Relevant bibliographies by topics / Docetaxel resistance

Contents

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

Academic literature on the topic 'Docetaxel resistance'

Author: Grafiati
Published: 2 November 2024
Last updated: 31 July 2025

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Journal articles on the topic "Docetaxel resistance"

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Alam, Md Rakibul, Amos Olalekan Akinyemi, Jianlin Wang, Mithu Howlader, Lixiang Gu, and Zhiguo Li. "Abstract 3071: Improving the docetaxel-based chemotherapy in therapy resistance prostate cancer." Cancer Research 85, no. 8_Supplement_1 (2025): 3071. https://doi.org/10.1158/1538-7445.am2025-3071.

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Prostate cancer is known to have a relatively good prognosis, but long-term hormone therapy can lead to castration-resistant prostate cancer (CRPC). Docetaxel, a third-generation chemotherapy drug based on inhibiting depolymerization of microtubules, provide excellent initial response in patients for the CRPC treatment. Despite the improved survival duration and reduction of tumor size observed in some patients, many have no response to the drugs or develop resistance over time. In this study, to elucidate the molecular basis of docetaxel resistance, we established docetaxel resistance prostat
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Kroon, Jan, Martin Puhr, Jeroen T. Buijs, et al. "Glucocorticoid receptor antagonism reverts docetaxel resistance in human prostate cancer." Endocrine-Related Cancer 23, no. 1 (2015): 35–45. http://dx.doi.org/10.1530/erc-15-0343.

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Resistance to docetaxel is a major clinical problem in advanced prostate cancer (PCa). Although glucocorticoids (GCs) are frequently used in combination with docetaxel, it is unclear to what extent GCs and their receptor, the glucocorticoid receptor (GR), contribute to the chemotherapy resistance. In this study, we aim to elucidate the role of the GR in docetaxel-resistant PCa in order to improve the current PCa therapies. GR expression was analyzed in a tissue microarray of primary PCa specimens from chemonaive and docetaxel-treated patients, and in cultured PCa cell lines with an acquired do
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Shen, Weiwei, Hailin Pang, Jiayu Liu, et al. "EpithelialMesenchymal Transition Contributes to Docetaxel Resistance in Human Non-Small Cell Lung Cancer." Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 22, no. 1 (2014): 47–55. http://dx.doi.org/10.3727/096504014x14098532393473.

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Lung cancer is an aggressive malignancy with high morbidity and mortality. Chemotherapy has always been the principal treatment measure, but its acquired resistance becomes a critical problem. In the current study, we established a new docetaxel-resistant human non-small lung cancer (NSCLC) cell line A549/Docetaxel. The resistance index (RI) of A549/Docetaxel cells and A549 induced by TGF- to docetaxel were 8.91 and 11.5, respectively. Compared to the parental A549 cells, the multiplication time of A549/Docetaxel was prolonged, the proportion of the cell cycle in the S phase decreased while th
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ILHAN, 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, no. 1 (2023): 53–67. http://dx.doi.org/10.58567/ci02010004.

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Although docetaxel treatment yields a high survival rate for prostate cancer (PCa), resistance eventually develops in many patients. Understanding the underlying mechanisms of docetaxel resistance is essential for improving treatment strategies. Cytokines, which play a role in cell signaling and immune responses, have been implicated in drug resistance mechanisms. The study revealed that interleukin-8 (IL-8) was consistently overexpressed in both docetaxel-resistant PCa cell lines. Thus, the expression levels of cytokines released from docetaxel-sensitive (PC-3- and DU-145) and resistant (PC-3
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Francini, Edoardo, Fang-Shu Ou, Justin Rhoades, et al. "Circulating Cell-Free DNA as Biomarker of Taxane Resistance in Metastatic Castration-Resistant Prostate Cancer." Cancers 13, no. 16 (2021): 4055. http://dx.doi.org/10.3390/cancers13164055.

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There are no biomarkers predictive of resistance to docetaxel or cabazitaxel validated for patients with metastatic castration-resistant prostate cancer (mCRPC). We assessed the association between ABCB1 amplification and primary resistance to docetaxel or cabazitaxel for patients with mCRPC, using circulating cell-free DNA (cfDNA). Patients with ≥1 plasma sample drawn within 12 months before starting docetaxel (cohort A) or cabazitaxel (cohort B) for mCRPC were identified from the Dana–Farber Cancer Institute IRB approved database. Sparse whole genome sequencing was performed on the selected
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Zu, Shulu, Weiming Ma, Pan Xiao, et al. "Evaluation of Docetaxel-Sensitive and Docetaxel-Resistant Proteomes in PC-3 Cells." Urologia Internationalis 95, no. 1 (2015): 114–19. http://dx.doi.org/10.1159/000351263.

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Objectives: Docetaxel was the first drug with proven survival benefit in men with castration-resistant prostate cancer. Acquired resistance to docetaxel precedes fatality in castration-resistant prostate cancer. The aims of this study were to evaluate docetaxel-sensitive and docetaxel-resistant proteomes in PC-3 cells, and to investigate the molecular mechanism of docetaxel-resistant PC-3 cells. Methods: Docetaxel-resistant PC-3 cells were developed by docetaxel dose escalation. The global profiling of the protein expression was investigated in docetaxel-sensitive and docetaxel-resistant prote
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Lima, Thiago S., Diego Iglesias-Gato, Luciano D. O. Souza, et al. "Molecular Profiling of Docetaxel-Resistant Prostate Cancer Cells Identifies Multiple Mechanisms of Therapeutic Resistance." Cancers 13, no. 6 (2021): 1290. http://dx.doi.org/10.3390/cancers13061290.

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Docetaxel—a taxane-based chemotherapeutic agent—was the first treatment to demonstrate significant improvements in overall survival in men with metastatic castration-resistant prostate cancer (mCRPC). However, the response to docetaxel is generally short-lived, and relapse eventually occurs due to the development of resistance. To explore the mechanisms of acquired docetaxel resistance in prostate cancer (PCa) and set these in the context of androgen deprivation therapy, we established docetaxel-resistant PCa cell lines, derived from the androgen-dependent LNCaP cell line, and from the LNCaP l
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Bukhari, Nedal, Kylea R. Potvin, D. Scott Ernst, Lori Sax, and Eric Winquist. "Early docetaxel-resistance in metastatic hormone-sensitive prostate cancer." Journal of Clinical Oncology 35, no. 6_suppl (2017): 260. http://dx.doi.org/10.1200/jco.2017.35.6_suppl.260.

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260 Background: The addition of docetaxel to standard androgen deprivation therapy (ADT) has been shown to improve the survival of men with metastatic hormone-sensitive prostate cancer (MHSPC) (Sweeney 2015, James 2016). We noticed PSA progression in some of our patients (pts) during docetaxel treatment and reviewed their outcomes. Methods: Men with MHSPC treated with docetaxel were identified from an electronic oncology pharmacy database. Eligible pts were prescribed docetaxel for metastatic adenocarcinoma of the prostate within 120 days of initiation of ADT. Pts with castration-resistant dis
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Gruber, Martina, Lavinia Ferrone, Martin Puhr, et al. "p300 is upregulated by docetaxel and is a target in chemoresistant prostate cancer." Endocrine-Related Cancer 27, no. 3 (2020): 187–98. http://dx.doi.org/10.1530/erc-19-0488.

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Administration of the microtubule inhibitor docetaxel is a common treatment for metastatic castration-resistant prostate cancer (mCRPC) and results in prolonged patient overall survival. Usually, after a short period of time chemotherapy resistance emerges and there is urgent need to find new therapeutic targets to overcome therapy resistance. The lysine-acetyltransferase p300 has been correlated to prostate cancer (PCa) progression. Here, we aimed to clarify a possible function of p300 in chemotherapy resistance and verify p300 as a target in chemoresistant PCa. Immunohistochemistry staining
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Zhao, Song, Ilsa Coleman, Roger Coleman, and Peter Nelson. "Association of PARP inhibitors and docetaxel resistance through suppressing a tumor microenvironment-associated secretory program." Journal of Clinical Oncology 31, no. 15_suppl (2013): e22212-e22212. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e22212.

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e22212 Background: Acquired resistance to therapeutics accounts for the majority of treatment failures in metastatic cancer. In response to genotoxic stress induced by therapeutics such as radiation and chemotherapy, tumor microenvironment (TME) undergoes marked molecular alterations manifested by increased secretion of cytokines and growth factors, which in turn promote tumor growth, facilitate epithelial-mesenchymal transition, and ultimately result in resistance to chemotherapy. Fibroblasts are a major component of TME and a primary source of cytokines and growth factor secretion following
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Dissertations / Theses on the topic "Docetaxel resistance"

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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.

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Kastl, Lena. "Molecular mechanisms of docetaxel resistance in breast cancer." Thesis, University of Aberdeen, 2007. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=158488.

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Docetaxel is a chemotherapy drug used to treat breast cancer, however as with many chemotherapeutic drugs, resistance commonly occurs and the underlying molecular mechanisms of drug resistance are not fully understood. Gene regulatory mechanisms like DNA methylation, histone deacetylation and miRNA expression have been shown to play an important role in cancer drug resistance. This study investigated the role of these mechanisms in two in vitro breast cancer cell line models (MCF-7 and MDA-MB-231) of acquired docetaxel resistance. Using inhibitors to DNA methylation and histone deacetylation,
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McDonald, 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.

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A model of docetaxel resistance in breast tumours was established in two breast cancer cell lines MCF-7 and MDA-MB-231. This was the first description of docetaxel resistant breast cancer cell lines. As an initial global analysis of the genetic events involved in docetaxel resistance, comparative genomic hybridisation (CGH) was used on the DNA extracted from the resistant cell compared to the parental cells. This allowed a unique insight into the specific chromosomal regions that were modified as resistance to docetaxel developed. The resistant cells exhibited a variety of chromosomal modifica
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Darcansoy, 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.

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Multidrug resistance phenotype of tumor cells describes resistance to wide range of structurally unrelated anticancer agents and is a serious limitation to effective chemotherapy. It is a multifactor yet not fully elucidated phenomenon by the involvement of diverse cellular pathways. Aim of this study was to investigate the resistance mechanisms developed against docetaxel and doxorubicin that are widely used in the treatment of breast cancer in model cell line MCF-7. Resistant sublines were developed by application of drugs in dose increments and effect of docetaxel and doxorubicin on drug
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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.

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IPPOLITO, 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.

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Tumor cells exhibit metabolic reprogramming according to microenvironmental scenarios (i.e. stroma composition and/or anticancer drugs burden) to meet their demands for energy, rapid proliferation, metastasis and progression. In our experimental model, a vicious metabolic synergy between CAFs and prostate cancer (PCa) cells has been described as a pivotal engine allowing cancer cells to achieve aggressive features and evolve their malignancy. Such metabolic crosstalk is mainly based on the OXPHOS rewiring of PCa cells induced by highly glycolytic CAFs through the establishment of tumor:
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Al, 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.

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La mise au point de modèles de laboratoire est d'une importance cruciale pour comprendre la biologie du cancer de la prostate, ainsi que pour évaluer les nouveaux traitements. Le développement de tels modèles est particulièrement difficile et reste à ce jour insuffisant car la majorité de ces modèles est d'origine métastatique ou obtenu in vitro d'une façon artificielle. C'est pourquoi, nous avons entrepris au laboratoire, l'établissement de nouveaux modèles à partir d'un cancer primaire de prostate tumorale et obtenu la lignée IGR-CaP1. La lignée IGR-CaP1 constitue un modèle adapté pour étudi
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RIZZUTI, 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.

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Solid tumors are complex biological structures which are composed of cellular and matrix components, everything being perfused by blood vessels. During tumor development, modifications of both biochemical and mechanical parameters are observed and can feedback on one another. Cancer cells constantly interact with their mechanical environment and the whole tissue is mostly confined by its surrounding. Compressive mechanical stress develops in part from cell proliferation and could eventually result in the clamping of blood vessels leading to increased interstitial fluid pressure (hydrostatic pr
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Len, Kateryna. "Vitamin D effects on prostate cancer progression." Electronic Thesis or Diss., Strasbourg, 2024. http://www.theses.fr/2024STRAJ028.

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Le cancer de la prostate (CaP) est l’un des cancers le plus mortel chez les hommes. Le CaP avancé est traité avec les inhibiteurs du récepteur des androgènes ou la chimiothérapie (chimiothérapie), mais la plupart des patients développent des résistances. Ainsi, des nouvelles stratégies thérapeutiques sont nécessaires pour améliorer la prise en charge du CaP. Les faibles niveaux circulants de la vitamine D ou de son récepteur VDR dans les cellules épithéliales prostatiques (PECs) sont corrélés avec la gravité du CaP, mais le mécanisme sous-jacent n'est pas décrit. Cette étu
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Hou, Pei-Shen, and 侯佩伸. "Molecular mechanisms of AMPK mediated docetaxel-resistance in human prostate cancer." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/69158788833945408088.

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碩士<br>高雄醫學大學<br>醫學研究所碩士班<br>105<br>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 remai
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Book chapters on the topic "Docetaxel resistance"

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Narita, Shintaro, and Tomonori Habuchi. "Intermittent Chemotherapy with Docetaxel for Metastatic Castration-Resistant Prostate Cancer." In Hormone Therapy and Castration Resistance of Prostate Cancer. Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-7013-6_36.

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Matsuyama, Hideyasu, Tomoyuki Shimabukuro, Isao Hara, et al. "Prediction of Optimal Number of Cycles in Docetaxel Regimen for Patients with mCRPC." In Hormone Therapy and Castration Resistance of Prostate Cancer. Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-7013-6_35.

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Petrylak, Daniel P., and Navid Hafez. "Docetaxel in Advanced and Castration Resistant Prostate Cancer." In Managing Metastatic Prostate Cancer In Your Urological Oncology Practice. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-31341-2_6.

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Bozkurt, Yunus Erol, and Turgay Turan. "Enzalutamide Therapy for Metastatic Prostate Cancer." In Current Management of Metastatic Prostate Cancer. Nobel Tip Kitabevleri, 2024. http://dx.doi.org/10.69860/nobel.9786053359142.7.

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Enzalutamide (ENZ), a potent androgen receptor pathway inhibitor, gained FDA approval in 2012 for metastatic castration-resistant prostate cancer (mCRPC) post-docetaxel chemotherapy. It exhibits high affinity to the androgen receptor (AR), disrupting AR signaling crucial for prostate cancer growth. Notably, ENZ’s mechanism inhibits AR nuclear translocation and exerts apoptotic effects, distinct from older antiandrogens like bicalutamide. Clinical trials demonstrate ENZ’s efficacy across various stages of prostate cancer, from metastatic hormone-sensitive disease to non-metastatic CRPC, prolong
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Szturz, Petr, and 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. Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-23175-9_13.

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AbstractIn the palliative management of patients with recurrent and/or metastatic squamous cell carcinoma of the head and neck who are not candidates for a complete resection or full-dose radiotherapy, systemic treatment has seen important advances over the past several decades. In general, there are six major factors impacting on the decision-making process. Four of them belong to a class of continuous functions and include overall health status (from fitness to frailty), disease burden (from high to low), pace of the disease (from fast to slow), and expression of programmed-death ligand 1 (P
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Kulkarni, 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. Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-33533-4_18.

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AbstractThe incidence of prostate cancer is ever increasing. After various time intervals, the disease almost always becomes resistant to the standard hormone treatment (castration-resistant prostate cancer, CRPC). Most patients with CRPC either already have metastases at diagnosis or develop them during the early months of follow-up, which is associated with a relatively poor prognosis. The taxane-based chemotherapy for metastatic CRPC (mCRPC), first line with docetaxel and second line using cabazitaxel, are associated with a high incidence of adverse effects. The novel androgen-axis drugs (N
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Lawal, Ismaheel O., Alfred Morgenstern, Otto Knoesen, Mariza Vorster, Frank Bruchertseifer, and 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. Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-33533-4_26.

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AbstractSince the first report in 2004 confirming the survival advantage conferred by docetaxel in the treatment of men with metastatic castration-resistant prostate cancer (mCRPC), many more agents have also been found to prolong life and are now in routine use in clinical practice. Despite the multitude of these effective agents, mCRPC remains a fatal disease with a poor prognosis. Efforts to develop more effective therapies are, therefore, ongoing. Targeting prostate-specific membrane antigen (PSMA) overexpressed on prostate cancer cells has become an attractive option for mCRPC treatment.
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Priya Muthaiah, Gnana Ruba, Motamarri Venkata Naga Lalitha Chaitanya, Seema Sajjan Singh Rathore, Maida Engels S.E., and 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. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815124699123010010.

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Currently, cancer has become one of the most dreadful diseases threatening human health. Natural plant sources play a vital role in the development of several anti-cancer drugs such as vincristine, vinblastine, vinorelbine, docetaxel, paclitaxel, camptothecin, etoposide, teniposide, etc. Various chemotherapies fail due to adverse reactions, target specificity, and drug resistance of some types of drugs. Researchers are attentive to developing drugs that overcome the problems stated above by using natural compounds that may affect multiple targets with reduced adverse effects and that are effec
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J. Suzuki, Yuichiro, Yasmine F. Ibrahim, Vladyslava Rybka, Jaquantey R. Bowens, Adenike S. Falade, and 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.

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Pulmonary arterial hypertension (PAH) is a fatal disease without a cure. By the time patients are diagnosed with PAH, thickening of pulmonary arterial (PA) walls and the narrowing of vascular lumen have already developed due to the abnormal growth of pulmonary vascular cells, contributing to the elevated pulmonary vascular resistance and the right ventricle (RV) damage. Therefore, agents that eliminate excess pulmonary vascular wall cells have therapeutic potential, and the apoptosis-based therapy using anti-cancer drugs may be promising for the treatment of PAH. However, cell death agents cou
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Siddiqui, Surayya, Sridevi I. Puranik, Aimen Akbar, and 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.

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Genetic polymorphism and prostate cancer (PC) are the most pernicious and recurrently malignancy worldwide. It is the most dominating cause of cancer related casualty among men in the US. Asian countries are inflicted with PC at an alarming rate though still the prevalence of PC is lower than European and American men. Some of the genetic and environmental factors that might play a role in PC risk include: age genetic predilection, family history, race/ethnicity, lifestyle, and dietary habits and non-dietary environmental risk factors such as smoking. Socio-economic factors including economic,
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Conference papers on the topic "Docetaxel resistance"

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Dahmani, Ahmed, Ludmilla De Plater, Charlotte Guyader, 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.

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Nagesh, Prashanth K. B., Pallabita Chowdhury, Elham Hatami, et al. "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.

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Sprowl, Jason A., та Amadeo Parissenti. "Abstract 3550: Role of TNFα in the cytotoxicity of docetaxel and in docetaxel resistance in MCF-7 cells". У 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.

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Peery, 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.

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Cotteret, Sophie, Nader Al Nakouzi, Catherine Gaudin, et al. "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.

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Duran, Ignacio, Clara Montagut, Emiliano Calvo, 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.

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Shimomura, Tatsuya, Evelyn Kono, Chau P. Tran, et al. "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.

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Lannér, Carita, Stephen Armstrong, Irina Kalatskaya, Baoqing Guo, and 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.

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Lichtenfels, Martina, Vivian Fontana, Francine Hickmann Nyland, et al. "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.

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Objective: Our preliminary study aimed to validate the efficacy of a novel in vitro chemoresistance platform to demonstrate tumor resistance in residual disease after neoadjuvant treatment for breast cancer. Methodology: Patients with invasive BC who presented residual disease after neoadjuvant chemotherapy (NACT) were included. Fresh tumor samples were collected during surgery and dissociated to obtain the tumor cells. The tumor cells were cultured in the chemoresistance platform with doxorubicin, epirubicin, paclitaxel, docetaxel, and cyclophosphamide, and after 72 h, cell viability was eval
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Watanabe, Mototsugu, Yasutaka Masada, Shinsuke Hashida, 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.

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Reports on the topic "Docetaxel resistance"

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Singh, Ajay. Exploring a Novel Mechanism of Docetaxel Resistance in Prostate Cancer. Defense Technical Information Center, 2013. http://dx.doi.org/10.21236/ada576367.

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Singh, Ajay. Exploring a Novel Mechanism of Docetaxel Resistance in Prostate Cancer. Defense Technical Information Center, 2014. http://dx.doi.org/10.21236/ada601299.

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Zhang, Ying, Xinjun Wang, Guangcheng Luo, Xiao Zhou, and 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, 2023. http://dx.doi.org/10.37766/inplasy2023.3.0018.

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Fan, 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, 2020. http://dx.doi.org/10.37766/inplasy2020.4.0076.

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You might also be interested in the extended bibliographies on the topic 'Docetaxel resistance' for particular source types:
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