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Добірка наукової літератури з теми "Docetaxel resistance"

Автор: Grafiati

Опубліковано: 2 листопада 2024

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Статті в журналах з теми "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, no. 1 (October 19, 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 docetaxel resistance (PC3-DR, DU145-DR, and 22Rv1-DR). We found a robust overexpression of the GR in primary PCa from docetaxel-treated patients and enhanced GR levels in cultured docetaxel-resistant human PCa cells, indicating a key role of the GR in docetaxel resistance. The capability of the GR antagonists (RU-486 and cyproterone acetate) to revert docetaxel resistance was investigated and revealed significant resensitization of docetaxel-resistant PCa cells for docetaxel treatment in a dose- and time-dependent manner, in which a complete restoration of docetaxel sensitivity was achieved in both androgen receptor (AR)-negative and AR-positive cell lines. Mechanistically, we demonstrated down-regulation of Bcl-xL and Bcl-2 upon GR antagonism, thereby defining potential treatment targets. In conclusion, we describe the involvement of the GR in the acquisition of docetaxel resistance in human PCa. Therapeutic targeting of the GR effectively resensitizes docetaxel-resistant PCa cells. These findings warrant further investigation of the clinical utility of the GR antagonists in the management of patients with advanced and docetaxel-resistant PCa.

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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 (June 14, 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/R-DU-145/R) PCa cells were compared. IL-8 was found to be commonly expressed in resistant cell lines. This finding led to the hypothesis that IL-8 could play a key role in mediating PCa cell resistance to docetaxel. IL-8 siRNA treatment increased docetaxel sensitivity in both resistant cells. To demonstrate the mechanism of IL-8-related resistance, MDR1 expression was evaluated. After IL-8 siRNA treatment MDR1 expression was reduced in both resistant cells suggesting that IL-8 regulates the docetaxel resistance of PCa cells via modulation of multidrug resistance 1 (MDR1). By expanding the knowledge of the cytokines and their effect mechanisms, novel approaches can be developed for the treatment of docetaxel-resistant prostate cancer. Further investigations into the role of IL-8 in docetaxel resistance could offer valuable insights into the development of effective treatment strategies for PCa patients.

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Shen, Weiwei, Hailin Pang, Jiayu Liu, Jing Zhou, Feng Zhang, Lele Liu, Ningqiang Ma, Ning Zhang, Helong Zhang, and Lili Liu. "EpithelialMesenchymal Transition Contributes to Docetaxel Resistance in Human Non-Small Cell Lung Cancer." Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 22, no. 1 (October 23, 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 that in the G1 phase increased, and apoptotic rate was much lower. The morphology of the resistant cells eventuated epithelialmesenchymal transition (EMT), which was confirmed by the higher expression of fibronectin, vimentin (mesenchymal markers), and lower expression of E-cadherin (epithelial marker) at mRNA and proteins levels. Furthermore, the representative markers for docetaxel resistance were examined, including ABCB1 (MDR1), Bcl-2, Bax, and tubulin, to figure out the mechanisms of the resistance of A549/Docetaxel. In summary, we have established a typical docetaxel-resistant human NSCLC cell line A549/Docetaxel, and it was suggested that the multidrug resistance of A549/Docetaxel was related to EMT.

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Francini, 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, no. 16 (August 12, 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 cfDNA samples and tumor fractions were estimated using the computational tool ichorCNA. We evaluated the association between ABCB1 amplification or other copy number alterations and primary resistance to docetaxel or cabazitaxel. Of the selected 176 patients, 45 samples in cohort A and 21 samples in cohort B had sufficient tumor content. No significant association was found between ABCB1 amplification and primary resistance to docetaxel (p = 0.58; odds ratio (OR) = 1.49) or cabazitaxel (p = 0.97; OR = 1.06). No significant association was found between exploratory biomarkers and primary resistance to docetaxel or cabazitaxel. In this study, ABCB1 amplification did not predict primary resistance to docetaxel or cabazitaxel for mCRPC. Future studies including ABCB1 amplification in a suite of putative biomarkers and a larger cohort may aid in drawing definitive conclusions.

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Zu, Shulu, Weiming Ma, Pan Xiao, Yazhou Cui, Tianjia Ma, Chunwen Zhou, and Huaiqiang Zhang. "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 proteomes in PC-3 cells using 2-dimensional polyacrylamide gel electrophoresis/matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. Results: Forty-nine differential proteins were found in docetaxel-resistant PC-3 cells in comparison with docetaxel-sensitive PC-3 cells. Expression in 29 proteins was upregulated, whereas expression in 20 proteins was downregulated. ATP synthase and galectin-1 were involved in the formation of tumor vessels; calreticulin, cathepsin D, and cofilin were involved in tumor metastasis, and GRP78 (78-kDa glucose-regulated protein) and microtubule-associated protein-6 were involved in drug resistance of tumor. Conclusion: It is suggested that a proteomic expression difference exists between docetaxel-sensitive and docetaxel-resistant PC-3 cells, which would be helpful for further understanding the molecular mechanisms of docetaxel resistance in PC-3 cells.

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Lima, Thiago S., Diego Iglesias-Gato, Luciano D. O. Souza, Jan Stenvang, Diego S. Lima, Martin A. Røder, Klaus Brasso, and José M. A. Moreira. "Molecular Profiling of Docetaxel-Resistant Prostate Cancer Cells Identifies Multiple Mechanisms of Therapeutic Resistance." Cancers 13, no. 6 (March 14, 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 lineage-derived androgen-independent C4-2B sub-line. We generated two docetaxel-resistant LNCaPR and C4-2BR sub-lines, with IC50 values 77- and 50-fold higher than those of the LNCaP and C4-2B parental cells, respectively. We performed gene expression analysis of the matched sub-lines and found several alterations that may confer docetaxel resistance. In addition to increased expression of ABCB1, an ATP-binding cassette (ABC) transporter, and a well-known gene associated with development of docetaxel resistance, we identified genes associated with androgen signaling, cell survival, and overexpression of ncRNAs. In conclusion, we identified multiple mechanisms that may be associated with the development of taxane drug resistance in PCa. Actioning these mechanisms could provide a potential approach to re-sensitization of docetaxel-resistant PCa cells to docetaxel treatment and thereby further add to the life-prolonging effects of this drug in men with mCRPC.

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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 (February 20, 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 disease (CRPC), other histologies, and those without metastatic disease were excluded. Demographic, clinical, treatment and outcome data were extracted retrospectively from electronic medical records. Results: 31 eligible pts with MHSPC treated with docetaxel between August 2014 and July 2016 were identified. Median age was 65 years (53-83) and 28 (90%) had high-volume disease as defined by Sweeney et al (2015). Nadir PSA levels 6-7 months from ADT initiation were < 0.2, 0.2-4, and > 4 ng/mL in 29.0%, 36.7% and 36.7%, respectively. At median follow up of 85 weeks, 45.2% of pts had progressed to CRPC and 22.6% had died. Median time to CRPC was 59 weeks and median overall survival was 85 weeks. Seven pts with high-volume disease (25%) had PSA progression while receiving docetaxel treatment. The median overall survival of this group was 26 weeks (17 to 106+) and six have died. Three had visceral metastases. Nadir PSA was < 0.2 (1 pt), 0.2-4 (2 pts) and > 4 ng/mL (4 pts). After docetaxel 2 pts received BSC alone and 5 pts had 1st-line CRPC therapy. No response to abiraterone/enzalutamide was seen (3 pts). Two pts who discontinued docetaxel immediately at PSA progression and were switched to alternative chemotherapy survived > 1 year. Conclusions: A subset of men with MHSPC has lethal docetaxel-resistant disease characterized by early PSA rise. It is important to recognize these patients, but it is not clear if standard CRPC therapies are effective. An immediate early switch to alternative chemotherapy may be helpful. Further research to predict early docetaxel resistance, characterize response to current therapies and identify more effective treatment is needed.

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Gruber, Martina, Lavinia Ferrone, Martin Puhr, Frédéric R. Santer, Tobias Furlan, Iris E. Eder, Natalie Sampson, Georg Schäfer, Florian Handle, and Zoran Culig. "p300 is upregulated by docetaxel and is a target in chemoresistant prostate cancer." Endocrine-Related Cancer 27, no. 3 (March 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 of tissue samples revealed significantly higher p300 protein expression in patients who received docetaxel as a neoadjuvant therapy compared to control patients. Elevated p300 expression was confirmed by analysis of publicly available patient data, where significantly higher p300 mRNA expression was found in tissue of mCRPC tumors of docetaxel-treated patients. Consistently, docetaxel-resistant PCa cells showed increased p300 protein expression compared to docetaxel-sensitive counterparts. Docetaxel treatment of PCa cells for 72 h resulted in elevated p300 expression. shRNA-mediated p300 knockdown did not alter colony formation efficiency in docetaxel-sensitive cells, but significantly reduced clonogenic potential of docetaxel-resistant cells. Downregulation of p300 in docetaxel-resistant cells also impaired cell migration and invasion. Taken together, we showed that p300 is upregulated by docetaxel, and our findings suggest that p300 is a possible co-target in treatment of chemoresistant PCa.

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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 (May 20, 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 damage. Preliminary results from our lab indicated PARP1 may be involved in regulating this secretory program. We hypothesized that PARP inhibition would suppress the TME-associated secretory program and thereby overcome chemotherapy resistance. Methods: Transcript profiles of cytokines and growth factors were analyzed with quantitative real-time PCR and cDNA microarrays in prostate fibroblasts after treatment with radiation or docetaxel, in combination with one of three PARP inhibitors (PARPi). We evaluated the effects of the docetaxel-induced fibroblast secretory program, in the absence or presence of PARPi, on the proliferation and drug sensitivity of prostate cancer cell lines. Results: Similar to radiation, docetaxel induced the secretion of cytokines and growth factors in prostate fibroblasts. PARP1 was activated by docetaxel treatment. Exposure to PARPi suppressed the docetaxel-induced secretory program. Further analysis suggested that PARPi abrogates activation of p38MAPK pathway. While conditioned medium from docetaxel-treated prostate fibroblasts stimulated growth and chemotherapy resistance, the addition of PARPi attenuated these effects. Conclusions: Docetaxel induces extracellular secretion of pro-tumorigenic cytokines and growth factors by components of the TME. PARP inhibitors attenuated docetaxel resistance through suppression of this secretory program, supporting a new mechanism of action for this class of drugs. Combinatorial use of cytotoxic agents and microenvironment-directed therapies may reduce treatment resistance.

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Wróbel, 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, no. 12 (October 2, 2020): 1544–56. http://dx.doi.org/10.1002/stem.3281.

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Abstract Combinations of metabolic blockers (including fenofibrate) with chemotherapeutic drugs interfere with the drug-resistance of prostate cancer cells. However, their effect on cancer stem cells-dependent microevolution of prostate cancer malignancy remains unaddressed. Here, we hypothesize that the combined docetaxel/fenofibrate treatment prompts the selective expansion of cancer stem cells that affects the microevolution of their progenies. Accordingly, we adapted a combined in vitro/in vivo approach to identify biological and therapeutic consequences of this process. Minute subpopulations of docetaxel-resistant CD133high and/or CD44high cancer stem cell-like (SCL) cells were found in prostate cancer DU145 and PC3 cell populations. When pretreated with docetaxel, they readily differentiated into docetaxel-resistant CD44negative “bulk” cells, thus accounting for the microevolution of drug-resistant cell lineages. Combined docetaxel/fenofibrate treatment induced the generation of poly(morpho)nuclear giant cells and drug-resistant CD44high SCL cells. However, the CD44negative offspring of docetaxel- and docetaxel/fenofibrate-treated SCLs remained relatively sensitive to the combined treatment, while retaining enhanced resistance to docetaxel. Long-term propagation of drug-resistant SCL-derived lineages in the absence of docetaxel/fenofibrate resulted in their reverse microevolution toward the drug-sensitivity and invasive phenotype. Consequently, prostate tumors were able to recover from the combined docetaxel/fenofibrate stress after the initial arrest of their expansion in vivo. In conclusion, we have confirmed the potential of fenofibrate for the metronomic treatment of drug-resistant prostate tumors. However, docetaxel/fenofibrate-induced selective expansion of hyper-resistant CD44high SCL prostate cells and their “bulk” progenies prompts the microevolution of prostate tumor drug-resistance. This process can limit the implementation of metabolic chemotherapy in prostate cancer treatment.

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Більше джерел

Дисертації з теми "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.

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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, response to docetaxel could be enhanced in both breast cancer cells and cDNA microarray expression analysis identified candidate genes that were re-expressed after treatment with both inhibitors, therefore being associated with docetaxel resistance. Decreased expression of one candidate gene, SERPINE1, was directly linked to docetaxel resistance whereby SERPINE1 modulation, using siRNA technology, directly altered response to docetaxel. Furthermore, miRNA expression profiling was performed in both docetaxel-sensitive and docetaxel-resistant cell lines where alterations of miRNAs were observed and associated with a docetaxel-resistant phenotype. In particular, increased expression of miR-34a was identified in docetaxel-resistant cells, which was associated with and with decreased BCL2 and cyclin D1 mRNA and protein expression in these cells. Modulation of miR-34a expression altered docetaxel response in both docetaxelsensitive and docetaxel-resistant cells, therefore identifying increased miR-34a as direct cause of docetaxel resistance in these cells. In addition, miR-34a was shown to directly target BCL2, which may present a mechanism through which miR-34a mediates docetaxel resistance. Overall, this study identified alterations in DNA methylation, histone deacetylation and miRNA expression as mechanisms through which gene expression is altered in docetaxel-resistant breast cancer cells.

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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 modifications from their parental cells. Most notable was the common region of gain of chromosome 7q and loss of chromosome 10q between the two resistant cell lines. Once modified chromosomal regions were identified, the subsequent aim of the study was to further characterise the regions and to identify candidate genes contained with in them. It was demonstrated that P-glycoprotein encoded on chromosome 7q21.1 was over expressed in the resistant cells and that this over expression contributed to the resistance. However it was discovered for the first time that, in addition to P-glycoprotein, the expression of additional genes (Hsp-27 and 14.3-3&'947;) contained on chromosome 7q, was altered. In addition, decreased expression of Bcl-2 was shown to be associated with docetaxel resistance. The identification of alteration of genomic regions and the modification of gene expression identified in this study make a significant original contribution to the understanding of the molecular events involved in docetaxel resistance.

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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 applied cells were investigated by cell viability assays. Expression analysis of P-gp, MRP1, BCRP, Bcl-2, Bax and &
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-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.

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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:stroma lactate shuttle. In the first part of this study, we highlighted a peculiar CAFs conditioning of PCa cells in terms of OXPHOS upgrading and enhancement. Indeed, we observed that CAFs induce a SIRT1/PGC-1α axis activation in PCa cells, leading to the accumulation of mitochondrial ROS and TCA cycle oncometabolites (succinate/fumarate) that are both closely related to EMT engagement and PCa invasiveness. Indeed, we found that CAFs-exacerbated mitochondrial ROS are crucial for the oxidation of critical targets (Src, PKM2) needed for the metabolic reprogramming toward OXPHOS established in CAFs-exposed PCa cells. On the other hand, succinate is able to maintain CAFs-induced HIF-1α activation and the HIF-1- dependent malignant phenotype of PCa cells. Furthermore, we intriguingly observed a mechanism of mitochondrial transfer elicited by CAFs in order to further boost OXPHOS exploitation, mitochondrial ROS generation and invasiveness of PCa cells. Among microenvironmental cues, chemotherapy resistance has been increasingly and finely associated to the metabolic reprogramming of resistant cancer cells. In the second part of this study, we metabolically characterized docetaxel-resistant PCa cells and we clearly outlined a metabolic adaptation of resistant cancer cells compared to the sensitive counterpart. Docetaxel-resistant PCa cells undergo a Warburg escape towards OXPHOS addiction in order to ensure metabolic advantages during acquisition of resistant phenotype. Together with lactate and glucose, we also found an higher glutamine mitochondrial exploitation by docetaxel-resistant cells. Furthermore, we appreciated a role of CAFs in modulating the response to drug exposure by protecting sensitive and resistant PCa cells. We found that such metabolic/resistant phenotype can be counteracted either by metformin (or other mitocans) treatment or by overexpressing miR-205, a downregulated miRNA orchestrating prostate tumor:stroma crosstalk. Taken together, all the data obtained in our study highlight the role of OXPHOS as an important shared metabolic state between chemotherapy resistance and symbiosis with microenvironment PCa cells.

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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 étudier les étapes précoces de la cancérogenèse prostatique. De plus, sa tumoroginicité et sa capacité à induire des métastases osseuses de nature mixtes ostéoblastiques et ostéolytiques font de ce modèles un outil potentiellement intéressant pour étudier les mécanismes métastatiques et rechercher de nouvelles cibles thérapeutiques. Depuis 2004, le traitement de référence des cancers de la prostate métastatiques hormono-résistants est une chimiothérapie par le Docetaxel. Cependant, malgré le bénéfice de survie obtenu, presque la moitié des patients traités par le Docetaxel développent une résistance à la chimiothérapie. Il est donc urgent d'identifier un biomarqueur prédictif pour sélectionner les patients qui vont bénéficier de cette chimiothérapie afin de contourner cette résistance. Dans le but d'étudier les mécanismes de résistance au Docetaxel dans le cancer de la prostate, nous avons établi plusieurs clones résistants au Docetaxel à partir de la lignée IGR-CaP1. Ces clones résistants nous ont permis de réaliser une analyse génomique à haut-débit par microarray comparant l'expression génique entre la lignée sensible et les clones résistants et d'identifier une signature de gènes potentiellement impliqués dans la résistance au Docetaxel. Parmi les gènes identifiés, nous nous sommes focalisés sur le gène LZTS1 sous-exprimé dans tous les clones résistants. LZTS1 est un suppresseur de tumeur qui contrôle le cycle cellulaire en interagissant avec la cycline Cdc25C. Nos résultats suggèrent que la déplétion de LZTS1 est potentiellement impliquée dans le mécanisme de résistance au Docetaxel. La finalité de notre projet est de valider nos résultats par immunohistochimie à partir des prélèvements tumoraux obtenus dans l'essai de phase III GETUG12. Nous espérons que notre étude permettra aux cliniciens de sélectionner les sous-groupes de patients susceptibles de profiter d'un traitement par Docetaxel.

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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 pressure). The consequent hypoperfusion poses important obstacles to drug delivery and nanomedicines. In fact, the tortuous tumor microvasculature has blood velocities up to one order of magnitude lower compared to healthy capillary networks. Moreover, the fast angiogenesis during tumor progression leads to high vascular density in solid tumors, large gaps exist between endothelial cells in tumor blood vessels, and tumor tissues show selective extravasation and retention of macromolecular drugs (Enhanced Permeation Retention – EPR – effect). These effects have served as a basis for the development of drug delivery systems which are aimed at enhancing tumor tissue targeting and drug therapeutic effectiveness. Over the last 15 years, a plethora of materials and different formulations have been proposed for the realization of nanomedicines. Yet, drug-loading efficiency, sequestration by phagocytic cells, and tumor accumulation of nanoparticle-loaded agents - nanomedicines - are sub-optimal. Starting from these considerations, during my PhD, I studied two complementary approaches: in the first two years my work was focused on implementing the characteristics of Discoidal Polymeric Nanoconstructs designed with controlled geometries and mechanical properties. In the last year, I investigated the role of mechanical stress on chemotherapeutic efficacy. More precisely, this work first reviews the use of deformable discoidal nanoconstructs (DPNs) as a novel delivery strategy for therapeutic and imaging agents. Inspired by blood cell behavior, these nanoconstructs are designed to efficiently navigate the circulatory system, minimize sequestration by phagocytic cells, and recognize the tortuous angiogenic microvasculature of neoplastic masses. In this work, the synthesis, drug loading and release, and physico-chemical characterization of DPNs were enhanced with particular emphasis on the ability to independently control size, shape, surface properties, and mechanical stiffness. Two different loading strategies were tested, namely the straightforward “direct loading” and the “absorbance loading”. In the former case, the agent was directly mixed with the polymeric paste to realize DPNs whereas, in the latter case, DPNs were first lyophilized and then rehydrated upon exposure to a concentrated aqueous solution of the agent. Under these two loading conditions, the encapsulation efficiencies and release profiles of three different molecules and their corresponding prodrugs were systematically assessed (1,2-Distearoyl-sn-glycero-3-phosphorylethanolamine lipid chains or 1 kDa PEG chains were directly conjugated with Cy5.5 or methotrexate and Doxorubicin). Moderately hydrophobic compounds with low molecular weight showed encapsulation efficiencies of 80%, with absorption loading (direct loading has efficiencies around 1%). The DOX-DPN showed on triple negative breast cancer cells a toxicity comparable to free DOX. Preliminary in vivo preliminary studies conducted with directly loaded Cy5-DPN demonstrated a fairly solid integration of the imaging compound with the polymer matrix of the particles. The second part of the work dissect what happens to free drugs or to drugs carried by nanovectors once they reach the tumor site. As we mention above, the elevated mechanical stress derived from tumor progression could result in blood vessels clamping with consequent reduction of drug efficacy. It is quite obvious to imagine that if the drug fails to reach the tumor it cannot act on it. Indeed, mechanical stress within the tumor site is present from the early stages of the disease. Our goal was to understand what happens when mechanical stress is not yet so large enough to fully collapse the blood vessels. Are there mechanical alterations that can affect the efficacy of a chemotherapeutic? We studied how mechanical perturbations of the tumor microenvironment could contribute to the mechanical-form of Gemcitabine drug resistance. Specifically, we developed a new in vitro strategy to mimic the mechanical compression stress induced by the stroma during tumor progression. We embedded pancreatic tumor spheroids into agarose polymeric matrix in order to demonstrate the effect of mechanical compressive stress on tumor proliferation. Then, we validated our results with other types of mechanical stresses. Finally, we investigated the therapeutic efficacy of a proliferation-based chemotherapy: Gemcitabine. Collectively, having the physical cues of cancer in mind, it can be important to cross-fertilize the fields of physical oncology and nanomedicine.

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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 étude montre que VDR réduit la prolifération des PECs dans un modèle murin de CaP, les souris Pten(i)pe-/-, via modération du stress oxydant. De plus, le VDR dans les PECs réduit le recrutement des neutrophiles, qui sont une cible thérapeutique pour la dissémination du CaP. Par ailleurs, la combinaison d'un agoniste de VDR avec le docétaxel réduit efficacement les volumes tumoraux du CaP chimiorésistant. Pour conclure, ce travail met en évidence comment la vitamine D ralentit la progression du CaP et suggère de nouvelles stratégies thérapeutiques pour cette maladie
Prostate 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

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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
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.

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Частини книг з теми "Docetaxel resistance"

Narita, Shintaro, and 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.

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Matsuyama, Hideyasu, Tomoyuki Shimabukuro, Isao Hara, Kazuhiro Suzuki, Hirotsugu Uemura, Munehisa Ueno, Yoshihiko Tomita, and 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.

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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, 77–92. Cham: 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, 79–88. Istanbul: 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, prolonging overall and radiographic progression-free survival. ENZ’s favorable outcomes in combination therapies highlight its role in advancing prostate cancer treatment paradigms.

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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, 199–215. Cham: 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 (PD-L1, from high to low). In addition, there are two categorical variables including disease site (e.g., locoregional recurrence versus metastatic) and platinum-sensitivity or resistance depending on disease-free interval after previous platinum-based therapy with a usual cut-off of 6 months. Taking into account these six factors and local drug policies, healthcare professionals opt either for 1) chemotherapy with or without cetuximab or 2) immunotherapy with or without chemotherapy. In platinum-sensitive cases, level I evidence based on data from the EXTREME and Keynote-048 randomized trials supports the use of the following three regimens. Biochemotherapy combining platinum, 5-fluorouracil, and cetuximab (the so-called EXTREME regimen) is suitable for fit patients with low PD-L1 expression measured as combined positive score (CPS). Higher CPS is predictive for improved overall survival when replacing cetuximab with the immune checkpoint inhibitor pembrolizumab, an anti-PD-1 antibody (immunochemotherapy regimen). Further, Keynote-048 demonstrated activity of single-agent pembrolizumab in patients with high CPS values. The latter (third) treatment retained its efficacy in the elderly, suggesting possible advantage in less fit patients who otherwise receive best supportive care only or single-agent cytotoxic chemotherapy with dubious impact on survival. In selected patients, the TPEx regimen consisting of cisplatin, docetaxel, and cetuximab represents an alternative to EXTREME. Treatment choice can also be influenced by disease extension (site). Compared with disseminated cancer cases, presence of locoregional recurrence without distant metastases may have a negative predictive value for immune checkpoint inhibitors, while favouring biochemotherapy. If the tumour is deemed platinum-resistant, the only evidence-based systemic approach is monotherapy with either pembrolizumab or nivolumab, another anti-PD-1 antibody. Alternatively, being especially pertinent to resource-limited countries, a taxane with or without cetuximab can be prioritized. Obviously, the list of different treatment schedules is longer, but the level of supporting evidence is proportionally lower. One of modern approaches to multidisciplinary management of SCCHN patients is treatment sequencing. It should be understood as a deliberate process of treatment planning typically starting in the locally advanced setting and reaching beyond several treatment failures. This has been enabled by a growing portfolio of effective anticancer modalities complemented by progress in supportive care. Finally, all therapeutic interventions impact somehow on quality of life, either in a positive or negative way, and the choice of anticancer agents should therefore not be reduced to a simple estimate of survival benefit but should contain an adequate appraisal and understanding of individual patient’s situation comprising emotional and spiritual dimensions, cultural and financial aspects, and environmental, social, and educational contexts.

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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, 181–85. Cham: 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 (NAAD) used after chemotherapy are androgen biosynthesis inhibitor abiraterone acetate (combined with prednisolone), the androgen receptor blockers enzalutamide as well as the newer generation apalutamide and darolutamide. However, these treatment regimens only provide a meager survival benefit in mCRPC. Radium-223 targets only the osteoblastic metastases and does not treat nodal or visceral metastases. Therefore, there has been an unmet need for targeted therapy.

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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, 255–65. Cham: 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. Ligands that bind to PSMA expressed on prostate cancer cells have been labeled to radionuclides for imaging and therapy in a theranostic approach to prostate cancer management. Actinium-225 (225Ac) is an alpha-emitting radionuclide that has been successfully labeled to PSMA ligands as 225Ac-PSMA for targeted alpha therapy (TAT) of mCRPC. The short path length of the highly energetic alpha particles causes deposition of massive energy in the tumor, leading to irreparable double-strand DNA damage, and consequently, tumor cell death while sparing surrounding normal tissues. When applied as a last-line therapy agent, 225Ac-PSMA therapy effectiveness is comparable or better than agents applied earlier in the treatment sequence of mCRPC. 225Ac-PSMA produces the most remarkable response in the chemotherapy-naïve setting, causing a high and sustained response in men with mCRPC. Xerostomia, a result of 225Ac-PSMA irradiation of the salivary gland parenchyma resulting from its intense accumulation in the glands, is the most worrisome complication of therapy. Different interventions, including dynamic dose de-escalation, combination therapy, and reduced administered activity, are being explored to ameliorate this adverse effect of treatment.

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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 could also exert adverse effects including cardiotoxicity, complicating the development of such therapies for PAH patients who already have the damaged heart. We tested the concept that programmed cell death-inducing anti-cancer drugs may reduce the PA wall thickening using rat models of PAH. We found that: (i) The treatment of PAH animals with anthracycline-, proteasome inhibitor- or Bcl-2 inhibitor-classes of anti-cancer drugs after the pulmonary vascular remodeling had already developed resulted in the reversal of PA wall thickening and opened up the lumen; (ii) These effects were accompanied by the apoptosis of PA wall cells in PAH rats, but not in normal healthy rats, suggesting the anti-cancer drugs selectively kill remodeled vascular cells; (iii) The RV affected by PAH was not further damaged by anthracyclines or proteasome inhibitors; (iv) While the left ventricle (LV) was damaged by these drugs, we identified cardioprotective agents that protect the heart against drug-induced cell death without affecting the efficacy to reverse the PA remodeling; and (v) docetaxel, not only reversed pulmonary vascular remodeling without exerting RV or LV toxicity, but also repaired the RV damage caused by PAH. Thus, the inclusion of programmed cell death-inducing anti-cancer drugs should be considered for treating PAH patients.

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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, 139–64. 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 effective against several cancer types. The development of a new drug is a highly complex, expensive, and time-consuming endeavour. In the traditional drug discovery process, ending with a new medicine ready for the market can take up to 15 years and cost more than one billion dollars. Fortunately, this situation has changed with the arrival of novel approaches recently. Many new technologies and methodologies have been developed to increase the efficiency of the drug discovery process, and computational methodologies utilise the existing data to generate knowledge that affords valuable understanding for addressing current complications and guiding the further research and development of new naturally derived drugs. Consequently, the application of in silico techniques and optimization algorithms in drug discovery ventures can provide versatile solutions to understand the molecular-level interactions of chemical constituents and identify the hits. Lead optimization techniques such as ligand-based or structure-based drug design are widely used in many discovery efforts. In this chapter, we first introduce the concepts of CADD, in silico tools, etc. we then describe how this virtual screening has been successfully applied. Furthermore, we review the concept of natural product anticancer therapies and present some of the most representative examples of molecules identified through this method.

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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, scholastic and intellectual factors do not, intrinsically seem to straight away influence the risk of acquiring PC. Other genetic changes that may support an increased risk of developing PC include HPC1, HPC2, HPCX, CAPB, ATM,s HOXB13 and mismatch repair genes. PC occurrence rates are highly variable. Almost all PC mortalities are due to metastatic disease, generally through tumors the progress to be hormone refractory or castrate resistant. PC, developing research has acknowledged a number of candidate genes and biological pathways associated with PC. Indirect pathways such as P13K/AKT signaling pathway is one of most well known alternate pathway in PC Vascular endothelial growth factor (VEGF) is widely known to be potent stimulator of angiogenesis. The over expression of EGFR in a very large majority of cases is accompanied by the succession of PC, implying that this may play a mechanistic role. Numerous occupational factors have been proposed to cause PC. Some of the risk factors include; farmers/agricultural workers, pesticides, shift work and flight personnel. PC treatment can be done through surgery, radical prostatectomy is the main type of surgery. Risks of injury are many – reactions to anesthesia, loss of blood, blood clumps in the legs/lungs, injury to surrounding organs, infection at the site of surgery and many more. The other treatments are hormone therapy, chemotherapy and radio therapy chemotherapy. Chemotherapeutic drugs are typically used one at a time for PC such as transurethral resection of prostate (TURP). Some of the chemotherapeutic drugs are Docetaxel, Cabazitaxel, Mitoxantrone and Estramustine. Among the score of biomarkers being studied, numerous markers and techniques deserve awareness and acceptability for both patients and urologists in clinical practice.

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Тези доповідей конференцій з теми "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.

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Nagesh, Prashanth K. B., Pallabita Chowdhury, Elham Hatami, Vivek K. Kashyap, Bilal B. Hafeez, Sheema Khan, Subhash C. Chauhan, Meena Jaggi, and 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.

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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, Frederic Commo, Shanna Rajpar, Sandra Lejuste, Nicolas Martin, Karim Fizazi, and 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.

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Lichtenfels, Martina, Vivian Fontana, Francine Hickmann Nyland, Bianca Silva Marques, Mário Casales Schorr, Júlia Caroline Marcolin, Caroline Brunetto de Farias, and 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.

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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 evaluated. The test result is defined based on cell viability as low (60%) resistance. Results: Samples from 20 patients with residual disease after NACT were tested in the chemoresistance platform. Regarding molecular subtypes: 9 tumors were triple-negative (45%), 6 luminal (30%), 4 LuminalHER2 (20%), and 1 HER2 (5%). A total of 16 (80%) patients responded partially to NACT, and 4 (20%) presented disease progression. Most (80%) of the patients used ACT (doxorubicin + cyclophosphamide + paclitaxel) chemotherapy regimen, 10% only paclitaxel, and 10% doxorubicin plus cyclophosphamide. The chemoresistance platform demonstrated that tumors treated with doxorubicin, paclitaxel, and cyclophosphamide in neoadjuvant setting presented high rates of resistance to the drugs (94.7% showed high resistance to paclitaxel, 58% to doxorubicin, and 52.6% to cyclophosphamide). In addition, we investigate if the tumor becomes more resistant to drugs from the same class (taxanes and adriamycin) of the treatment already used by the patients and evidenced 93.7% of high resistance to docetaxel and 50% to epirubicin. Conclusion: This preliminary finding highlighted the efficacy of the in vitro chemoresistance platform to demonstrate the acquisition of resistance during NACT and suggested a role of acquired resistance in the worse prognosis of patients with residual disease after NACT.

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Duran, 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.

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Shimomura, Tatsuya, Evelyn Kono, Chau P. Tran, Joyce Yamashiro, Shu Lin, Sean Hyung-Kwon Lee, Zev A. Wainberg, and 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.

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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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Watanabe, 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.

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Звіти організацій з теми "Docetaxel resistance"

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

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Singh, Ajay. Exploring a Novel Mechanism of Docetaxel Resistance in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 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, March 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, April 2020. http://dx.doi.org/10.37766/inplasy2020.4.0076.

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