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Jan Kroon, Martin Puhr, Jeroen T Buijs, Geertje van der Horst, Daniëlle M Hemmer, Koen A Marijt, Ming S Hwang, Motasim Masood, Stefan Grimm, Gert Storm, Josbert M Metselaar, Onno C Meijer, Zoran Culig, and Gabri van der Pluijm

unresponsive to current cytotoxic treatments. Docetaxel (Taxotere, Sanofi-Aventis, Paris, France) is a microtubule-stabilizing agent that is clinically approved for a range of malignancies, including castration-resistant PCa (CRPC) for which it is the standard

Open access

Martina Gruber, Lavinia Ferrone, Martin Puhr, Frédéric R Santer, Tobias Furlan, Iris E Eder, Natalie Sampson, Georg Schäfer, Florian Handle, and Zoran Culig

) include inhibitors of androgen synthesis and antiandrogens such as enzalutamide and apalutamide as well as the chemotherapeutic compound docetaxel (Taxotere®). In 2004, the landmark study TAX327 showed a significant survival benefit of 2.4 months for

Free access

Wei Guan, Junhui Hu, Lu Yang, Ping Tan, Zhuang Tang, Brian L West, Gideon Bollag, Hua Xu, and Lily Wu

( Silberstein et al . 2016 ). Potential mechanisms of resistance include AR mutations, amplification and splice variant ( Antonarakis et al . 2014 , Azad et al . 2015 , Romanel et al . 2015 ). Docetaxel has been established as the standard first

Free access

Juliang Zhang, Huimin Meng, Mingkun Zhang, Cun Zhang, Meiling Huang, Changjiao Yan, Zhe Wang, Lan Hou, Liu Yang, and Rui Ling

taxanes (docetaxel (DTX) and paclitaxel) are a group of antimicrotubule therapeutic agents that cause apoptosis by inhibiting the depolymerisation of the β-tubulin subunit of microtubules. Compared to paclitaxel, DTX displays less side-effects ( Kastl et

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Anton Neschadim, Laura B Pritzker, Kenneth P H Pritzker, Donald R Branch, Alastair J S Summerlee, John Trachtenberg, and Joshua D Silvertown

growth of aggressive, androgen-independent human prostate cancer tumor xenografts. We further show that AT-001 treatment synergistically combines with standard first-line chemotherapy, docetaxel ( Garmey et al . 2008 , Carles et al . 2012 ), and that

Open access

K M Biernacka, R A Persad, A Bahl, D Gillatt, J M P Holly, and C M Perks

dosed with Docetaxel (0–60 nM), Metformin (0–10 mM) and Compound C (2 µM) according to the respective figure legends. Dead cells were assessed using trypan blue cell counting as described previously ( Thomas et al . 2010 ). Images were taken with a 10

Free access

Claudio Festuccia, Giovanni Luca Gravina, Anna Maria D'Alessandro, Paola Muzi, Danilo Millimaggi, Vincenza Dolo, Enrico Ricevuto, Carlo Vicentini, and Mauro Bologna

clinical trials indicated that docetaxel (DTX)-based chemotherapy improved survival in patients with hormone-refractory prostate cancer, HRPC ( Patel et al . 2005 , Armstrong et al . 2007 ). Docetaxel and mitoxantrone are two food and drug administration

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Giovanni Luca Gravina, Francesco Marampon, Foteini Petini, Leda Biordi, David Sherris, Emmanuele A Jannini, Vincenzo Tombolini, and Claudio Festuccia

third highest of all cancers ( Desireddi et al . 2007 , Svatek et al . 2008 ). Although chemotherapy historically has had limited utility in treating advanced PCa, the results from two recent randomized clinical trials indicated that docetaxel (DTX

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C Ferlini, M Di Stefano, M Marone, C Gaggini, G Ferrandina, A Riva, E Bombardelli, A De Pasqua, S Mancuso, and G Scambia


Docetaxel is a semi-synthetic drug that has been shown to be effective in refractory advanced breast cancer. Its main mechanism of action seems to be to block microtubule depolymerisation. In this study we investigated the interaction between docetaxel and the pure anti-oestrogen ICI 182,780 on different oestrogen receptor-negative cancer cells, some of which express the classical multi-drug resistance (MDR) phenotype. ICI 182,780 potentiated the anti-proliferative effect of docetaxel only in the MDR-positive cells. Isobolic analysis demonstrated that this chemosensitising effect was a synergism. In the same conditions where synergism was detected, cell cycle analysis demonstrated an augmentation of cells blocked at the G2/M phase of the cell cycle, suggesting that ICI 182,780 increases the activity of docetaxel. In order to test this hypothesis, we performed bcl-2 western blot analysis and demonstrated that the addition of ICI 182,780 to docetaxel induced bcl-2 phosphorylation only in MDR-positive cells. The functional inactivation of bcl-2 is probably responsible for the commitment to apoptosis, since the combined docetaxel/ICI 182,780 treatment was able to foster a massive apoptosis in MDR-bearing cells as demonstrated by morphological analysis.

Our results suggest that the synergism between docetaxel and ICI 182,870 is due to a block in P-glycoprotein activity, thus determining cell cycle block, bcl-2 inactivation and apoptosis induced by docetaxel accumulation.

Open access

Simon Linder, Henk G van der Poel, Andries M Bergman, Wilbert Zwart, and Stefan Prekovic

approaches aimed to overcome therapy resistance (5). Figure 2 Graphical summary capturing the topics discussed in this review. Docetaxel has been the first agent showing a survival benefit in mCRPC patients (1). Despite initial responses upon docetaxel