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Relevant bibliographies by topics / Neuroendocrine transdifferentiation

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Journal articles
Dissertations / Theses
Conference papers

Academic literature on the topic 'Neuroendocrine transdifferentiation'

Author: Grafiati

Published: 21 September 2024

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Journal articles on the topic "Neuroendocrine transdifferentiation"

1

Sergeant, Camille, Christel Jublanc, Delphine Leclercq, et al. "Transdifferentiation of Neuroendocrine Cells." American Journal of Surgical Pathology 41, no. 6 (2017): 849–53. http://dx.doi.org/10.1097/pas.0000000000000803.

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2

Stone, Louise. "A novel mechanism of neuroendocrine transdifferentiation." Nature Reviews Urology 15, no. 5 (2018): 263. http://dx.doi.org/10.1038/nrurol.2018.40.

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3

Cordeiro-Rudnisky, Fernanda, Yue Sun, and Rayan Saade. "Prostate Carcinoma With Overlapping Features of Small Cell and Acinar Adenocarcinoma: A Case Report." American Journal of Clinical Pathology 152, Supplement_1 (2019): S66—S67. http://dx.doi.org/10.1093/ajcp/aqz113.072.

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Abstract Introduction Prostate neuroendocrine (NE) cells can stimulate prostate adenocarcinoma (PA) cell growth, but occasionally adenocarcinoma cells themselves acquire NE characteristics, a phenomenon known as NE transdifferentiation of prostate adenocarcinoma. During this process, tumor cells acquire small cell-like morphology and become positive for neuroendocrine markers. NE transdifferentiation is associated with decreased androgen receptor (AR) signaling, a mechanism of resistance to AR-targeted treatments. Case A 74-year-old male with a history of cirrhosis, splenomegaly, and thrombocy

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4

Quintanal-Villalonga, Alvaro, Hirokazu Taniguchi, Yingqian A. Zhan, et al. "AKT inhibition as a therapeutic strategy to constrain histological transdifferentiation in EGFR-mutant lung adenocarcinoma." Journal of Clinical Oncology 40, no. 16_suppl (2022): e21166-e21166. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.e21166.

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e21166 Background: In lung adenocarcinomas (LUADs), lineage plasticity drives neuroendocrine (NE) and squamous cell (LUSC) transdifferentiation in the context of acquired resistance to targeted inhibition of driver mutations, with up to 14% and 9% incidences in EGFR-mutant tumors relapsed on EGFR inhibitors, respectively. Notably, survival of patients with NE- or LUSC-transdifferentiated tumors is remarkably lower than those of LUAD or de novo LUSC patients. The paucity of transforming clinical specimens amenable for molecular analyses has hindered the identification of histological transforma

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5

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 (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 revie

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Von Amsberg, Gunhild, Sergey Dyshlovoy, Jessica Hauschild, et al. "Long-term taxane exposure and transdifferentiation of prostate cancer in vitro." Journal of Clinical Oncology 41, no. 6_suppl (2023): 254. http://dx.doi.org/10.1200/jco.2023.41.6_suppl.254.

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254 Background: Development of aggressive variants of metastatic castration-resistant prostate cancer (AVPC) is a major challenge in the course of therapy but the underlying mechanisms of aggressive transdifferentiation are not completely understood and appropriate tumor models are missing. Here, we investigated the consequences of long-term taxane exposure on hormone-independent, BRCA2-mutated, AR-V7-positive 22Rv1 cells. Methods: 22Rv1 cells were treated with stepwise increased taxane concentrations for 10 months. Individual clones were picked and further cultured in media containing either

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7

Quintanal-Villalonga, Alvaro, Hirokazu Taniguchi, Yingqian A. Zhan, et al. "Abstract 658: AKT pathway as a therapeutic target to constrain lineage plasticity leading to histological transdifferentiation." Cancer Research 82, no. 12_Supplement (2022): 658. http://dx.doi.org/10.1158/1538-7445.am2022-658.

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Abstract Lineage plasticity contributes to therapeutic resistance in cancer. In lung adenocarcinomas (LUADs), this phenomenon drives neuroendocrine (NE) and squamous cell (LUSC) histologic transdifferentiation in the context of acquired resistance to targeted inhibition of driver mutations, with up to 14% and 9% incidences in EGFR-mutant tumors relapsed on EGFR inhibitors, respectively. Notably, survival of patients with NE- or LUSC-transdifferentiated tumors is lower than that of either LUAD or de novo LUSC patients. To date, little is known about the molecular effectors enhancing lineage pla

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8

Frigo, Daniel E., and Donald P. McDonnell. "Differential effects of prostate cancer therapeutics on neuroendocrine transdifferentiation." Molecular Cancer Therapeutics 7, no. 3 (2008): 659–69. http://dx.doi.org/10.1158/1535-7163.mct-07-0480.

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9

Patel, Girijesh, Sayanika Dutta, Mosharaf Mahmud Syed, et al. "TBX2 Drives Neuroendocrine Prostate Cancer through Exosome-Mediated Repression of miR-200c-3p." Cancers 13, no. 19 (2021): 5020. http://dx.doi.org/10.3390/cancers13195020.

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Deciphering the mechanisms that drive transdifferentiation to neuroendocrine prostate cancer (NEPC) is crucial to identifying novel therapeutic strategies against this lethal and aggressive subtype of advanced prostate cancer (PCa). Further, the role played by exosomal microRNAs (miRs) in mediating signaling mechanisms that propagate the NEPC phenotype remains largely elusive. The unbiased differential miR expression profiling of human PCa cells genetically modulated for TBX2 expression led to the identification of miR-200c-3p. Our findings have unraveled the TBX2/miR-200c-3p/SOX2/N-MYC signal

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10

Turner, Leo, Andrew Burbanks, and Marianna Cerasuolo. "Mathematical insights into neuroendocrine transdifferentiation of human prostate cancer cells." Nonlinear Analysis: Modelling and Control 26, no. 5 (2021): 884–913. http://dx.doi.org/10.15388/namc.2021.26.24441.

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Prostate cancer represents the second most common cancer diagnosed in men and the fifth most common cause of death from cancer worldwide. In this paper, we consider a nonlinear mathematical model exploring the role of neuroendocrine transdifferentiation in human prostate cancer cell dynamics. Sufficient conditions are given for both the biological relevance of the model’s solutions and for the existence of its equilibria. By means of a suitable Liapunov functional the global asymptotic stability of the tumour-free equilibrium is proven, and through the use of sensitivity and bifurcation analys

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Dissertations / Theses on the topic "Neuroendocrine transdifferentiation"

1

Guo, Yingbo. "Rôle du cil primaire au cours de la transdifferentiation neuroendocrine du cancer de la prostate." Electronic Thesis or Diss., Université Côte d'Azur, 2024. http://www.theses.fr/2024COAZ6005.

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Le cancer de la prostate est l’un des cancers malins les plus répandus dans le monde, avec 95 % des patients diagnostiqués présentant un adénocarcinome de la prostate sans marqueurs neuroendocriniens. Le cancer neuroendocrinien de la prostate de novo représente un sous-type rare et agressif. Environ 20 % des cas d’adénocarcinome de la prostate évoluent vers le cancer neuroendocrinien de la prostate après un traitement de privation androgénique. Le traitement de privation androgénique bien qu’efficace, peut également induire une différenciation neuroendocrinienne de l'adénocarcinome de la prost

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Conference papers on the topic "Neuroendocrine transdifferentiation"

1

Li, Yinan. "Abstract 4473: SRRM4 drives treatment-induced neuroendocrine transdifferentiation of prostate adenocarcinoma under androgen receptor pathway inhibition." 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.am2017-4473.

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Beshiri, Mike L., Caitlin M. Tice, Adam G. Sowalsky, et al. "Abstract 5020: A patient-derived organoid model of neuroendocrine prostate cancer transdifferentiation informing the role of the BAF complex component ARID1A." 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.am2018-5020.

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