Relevant bibliographies by topics / Cancer de la prostate neuroendocrine

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Cancer de la prostate neuroendocrine'

Author: Grafiati
Published: 17 September 2021
Last updated: 18 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Cancer de la prostate neuroendocrine.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

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

1

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
2

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
3

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
4

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
5

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
6

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
7

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
8

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
9

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Cancer de la prostate neuroendocrine"

1

Vias, Maria. "Neuroendocrine differentiation in hormone resistant prostate cancer cells." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612330.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Yeung, Jake. "Identification of RNA binding proteins associated with differential splicing in neuroendocrine prostate cancer." Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/46688.

Full text
Abstract:
Alternative splicing is a tightly regulated process that can be disrupted in cancer. Established cancer genes express splice isoforms with distinct properties and their differential expression is associated with tumour progression. Although prostate adenocarcinoma (PCa) is effectively managed at early stage by therapies targeting the androgen receptor signaling axis, up to 30% of late stage prostate cancers progress to a treatment-resistant form of the disease called neuroendocrine prostate cancer (NEPC), for which there are few therapeutic options. It is histologically distinct from PCa, expresses a neuronal gene signature and is associated with poor survival (<1 year). We hypothesize that alternative splicing has an important role in driving transformation of PCa tumours towards the NEPC phenotype and we seek to identify regulators of aberrant alternative splicing. We integrated a number of bioinformatics tools to investigate alternative splicing in NEPC. Analyzing RNA-Seq data from a patient-derived xenograft model of neuroendocrine transdifferentiation, we compared splicing profiles between NEPC and PCa and identified a set of differentially spliced cassette exons. We found these cassette exons to code for protein segments containing DNA-binding domains, protein-binding regions and posttranslational modification sites. We discovered evolutionarily conserved motifs around intronic regions of the cassette exons and implicated them with RNA recognition motifs of tissue-specific RNA binding proteins. We corroborated our findings by analyzing RNA-Seq data from a patient-tumour cohort and found recurrent RNA binding proteins associated with cassette exon inclusion. Our integrated analysis suggests that splicing changes between PCa and NEPC are mediated by tissue-specific RNA binding proteins, which may be of therapeutic or diagnostic value.
APA, Harvard, Vancouver, ISO, and other styles
3

Chen, Ruiqi. "Implications of PI3K/AKT inhibition on REST protein stability and neuroendocrine prostate cancer." Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/62099.

Full text
Abstract:
Treatment-induced neuroendocrine (NE) prostate cancer (t-NEPC) is an aggressive subtype of prostate cancer (PCa) that can arise as a consequence of rigorous androgen receptor pathway inhibition (ARPI) therapies now used to treat castration resistant disease (CRPC). While the PI3K/AKT pathway has been investigated as a co-therapeutic target with ARPI for advanced prostate adenocarcinoma, whether this strategy has implications on t-NEPC progression remains unknown. Findings from this work indicate that PI3K/AKT inhibition alone reduces protein expression of the RE-1 silencing transcription factor (REST) and induces multiple NE markers in PCa cells. The loss of REST by PI3K/AKT inhibition is through protein degradation mediated by the E3-ubiquitin ligase β-TRCP and REST phosphorylations at the S1024, S1027, and S1030 sites. Since AR inhibition was previously reported to deplete REST, results from this project reveal that the combined inhibition of PI3K/AKT and AR further aggravates REST protein reduction. Upon profiling the transcriptomes of AKT inhibition, AR inhibition, and AKT/AR co-inhibition in the LNCaP cell model, Gene Set Enrichment Analysis (GSEA) shows that these transcriptomes are highly correlated with the REST-regulated gene signature. Co-targeting AKT and AR resulted in an even higher correlation comparing to those of single treatment. Comparing these transcriptomes to the RNA-seq gene signature of t-NEPC patients by GSEA, it was observed that adding AKT inhibition to AR blockade enhanced the expression of neurogenesis-related genes and resulted in a stronger and broader upregulation of REST-regulated genes specific to t-NEPC. Collectively, these results indicate that AKT pathway inhibition can induce NE transdifferentiation in PCa cells via REST protein degradation. It delineates a potential risk for the AR and PI3K/AKT co-targeting strategy as it may further facilitate t-NEPC development.
Medicine, Faculty of
Experimental Medicine, Division of
Medicine, Department of
Graduate
APA, Harvard, Vancouver, ISO, and other styles
4

Goodin, Jeremy Lee. "Characterization of Gene Expression During Adenosine 3':5'-Cyclic Monophosphate Induced Neuroendocrine Differentiation in Human Prostatic Adenocarcinoma." Diss., Virginia Tech, 2002. http://hdl.handle.net/10919/26791.

Full text
Abstract:
The LNCaP cell line is a versatile and useful model that is suitable for the study of human prostate cancer in vitro. The elevation of LNCaP intracellular cAMP levels through the addition of membrane permeable cAMP analogues, phosphodiesterase inhibitors, adenylate cyclase activators, or components of the cAMP signal transduction pathway can induce reversible neuroendocrine differentiation. Elucidation of those genes that are differentially expressed between undifferentiated prostate cancer cells and prostate cancer cells that have been induced to differentiate may present new insights for the molecular mechanisms governing neuroendocrine differentiation, early detection of prostate cancer, and/or potential targets for gene therapy. In this study, differential display PCR was used to identify 226 differentially expressed PCR products. Twelve of the differential display PCR products were confirmed by Northern blot analysis and cloned. DNA sequencing and database comparisons were performed. Among the differentially expressed genes, the human ribosomal S3a gene was identified as down regulated in response to LNCaP differentiation. In order to better ascertain the mechanism by which HRS3a gene expression is decreased during differentiation, the promoter region for this gene was analyzed. Electrophoretic mobility shift assay, antibody supershift assays, site-directed mutagenesis, and luciferase reporter gene analysis were employed to authenticate the roles of several transcription factors in the regulation of the HRS3a gene. Two cyclic AMP response elements, a Sp1 element and a GA-binding protein element, were involved in the regulation of HRS3a gene expression. In order to ascertain the effect of HRS3a down regulation in LNCaP cells, antisense phosphorothioate oligonucleotides were designed to inhibit HRS3a gene expression. Treatment of LNCaP cells with antisense HRS3a oligonucleotides did not influence cAMP induced neuroendocrine differentiation but antisense treatment did result in a decrease in LNCaP cell growth. In addition, it was determined that morphological changes associated with cAMP induced differentiation of LNCaP cells from the epithelial to the neuroendocrine state may not require alterations in gene expression nor the expression of novel proteins.
Ph. D.
APA, Harvard, Vancouver, ISO, and other styles
5

Hirth, Carlos Gustavo. "The prognostic value of neuroendocrine differentiation and stem cells markers for localized prostate cancer." Universidade Federal do CearÃ, 2016. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=18238.

Full text
Abstract:
This study aimed to evaluate the new immunohistochemical markers related to neuroendocrine differentiation induction and stem cells with prognostic factors and biochemical recurrence in patients submitted to radical prostatectomy. Therefore, patients operated at the Hospital Walter CantÃdio, Federal University of CearÃ, in the period of 2008-2013, underwent clinical and outpatient follow-up, between the years 2008-2016. Biochemical recurrence was evaluated and was correlated with pathological characteristics and immunohistochemical reactions. Chromogranin (neuroendocrine differentiation), Aurora Kinase A (AURKA), N-MYC, C-MYC and CD44s were performad in paraffined material. From 74 patients underwent surgery was obtained the followup of 69, in a median period of 41 (2-89) months. Neoplastic neuroendocrine differentiation was associated with seminal vesicles infiltration (p = 0.032) and stage (p = 0.030). C-MYC was associated with Gleason score (p = 0.001) and seminal vesicles infiltration (p = 0.014). AURKA was expressed in rare cases. N-MYC protein was negative in all patients. CD44s was associated with lower preoperative PSA levels and lower Gleason scores. Biochemical recurrence was observed in 27.0% of patients. Recurrence was associated with serum preoperative PSA, Gleason score, seminal vesicle invasion and staging at least in one form of analysis. There was no significant association between recurrence and neuroendocrine differentiation, C-MYC and CD44s expression. Therefore, immunohistochemical detection of neuroendocrine differentiation, expression of C-MYC and loss of CD44s were related to more aggressive carcinomas (PSA, Gleason, seminal vesical invasion and/or stage), but no association with biochemical recurrence. Classic prognostic factors were affirmed like biochemical recurrence predictores.
Este estudo objetivou avaliar novos marcadores imuno-histoquÃmicos relacionados à induÃÃo da diferenciaÃÃo neuroendÃcrina e cÃlulas-tronco com fatores de prognÃstico e recorrÃncia bioquÃmica, em pacientes submetidos à prostatectomia radical. Para tanto, pacientes operados no Hospital Walter CantÃdio, Universidade Federal do CearÃ, no perÃodo de 2008 a 2013, foram submetidos a acompanhamento clÃnico-ambulatorial, entre os anos de 2008 a 2016. Avaliou-se a proporÃÃo daqueles que apresentaram recorrÃncia bioquÃmica, bem como as caracterÃsticas clÃnico-patolÃgicas e a marcaÃÃo em reaÃÃes de imuno-histoquÃmica para cromogranina (diferenciaÃÃo neuroendÃcrina), Aurora quinase A (AURKA), N-MYC, C-MYC e CD44s, em material parafinado. De 74 pacientes submetidos à cirurgia, obteve-se acompanhamento de 69, com tempo de seguimento de 41 (2-89) meses; diferenciaÃÃo neuroendÃcrina na neoplasia se associou com infiltraÃÃo de vesÃculas seminais (p=0,032) e estadiamento (p=0,030). C-MYC associou-se com escore de Gleason (p=0,001) e infiltraÃÃo de vesÃculas seminais (p=0,014). AURKA expressou-se em raros casos. N-MYC foi negativo em todos os pacientes. CD44s se associou com menores nÃveis de PSA prÃ-operatÃrio e menores escores de Gleason. Observou-se recorrÃncia bioquÃmica em 27,0% dos pacientes. RecorrÃncia se associou, em pelo menos uma das formas de anÃlise, com nÃveis sÃricos de PSA prÃ-operatÃrio, escore de Gleason, invasÃo de vesÃculas seminais e estadiamento. NÃo houve associaÃÃo significativa entre recorrÃncia e diferenciaÃÃo neuroendÃcrina, C-MYC e CD44s. Dessa forma, nesse estudo, a detecÃÃo imuno-histoquÃmica da diferenciaÃÃo neuroendÃcrina; a expressÃo de C-MYC e a perda da expressÃo de CD44s relacionaram-se com carcinomas mais agressivos (PSA, Gleason, infiltraÃÃo de vesÃcula seminal e/ou estadiamento), porÃm sem associaÃÃo com a recorrÃncia bioquÃmica; bem como confirma a importÃncia de fatores prognÃsticos considerados como clÃssicos em sÃrie regional de pacientes com cÃncer de prÃstata.
APA, Harvard, Vancouver, ISO, and other styles
6

Nip, Ka Mun. "TNIK, a novel androgen receptor-repressed gene, is a potential biomarker for neuroendocrine prostate cancer." Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/64148.

Full text
Abstract:
Traf2- and Nck-interacting kinase (TNIK) is a serine/threonine kinase upregulated and amplified in pancreatic and gastric cancer respectively. TNIK has also been identified as a potential therapeutic target of colorectal cancer. However, the role of TNIK in prostate cancer (PCa) has not been investigated. Interrogating public human PCa patient data, we found that TNIK expression is associated with an aggressive form of PCa termed neuroendocrine prostate cancer (NEPC). Treatment-induced NEPC can arise as a consequence of strong selective pressure from androgen receptor (AR) pathway inhibition. Clinically, TNIK expression is positively correlated with neuroendocrine (NE) markers and inversely correlated with androgen regulated genes. In agreement, our in vitro studies reveal that TNIK expression is increased under AR pathway inhibition. We found that TNIK is transcriptionally repressed by androgen via direct binding of the AR at the TNIK locus. Through gain of function studies, we demonstrated that TNIK is not required for NE differentiation. Likewise, loss of function studies using siRNA or small molecule inhibitors targeting TNIK did not have significant effect on the growth of Enzalutamide-resistant cells with NE phenotype in vitro. Overall, our results indicate that TNIK may serve as a possible biomarker for NEPC.
Medicine, Faculty of
Experimental Medicine, Division of
Medicine, Department of
Graduate
APA, Harvard, Vancouver, ISO, and other styles
7

Blanc, Charly. "La Neuropiline-1, un nouveau biomarqueur de résistance thérapeutique du cancer de la prostate." Thesis, Paris Est, 2016. http://www.theses.fr/2016PESC0072.

Full text
Abstract:
Le cancer de la prostate représente actuellement un problème majeur de santé publique. L’hormonothérapie, par privation de l’axe androgénique, constitue aujourd’hui la seule arme thérapeutique efficace pour les formes avancées. Malgré un taux important de réponse initiale, une forme de résistance survient inéluctablement, conduisant pour la plupart au décès du patient. La progression tumorale vers la résistance à la castration est un processus multifactoriel. Elle peut être associée à une dérégulation de l’axe du récepteur des androgènes, l’activation de voies de survie cellulaire, et favoriser une différenciation cellulaire vers l’acquisition d’un phénotype neuroendocrine androgéno-indépendant. L’objectif de la recherche actuelle repose donc sur l’identification de nouveaux biomarqueurs de résistance thérapeutique afin de proposer de nouvelles cibles permettant de contrecarrer la résistance à la castration. La caractérisation d’une signature moléculaire associée à l’émergence d’une différenciation neuroendocrine du cancer de la prostate résistant à la castration a permis d’identifier la Neuropiline-1, une glycoprotéine transmembranaire impliquée dans le développement neuronal et vasculaire. La répression de la voie du récepteur des androgènes au cours de l’hormonothérapie régule dynamiquement l’expression de la Neuropiline-1 et favorise la résistance à la castration associée à une différenciation neuroendocrine. La Neuropiline-1 joue donc un rôle important dans la résistance thérapeutique puisqu’elle favorise la neuro-transdifférenciation, l’activation de voie de survie cellulaire et altère la sensibilité des cellules cancéreuses à la chimiothérapie. L’étude des voies de signalisation associées à la Neuropiline-1 a permis d’identifier la voie des PKCs, impliquée dans la régulation de la différenciation neuroendocrine du cancer de la prostate. Par conséquent, nous montrons pour la première fois que le ciblage de cette voie activée par la Neuropiline-1 bloque l’évolution tumorale vers la résistance à la castration et augmente l’efficacité d’une chimiothérapie à base de docétaxel sur des modèles précliniques in vivo. Parallèlement, la caractérisation des ligands de la Neuropiline a permis d’identifier de nouveaux partenaires dont la Pléiotrophine, comme nouveau ligand associé aux activités biologiques de la Neuropiline-1 dans la carcinogenèse prostatique. L’ensemble de ces travaux apporte de nouvelles connaissances sur la caractérisation de la résistance thérapeutique du cancer de la prostate, et fournit un réel intérêt clinique porteur d’espoir dans la prise en charge de la maladie neuroendocrine résistante à la castration
Prostate cancer currently represents a major public health problem. Hormone therapy, by deprivation of androgen signaling axis represents the only efficient treatment for advanced forms. Despite effective initial response, a form of resistance inevitably occurs, leading mostly to patient's death. Tumor progression to castration resistance is a multifactorial process. It can be associated to dysregulation of the androgen receptor axis and activation of cell survival pathways, and thus promotes cell differentiation towards the acquisition of an androgen-independent neuroendocrine phenotype. Therefore, the goal of current research is based on the identification of new biomarkers of therapeutic resistance to propose new targets to counteract the castration resistance. The characterization of a molecular signature associated with the emergence of a neuroendocrine castration-resistant prostate cancer identified Neuropilin-1, a transmembrane glycoprotein involved in vascular and neuronal development. Down-regulation of androgen receptor axis during hormone therapy dynamically regulates the expression of Neuropilin-1 and promotes resistance to castration associated with neuroendocrine differentiation. Thus, Neuropilin-1 plays an important role in the therapeutic resistance since it favors the neuro-transdifferentiation, activation of cell survival pathway and alters the sensitivity of cancer cells to chemotherapy. Moreover, the study of signaling pathways associated with Neuropilin-1 and involved in the regulation of the neuroendocrine differentiation of prostate cancer has identified the PKCs pathway. We show for the first time that targeting this pathway activated by Neuropilin-1 blocks tumor evolution towards resistance to castration and increases the efficacy of docetaxel-based chemotherapy in preclinical models in vivo. In parallel, the characterization of Neuropilin’s ligands identified new partners, including Pleiotrophin, as a new ligand associated with Neuropilin-1 biological activities in prostate carcinogenesis. All this work provides new knowledge in the characterization of therapeutic resistance in prostate cancer, and supports a real promising clinical value in the treatment of neuroendocrine castration-resistant form of the disease
APA, Harvard, Vancouver, ISO, and other styles
8

Soori, Mehrnoosh. "Neuroendocrine differentiation of prostate cancer cells a survival mechanism during early stages of metastatic colonization of bone /." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 105 p, 2009. http://proquest.umi.com/pqdweb?did=1654490661&sid=6&Fmt=2&clientId=8331&RQT=309&VName=PQD.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Berenguer, Caroline. "Rôle de l'adrénomédulline dans le cancer de la prostate : implication dans la différenciation neuroendocrine et dans la progression tumorale." Aix-Marseille 2, 2006. http://www.theses.fr/2006AIX20691.

Full text
Abstract:
Les cancers prostatiques (CaP) sont des pathologies des plus fréquentes et représentent donc un problème de santé publique. Ils constituent actuellement un enjeu thérapeutique puisque 25% des patients traités par hormonothérapie sont victimes à plus ou moins longue échéance d’une baisse de l’efficacité du traitement : « échappement hormonal ou androgéno-indépendance ». Une meilleure compréhension des mécanismes impliqués dans ce phénomène est donc indispensable. Plusieurs études suggèrent un rôle des cellules neuroendocrines dans l’émergence de l’hormonoindépendance des CaP. Ces cellules neuroendocrines présentent dans la prostate ne sont pas dépendantes des androgènes pour leur croissance et leur survie. Elles synthétisent une variété de neuropeptides spécifiques des cellules neuronales (ChgA, NSE, 5-HT) et des peptides bioactifs (somatostatine, bombésine, CGRP…). Parmi les différents facteurs de régulation, nous nous sommes intéressés aux peptides bioactifs, amidés en C-terminal par l’enzyme bifonctionnelle : Peptidylglycine-α-Amitating Monooxygénase (PAM), et décrits comme étant capables d’induire et de stimuler la croissance tumorale. Parmi les peptides amidés criblés, nous avons retenu comme candidat l’Adrénomédulline (AM), peptide mitogénique et angiogénique. Dans cette étude, nous avons émis l’hypothèse selon laquelle l’AM peut jouer un rôle dans l’évolution du CaP vers l’androgéno-indépendance et plus spécifiquement dans la composante neuroendocrine associée à cette phase de résistance thérapeutique. Nous avons également mis en évidence une augmentation de l’expression et de la synthèse de l’AM dans les cellules hormonodépendantes LNCaP en absence d’androgènes. L’analyse morphologique, histologique et moléculaire des cellules privées d’hormones, a mis en évidence une relation directe entre le phénotype neuroendocrine (prolongements cytoplasmiques, marqueurs neuroendocrines : NSE et ChgA) et le sysytème AM/Récepteur de l’AM. Confortant notre l’hypothèse sur le rôle de l’AM dans la composante neuroendocrine observée et décrite dans le CaP évoluant vers l’hormonorésistance. La deuxième partie de ce travail est dédiée à l’étude de l’AM au cours de l’hormonoindépendance. Nous avons ainsi mis en évidence un rôle de l’AM sur la croissance tumorale, sur la vascularisation intratumorale, chez des souris xénogreffées avec des cellules hormonoindépendantes DU145. Dans les tumeurs traitées par l’anticorps anti-AM, outre la diminution du volume tumoral, les structures vasculaires sont profondément modifiées. Ces résultats montre l’implication de l’AM dans les interactions entre les différents compartiments cellulaires (stroma/épithélium) et le microenvironnement tumoral. En conséquence, l'AM constitue une voie de recherche stimulante visant à améliorer la thérapie anti-cancéreuse au niveau de la prostate mais aussi au niveau d'autres types de tumeurs présentant une forte expression de ce peptide amidé.
APA, Harvard, Vancouver, ISO, and other styles
10

Maina, Peterson Kariuki. "Novel oncogenic roles and regulations of histone demethylase PHF8 in prostate cancer." Diss., University of Iowa, 2017. https://ir.uiowa.edu/etd/5562.

Full text
Abstract:
Prostate cancer (PCa) is the most common cancer in American men. Although initial androgen deprivation therapy (ADT) confers a five year survival rate of 99%, the relapse of metastatic and drug resistant PCa (CRPC- Castration-Resistant PCa) continues to account for most deaths. How certain PCa cells develop into CRPC is the key question in the field. In addressing it, attention has focused on epigenetic factors that contribute to CRPC development. Herein we investigated the role and regulation of histone demethylase PHF8 during PCa neuroendocrine differentiation (NED) and progression into CRPC. We utilized bioinformatic analyses and biochemical approaches in PCa/CRPC cell line and mouse models to unravel the following results: First, we discovered that PHF8 post-transcriptionally clusters with cell cycle genes during NED and into CRPC via an AR/MYC/miR-22 regulatory axis. We showed that this axis is dysregulated in CRPC cells to allow enhanced cell proliferation and resistance to the clinical AR antagonist drug Xtandi® (enzalutamide). Second, we revealed that PHF8 is necessary for hypoxia induced NED by demethylating repressive H3K9me2 and H3K27me2, above maintaining active H3K4me3 on select NED genes. Importantly, we unveiled that PHF8 sustains HIF1α expression in CRPC cells via a regulatory role associated with full length AR. Third, we recapitulated the role of PHF8 in vivo by excising its floxed allele in the prostate of TRAMP mice -Transgenic Adenocarcinoma of the Mouse Prostate. We observed that KO of Phf8 lowered tumor burden in part by sustaining Ezh2 expression during NED transition into CRPC. In conclusion, our data implicates PHF8 in multiple oncogenic roles and regulations during PCa NED into CRPC. Our results lay a foundation for understanding the dynamics of histone modifying enzymes during PCa progression and hint at designing small molecule inhibitors against PHF8 as a novel CRPC therapeutic target.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Cancer de la prostate neuroendocrine"

1

Prostate cancer. New York, NY: Demos Medical Pub., 2011.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Mason, Malcolm. Prostate Cancer. Oxford: Oxford University Press, 2003.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Chen, Allen. Prostate cancer. New York: Demos Medical, 2011.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Kirby, R. S. Prostate cancer. 2nd ed. London: Mosby, 2001.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Sheen, Barbara. Prostate cancer. Detroit: Lucent Books, 2008.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Prostate cancer. Pittsburgh, Pa: Oncology Nursing Society, 2009.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Vijayakumar, Srinivasan. Prostate cancer. New York: Demos Medical, 2011.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Feneley, Mark R., and Heather A. Payne. Prostate cancer. Oxford: Clinical Pub., 2007.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

I, Patel Manish, ed. Prostate cancer. 7th ed. Abingdon: Health Press, 2011.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Prostate cancer. Oxford: Oxford University Press, 2011.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Cancer de la prostate neuroendocrine"

1

Beg, Shaham, and Juan Miguel Mosquera. "Neuroendocrine Prostate Cancer." In Molecular Pathology Library, 323–41. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-64096-9_19.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Beltran, Himisha, Juan Miguel Mosquera, and Mark A. Rubin. "Neuroendocrine Prostate Cancer." In Prostate Cancer: A Comprehensive Perspective, 277–82. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-2864-9_22.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Franco, Renato, Paolo Chieffi, Sisto Perdonà, Gaetano Facchini, and Michele Caraglia. "Neuroendocrine Differentiation in Prostate Cancer." In Prostate Cancer: Shifting from Morphology to Biology, 87–109. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-7149-9_5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Akamatsu, Shusuke. "Molecular Basis of Neuroendocrine Prostate Cancer." In Hormone Therapy and Castration Resistance of Prostate Cancer, 387–96. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-7013-6_39.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Beltran, Himisha, Gurveen Kaur, Myriam Kossai, David M. Nanus, and Scott T. Tagawa. "Undifferentiated Prostate Cancer and the Neuroendocrine Phenotype." In Management of Castration Resistant Prostate Cancer, 297–304. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1176-9_21.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Marshall, James R., and David P. Wood. "Prostate." In Cancer Precursors, 333–43. New York, NY: Springer New York, 2002. http://dx.doi.org/10.1007/0-387-21605-7_21.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Güler, E. Nilüfer, Murat Fani Bozkurt, Serdar Ozbas, and Suayib Yalcin. "Thyroid Cancer." In Neuroendocrine Tumours, 353–88. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-45215-8_21.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Duran, Ignacio, and Lillian L. Siu. "Neuroendocrine Carcinoma." In Encyclopedia of Cancer, 2482–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_4029.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Schmitt-Graeff, Annette. "Neuroendocrine Tumors." In Encyclopedia of Cancer, 2486–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_4032.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Duran, Ignacio, and Lillian L. Siu. "Neuroendocrine Carcinoma." In Encyclopedia of Cancer, 1–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_4029-4.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Cancer de la prostate neuroendocrine"

1

Puca, Loredana, Dong Gao, Myriam Kossai, Clarisse Marotz, Juan Miguel Mosquera, Theresa Y. MacDonald, Kyung Park, et al. "Abstract 3844: Targeting EZH2 in neuroendocrine prostate cancer." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3844.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Dardenne, Etienne, Himisha Beltran, Kaitlyn Gayvert, Matteo Benelli, Adeline Berger, Loredana Puca, Joanna Cyrta, et al. "Abstract 887: N-Myc drives neuroendocrine prostate cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-887.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Sanders, Danielle N., Magdalena Grabowska, and Robert Matusik. "Abstract B23: Neuroendocrine differentiation in prostate cancer and development." In Abstracts: Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; November 13-16, 2015; Atlanta, Georgia. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7755.disp15-b23.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Ferguson, Alison M., Bhavneet Bhinder, Vincenza Conteduca, Michael Sigouros, Andrea Sboner, David Nanus, Scott Tagawa, David Rickman, Olivier Elemento, and Himisha Beltran. "Abstract 134: Immunogenomic landscape of neuroendocrine prostate cancer (NEPC)." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-134.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Ferguson, Alison M., Bhavneet Bhinder, Vincenza Conteduca, Michael Sigouros, Andrea Sboner, David Nanus, Scott Tagawa, David Rickman, Olivier Elemento, and Himisha Beltran. "Abstract 134: Immunogenomic landscape of neuroendocrine prostate cancer (NEPC)." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-134.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Marhold, Maximilian, Erwin Tomasich, Simon Udovica, Gerwin Heller, Corinna Altenberger, Andreas Spittler, Reinhard Horvat, Peter Horak, and Michael Krainer. "Abstract 2407: Neuroendocrine and luminal progenitors drive cancer progression in prostate cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2407.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Connelly, Zachary, Shu Yang, Anthony Blankenship, and Xiuping Yu. "Abstract 1514: Role of polycomb proteins in neuroendocrine prostate cancer." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1514.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Puca, Loredana, Rohan Bareja, Reid Shaw, Wouter Karthaus, Dong Gao, Chantal Pauli, Juan Miguel Mosquera, et al. "Abstract 992: Patient-derived tumor organoids of neuroendocrine prostate cancer." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-992.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Wang, Jing, Jingjing Li, Boyang Wu, and Lijuan Yin. "Abstract 2612: Neuropilin-2 promotes enzalutamide-resistant neuroendocrine prostate cancer." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2612.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Khalil, Md Imtiaz, Shu Yang, Anthony Blankenship, Zachary Connelly, and Xiuping Yu. "Abstract 5191: Functional role of EZH2 in neuroendocrine prostate cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-5191.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Cancer de la prostate neuroendocrine"

1

Hu, Chang-Deng, Xuehong Deng, and Gyeon Oh. Targeting Neuroendocrine Differentiation for Prostate Cancer Radiosensitization. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613326.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Evans, Christopher P. Castration Induced Neuroendocrine Mediated Progression of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2008. http://dx.doi.org/10.21236/ada492892.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Evans, Christopher P. Castration-Induced Neuroendocrine Mediated Progression of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2005. http://dx.doi.org/10.21236/ada446371.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Huang, Jiaoti. The Function of Neuroendocrine Cells in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada580194.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Huang, Jiaoti. The Function of Neuroendocrine Cells in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2014. http://dx.doi.org/10.21236/ada604606.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Huang, Jiaoti. The Function of Neuroendocrine Cells in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2012. http://dx.doi.org/10.21236/ada590965.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Huang, Jiaoti. The Function of Neuroendocrine Cells in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2015. http://dx.doi.org/10.21236/ada621366.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Evans, Christopher P. Castration Induced Neuroendocrine Mediated Progression of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2007. http://dx.doi.org/10.21236/ada476920.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Huang, Jiaoti. Function of PTP1B in Neuroendocrine Differentiation of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 2008. http://dx.doi.org/10.21236/ada481731.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Kim, Isaac. Neuroendocrine Differentiation in Prostate Cancer: Role of Bone Morphogenetic Protein-6 and Macrophages. Fort Belvoir, VA: Defense Technical Information Center, July 2011. http://dx.doi.org/10.21236/ada555480.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Cancer de la prostate neuroendocrine' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography