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Artykuły w czasopismach na temat „Docetaxel resistance”

Autor: Grafiati

Data publikacji: 2 listopada 2024

Data aktualizacji: 31 lipca 2025

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1

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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2

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Wróbel, Tomasz, Marcin Luty, Jessica Catapano, et al. "CD44+ cells determine fenofibrate-induced microevolution of drug-resistance in prostate cancer cell populations." Stem Cells 38, no. 12 (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 subpopulati

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12

Liu, Rong-Zong, Mansi Garg, Xiao-Hong Yang, and Roseline Godbout. "Docetaxel-Induced Cell Death Is Regulated by a Fatty Acid-Binding Protein 12-Slug-Survivin Pathway in Prostate Cancer Cells." International Journal of Molecular Sciences 25, no. 17 (2024): 9669. http://dx.doi.org/10.3390/ijms25179669.

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Chemotherapy is an important treatment option for advanced prostate cancer, especially for metastatic prostate cancer (PCa). Resistance to first-line chemotherapeutic drugs such as docetaxel often accompanies prostate cancer progression. Attempts to overcome resistance to docetaxel by combining docetaxel with other biological agents have been mostly unsuccessful. A better understanding of the mechanisms underlying docetaxel resistance may provide new avenues for the treatment of advanced PCa. We have previously found that the fatty acid-binding protein 12 (FABP12)-PPARγ pathway modulates lipid

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13

Gjyrezi, Ada, Fang Xie, Daniel E. Fein, et al. "Abstract 3081: The multiciliated transcription factor FOXJ1 modulates microtubule dynamics and mediates taxane resistance in prostate cancer." Cancer Research 85, no. 8_Supplement_1 (2025): 3081. https://doi.org/10.1158/1538-7445.am2025-3081.

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Abstract Docetaxel is the first-line chemotherapy for metastatic castration-resistant prostate cancer, but clinically meaningful mechanisms of resistance remain to be established. We generated an in vivo model of docetaxel resistance using castration-resistant patient-derived xenografts and found increased expression of genes that drive development of multiciliated cells, including FOXJ1 and its effector genes, many of which regulate ciliary microtubules. Mechanistically, FOXJ1 overexpression conferred docetaxel resistance in vitro and in vivo, which was associated with decreased docetaxel-med

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14

Shimizu, Yasuomi, Satoshi Tamada, Minoru Kato, et al. "Androgen Receptor Splice Variant 7 Drives the Growth of Castration Resistant Prostate Cancer without Being Involved in the Efficacy of Taxane Chemotherapy." Journal of Clinical Medicine 7, no. 11 (2018): 444. http://dx.doi.org/10.3390/jcm7110444.

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Expression of androgen receptor (AR) splice variant 7 (AR-V7) has been identified as the mechanism associated with the development of castration-resistant prostate cancer (CRPC). However, a potential link between AR-V7 expression and resistance to taxanes, such as docetaxel or cabazitaxel, has not been unequivocally demonstrated. To address this, we used LNCaP95-DR cells, which express AR-V7 and exhibit resistance to enzalutamide and docetaxel. Interestingly, LNCaP95-DR cells showed cross-resistance to cabazitaxel. Furthermore, these cells had increased levels of P-glycoprotein (P-gp) and thei

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15

Liu, Xiao Dong, Yi Ju Hou, Lin Zhang, and Hui Ling Cao. "Compound Injection of Shenqi as a Reversal Drug on Docetaxel Resistant Human Lung Adenocarcinoma Cell A549/DTX." Advanced Materials Research 926-930 (May 2014): 1054–57. http://dx.doi.org/10.4028/www.scientific.net/amr.926-930.1054.

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To investigate the effect and the mechanism of compound injection of Shenqi (Codonopsis and Astragalus) on Docetaxel resistance of human lung adenocarcinoma cell A549/ DTX. The cytotoxicities of Shenqi Injection were assayed with the MTT method, the effects of Shenqi Injection on apoptosis induced by Docetaxel in A549/ DTX was examined by flow cytometry (FCM). The expression levels of apoptosis regulator Bc1-2 and Bax were detected by Western blot. After treatment with Shenqi Injection for 24 hours, results showed that 15 μL / mL Shenqi Injection significantly increased toxicity of Docetaxel o

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16

Song, Liankun, Vyvyan Nguyen, Jun Xie, et al. "Abstract 1687: ATPase copper transporting beta (ATP7B) contributes to acquired docetaxel resistance in human prostate cancer." Cancer Research 83, no. 7_Supplement (2023): 1687. http://dx.doi.org/10.1158/1538-7445.am2023-1687.

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Abstract Docetaxel has been the standard first-line chemotherapy for lethal metastatic prostate cancer (mPCa) since 2004, but the resistance to docetaxel treatment is common. The molecular mechanisms of docetaxel resistance remain largely unknown and could be amenable to interventions that mitigate resistance. We have recently discovered that several docetaxel resistant mPCa cell lines exhibit less uptake of cellular copper and express markedly higher levels of ATP7B protein without significant changes in the protein expression levels of other copper transporters, such as ATPase copper transpo

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17

Yin, Beibei, Ping Lu, Jing Liang, et al. "The ABCB1 3435C > T polymorphism influences docetaxel transportation in ovarian cancer." Journal of International Medical Research 47, no. 10 (2019): 5256–69. http://dx.doi.org/10.1177/0300060519870354.

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Objective To investigate the effect of the ATP-binding cassette transporter superfamily B member 1 gene ( ABCB1) 3435C > T single nucleotide polymorphism (SNP) on docetaxel transportation in ovarian cancer cells. Methods ES-2 and SKOV3 cells were transfected with an ABCB1 3435C > T recombinant plasmid, and mRNA expression was detected by real-time PCR. The MTT assay was used to detect the toxicity of docetaxel. High-performance liquid chromatography determined the drug concentration in different cell models to evaluate intracellular accumulation, and a transmembrane resistance experiment

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Guo, Yanxia, Shikang Wang, Qun Liu, Yan Dong, and Yongqing Liu. "St-N, a novel alkaline derivative of stevioside, reverses docetaxel resistance by targeting lysosomes in vitro and in vivo." PLOS ONE 19, no. 12 (2024): e0316268. https://doi.org/10.1371/journal.pone.0316268.

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Drug resistance of cancers remains a major obstacle due to limited therapeutics. Lysosome targeting is an effective method for overcoming drug resistance in cancer cells. St-N (ent-13-hydroxy-15-kaurene-19-acid N-methylpiperazine ethyl ester) is a novel alkaline stevioside derivative with an amine group. In this study, we found that docetaxel (Doc)-resistant prostate cancer (PCa) cells were sensitive to St-N. Mechanistically, the alkaline characteristic of St-N led to targeting lysosomes, as evidenced by lysosomal swelling and rupture through transmission electron microscopy and Lyso-tracker R

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Riedel, R. F., A. Porrello, E. Chenette, A. Potti, J. R. Nevins, and P. G. Febbo. "A genomic approach to identify mechanisms associated with chemotherapy resistance." Journal of Clinical Oncology 25, no. 18_suppl (2007): 2534. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.2534.

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2534 Background: Gene expression profiling has shown an ability to predict chemotherapeutic response (Potti et al. Nature Medicine 2006). Building on this work, we used a genomic strategy to explore the biology associated with the development of chemotherapy resistance and sought to determine if disease context impacted results. Methods: Gene set enrichment analysis (GSEA) was performed on expression data for NCI60 cell lines sensitive and resistant to specific chemotherapeutic agents (adriamycin, cyclophosphamide, docetaxel, etoposide, 5-fluoruracil, paclitaxel, topotecan). GSEA was additiona

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AHMEDLİ, Dilay, Zehra GÜMÜŞ, Rana YETKİN, Gonca KABAK, and Yavuz SİLİĞ. "The Effect of Combined Treatment with Mentha longifolia L. and Docetaxel on Drug Resistance in Colon Cancer." MAS Journal of Applied Sciences 9, no. 2 (2024): 459–65. https://doi.org/10.5281/zenodo.12167759.

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This study investigates the effects of <em>Mentha longifolia</em> L. and the chemotherapeutic drug docetaxel on drug resistance in colon cancer. One of the major challenges in colon cancer treatment is the resistance of cancer cells to chemotherapy drugs. The primary mechanism of this resistance involves the overexpression of multi-drug resistance (MDR/ABCB1) genes. MDR<em> </em>genes reduce the intracellular accumulation of chemotherapeutic agents in cancer cells. The study examined the effects of <em>Mentha longifolia</em> L. extract and docetaxel on ABCB1 gene expression in the HT-29 colon

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Ando, Masashi, Toru Watanabe, Kazuhiro Nagata, Masaru Narabayashi, Isamu Adachi, and Noriyuki Katsumata. "Efficacy of Docetaxel 60 mg/m2 in Patients With Metastatic Breast Cancer According to the Status of Anthracycline Resistance." Journal of Clinical Oncology 19, no. 2 (2001): 336–42. http://dx.doi.org/10.1200/jco.2001.19.2.336.

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PURPOSE: To evaluate the efficacy of docetaxel 60 mg/m2 in metastatic breast cancer (MBC) according to the status of anthracycline resistance. PATIENTS AND METHODS: Ninety-nine patients with anthracycline-resistant MBC were treated with docetaxel 60 mg/m2 intravenously for a 90-minute period every 3 to 4 weeks. Anthracycline resistance was defined as primary and secondary resistance. Primary resistance was defined as progression during or within 6 months after completion of adjuvant anthracycline, and no MBC response to a first-line regimen that contained anthracycline. Secondary resistance wa

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Şumnulu, Deniz, and Zeynep Doğanlar. "Aba enhances the apoptotic effect of docetaxel in the multidrug-resistant DU145 prostate cancer cell line." Archives of Biological Sciences, no. 00 (2024): 31. http://dx.doi.org/10.2298/abs240812031s.

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This study aimed to induce drug resistance in DU145 prostate cancer cells by exposing them to docetaxel and mitoxantrone, and to examine the effects of combining docetaxel and abscisic acid (ABA). The IC50 values for docetaxel and mitoxantrone in non-resistant cells were 54.57 nM and 6.25 nM, respectively, rising to 808.53 nM and 50.07 nM after resistance had developed. RT-PCR analysis showed that treatment of resistant cells with 50.07 nM docetaxel and 500 ?M ABA (ABA) resulted in the following changes in gene expression: heat shock protein (HSP) 70 (0.63-fold), glucose-regulated protein 94 (

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Shimizu, Yasuomi, Minoru Kato, Yuji Takeyama, et al. "The effect of androgen receptor splice variant 7 on the growth of castration-resistant prostate cancer and the efficacy of taxane chemotherapy." Journal of Clinical Oncology 37, no. 7_suppl (2019): 302. http://dx.doi.org/10.1200/jco.2019.37.7_suppl.302.

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302 Background: Expression of androgen receptor (AR) splice variant 7 (AR-V7) has been identified as a mechanism associated with the development of castration-resistant prostate cancer (CRPC), but a potential link between AR-V7 expression and resistance to taxanes, such as docetaxel or cabazitaxel, has not been unequivocally demonstrated. We clarify the relationship between AR-V7 expression and resistance to taxanes. Furthermore, we assess the inhibitory effect of EPI-002, an antagonist of AR amino-terminal domain (NTD), to an AR-V7 driven CRPC cell line with acquired resistance to docetaxel.

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Byun, Woong Sub, Eun Seo Bae, Jinsheng Cui, Hyen Joo Park, Dong-Chan Oh, and Sang Kook Lee. "Antitumor Activity of Pulvomycin via Targeting Activated-STAT3 Signaling in Docetaxel-Resistant Triple-Negative Breast Cancer Cells." Biomedicines 9, no. 4 (2021): 436. http://dx.doi.org/10.3390/biomedicines9040436.

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Although docetaxel-based regimens are common and effective for early-stage triple-negative breast cancer (TNBC) treatment, acquired drug resistance frequently occurs. Therefore, a novel therapeutic strategy for docetaxel-resistant TNBC is urgently required. Signal transducer and activator of transcription 3 (STAT3) plays a pivotal role in the tumorigenesis and metastasis of numerous cancers, and STAT3 signaling is aberrantly activated in TNBC cells. In this study, a docetaxel-resistant TNBC cell line (MDA-MB-231-DTR) was established, and mechanisms for the antitumor activity of pulvomycin, a n

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Schaaf, Zachary A., Shu Ning, Amy R. Leslie, et al. "Therapeutic Resistance Models and Treatment Sequencing in Advanced Prostate Cancer." Cancers 15, no. 21 (2023): 5273. http://dx.doi.org/10.3390/cancers15215273.

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Current common treatments for castration-resistant prostate cancer (CRPC) typically belong to one of three major categories: next-generation anti-androgen therapies (NGAT) including enzalutamide, abiraterone acetate, apalutamide, and darolutamide; taxane therapy represented by docetaxel; and PARP inhibitors (PARPi) like olaparib. Although these treatments have shown efficacy and have improved outcomes for many patients, some do not survive due to the emergence of therapeutic resistance. The clinical landscape is further complicated by limited knowledge about how the sequence of treatments impa

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Lohiya, Vipin, Jeanny B. Aragon-Ching, and Guru Sonpavde. "Role of Chemotherapy and Mechanisms of Resistance to Chemotherapy in Metastatic Castration-Resistant Prostate Cancer." Clinical Medicine Insights: Oncology 10s1 (January 2016): CMO.S34535. http://dx.doi.org/10.4137/cmo.s34535.

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Chemotherapy using the taxanes, docetaxel and cabazitaxel, remains an important therapeutic option in metastatic castration-resistant prostate cancer (CRPC). However, despite the survival benefits afforded by these agents, the survival increments are modest and resistance occurs universally. Efforts to overcome resistance to docetaxel by combining with biologic agents have heretofore been unsuccessful. Indeed, resistance to these taxanes is also associated with cross-resistance to the antiandrogen drugs, abiraterone and enzalutamide. Here, we discuss the various mechanisms of resistance to che

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Sanchez, Bertha E., Nilesh Gupta, Meredith Mahan, Evelyn R. Barrack, Prem-veer Reddy та Clara Hwang. "βIII-tubulin expression as a predictor of docetaxel resistance in metastatic castrate-resistant prostate cancer." Journal of Clinical Oncology 30, № 15_suppl (2012): e15174-e15174. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e15174.

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e15174 Background: Docetaxel is a tubulin-targeting cytotoxic that remains first-line therapy in metastatic castrate-resistant prostate cancer (mCRPC) patients (pts) even though half of pts are reported to be non-responders. A predictive marker to identify those who will benefit from docetaxel-therapy will assist clinical decision making. High βIII-tubulin (TUBB3) expression has previously been reported to correlate with lack of response to taxanes in other cancers. We evaluated TUBB3 expression as a predictor of docetaxel-resistance in mCRPC. Methods: mCRPC pts treated with at least 3 cycles

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Mu, Chao-Feng, Fude Cui, Yong-Mei Yin, Hyun-Jong Cho, and Dae-Duk Kim. "Docetaxel-Loaded Chitosan-Cholesterol Conjugate-Based Self-Assembled Nanoparticles for Overcoming Multidrug Resistance in Cancer Cells." Pharmaceutics 12, no. 9 (2020): 783. http://dx.doi.org/10.3390/pharmaceutics12090783.

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Cholesteryl hemisuccinate (CHS)-conjugated chitosan (CS)-based self-assembled nanoparticles (NPs) were developed for enhancing the intracellular uptake of docetaxel in multidrug resistance (MDR)-acquired cancer cells. CHS-CS was successfully synthesized and self-aggregation, particle size, zeta potential, drug entrapment efficiency, and in vitro drug release of docetaxel-loaded CHS-CS NPs were tested. The optimized NPs had a mean hydrodynamic diameter of 303 nm, positive zeta potential of 21.3 mV, and spherical shape. The in vitro release of docetaxel from the optimized CHS-CS NPs in different

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Qian, Jiang, Sheliang Shen, Wei Chen та Nianping Chen. "Propofol Reversed Hypoxia-Induced Docetaxel Resistance in Prostate Cancer Cells by Preventing Epithelial–Mesenchymal Transition by Inhibiting Hypoxia-Inducible Factor 1α". BioMed Research International 2018 (2018): 1–9. http://dx.doi.org/10.1155/2018/4174232.

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Prostate cancer is the second most frequently diagnosed cancer worldwide. Hypoxia-induced epithelial–mesenchymal transition (EMT), driven by hypoxia-inducible factor 1α (HIF-1α), is involved in cancer progression and metastasis. The present study was designed to explore the role of propofol in hypoxia-induced resistance of prostate cancer cells to docetaxel. We used the Cell Counting Kit-8 and 5-ethynyl-2′-deoxyuridine incorporation assay to measure cell viability and cell proliferation, respectively, in prostate cancer cell lines. Then, we detected HIF-1α, E-cadherin, and vimentin expression

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Ando, Takayuki, Ayumu Hosokawa, Kohei Ogawa, et al. "Efficacy of weekly paclitaxel in patients with advanced gastric cancer with prior docetaxel-containing chemotherapy." Journal of Clinical Oncology 30, no. 4_suppl (2012): 127. http://dx.doi.org/10.1200/jco.2012.30.4_suppl.127.

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127 Background: Efficacy of paclitaxel for docetaxel-refractory gastric cancer is not known, although partial cross-resistance between docetaxel and paclitaxel has been demonstrated in breast and ovary cancers. Therefore, we retrospectively evaluated the efficacy of paclitaxel in gastric cancer patients who had been refractory to docetaxel-containing chemotherapy. Methods: The patients who had received docetaxel-containing regimen were categorized as prior-docetaxel group, and the patients who had never received docetaxel were categorized as non-docetaxel group. Paclitaxel at 80 mg/m2 was admi

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Postigo-Corrales, Fátima, Asunción Beltrán-Videla, Antonio David Lázaro-Sánchez, et al. "Docetaxel Resistance in Breast Cancer: Current Insights and Future Directions." International Journal of Molecular Sciences 26, no. 15 (2025): 7119. https://doi.org/10.3390/ijms26157119.

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Docetaxel is a chemotherapeutic agent widely used for breast cancer treatment; however, its efficacy is often limited by drug resistance and associated toxicity. This review examines the molecular mechanisms of docetaxel resistance in breast cancer and discusses research advances and future directions for overcoming this challenge. Key resistance mechanisms include alterations in drug targets (microtubules), increased drug efflux, suppression of apoptosis, activation of survival signalling pathways, epithelial-to-mesenchymal transition (EMT), and cancer stem cell enrichment. An evolutionary pe

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Bowers, Laura, Aneesha Kulkarni, and Stephen Hursting. "Obesity-Associated Leptin Signaling Promotes Chemotherapy Resistance in Basal-Like Breast Cancer: The Role of Tumor-Associated Macrophages." Current Developments in Nutrition 4, Supplement_2 (2020): 311. http://dx.doi.org/10.1093/cdn/nzaa044_010.

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Abstract Objectives Obesity is associated with a reduced response to cytotoxic chemotherapies. Given that the adipokine leptin has been shown to promote macrophage production of pro-tumor cytokines, we hypothesized that leptin-induced pro-tumor macrophage polarization is a key mediator of obesity-associated docetaxel resistance. Methods Wild-type C57BL/6 mice were fed a low-fat control (10% kcal from fat) or high-fat diet-induced obesity (DIO; 60% kcal from fat) diet for 15 weeks, then orthotopically injected with 2 mouse mammary tumor cell lines: EWnt-S (scrambled shRNA) and EWnt-L (shRNA to

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&NA;. "Aberdeen researchers develop probe for docetaxel resistance." Oncology Times UK 4, no. 11 (2007): 7. http://dx.doi.org/10.1097/01434893-200711000-00007.

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Fenner, Annette. "Antiandrogens reverse docetaxel resistance via ABCB1 inhibition." Nature Reviews Urology 12, no. 7 (2015): 361. http://dx.doi.org/10.1038/nrurol.2015.135.

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Miyazawa, Yoshiyuki, Nobuaki Shimizu, Yutaka Takezawa, et al. "Exploratory study of prognostic factors in mCRPC patients who administered enzalutamide focusing on early PSA decline and PSA kinetics at PSA progression: Results of retrospective multicenter study." Journal of Clinical Oncology 37, no. 7_suppl (2019): 292. http://dx.doi.org/10.1200/jco.2019.37.7_suppl.292.

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292 Background: Recent studies have shown that an early PSA response to AR-targeting agents in mCRPC is associated with a better prognosis. We analyzed the early PSA response to enzalutamide (ENZ) by measuring the PSA doubling time (PSADT) and PSA Velocity while monitoring oncologic outcomes and survival in Japanese patients. Methods: A total of 241 patients with mCRPC treated with ENZ were analyzed. Patients’ median age is 75±7.9 (range 53-93). The patients pre-docetaxel settings were 171 cases (71 %), post-docetaxel settings were 70 cases (29 %). The PSA-PFS and OS were assessed according to

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Komura, Kazumasa, Seong Ho Jeong, Kunihiko Hinohara, et al. "Resistance to docetaxel in prostate cancer is associated with androgen receptor activation and loss of KDM5D expression." Proceedings of the National Academy of Sciences 113, no. 22 (2016): 6259–64. http://dx.doi.org/10.1073/pnas.1600420113.

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The androgen receptor (AR) plays an essential role in prostate cancer, and suppression of its signaling with androgen deprivation therapy (ADT) has been the mainstay of treatment for metastatic hormone-sensitive prostate cancer for more than 70 y. Chemotherapy has been reserved for metastatic castration-resistant prostate cancer (mCRPC). The Eastern Cooperative Oncology Group-led trial E3805: ChemoHormonal Therapy Versus Androgen Ablation Randomized Trial for Extensive Disease in Prostate Cancer (CHAARTED) showed that the addition of docetaxel to ADT prolonged overall survival compared with AD

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Halder, Sushanta, Sakthivel Muniyan, Ramakanth Chirravuri-Venkata, et al. "Abstract 1756: Targeting LIFR/c-Myc Axis to Overcome Docetaxel Resistance in Prostate Cancer." Cancer Research 83, no. 7_Supplement (2023): 1756. http://dx.doi.org/10.1158/1538-7445.am2023-1756.

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Abstract Background: Docetaxel has been the most effective chemotherapeutic option after the emergence of Castration-resistant prostate cancer (CRPC). However, more than 50% of patients develop Docetaxel Resistance (DoceR) within three years of treatment. It also shows severe adverse effects that lead to dose reduction and treatment failure. Thus, targeting the underlying mechanism of DoceR could improve survival benefits for CRPC patients. In this study, we identified leukemia inhibitory factor receptor (LIFR) as a candidate for DoceR. We targeted it with EC914, a first-in-class oral small mo

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Ding, Adeline B., Erika Heninger, Shannon R. Reese, et al. "Abstract 635: Osteoclasts mediate chemotherapy resistance in a fully humanized microphysiologic system of prostate cancer bone metastases." Cancer Research 84, no. 6_Supplement (2024): 635. http://dx.doi.org/10.1158/1538-7445.am2024-635.

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Abstract Bone metastases (BM) are the most common sites of metastases in prostate cancer, occurring in ~85% of patients. Overall survival of men with castrate resistant prostate cancer with BM is less than 24 months. Docetaxel is the most commonly used therapy for patients with prostate cancer, but the response rate is only 30-40% and median duration of response is less than 9 months. Non-tumor components of the Tumor Microenvironment (TME) have been proposed to mediate treatment resistance, but few pre-clinical models capture the complex physiology of the human bone TME. We report the develop

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Glynn, Sharon A., Aidan Toner, Joe Lewis, et al. "Prostate cancer inhibitory activity of a novel dual inhibitor, EL102, in combination with docetaxel, and its effects on MDR1-mediated drug resistance in vitro." Journal of Clinical Oncology 30, no. 15_suppl (2012): e15126-e15126. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e15126.

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e15126 Background: EL102 is a dual-action drug promoting apoptosis and inhibiting angiogenesis. It exerts its action though the inhibition of Hif1a induced hypoxic signalling and induction of the Caspase 3/7 apoptotic cascade. The drug has equal activity in normoxia and hypoxia indicating it may be equally active in these different tumor compartments. We tested its ability to circumvent chemotherapeutic drug resistance. Methods: We assessed the ability of EL102 to inhibit prostate cancer cell proliferation and motility in vitro, calculating IC50s for CWR22, 22Rv2, PC3 and DU145 prostate cancer

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Thangaretnam, Krishnapriya, Islam MD Obaidul, Heng Lu, et al. "Abstract 375: Smoking induces Wee1 expression through miRNA deregulation, promoting docetaxel resistance in esophageal adenocarcinoma." Cancer Research 83, no. 7_Supplement (2023): 375. http://dx.doi.org/10.1158/1538-7445.am2023-375.

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Abstract Esophageal Adenocarcinoma (EAC) is the most common subtype of Esophageal Cancer in Western countries, and its incidence rate has increased over the past few decades. The overall five-year survival rate of EAC is less than 20%. Smoking is a major risk factor for EAC development. WEE1 kinase plays a crucial role in the cell cycle by regulating the G2/M checkpoint, providing a time frame for the cells to repair DNA damage. Thus, targeting WEE1 using an inhibitor could potentiate the effect of chemotherapeutic drugs. This study investigated how smoking induces WEE1 protein expression, pro

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Deshmukh, Chetan Dilip, Ganesh Divekar, Minish Mahendra Jain, Shailesh Arjun Bondarde, and Niraj Bhatt. "Pharmacologic differences in taxanes leading to difference in clinical activity and toxicity." Journal of Clinical Oncology 31, no. 15_suppl (2013): e13567-e13567. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e13567.

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e13567 Background: Paclitaxel and docetaxel share major parts of their structures and mechanism of action, but differ in several aspects. Both paclitaxel and docetaxel act at microtubule causing tubulin polymer generation but exhibit pharmacodynamic differences. These pharmacological differences may account for the differences observed between taxanes in their clinical activity and toxicity. Methods: Review of articles providing details of taxane pharmacology was conducted to evaluate pharmacological basis. Results: Greater uptake and slower efflux of docetaxel from tumor cells leads to longer

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Li, Jia, Jing Ke, Cheng-lin Qin, and Xun Zhu. "LINC00680 modulates docetaxel resistance in breast cancer via the miR-320b/CDKL5 axis." International Journal of Immunopathology and Pharmacology 36 (January 2022): 039463202211056. http://dx.doi.org/10.1177/03946320221105608.

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Introduction: Increasing evidence has indicated that LINC00680 represents an oncogenic factor in cancer; however, the mechanism by which LINC00680 contributes to breast cancer (BC) remains unknown. Methods: A dual-luciferase reporter assay was used to explore the relationship between LINC00680, miR-320b, and cyclin-dependent kinase 5 (CDKL5). A CCK-8 assay and transwell assay were utilized to evaluate the proliferation and invasion in docetaxel-resistant BC cells, respectively. Results: LINC00680 and CDKL5 protein levels were both upregulated when induced by different concentrations of docetax

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Thomson, Alastair, Adam Pollard, and Frances May Mark. "Timing of docetaxel chemotherapy and impact on outcomes in metastatic castrate-resistant prostate cancer (MCRPC)." Journal of Clinical Oncology 37, no. 7_suppl (2019): 298. http://dx.doi.org/10.1200/jco.2019.37.7_suppl.298.

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298 Background: Docetaxel use has led to a significant prolongation in overall survival (OS) in metastatic prostate cancer after castrate resistance, with a more substantial OS gain when used in combination with initial androgen deprivation therapy (ADT). There is however limited information on outcomes in patients who initially do not receive chemotherapy, perhaps through patient choice or impaired performance status, who become suitable for docetaxel, comparing earlier with later docetaxel treatment. Methods: We retrospectively reviewed patients’ electronic clinical and prescribing records d

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Mukherji, Deborah, Carmel Jo Pezaro, Diletta Bianchini, Andrea Zivi, and Johann Sebastian De Bono. "Response to abiraterone acetate in the postchemotherapy setting in patients with castration-resistant prostate cancer whose disease progresses early on docetaxel." Journal of Clinical Oncology 30, no. 5_suppl (2012): 17. http://dx.doi.org/10.1200/jco.2012.30.5_suppl.17.

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17 Background: Abiraterone acetate (AA) has recently been approved for men with metastatic castration-resistant prostate cancer (CRPC) following docetaxel chemotherapy. AA inhibits CYP17, reducing androgen production and thereby impacting androgen receptor (AR) signalling. Recent evidence suggests taxanes also impact AR signalling, raising concerns about potential cross-resistance. We have previously shown that docetaxel has no antitumor activity in AA refractory patients. We have now evaluated the antitumor activity of AA post-docetaxel to determine the activity of AA in docetaxel refractory

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van Soest, Robert J., Martin E. van Royen, Ellen S. de Morrée, et al. "Effects on androgen receptor nuclear import by docetaxel, cabazitaxel, abiraterone, and enzalutamide: Potential mechanism for cross-resistance in castration-resistant prostate cancer (CRPC)." Journal of Clinical Oncology 31, no. 15_suppl (2013): 5064. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.5064.

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5064 Background: Recent reports have suggested that paclitaxel and docetaxel, which exert their therapeutic activity primarily through inhibition of microtubule function and mitosis, also impair androgen receptor (AR) signaling. AR signaling is the key therapeutic target for the newly available agents abiraterone and enzalutamide. A recent study suggested impaired efficacy of docetaxel when given after progression on abiraterone in patients with CRPC. To identify potential mechanisms of cross-resistance, we investigated whether and to what extent AR nuclear translocation is affected by docetax

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Pudova, Elena, Anastasiya Kobelyatskaya, Irina Katunina та ін. "Docetaxel Resistance in Castration-Resistant Prostate Cancer: Transcriptomic Determinants and the Effect of Inhibiting Wnt/β-Catenin Signaling by XAV939". International Journal of Molecular Sciences 23, № 21 (2022): 12837. http://dx.doi.org/10.3390/ijms232112837.

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Castration-resistant prostate cancer (CRPC) is a common form of prostate cancer in which docetaxel-based chemotherapy is used as the first line. The present study is devoted to the analysis of transcriptome profiles of tumor cells in the development of resistance to docetaxel as well as to the assessment of the combined effect with the XAV939 tankyrase inhibitor on maintaining the sensitivity of tumor cells to chemotherapy. RNA-Seq was performed for experimental PC3 cell lines as well as for plasma exosome samples from patients with CRPC. We have identified key biological processes and identif

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Haldar, Subhash, Rajeev Mishra, Sandrine Billet, et al. "Cancer epithelia-derived mitochondrial DNA is a targetable initiator of a paracrine signaling loop that confers taxane resistance." Proceedings of the National Academy of Sciences 117, no. 15 (2020): 8515–23. http://dx.doi.org/10.1073/pnas.1910952117.

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Stromal-epithelial interactions dictate cancer progression and therapeutic response. Prostate cancer (PCa) cells were identified to secrete greater concentration of mitochondrial DNA (mtDNA) compared to noncancer epithelia. Based on the recognized coevolution of cancer-associated fibroblasts (CAF) with tumor progression, we tested the role of cancer-derived mtDNA in a mechanism of paracrine signaling. We found that prostatic CAF expressed DEC205, which was not expressed by normal tissue-associated fibroblasts. DEC205 is a transmembrane protein that bound mtDNA and contributed to pattern recogn

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Rushworth, Linda K., Victoria Harle, Peter Repiscak, et al. "In vivo CRISPR/Cas9 knockout screen: TCEAL1 silencing enhances docetaxel efficacy in prostate cancer." Life Science Alliance 3, no. 12 (2020): e202000770. http://dx.doi.org/10.26508/lsa.202000770.

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Docetaxel chemotherapy in metastatic prostate cancer offers only a modest survival benefit because of emerging resistance. To identify candidate therapeutic gene targets, we applied a murine prostate cancer orthograft model that recapitulates clinical invasive prostate cancer in a genome-wide CRISPR/Cas9 screen under docetaxel treatment pressure. We identified 17 candidate genes whose suppression may enhance the efficacy of docetaxel, with transcription elongation factor A–like 1 (Tceal1) as the top candidate. TCEAL1 function is not fully characterised; it may modulate transcription in a promo

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Scherbakov, Alexander M., Anna A. Basharina, Danila V. Sorokin, et al. "Targeting hormone-resistant breast cancer cells with docetaxel: a look inside the resistance." Cancer Drug Resistance 6, no. 1 (2023): 103–15. http://dx.doi.org/10.20517/cdr.2022.96.

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Aim: The study aims to analyze the effect of long-term incubation of ERα-positive MCF7 breast cancer cells with 4-hydroxytamoxifen (HT) on their sensitivity to tubulin polymerization inhibitor docetaxel. Methods: The analysis of cell viability was performed by the MTT method. The expression of signaling proteins was analyzed by immunoblotting and flow cytometry. ERα activity was evaluated by gene reporter assay. To establish hormone-resistant subline MCF7, breast cancer cells were treated with 4-hydroxytamoxifen for 12 months. Results: The developed MCF7/HT subline has lost sensitivity to 4-hy

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Pouptsis, Athanasios, Styliani Germanou, Nick Waldron, et al. "Primary resistance in docetaxel and androgen deprivation therapy in metastatic castrate sensitive prostate cancer patients." Journal of Clinical Oncology 36, no. 6_suppl (2018): 342. http://dx.doi.org/10.1200/jco.2018.36.6_suppl.342.

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342 Background: Docetaxel chemotherapy combined with androgen deprivation therapy (ADT) has become the new standard of care in patients with metastatic castrate sensitive prostate cancer as it has shown significant benefit in terms of overall survival (OS) and response rates (Sweeney 2015, James 2016). However a subgroup of patients still experience early progression. Methods: We searched the hospital database for patients treated with docetaxel in the castrate sensitive setting. Eligible patients included those with newly diagnosed metastatic prostate adenocarcinoma and also patients with rel

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