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Nicola Normanno, Alessandro Morabito, Antonella De Luca, Maria Carmela Piccirillo, Marianna Gallo, Monica R Maiello, and Francesco Perrone

-talk between ER and the ErbB-2 pathway, and the observation that ErbB-2 overexpression is associated with preclinical and clinical resistance to hormonal therapy, suggested that combining treatments targeting both pathways may provide additional benefits for

Open access

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

of DEX has been described in preclinical ( Kroon et al . 2015 ) and clinical studies ( Venkitaraman et al . 2008 ). On the other hand, GC usage seems to be associated with the resistance to antiandrogen therapy ( Arora et al . 2013 , Isikbay et

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J M W Gee, A Howell, W J Gullick, C C Benz, R L Sutherland, R J Santen, L-A Martin, F Ciardiello, W R Miller, M Dowsett, P Barrett-Lee, J F R Robertson, S R Johnston, H E Jones, A E Wakeling, R Duncan, and R I Nicholson

the breast cancer patient, a pervading problem with all conventional therapies is development of resistance and the new anti-hormonal agents do not appear to be spared this limitation. Thus, in addition to those patients who are refractory to therapy

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Thomas Cuny, Wouter de Herder, Anne Barlier, and Leo J Hofland

metastasis. Another source of uncertainty related to angiogenesis concerns the adaptative mechanisms that occur during the antiangiogenic therapy regimen of certain patients with GEP-NETs, responsible for an escape and, ultimately, a resistance to this

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Dara Hope Cohen and Derek LeRoith

pursued target for cancer therapy. In fact, activation of mTOR has been seen in breast cancer cells and has been linked to resistance to trastuzumab and tamoxifen, both chemotherapeutic agents ( Yakar et al . 2005 ). Insulin resistance In obesity and T2D

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Belinda van Zyl, Denise Tang, and Nikola A Bowden

profiles of 23 patient-matched treatment – naïve and platinum-resistant (after several lines of platinum therapy) HGSOC tumour samples. A resistance gene expression signature indicative of TGFβ-mediated EMT was identified and confirmed in a validation set

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Antonino Belfiore and Roberta Malaguarnera

resistance to anti-IGF1R therapies in Ewing's sarcomas. Cells that have developed resistance to specific IGF1R inhibitors, either antibodies or tyrosine kinase inhibitors, showed enhanced IR-A homodimers and/or IGF2 production. These resistant cells thus

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Wei Wei and Michael T Lewis

these are the issues of treatment resistance, disease recurrence, and metastasis. For example, whereas many ER + tumors respond to ER-targeted therapies (antiestrogens such as tamoxifen and aromatase inhibitors such as anastrozole, letrozole, and

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Stephanie Metcalf, Belinda J Petri, Traci Kruer, Benjamin Green, Susan Dougherty, James L Wittliff, Carolyn M Klinge, and Brian F Clem

lead to better patient outcomes, significant clinical hurdles remain in managing ER+ BC ( Clarke et al. 2015 ). These largely stem from resistance to endocrine therapies, which can be classified as either innate or acquired resistance. Innate, or de

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Giorgio Secreto, Paola Muti, Milena Sant, Elisabetta Meneghini, and Vittorio Krogh

of de novo or acquired resistance to anti-estrogens, that prevents about 50% of patients to benefit with the therapy ( Rechoum et al. 2014 , Fuji et al. 2014 , Ciupek et al . 2015 ) and occurrence of late relapse after anti-estrogens have been