Auswahl der wissenschaftlichen Literatur zum Thema „Neuroendocrine transdifferentiation“
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Zeitschriftenartikel zum Thema "Neuroendocrine transdifferentiation"
Sergeant, Camille, Christel Jublanc, Delphine Leclercq, Anne-Laure Boch, Franck Bielle, Gerald Raverot, Adrian F. Daly, Jacqueline Trouillas und Chiara Villa. „Transdifferentiation of Neuroendocrine Cells“. American Journal of Surgical Pathology 41, Nr. 6 (Juni 2017): 849–53. http://dx.doi.org/10.1097/pas.0000000000000803.
Der volle Inhalt der QuelleStone, Louise. „A novel mechanism of neuroendocrine transdifferentiation“. Nature Reviews Urology 15, Nr. 5 (20.03.2018): 263. http://dx.doi.org/10.1038/nrurol.2018.40.
Der volle Inhalt der QuelleCordeiro-Rudnisky, Fernanda, Yue Sun und Rayan Saade. „Prostate Carcinoma With Overlapping Features of Small Cell and Acinar Adenocarcinoma: A Case Report“. American Journal of Clinical Pathology 152, Supplement_1 (11.09.2019): S66—S67. http://dx.doi.org/10.1093/ajcp/aqz113.072.
Der volle Inhalt der QuelleQuintanal-Villalonga, Alvaro, Hirokazu Taniguchi, Yingqian A. Zhan, Jacklynn V. Egger, Umesh Bhanot, Juan Qiu, Elisa de Stanchina et al. „AKT inhibition as a therapeutic strategy to constrain histological transdifferentiation in EGFR-mutant lung adenocarcinoma.“ Journal of Clinical Oncology 40, Nr. 16_suppl (01.06.2022): e21166-e21166. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.e21166.
Der volle Inhalt der QuelleYuan, Ta-Chun, Suresh Veeramani und Ming-Fong Lin. „Neuroendocrine-like prostate cancer cells: neuroendocrine transdifferentiation of prostate adenocarcinoma cells“. Endocrine-Related Cancer 14, Nr. 3 (September 2007): 531–47. http://dx.doi.org/10.1677/erc-07-0061.
Der volle Inhalt der QuelleVon Amsberg, Gunhild, Sergey Dyshlovoy, Jessica Hauschild, Verena Sailer, Sven Perner, Anne Offermann, Lina Merkens et al. „Long-term taxane exposure and transdifferentiation of prostate cancer in vitro.“ Journal of Clinical Oncology 41, Nr. 6_suppl (20.02.2023): 254. http://dx.doi.org/10.1200/jco.2023.41.6_suppl.254.
Der volle Inhalt der QuelleQuintanal-Villalonga, Alvaro, Hirokazu Taniguchi, Yingqian A. Zhan, Fathema Uddin, Viola Allaj, Parvathy Manoj, Nisargbhai S. Shah et al. „Abstract 658: AKT pathway as a therapeutic target to constrain lineage plasticity leading to histological transdifferentiation“. Cancer Research 82, Nr. 12_Supplement (15.06.2022): 658. http://dx.doi.org/10.1158/1538-7445.am2022-658.
Der volle Inhalt der QuelleFrigo, Daniel E., und Donald P. McDonnell. „Differential effects of prostate cancer therapeutics on neuroendocrine transdifferentiation“. Molecular Cancer Therapeutics 7, Nr. 3 (März 2008): 659–69. http://dx.doi.org/10.1158/1535-7163.mct-07-0480.
Der volle Inhalt der QuellePatel, Girijesh, Sayanika Dutta, Mosharaf Mahmud Syed, Sabarish Ramachandran, Monica Sharma, Venkatesh Rajamanickam, Vadivel Ganapathy et al. „TBX2 Drives Neuroendocrine Prostate Cancer through Exosome-Mediated Repression of miR-200c-3p“. Cancers 13, Nr. 19 (07.10.2021): 5020. http://dx.doi.org/10.3390/cancers13195020.
Der volle Inhalt der QuelleTurner, Leo, Andrew Burbanks und Marianna Cerasuolo. „Mathematical insights into neuroendocrine transdifferentiation of human prostate cancer cells“. Nonlinear Analysis: Modelling and Control 26, Nr. 5 (01.09.2021): 884–913. http://dx.doi.org/10.15388/namc.2021.26.24441.
Der volle Inhalt der QuelleDissertationen zum Thema "Neuroendocrine transdifferentiation"
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.
Der volle Inhalt der QuelleProstate cancer is one of the most common malignancy cancers worldwide. 95% of PCa patients are diagnosed with adenocarcinoma of the prostate showing no expression of neuroendocrine markers. De novo neuroendocrine prostate cancer is a rare and aggressive subtype of prostate cancer, characterized by neuroendocrine markers expression. Approximatively 20% of adenocarcinoma cases progress to neuroendocrine prostate cancer following androgen deprivation therapy. The potential side effect of androgen deprivation therapy, resulting in neuroendocrine differentiation of adenocarcinoma of the prostate, brings a novel challenge for prostate cancer treatment. While many molecular mechanisms of neuroendocrine differentiation have been described, the timing of the neuroendocrine differentiation occurrence and how these driving factors result in neuroendocrine differentiation remain unclear.The primary cilium is a non-motile organelle present in nearly all human cells. Loss of primary cilium has been observed in various cancers, including clear cell Renal Cell Carcinoma (ccRCC) and PCa. Previous findings from our research team identified a distinct subgroup of pataients within ccRCC, which retained primary cilium and exhibited resistance to therapy. The presence of primary cilium was characterized by the GLI1+/IFT20+ signature. Under hypoxic conditions, primary cilium was inhibited due to stabilization of HIF-1α, correlating with increased aggressiveness of ccRCC. Considering that both ccRCC and prostate cancer are typically described as cancer lacking PC, we postulated the existence of a unique subgroup in prostate cancer exhibiting primary cilium presence associated with higher aggressiveness.We developed multiple approaches to enhance in the number of primary cilium numbers in both normal prostate cells and prostate cancer-like cells in 2D or 3D cell culture settings. This increase was correlated with a reduction in proliferation and growth of 3D structures. Notably, these methods maintained their effectiveness in inducing primary cilium numbers even under hypoxic conditions. Our findings confirmed the robustness of the GLI1+/IFT20+ signature in increasing primary cilium numbers in normal cells, while this signature was less pronounced in prostate cancer-like cells. In parallel, we discovered that the restoration of primary cilium in prostate cancer cells is associated to the neuroendocrine transdifferentiation of prostate cancer. Furthermore, the regulation of primary cilium is linked to the cancer aggressiveness.Our research provides evidence that primary cilium is present in a more aggressive subgroup of prostate cancer patients, similar to what is observed in ccRCC. Analyzing the role of primary cilium in the transdifferentiation of prostate cancer provides new insights into potential treatment strategies
Konferenzberichte zum Thema "Neuroendocrine transdifferentiation"
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.
Der volle Inhalt der QuelleBeshiri, Mike L., Caitlin M. Tice, Adam G. Sowalsky, Crystal Tran, Fatima Karzai, William Dahut und Kathy Kelly. „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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