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Auswahl der wissenschaftlichen Literatur zum Thema „Docetaxel resistance“
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Zeitschriftenartikel zum Thema "Docetaxel resistance"
Kroon, Jan, Martin Puhr, Jeroen T. Buijs, Geertje van der Horst, Daniëlle M. Hemmer, Koen A. Marijt, Ming S. Hwang et al. „Glucocorticoid receptor antagonism reverts docetaxel resistance in human prostate cancer“. Endocrine-Related Cancer 23, Nr. 1 (19.10.2015): 35–45. http://dx.doi.org/10.1530/erc-15-0343.
Der volle Inhalt der QuelleILHAN, Suleyman. „Effect of interleukin-8 on docetaxel resistance in prostate cancer cells: insights into the role of multidrug resistance 1 protein modulation“. Cancer Insight 2, Nr. 1 (14.06.2023): 53–67. http://dx.doi.org/10.58567/ci02010004.
Der volle Inhalt der QuelleShen, Weiwei, Hailin Pang, Jiayu Liu, Jing Zhou, Feng Zhang, Lele Liu, Ningqiang Ma, Ning Zhang, Helong Zhang und Lili Liu. „EpithelialMesenchymal Transition Contributes to Docetaxel Resistance in Human Non-Small Cell Lung Cancer“. Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 22, Nr. 1 (23.10.2014): 47–55. http://dx.doi.org/10.3727/096504014x14098532393473.
Der volle Inhalt der QuelleFrancini, Edoardo, Fang-Shu Ou, Justin Rhoades, Eric G. Wolfe, Edward P. O’Connor, Gavin Ha, Gregory Gydush et al. „Circulating Cell-Free DNA as Biomarker of Taxane Resistance in Metastatic Castration-Resistant Prostate Cancer“. Cancers 13, Nr. 16 (12.08.2021): 4055. http://dx.doi.org/10.3390/cancers13164055.
Der volle Inhalt der QuelleZu, Shulu, Weiming Ma, Pan Xiao, Yazhou Cui, Tianjia Ma, Chunwen Zhou und Huaiqiang Zhang. „Evaluation of Docetaxel-Sensitive and Docetaxel-Resistant Proteomes in PC-3 Cells“. Urologia Internationalis 95, Nr. 1 (2015): 114–19. http://dx.doi.org/10.1159/000351263.
Der volle Inhalt der QuelleLima, Thiago S., Diego Iglesias-Gato, Luciano D. O. Souza, Jan Stenvang, Diego S. Lima, Martin A. Røder, Klaus Brasso und José M. A. Moreira. „Molecular Profiling of Docetaxel-Resistant Prostate Cancer Cells Identifies Multiple Mechanisms of Therapeutic Resistance“. Cancers 13, Nr. 6 (14.03.2021): 1290. http://dx.doi.org/10.3390/cancers13061290.
Der volle Inhalt der QuelleBukhari, Nedal, Kylea R. Potvin, D. Scott Ernst, Lori Sax und Eric Winquist. „Early docetaxel-resistance in metastatic hormone-sensitive prostate cancer.“ Journal of Clinical Oncology 35, Nr. 6_suppl (20.02.2017): 260. http://dx.doi.org/10.1200/jco.2017.35.6_suppl.260.
Der volle Inhalt der QuelleGruber, Martina, Lavinia Ferrone, Martin Puhr, Frédéric R. Santer, Tobias Furlan, Iris E. Eder, Natalie Sampson, Georg Schäfer, Florian Handle und Zoran Culig. „p300 is upregulated by docetaxel and is a target in chemoresistant prostate cancer“. Endocrine-Related Cancer 27, Nr. 3 (März 2020): 187–98. http://dx.doi.org/10.1530/erc-19-0488.
Der volle Inhalt der QuelleZhao, Song, Ilsa Coleman, Roger Coleman und Peter Nelson. „Association of PARP inhibitors and docetaxel resistance through suppressing a tumor microenvironment-associated secretory program.“ Journal of Clinical Oncology 31, Nr. 15_suppl (20.05.2013): e22212-e22212. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e22212.
Der volle Inhalt der QuelleWróbel, Tomasz, Marcin Luty, Jessica Catapano, Elżbieta Karnas, Małgorzata Szczygieł, Katarzyna Piwowarczyk, Damian Ryszawy et al. „CD44+ cells determine fenofibrate-induced microevolution of drug-resistance in prostate cancer cell populations“. Stem Cells 38, Nr. 12 (02.10.2020): 1544–56. http://dx.doi.org/10.1002/stem.3281.
Der volle Inhalt der QuelleDissertationen zum Thema "Docetaxel resistance"
Sangrithi-Wallace, Jay N. „An investigation of the molecular mechanisms of docetaxel resistance in breast cancer cells“. Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources, 2009. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=56251.
Der volle Inhalt der QuelleKastl, Lena. „Molecular mechanisms of docetaxel resistance in breast cancer“. Thesis, University of Aberdeen, 2007. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=158488.
Der volle Inhalt der QuelleMcDonald, Sarah L. „Characterization of genetic events involved in docetaxel resistance in breast cancer“. Thesis, University of Aberdeen, 2005. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU487906.
Der volle Inhalt der QuelleDarcansoy, Iseri Ozlem. „Investigation Of Docetaxel And Doxorubicin Resistance In Mcf-7 Breast Carcinoma Cell Line“. Phd thesis, METU, 2009. http://etd.lib.metu.edu.tr/upload/3/12610422/index.pdf.
Der volle Inhalt der Quelle#946
-tubulin isotypes were performed by RT-PCR, qPCR, Western blot and immunocytochemistry. Genome-wide expression analysis was also performed by cDNA microarray. According to cell viability assays, drug applied cells developed varying degree of resistance to docetaxel and doxorubicin. Gene expression analysis demonstrated that de novo expression of P-gp contributed significantly to drug resistance. Expression levels of class II, III and V &
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-tubulin isotypes increased in docetaxel resistant sublines. According to microarray analysis, a variety of genes showed significantly altered expression levels particularly drug metabolizing and detoxification enzymes (i.e. increased GPX1 and GSTP1 with decreased POR), survival proteins (e.g. decreased TRAIL together with increased decoy receptors and CD40), extracellular matrix components (e.g. increased integrin signaling), growth factors and cytokines (e.g. EGFR1, FGFR1, CTGF, IL6, IL8 and IL18 overexpression), epithelial-mesenchymal transition proteins (i.e. increased vimentin and N-cadherin with decreased E-cadherin and occludin) and microtubule dynamics related proteins (e.g. increased MAP1B and decreased MAP7). Development of cross-resistance and combined drug effects on resistant sublines were also studied. Results demonstrated that docetaxel and doxorubicin resistant cells developed cross-resistance to paclitaxel, vincristine, ATRA, tamoxifen and irradiation. Finally, modulatory effects of verapamil and promethazine in combined drug applications were investigated and verapamil and promethazine were shown to decrease MDR1 expression level thus reverse the MDR. They also showed synergic and additive effects in combined docetaxel and doxorubicin applications. Identification of resistance mechanisms may personalize chemotherapy potentially increasing efficacy of chemotherapy and life quality of patients.
Pruitt, Freddie Lee III. „Chemoresistance of prostate cancer cells to docetaxel is modified by extracellular matrix substratum“. Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 92 p, 2008. http://proquest.umi.com/pqdweb?did=1459903001&sid=4&Fmt=2&clientId=8331&RQT=309&VName=PQD.
Der volle Inhalt der QuelleIPPOLITO, LUIGI. „OXPHOS - a metabolic switch driven by tumor microenvironment and resistance to therapy in prostate carcinoma“. Doctoral thesis, Università di Siena, 2016. http://hdl.handle.net/11365/1006820.
Der volle Inhalt der QuelleAl, Nakouzi Nader. „Etablissement d'un nouveau modèle pérclinique de cancer de la prostate et identification de biomarqueurs de résistance au docetaxel“. Phd thesis, Université Paris Sud - Paris XI, 2011. http://tel.archives-ouvertes.fr/tel-00739261.
Der volle Inhalt der QuelleRIZZUTI, ILARIA FRANCESCA. „STRENGTHEN OF DPNS FEATURES FOR THERANOSTIC APPLICATIONS AND MECHANICAL-CONTROL OF CHEMOTHERAPEUTIC EFFICACY THROUGH MODULATION OF CELL PROLIFERATION“. Doctoral thesis, Università degli studi di Genova, 2020. http://hdl.handle.net/11567/1000310.
Der volle Inhalt der QuelleLen, Kateryna. „Vitamin D effects on prostate cancer progression“. Electronic Thesis or Diss., Strasbourg, 2024. http://www.theses.fr/2024STRAJ028.
Der volle Inhalt der QuelleProstate cancer (PCa) is one of the leading causes of cancer-related deaths in men. Androgen receptor signaling inhibitors are the gold standard treatment for advanced PCa, but most patients develop castration-resistant prostate cancer (CRPC). The treatment of choice for CRPC is the chemotherapy (docetaxel), but the overall survival is only about one year. Thus, novel therapeutic strategies are required to improve PCa care. Low circulating vitamin D levels and reduced expression of its receptor VDR in prostatic epithelial cells (PECs) correlate with PCa severity, but the underlying mechanism is unclear. This study shows that VDR in PECs of Pten(i)pe-/- mice, a model of PCa, reduces cell proliferation via oxidative stress attenuation. Furthermore, VDR in PECs limits the recruitment of neutrophils, that are shown to be therapeutic target for PCa dissemination. Additionally, combining a VDR agonist with docetaxel effectively reduces tumor volumes in chemoresistant CRPC xenografts. Overall, this work highlights how vitamin D signaling slows PCa progression and suggests new therapeutic strategies for advanced PCa
Hou, Pei-Shen, und 侯佩伸. „Molecular mechanisms of AMPK mediated docetaxel-resistance in human prostate cancer“. Thesis, 2017. http://ndltd.ncl.edu.tw/handle/69158788833945408088.
Der volle Inhalt der Quelle高雄醫學大學
醫學研究所碩士班
105
Docetaxel is the first-line chemotherapeutic agent for patients with castration resistant prostate cancer (CRPC). Unfortunately, clinical treatment with docetaxel often encounters a number of undesirable side effects, including drug resistance. AMP-activated protein kinase (AMPK) is the cellular energy sensor, which can regulate metabolism and maintain energy homeostasis involving glycolysis. Recently, we found AMPK was associated with the development of docetaxel resistance in PC. However, the mechanisms of AMPK-mediated docetaxel-resistance in PC were remained unclear. Our results showed that the level of phospho-AMPK (S487) was significantly higher expression in PC/DX25 cells (a docetaxel resistance PC cell line) than in parental PC3 cells by Western blotting analysis. The expression of phospho-AMPK (S487) was gradually increased by docetaxel treatment in a dose-dependent manner in PC3 cells. Knockdown of AMPK expression reversed docetaxel sensitivity in PC/DX25 cells by MTT assay. However, using the AMPK agonist 2-Deoxy-D-glucose (2DG) and 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR) enhanced the docetaxel resistance in PC/DX25 cells. We also found the expression of HIF-1α and PFKFB4 were reduced via AMPK in PC/DX25 cells. Downregulation of HIF-1α and PFKFB4 were associated with PC/DX25 cell proliferation. The phospho-AMPK (S487) was overexpressed in clinical cancer samples of castration-resistant prostate cancer (CRPC). According to the above results, AMPK may play an important role in regulating chemoresistane in docetaxel-resistant prostate cancer.
Buchteile zum Thema "Docetaxel resistance"
Narita, Shintaro, und Tomonori Habuchi. „Intermittent Chemotherapy with Docetaxel for Metastatic Castration-Resistant Prostate Cancer“. In Hormone Therapy and Castration Resistance of Prostate Cancer, 357–68. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-7013-6_36.
Der volle Inhalt der QuelleMatsuyama, Hideyasu, Tomoyuki Shimabukuro, Isao Hara, Kazuhiro Suzuki, Hirotsugu Uemura, Munehisa Ueno, Yoshihiko Tomita und Nobuaki Shimizu. „Prediction of Optimal Number of Cycles in Docetaxel Regimen for Patients with mCRPC“. In Hormone Therapy and Castration Resistance of Prostate Cancer, 345–55. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-7013-6_35.
Der volle Inhalt der QuellePetrylak, Daniel P., und Navid Hafez. „Docetaxel in Advanced and Castration Resistant Prostate Cancer“. In Managing Metastatic Prostate Cancer In Your Urological Oncology Practice, 77–92. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-31341-2_6.
Der volle Inhalt der QuelleBozkurt, Yunus Erol, und Turgay Turan. „Enzalutamide Therapy for Metastatic Prostate Cancer“. In Current Management of Metastatic Prostate Cancer, 79–88. Istanbul: Nobel Tip Kitabevleri, 2024. http://dx.doi.org/10.69860/nobel.9786053359142.7.
Der volle Inhalt der QuelleSzturz, Petr, und Jan B. Vermorken. „Systemic Treatment Sequencing and Prediction of First-line Therapy Outcomes in Recurrent or Metastatic Head and Neck Cancer“. In Critical Issues in Head and Neck Oncology, 199–215. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-23175-9_13.
Der volle Inhalt der QuelleKulkarni, Harshad R. „PSMA Radioligand Therapy: A Revolution in the Precision Radiomolecular Oncology of Prostate Cancer“. In Beyond Becquerel and Biology to Precision Radiomolecular Oncology: Festschrift in Honor of Richard P. Baum, 181–85. Cham: Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-33533-4_18.
Der volle Inhalt der QuelleLawal, Ismaheel O., Alfred Morgenstern, Otto Knoesen, Mariza Vorster, Frank Bruchertseifer und Mike M. Sathekge. „Therapy of Castration-Resistant Prostate Cancer: Where Is the Place of 225Ac-PSMA?“ In Beyond Becquerel and Biology to Precision Radiomolecular Oncology: Festschrift in Honor of Richard P. Baum, 255–65. Cham: Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-33533-4_26.
Der volle Inhalt der QuelleJ. Suzuki, Yuichiro, Yasmine F. Ibrahim, Vladyslava Rybka, Jaquantey R. Bowens, Adenike S. Falade und Nataliia V. Shults. „Strategies to Treat Pulmonary Hypertension Using Programmed Cell Death-Inducing Anti-Cancer Drugs without Damaging the Heart“. In Muscle Cell and Tissue - Novel Molecular Targets and Current Advances [Working Title]. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.95264.
Der volle Inhalt der QuellePriya Muthaiah, Gnana Ruba, Motamarri Venkata Naga Lalitha Chaitanya, Seema Sajjan Singh Rathore, Maida Engels S.E. und Vishnu Nayak Badavath. „Importance of In silico Tools in Anticancer Drug Discovery from Nature“. In Alternative Remedies and Natural Products for Cancer Therapy: An Integrative Approach, 139–64. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815124699123010010.
Der volle Inhalt der QuelleSiddiqui, Surayya, Sridevi I. Puranik, Aimen Akbar und Shridhar C. Ghagane. „Genetic Polymorphism and Prostate Cancer: An Update“. In Genetic Polymorphisms - New Insights [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.99483.
Der volle Inhalt der QuelleKonferenzberichte zum Thema "Docetaxel resistance"
Dahmani, Ahmed, Ludmilla De Plater, Charlotte Guyader, Jean‐Jacques Fontaine, Aurélie Berniard, Franck Assayag, Philippe Beuzeboc et al. „Abstract A27: Efficacy of estramustine + docetaxel in docetaxel‐resistant human prostate cancer xenograft: a preclinical model of docetaxel resistance reversion“. In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-a27.
Der volle Inhalt der QuelleNagesh, Prashanth K. B., Pallabita Chowdhury, Elham Hatami, Vivek K. Kashyap, Bilal B. Hafeez, Sheema Khan, Subhash C. Chauhan, Meena Jaggi und Murali M. Yallapu. „Abstract 4657: Docetaxel nanoformulation reverts drug resistance in 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.am2018-4657.
Der volle Inhalt der QuelleSprowl, Jason A., und Amadeo Parissenti. „Abstract 3550: Role of TNFα in the cytotoxicity of docetaxel and in docetaxel resistance in MCF-7 cells“. In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3550.
Der volle Inhalt der QuellePeery, Robert C. „Abstract 4396: Targeting survivin to overcome docetaxel resistance in 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.am2018-4396.
Der volle Inhalt der QuelleCotteret, Sophie, Nader Al Nakouzi, Catherine Gaudin, Frederic Commo, Shanna Rajpar, Sandra Lejuste, Nicolas Martin, Karim Fizazi und Anne Chauchereau. „Abstract 956: Role of the cell cycle regulator LZTS1 in docetaxel resistance of prostate cancer cells and overcoming the docetaxel resistance by cell cycle pharmacological inhibitors.“ In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-956.
Der volle Inhalt der QuelleLichtenfels, Martina, Vivian Fontana, Francine Hickmann Nyland, Bianca Silva Marques, Mário Casales Schorr, Júlia Caroline Marcolin, Caroline Brunetto de Farias und José Luiz Pedrini. „What happens in residual disease after neoadjuvant chemotherapy? Efficacy of a novel in vitro breast cancer chemoresistance platform to demonstrate high resistance to drugs“. In Brazilian Breast Cancer Symposium 2023. Mastology, 2023. http://dx.doi.org/10.29289/259453942023v33s1010.
Der volle Inhalt der QuelleDuran, Ignacio, Clara Montagut, Emiliano Calvo, Alicia Navarrete, Antonia Garcia, Manuel Hidalgo, Jesus Rodriguez-Pascual et al. „Abstract C65: Overcoming docetaxel resistance through m-TOR inhibition: A phase I study of the combination of docetaxel and temsirolimus.“ In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-c65.
Der volle Inhalt der QuelleShimomura, Tatsuya, Evelyn Kono, Chau P. Tran, Joyce Yamashiro, Shu Lin, Sean Hyung-Kwon Lee, Zev A. Wainberg und Robert E. Reiter. „Abstract 3310: N-cadherin promotes docetaxel resistance through upregulated TLR4 signaling in castration resistant prostate cancers“. In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3310.
Der volle Inhalt der QuelleLannér, Carita, Stephen Armstrong, Irina Kalatskaya, Baoqing Guo und Amadeo Parissenti. „Abstract 1716: Mechanisms of resistance in carboplatin, docetaxel and dual drug resistant ovarian cancer cell lines“. In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1716.
Der volle Inhalt der QuelleWatanabe, Mototsugu, Yasutaka Masada, Shinsuke Hashida, Tomoaki Ohtsuka, Ken Suzawa, Yuho Maki, Hiromasa Yamamoto et al. „Abstract 358: The role of GDF-15 on docetaxel resistance in lung 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.am2015-358.
Der volle Inhalt der QuelleBerichte der Organisationen zum Thema "Docetaxel resistance"
Singh, Ajay. Exploring a Novel Mechanism of Docetaxel Resistance in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, März 2013. http://dx.doi.org/10.21236/ada576367.
Der volle Inhalt der QuelleSingh, Ajay. Exploring a Novel Mechanism of Docetaxel Resistance in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, Mai 2014. http://dx.doi.org/10.21236/ada601299.
Der volle Inhalt der QuelleZhang, Ying, Xinjun Wang, Guangcheng Luo, Xiao Zhou und Ran Xu. Neutrophil-to-lymphocyte ratio as a prognostic factor in patients with castration-resistant prostate cancer treated with docetaxel-based chemotherapy:A meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, März 2023. http://dx.doi.org/10.37766/inplasy2023.3.0018.
Der volle Inhalt der QuelleFan, Long-wen. Efficacy of docetaxel combined carboplatin for the treatment of patients with castration-resistant prostate cancer: a protocol of systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review Protocols, April 2020. http://dx.doi.org/10.37766/inplasy2020.4.0076.
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