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Parvesh Chaudhry and Eric Asselin

phenomenon of therapeutic resistance in endometrial cancer. The endometrium is a hormone-responsive tissue so it is important to consider hormone therapy and further acquired resistance in this process. We then elucidated some of the recently established

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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

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Phungern Khongthong, Antonia K Roseweir, and Joanne Edwards

testosterone conversion to oestrogens both in the tumour and peripheral tissue ( Baum et al. 2003 ). However, a significant number of the patient fail to respond to endocrine therapies as a result of either de novo or acquired resistance ( Liu et al. 2017

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Suleiman Massarweh and Rachel Schiff

manipulation ( de novo resistance) and a substantial number of patients who do respond will develop disease progression or recurrence while on therapy (acquired resistance). While some of the predictors of endocrine therapy failure are clinical factors, such

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Roberto Bianco, Teresa Troiani, Giampaolo Tortora, and Fortunato Ciardiello

to 35% of breast cancer patients with ErbB-2 overxpressing tumors respond to therapy with trastuzumab and the development of resistance is a common clinical problem. Trastuzumab is able to inhibit the growth of ErbB-2 overexpressing and IGF

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K-M Rau, H-Y Kang, T-L Cha, S A Miller, and M-C Hung

) receptorpositive, hormone-independent; and (3) receptornegative, hormone-independent. Several mechanisms have been proposed for these phenotypes. However, a common scenario is that once the tumor develops resistance to antihormone therapy it will become more

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Patricia V Elizalde, Rosalía I Cordo Russo, Maria F Chervo, and Roxana Schillaci

. 2004 ) strongly support nuclear ErbB-2’s role in BC metastasis. Nuclear ErbB-2’s role in the response to BC therapies Full-length ErbB-2 located in the nuclear compartment was found to participate in the mechanisms of BC resistance to

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Ton van Agthoven, Anieta M Sieuwerts, Danielle Meijer, Marion E Meijer-van Gelder, Thecla L A van Agthoven, Roya Sarwari, Stefan Sleijfer, John A Foekens, and Lambert C J Dorssers

of resistance to endocrine therapy for breast cancer . Cancer Cell 13 91 – 104 . Jaiyesimi IA Buzdar AU Decker DA Hortobagyi GN 1995 Use of tamoxifen for breast cancer: twenty-eight years later . Journal

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R I Nicholson, I R Hutcheson, S E Hiscox, J M Knowlden, M Giles, D Barrow, and J M W Gee

extensive growth inhibition. Indeed, extension of the growth studies to 3 months clearly demonstrates that while tumour cell re-growth is evident in the mono-therapy arms of the experiment, indicating the initiation of drug resistance, the combination of

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M Dowsett

Hormonal therapy leads to improved survival in oestrogen receptor (ER) positive early breast cancer and long-term responses in advanced disease. However, resistance to such therapy is a serious clinical problem. This article considers the data for and against there being a significant role for the oncogene HER-2 in such resistance. Transfection of HER-2 into MCF-7 cells leads to resistance to tamoxifen but data differ in relation to the oestrogen dependence of such cells. A number of retrospective studies have been conducted of HER-2 status in adjuvant trials of tamoxifen. Most of these also suggest a negative role but individually the studies do not have the statistical power to be conclusive. Recent studies in the neoadjuvant context have shown a significant antiproliferative effect of endocrine therapy in HER-2 positive/ER positive tumours but this is much less than in HER-2 negative/ER positive tumours. It is concluded that incomplete hormonal resistance results from co-expression of HER-2 and ER and that this may differ between different hormonal agents.