protein was identified. Immunocytochemical techniques indicate that this protein, 25.1, and intracellular IGF-binding protein-related protein 1 colocalize in the nucleus. When 25.1 is transiently expressed in a stable prostate cancer cell line overexpressing IGF-binding protein-related protein 1, cells assume a neuritic-like morphology with long dendritic-like processes and express the neuroendocrine markers chromogranin A and neuron-specific enolase. We propose that 25.1 (neuroendocrine differentiation factor) together with IGF-binding protein-related protein 1 can induce neuroendocrine cell differentiation in prostate cancer cells.

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Abbasova, Daria V., Svetlana B. Polikarpova, Nikolai A. Kozlov, Madina P. Baranova, Irina P. Kovalenko, and Elena I. Ignatova. "Neuroendocrine carcinoma of the prostate (review of the literature)." Journal of Modern Oncology 21, no. 3 (September 15, 2019): 52–55. http://dx.doi.org/10.26442/18151434.2019.3.190673.

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Neuroendocrine neoplasia (NEC) of the prostate gland is a rather rare extrapulmonary neuroendocrine carcinoma and makes up only 0.5 to 1% of all malignant neoplasms of this localization. NEC of the prostate gland is a tumor of epithelial origin, histologically and immunohistochemically identical to analogues in the lungs and digestive system. When stained with hemotoxylin-eosin, neuroendocrine cells cannot always be visualized; they are best recognized by the immunohistochemical method of investigation using specific markers. Currently, a number of neuroendocrine markers are used, the expression of which may indicate a neuroendocrine nature. Androgen neuroendocrine cells themselves are independent and do not cause an increase in the concentration of prostate-specific antigen. Prostate NECs are represented by some histological forms according to WHO classification (2015): 1. Adenocarcinoma with focal neuroendocrine differentiation. 2. Well-differentiated neuroendocrine tumor. 3. Small cell neuroendocrine cancer is a high - grade tumor with high malignant potential. 4. Large cell neuroendocrine cancer is a high - grade tumor. Due to the rarity of NEC of the prostate, a specific algorithm for diagnosis and treatment has not been developed, as a rule, they are similar to methods of other malignant forms of prostate cancer and neuroendocrine tumors.

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Tabrizi, Shervin, Mohammed Alshalalfa, Brandon Arvin Virgil Mahal, Elai Davicioni, Yang Liu, Kent William Mouw, Felix Y. Feng, Paul L. Nguyen, and Vinayak Muralidhar. "Doublecortin expression in prostate adenocarcinoma and neuroendocrine tumors." Journal of Clinical Oncology 38, no. 6_suppl (February 20, 2020): 161. http://dx.doi.org/10.1200/jco.2020.38.6_suppl.161.

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161 Background: Recent work using prostate cancer mouse models implicated doublecortin (DCX)-expressing neural progenitor cells in prostate adenocarcinoma, reporting a strong association between DCX expression and disease progression and outcome. We sought to evaluate the relationship between DCX expression and these outcomes in human prostate cancer. Methods: DCX expression was measured in transcriptome-wide microarray data from 18,501 patients with localized prostate cancer and 290 patients with metastatic castration-resistant prostate cancer (mCRPC). Pairwise comparisons were performed using the Mann–Whitney U test. Metastasis-free survival (MFS) and overall survival (OS) were analyzed using Cox-proportional hazards. Results: DCX expression was not significantly different between normal prostate (n=29), primary prostate cancer (n=131), or metastases (n=19) (p > 0.5), and did not differ across Gleason score in a large cohort of RP samples (n=17,967, p=0.21). The lack of difference persisted after adjusting for stromal contribution using a 141-gene stromal signature. Those with DCX expression above and below the median did not have significant differences in MFS (HR 1.2 [0.84-1.7], p=0.3) or OS (HR 1.15 [0.7-1.84], p =0.56). In a cohort of untreated prostate cancer, DCX expression was higher in neuroendocrine tumors (n=10) compared to Gleason 9-10 prostate adenocarcinoma (n=110) (p=0.007). Similarly, in two cohorts with mCRPC (n=290), DCX expression was higher in lesions with neuroendocrine features than adenocarcinoma (p<0.001). Consistently, in a patient-derived xenograft model subjected to host castration, DCX expression was initially low, but increased significantly once tumors underwent neuroendocrine differentiation and treatment escape. Conclusions: Contrary to recent data using mouse models, DCX expression did not differ by disease state, grade, or outcome in a dataset of human patients with prostate adenocarcinoma. However, DCX expression appeared to correlate with neuroendocrine prostate cancers, a subgroup that can arise de novo or in the castrate-resistant setting. Further work is needed to define the role of DCX expression and its prognostic significance in prostate cancer.

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Krušlin, Božo, Lucija Škara, Tonći Vodopić, Borna Vrhovec, Jure Murgić, Goran Štimac, Ana Fröbe, Cvjetko Lež, Monika Ulamec, and Koraljka Gall-Trošelj. "Genetics of Prostate Carcinoma." Acta Medica Academica 50, no. 1 (May 26, 2021): 71. http://dx.doi.org/10.5644/ama2006-124.327.

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The aim of this review is to provide a brief overview of some current approaches regarding diagnostics, pathologic features, treatment, and genetics of prostate carcinoma (PCa). Prostate carcinoma is the most common visceral tumor and the second most common cancer-related cause of death in males. Clinical outcomes for patients with localized prostate cancer are excellent, but despite advances in prostate cancer treatments, castrate-resistant prostate cancer and metastatic prostate cancer patients have a poor prognosis. Advanced large-scale genomic studies revealed a large number of genetic alterations in prostate cancer. The meaning of these alterations needs to be validated in the specific prostate cancer molecular subtype context. Along these lines, there is a critical need for establishing genetically engineered mouse models, which would include speckle type BTB/POZ protein and isocitrate Dehydrogenase (NADP (+)) 1 mutant, as well as androgen receptor neuroendocrine subtypes of prostate cancer. Another urgent need is developing highly metastatic prostate cancer models, as only up to 17% of available models dis- play bone metastases and exhibit a less typical neuroendocrine prostate cancer or sarcomatoid carcinoma. Moreover, androgen deprivation and relapse should be mimicked in the genetically engineered mouse models, as androgen independence may yield a better model for metastatic castrate-resistant prostate cancer. The development of such refined animal models should be guid- ed by comparative genomics of primary versus corresponding metastatic tumors. Such an approach will have the potential to illuminate the key genetic events associated with specific molecular prostate cancer subsets and indicate directions for effective therapy.Conclusion. Despite excellent results in the treatment of localized prostatic carcinoma, castrate-resistant prostate can- cer and metastatic prostate cancer have a poor prognosis. Advanced large-scale genomic studies revealed a large number of ge- netic alterations in PCa. Experimental models of prostate carcinoma in genetically modified mice could provide new data about the genetic changes in such cancers and help in developing better animal models for treatment resistant prostate carcinomas.

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Puca, Loredana, Katie Gavyert, Verena Sailer, Vincenza Conteduca, Etienne Dardenne, Michael Sigouros, Kumiko Isse, et al. "Delta-like protein 3 expression and therapeutic targeting in neuroendocrine prostate cancer." Science Translational Medicine 11, no. 484 (March 20, 2019): eaav0891. http://dx.doi.org/10.1126/scitranslmed.aav0891.

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Histologic transformation to small cell neuroendocrine prostate cancer occurs in a subset of patients with advanced prostate cancer as a mechanism of treatment resistance. Rovalpituzumab tesirine (SC16LD6.5) is an antibody-drug conjugate that targets delta-like protein 3 (DLL3) and was initially developed for small cell lung cancer. We found that DLL3 is expressed in most of the castration-resistant neuroendocrine prostate cancer (CRPC-NE) (36 of 47, 76.6%) and in a subset of castration-resistant prostate adenocarcinomas (7 of 56, 12.5%). It shows minimal to no expression in localized prostate cancer (1 of 194) and benign prostate (0 of 103). DLL3 expression correlates with neuroendocrine marker expression,RB1loss, and aggressive clinical features. DLL3 in circulating tumor cells was concordant with matched metastatic biopsy (87%). Treatment of DLL3-expressing prostate cancer xenografts with a single dose of SC16LD6.5 resulted in complete and durable responses, whereas DLL3-negative models were insensitive. We highlight a patient with neuroendocrine prostate cancer with a meaningful clinical and radiologic response to SC16LD6.5 when treated on a phase 1 trial. Overall, our findings indicate that DLL3 is preferentially expressed in CRPC-NE and provide rationale for targeting DLL3 in patients with DLL3-positive metastatic prostate cancer.

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Mijovic, Milica, Aleksandar Corac, Sonja Smiljic, Sladjana Savic, Predrag Mandic, Leonida Vitkovic, Snezana Lestarevic, and Snezana Janicijevic-Hudomal. "Correlation of focal neuroendocrine differentiation in prostate cancer with the parameters of predictive value." Vojnosanitetski pregled 76, no. 11 (2019): 1115–26. http://dx.doi.org/10.2298/vsp170930019m.

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Background/Aim. Neuroendocrine (NE) cells are one of the epithelial populations in the prostate. It is well-known that the focal neuroendocrine differentiation (FNED) in prostate cancer (PC) is an aggressive subtype that most commonly evolves from preexisting PC which does not respond to hormone therapy (androgen independed PC). The incidence and clinical importance of FNED in PC is not clearly understood because of conflicting results in the studies, and evaluation of FNED is not routinely performed in clinical practice. The aim of the present study is to determine the importance of FNED presence in the examined prostate changes with special reference to the relationship of FNED degree in PC with some parameters of predictive value [Gleason score, preoperative serum total prostata specific antigen (PSA) value, tumor volume and tumor stage]. Methods. The study included the biopsy material from 100 untreated consecutive prostate pathological changes: 70 PC, 20 prostatic intraepithelial neoplasia (PIN) and 10 benign prostatic hyperplasia (BPH). The patients with PIN and BPH were the control groups. A block containing part of the main bulk of pathological change was chosen as representative based on hematoxylin-eosin appearance, and a section of this block was immunohistochemically stained for the tissue PSA (to mark prostatic secretory cells) and chromogranin A, serotonin and synaptophysin (to mark NE cells). Results. We found a very pronounced degree of FNED differentiation in 16 (22.9%) PC. Ten (62.5%) of them had Gleason score ? 7, the average serum PSA level was 32.62 ? 30.80 ng/mL, average tumor volume was 43.18 ? 31.45 mL and 6 (37.5%) of this PC were detected in D clinical stage with distant hematogenous metastases. The FNED is negatively correlated with the serum PSA level, Gleason score and clinical stage positively correlated with the tumor volume, but without statistically significant differences. Conclusion. The FNED has no significant role in the prognosis of PC.

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Xiang, Qian, Zhiguo Zhu, Lianmin Luo, Jiamin Wang, Yangzhou Liu, Yihan Deng, Mingda Zhou, and Zhigang Zhao. "The Correlation between PSCA Expression and Neuroendocrine Differentiation in Prostate Cancer." BioMed Research International 2020 (September 24, 2020): 1–9. http://dx.doi.org/10.1155/2020/5395312.

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The prostate stem cell antigen (PSCA), as a predominantly prostate-specific marker, is overexpressed in most prostate cancer specimens, is positively correlated with prostate cancer androgen independence, and has the potential to be treated with castration-resistant prostate cancer (CRPC) as a gene therapy target. Using the typical androgen deprivation therapy, most tumors will progress to CRPC, as well as develop into neuroendocrine prostate cancer (NEPC) characterized by the expression of neuroendocrine markers such as enolase 2 (NSE). Our study was aimed at investigating the expressions of PSCA and NSE and the relationship between the two markers, as well as the correlation between the PSCA and NSE expressions and the clinicopathological parameters in prostate cancer specimens from 118 patients by using immunohistochemistry. Our results demonstrated that the PSCA and NSE protein expressions did not correlate with the prostate cancer patients’ age or the hormone therapy but showed a significant correlation with the pathological tumor stage of prostate cancer, the Gleason score, and the presence of metastasis. There is a positive association between PSCA and NSE but a negative one between the prostate-specific antigen (PSA) and PSCA or between PSA and NSE. High PSCA and NSE expressions correlated with a poor prognosis in prostate cancer patients. PSCA may play an important role in the progression of neuroendocrine prostate cancer (NEPC).

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Davies, Alastair, Amina Zoubeidi, and Luke A. Selth. "The epigenetic and transcriptional landscape of neuroendocrine prostate cancer." Endocrine-Related Cancer 27, no. 2 (February 2020): R35—R50. http://dx.doi.org/10.1530/erc-19-0420.

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Tumours adapt to increasingly potent targeted therapies by transitioning to alternative lineage states. In prostate cancer, the widespread clinical application of androgen receptor (AR) pathway inhibitors has led to the insurgence of tumours relapsing with a neuroendocrine phenotype, termed neuroendocrine prostate cancer (NEPC). Recent evidence suggests that this lineage reprogramming is driven largely by dysregulation of the epigenome and transcriptional networks. Indeed, aberrant DNA methylation patterning and altered expression of epigenetic modifiers, such as EZH2, transcription factors, and RNA-modifying factors, are hallmarks of NEPC tumours. In this review, we explore the nature of the epigenetic and transcriptional landscape as prostate cancer cells lose their AR-imposed identity and transition to the neuroendocrine lineage. Beyond addressing the mechanisms underlying epithelial-to-neuroendocrine lineage reprogramming, we discuss how oncogenic signaling and metabolic shifts fuel epigenetic/transcriptional changes as well as the current state of epigenetic therapies for NEPC.

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Sciarra, Alessandro, Michele Innocenzi, Michele Ravaziol, Francesco Minisola, Andrea Alfarone, Susanna Cattarino, Giuseppe Monti, Vincenzo Gentile, and Franco Di Silverio. "Neuroendocrine target therapies for prostate cancer." Rivista Urologia 78, no. 2 (2011): 137–41. http://dx.doi.org/10.5301/ru.2011.8335.

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Kim, J., H. Jin, J. C. Zhao, Y. A. Yang, Y. Li, X. Yang, X. Dong, and J. Yu. "FOXA1 inhibits prostate cancer neuroendocrine differentiation." Oncogene 36, no. 28 (March 20, 2017): 4072–80. http://dx.doi.org/10.1038/onc.2017.50.

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Thoma, Clemens. "Targeting DLL3 in neuroendocrine prostate cancer." Nature Reviews Urology 16, no. 6 (April 30, 2019): 330. http://dx.doi.org/10.1038/s41585-019-0190-6.

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Conteduca, Vincenza, Clara Oromendia, Kenneth W. Eng, Rohan Bareja, Michael Sigouros, Ana Molina, Bishoy M. Faltas, et al. "Clinical features of neuroendocrine prostate cancer." European Journal of Cancer 121 (November 2019): 7–18. http://dx.doi.org/10.1016/j.ejca.2019.08.011.

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Mather, Rebecca L., Henry Andrews, Hardev Pandha, Elena Jachetti, Jake Micallef, Yuzhuo Wang, and Francesco Crea. "The Open University's first one-day symposium on treatment-emergent neuroendocrine prostate cancer." Future Oncology 16, no. 6 (February 2020): 147–49. http://dx.doi.org/10.2217/fon-2019-0718.

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The Open University's first one-day symposium on treatment-emergent neuroendocrine prostate cancer attracted world-leading figures, early career researchers and industry colleagues. The symposium proved insightful into the ‘real-world’ impact and current problems faced in the diagnosis and treatment of neuroendocrine prostate cancer. It was important for this meeting to take place as the incidence of neuroendocrine prostate cancer is increasing due to the widespread use of next-generation androgen deprivation drugs. The symposium discussions proposed new molecularly driven deadlines to accelerate research and improved the treatment of this deadly and poorly recognized malignancy.

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Moparthi, Lavanya, Giulia Pizzolato, and Stefan Koch. "Wnt activator FOXB2 drives the neuroendocrine differentiation of prostate cancer." Proceedings of the National Academy of Sciences 116, no. 44 (October 14, 2019): 22189–95. http://dx.doi.org/10.1073/pnas.1906484116.

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The Wnt signaling pathway is of paramount importance for development and disease. However, the tissue-specific regulation of Wnt pathway activity remains incompletely understood. Here we identify FOXB2, an uncharacterized forkhead box family transcription factor, as a potent activator of Wnt signaling in normal and cancer cells. Mechanistically, FOXB2 induces multiple Wnt ligands, including WNT7B, which increases TCF/LEF-dependent transcription without activating Wnt coreceptor LRP6 or β-catenin. Proximity ligation and functional complementation assays identified several transcription regulators, including YY1, JUN, and DDX5, as cofactors required for FOXB2-dependent pathway activation. Although FOXB2 expression is limited in adults, it is induced in select cancers, particularly advanced prostate cancer. RNA-seq data analysis suggests that FOXB2/WNT7B expression in prostate cancer is associated with a transcriptional program that favors neuronal differentiation and decreases recurrence-free survival. Consistently, FOXB2 controls Wnt signaling and neuroendocrine differentiation of prostate cancer cell lines. Our results suggest that FOXB2 is a tissue-specific Wnt activator that promotes the malignant transformation of prostate cancer.

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Nappi, Lucia, Claudia Kesch, Sepideh Vahid, Ladan Fazli, Bernhard J. Eigl, Christian K. Kollmannsberger, Martin Gleave, Amina Zoubeidi, Alexander William Wyatt, and Kim N. Chi. "Immunogenomic landscape of neuroendocrine small cell prostate cancer." Journal of Clinical Oncology 37, no. 7_suppl (March 1, 2019): 217. http://dx.doi.org/10.1200/jco.2019.37.7_suppl.217.

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217 Background: Neuroendocrine small cell prostate cancer (NEPC) is a lethal variant of prostate cancer (PCa) unresponsive to hormone therapy and associated with poor prognosis. Cisplatin induces short-lived responses and therefore alternative novel therapeutic options are urgently needed. Methods: Prostate specimens from radical prostatectomy or transurethral resection (benign prostate specimens n = 4, primary untreated or neoadjuvant hormone-treated adenocarcinoma n = 30, castrate-resistant prostate cancer-CRPC n = 38 and NEPC n = 16) were evaluated for PD-L1 (SpringBio, M4420), AR, chromogranin A, synaptophysin, NSE and CD56 expression by immunohistochemistry (IHC). Archival tissue from liver, lymph nodes and prostate from 30 additional patients with de novo and treatment emergent NEPC were analyzed for PD-L1 expression by IHC. The intensity was assessed as percentage of positive cells / mm2 of tissue. Targeted and whole exome sequencing of the high-density tumor areas were performed and correlated to the PD-L1 status (PD-L1+ve: > 1% of positive cells). OS was calculated from the date of diagnosis of NEPC to death. We set out to define PD-L1 expression and immunogenomic characteristics of NEPC. Results: PD-L1 was expressed in 0%, 5%, 10% and 41% of benign, adenocarcinoma, CRPC and NEPC specimens, respectively. The PD-L1 expression intensity was significantly higher in patients with NEPC (mean: 40%, range: 5-100%) compared to benign, adenocarcinoma and CRPC samples (mean: 0%, 2% and 8%, respectively, P < 0.0001). There was a higher prevalence of biallelic DNA Repair Defects (DRD) in the PD-L1+ve vs PD-L1-ve patients (65% vs 0%, P = 0.005). The median OS of the NEPC patients was 8.5 months vs 10.5 months in PD-L1+ve vs PD-L1-ve tumors (HR 1.24, 95% CI: 0.59-2.75, p = 0.55). Conclusions: NEPC have greater PD-L1 expression than adenoCa and CRPC. Biallelic DRD was exclusively observed in PD-L1+ve patients. Since PD-L1 expression and DRD have been associated to response to PARP and PD1/PD-L1 inhibitors in prostate and other cancers, further studies evaluating the activity of those agents in NEPC patients are warranted.

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Beltran, Himisha, and Francesca Demichelis. "Therapy considerations in neuroendocrine prostate cancer: what next?" Endocrine-Related Cancer 28, no. 8 (August 1, 2021): T67—T78. http://dx.doi.org/10.1530/erc-21-0140.

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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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Park, Jung Wook, John K. Lee, Katherine M. Sheu, Liang Wang, Nikolas G. Balanis, Kim Nguyen, Bryan A. Smith, et al. "Reprogramming normal human epithelial tissues to a common, lethal neuroendocrine cancer lineage." Science 362, no. 6410 (October 4, 2018): 91–95. http://dx.doi.org/10.1126/science.aat5749.

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The use of potent therapies inhibiting critical oncogenic pathways active in epithelial cancers has led to multiple resistance mechanisms, including the development of highly aggressive, small cell neuroendocrine carcinoma (SCNC). SCNC patients have a dismal prognosis due in part to a limited understanding of the molecular mechanisms driving this malignancy and the lack of effective treatments. Here, we demonstrate that a common set of defined oncogenic drivers reproducibly reprograms normal human prostate and lung epithelial cells to small cell prostate cancer (SCPC) and small cell lung cancer (SCLC), respectively. We identify shared active transcription factor binding regions in the reprogrammed prostate and lung SCNCs by integrative analyses of epigenetic and transcriptional landscapes. These results suggest that neuroendocrine cancers arising from distinct epithelial tissues may share common vulnerabilities that could be exploited for the development of drugs targeting SCNCs.

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Ferguson, Alison, Bhavneet Bhinder, Vincenza Conteduca, Michael Sigouros, Andrea Sboner, David M. Nanus, Scott T. Tagawa, David Rickman, Olivier Elemento, and Himisha Beltran. "Immunogenomic landscape of neuroendocrine prostate cancer (NEPC)." Journal of Clinical Oncology 37, no. 7_suppl (March 1, 2019): 224. http://dx.doi.org/10.1200/jco.2019.37.7_suppl.224.

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224 Background: Prostate cancer (PCa) shows limited clinical benefit from current immunotherapy strategies. NEPC is a histologic subtype of advanced PCa that most often arises clonally from castrate resistant prostate adenocarcinoma (CRPC) as a mechanism of resistance, but shares pathologic, clinical, and molecular features with small cell lung carcinoma (SCLC). We investigated the immune landscape of NEPC in relation to other PCa subtypes and SCLC to identify potential immunological targets. Methods: We evaluated RNA-seq from 190 patients comprising benign prostate (n = 29; 25 PCa matched), localized PCa (n = 68), hormone-naïve metastatic prostate adenocarcinoma (mPCa; n = 11), CRPC (n = 54), NEPC (n = 25) with follow-up data, and SCLC (n = 28) (Rudin et al., Nat Gen 2012). Additionally, 290 patients had WES data available for tumor mutational burden (TMB). Unsupervised clustering of FPKMs was performed to identify an immune rich cluster of 232 genes, which was used to categorize immune status and prioritize validation of select targets by IHC. Results: Median TMB of NEPC was similar to CRPC (38.0 vs 37.0 p= 0.44) but significantly lower than SCLC (38.0 vs 142.5, p< 0.001). Unsupervised assessment of T-cell related gene expression identified a predominantly cold immune status across subtypes, with hot (n = 8) tumors associated with metastatic tumors of the LN and bone. Worse overall survival was seen with intermediate vs cold T-cell immune status (66.5 mo vs 101.5 mo; p < 0.001). Further analysis of NEPC showed lower expression of cytokines ( p< 0.01) and variation in checkpoint markers. Specifically, NEPC had significantly lower expression of PD1 in relation to CRPC ( p= 0.0001) and SCLC ( p = < 0.0001), higher PDL1 than CRPC ( p= 0.05) but comparable with SCLC ( p= 0.93) and lower PDL2 than PCa and SCLC ( p= 0.03; < 0.001, respectively). Conclusions: NEPC is characterized by a relatively ‘cold’ tumor immune microenvironment similar to other metastatic prostate cancer subtypes but higher PDL1 expression comparable to SCLC. The inverse correlation between survival outcome and immune infiltration, as well as the novel expression changes in cytokines and checkpoint markers support further investigation into the immune landscape and potential targets for NEPC.

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Crea, Francesco. "Neuroendocrine prostate cancer: long noncoding RNAs to treat an incurable cancer – an interview with Dr Francesco Crea." Epigenomics 11, no. 13 (October 2019): 1461–62. http://dx.doi.org/10.2217/epi-2019-0236.

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Francesco Crea speaks to Lucy Chard, Commissioning Editor. Dr Crea’s lab studies the role of epigenetic factors and noncoding RNA in cancer initiation and progression. While working at the National Cancer Institute (USA), Dr Crea has demonstrated that polycomb-targeting drugs eradicate prostate cancer stem cells. While working at the BC Cancer Agency (Canada), Dr Crea discovered and patented PCAT18, a long noncoding RNA involved in prostate cancer metastasis. Dr Crea has received awards from the American Society of Clinical Oncology, from the Prostate Cancer Program and from Prostate Cancer Foundation BC. He is also an Editorial Board member for Epigenomics. His team is currently working on developing new biomarkers and therapeutic targets for incurable prostate and breast cancers.

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Hu, Jing, Bo Han, and Jiaoti Huang. "Morphologic Spectrum of Neuroendocrine Tumors of the Prostate: An Updated Review." Archives of Pathology & Laboratory Medicine 144, no. 3 (October 23, 2019): 320–25. http://dx.doi.org/10.5858/arpa.2019-0434-ra.

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Context.— The incidence of neuroendocrine tumors of the prostate increases after hormonal therapy. Neuroendocrine tumors possess a broad spectrum of morphologic features and pose challenges in the pathologic diagnosis and clinical management of patients. Objective.— To present a brief updated summary of neuroendocrine tumors of the prostate with an overview of their histopathologic and immunohistochemical profiles and differential diagnoses. Data Sources.— Literature review, personal experience in the daily practice of pathologic diagnosis, and laboratory research. Conclusions.— Our understanding of neuroendocrine tumors of the prostate classification and diagnosis continues to evolve. These advances benefit the risk stratification and management of prostate cancer.

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Apolikhin, O. I., A. V. Sivkov, and N. G. Keshishev. "P080 Castration-refractory prostate cancer – neuroendocrine tumor?" European Urology Supplements 11, no. 5 (November 2012): 217–18. http://dx.doi.org/10.1016/s1569-9056(13)60452-2.

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ITO, Takaaki, Taku AIZAWA, Shinichi KITSUKAWA, Yoshimi MAMIYA, and Makoto MIKI. "Appearance of Neuroendocrine Cells in Prostate Cancer." Nihon Gekakei Rengo Gakkaishi (Journal of Japanese College of Surgeons) 24, no. 4 (1999): 592–95. http://dx.doi.org/10.4030/jjcs1979.24.4_592.

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Abrahamsson, Per-Anders. "Neuroendocrine differentiation and hormone-refractory prostate cancer." Prostate 29, S6 (1996): 3–8. http://dx.doi.org/10.1002/(sici)1097-0045(1996)6+<3::aid-pros2>3.0.co;2-t.

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Hope, Thomas A., Rahul Aggarwal, Jeff P. Simko, Henry F. VanBrocklin, and Charles J. Ryan. "Somatostatin Imaging of Neuroendocrine-Differentiated Prostate Cancer." Clinical Nuclear Medicine 40, no. 6 (June 2015): 540–41. http://dx.doi.org/10.1097/rlu.0000000000000776.

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Carlson, Robert H. "The Treatment Challenges of Neuroendocrine Prostate Cancer." Oncology Times 37, no. 4 (February 2015): 1. http://dx.doi.org/10.1097/01.cot.0000461860.84751.a3.

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Chen, Ruiqi, Xuesen Dong, and Martin Gleave. "Molecular model for neuroendocrine prostate cancer progression." BJU International 122, no. 4 (April 24, 2018): 560–70. http://dx.doi.org/10.1111/bju.14207.

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VanDeusen, Halena R., Johnny R. Ramroop, Katherine L. Morel, Song Yi Bae, Anjali V. Sheahan, Zoi Sychev, Nathan A. Lau, et al. "Targeting RET Kinase in Neuroendocrine Prostate Cancer." Molecular Cancer Research 18, no. 8 (May 27, 2020): 1176–88. http://dx.doi.org/10.1158/1541-7786.mcr-19-1245.

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Bland, Tyler, Jing Wang, Lijuan Yin, Tianjie Pu, Jingjing Li, Jin Gao, Tzu-Ping Lin, Allen C. Gao, and Boyang Jason Wu. "WLS-Wnt signaling promotes neuroendocrine prostate cancer." iScience 24, no. 1 (January 2021): 101970. http://dx.doi.org/10.1016/j.isci.2020.101970.

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Zhang, Dingxiao, and Dean G. Tang. "“Splice” a way towards neuroendocrine prostate cancer." EBioMedicine 35 (September 2018): 12–13. http://dx.doi.org/10.1016/j.ebiom.2018.08.037.

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Guerriero, Ilaria, Håkon Ramberg, Krizia Sagini, Manuel Ramirez-Garrastacho, Kristin A. Taskén, and Alicia Llorente. "Implication of β2-adrenergic receptor and miR-196a correlation in neurite outgrowth of LNCaP prostate cancer cells." PLOS ONE 16, no. 6 (June 30, 2021): e0253828. http://dx.doi.org/10.1371/journal.pone.0253828.

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The β2-adrenergic receptor has been shown to be involved in neuroendocrine differentiation and to contribute to the development of aggressive prostate cancer. In this study we have investigated whether miR-196a plays a role in the regulation of the β2-adrenergic receptor in the LNCaP prostate cancer cell line. Our results show that the expression of miR-196a is elevated in LNCaP prostate cancer cells with reduced levels of β2-adrenergic receptor after stably transfection with three different shRNAs. Furthermore, treatment with β-blockers showed that this upregulation is strictly related to the low levels of β2-adrenergic receptor and not to the inhibition of the receptor signaling activity. Finally, we found that the reduced ability of LNCaP cells with low levels of β2-adrenergic receptor to initiate neuroendocrine differentiation under androgen depletion conditions is mediated by miR-196a. In conclusion, this study provides the rational for a role of miR-196a in the β2-adrenergic receptor mediated neuroendocrine differentiation of LNCaP prostate cancer cells.

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Balážová, Zuzana, Igor Černý, and Petr Vyškovský. "Incidental Accumulation of Fluciclovine in Neuroendocrine Tumour in a Patient with Oncological Duplicity." Case Reports in Oncology 13, no. 1 (April 21, 2020): 431–35. http://dx.doi.org/10.1159/000506829.

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18F-fluciclovine is a PET radiopharmaceutical used for the detection of recurrent prostate cancer in adult men after primary curative treatment with suspicion of recurrence based on elevated prostate-specific antigen level. Several incidental uptakes of 18F-fluciclovine in other tumour types have been described in the literature so far – in breast cancer, hepatocellular carcinoma, and malignant melanoma. Our case report presents a patient with oncological duplicity (prostate gland carcinoma and newly diagnosed neuroendocrine tumour) and with accumulation of fluciclovine in pathologically proved neuroendocrine tumour, later imagined also by octreotide SPECT/CT. To our knowledge, this is the first case of fluciclovine accumulated in a neuroendocrine tumour described in the literature.

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Chmelenský, Tomáš, Pavel Hanek, Karel Franěk, Josef Rejlek, and Jiří Zvěřina. "Neuroendocrine prostate cancer with primary origin in the lungs." Urologie pro praxi 17, no. 2 (April 23, 2016): 94–95. http://dx.doi.org/10.36290/uro.2016.025.

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Samiea, Abrar, Jeff S. J. Yoon, Christopher J. Ong, Amina Zoubeidi, Thomas C. Chamberlain, and Alice L. F. Mui. "Interleukin-10 Induces Expression of Neuroendocrine Markers and PDL1 in Prostate Cancer Cells." Prostate Cancer 2020 (July 31, 2020): 1–12. http://dx.doi.org/10.1155/2020/5305306.

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Interleukin-10 (IL10) is best studied for its inhibitory action on immune cells and ability to suppress an antitumour immune response. But IL10 also exerts direct effects on nonimmune cells such as prostate cancer epithelial cells. Elevated serum levels of IL10 observed in prostate and other cancer patients are associated with poor prognosis. After first-line androgen-deprivation therapy, prostate cancer patients are treated with androgen receptor antagonists such as enzalutamide to inhibit androgen-dependent prostate cancer cell growth. However, development of resistance inevitably occurs and this is associated with tumour differentiation to more aggressive forms such as a neuroendocrine phenotype characterized by expression of neuron specific enolase and synaptophysin. We found that treatment of prostate cancer cell lines in vitro with IL10 or enzalutamide induced markers of neuroendocrine differentiation and inhibited androgen receptor reporter activity. Both also upregulated the levels of PDL1, which could promote tumour survival in vivo through its interaction with the immune cell inhibitory receptor PD1 to suppress antitumour immunity. These findings suggest that IL10’s direct action on prostate cancer cells could contribute to prostate cancer progression independent of IL10’s suppression of host immune cells.

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Journal articles on the topic 'Cancer de la prostate neuroendocrine'

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