neoadjuvant setting, clinical response rates range from 50 to 70% of patients ( Colleoni & Montagna 2012 ). Almost all patients with advanced or metastatic ER+ breast cancer will relapse if treated with endocrine therapy alone during the first few years of
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Anastasia Alataki and Mitch Dowsett
Leonardo Oliveira Reis
parameter of disease independently ( Scher et al . 1997 , Suzuki et al . 2008 ). The specific hormone therapy administered and the response to that therapy can influence the biology of the relapsing tumor and the sensitivity to subsequent therapies, and
Miguel A Zaballos, Adrián Acuña-Ruiz, Marta Morante, Piero Crespo, and Pilar Santisteban
response to these drugs is only temporary and relapse of the tumor due to the emergence of resistance is common. Additionally, systemic inhibition of the ERK pathway generates toxicity, especially in highly proliferative tissues. Currently, there is a lack
Susanna Leskelä, Luis J Leandro-García, Marta Mendiola, Jorge Barriuso, Lucía Inglada-Pérez, Iván Muñoz, Beatriz Martínez-Delgado, Andrés Redondo, Javier de Santiago, Mercedes Robledo, David Hardisson, and Cristina Rodríguez-Antona
disease 4 7 Unknown 1 2 Pathological response Complete response 14 25 Stable disease 10 17 Unknown 33 58 Debulking status Optimal (<1 cm) 24 42 Suboptimal (>1 cm) 12 21 Unknown 21 37 Relapse/progression Yes 47 83 No 8 14 Unknown 2 3 Progression
Anika Nagelkerke, Anieta M Sieuwerts, Johan Bussink, Fred C G J Sweep, Maxime P Look, John A Foekens, John W M Martens, and Paul N Span
95 31 0.0072 0.016 Dominant site of relapse 0.034 d Soft tissue (LRR) 35 12 0.0103 0.020 Bone 157 52 0.0042 0.010 Viscera (other) 112 37 0.0057 0.013 ERBB2 mRNA 0.036 b Low 257 85 0.0044 0.010 High 40 13 0.0095 0.017 Unknown 7 2 ER mRNA ( r s
Georgios P Skliris, Zoann J Nugent, Brian G Rowan, Carla R Penner, Peter H Watson, and Leigh C Murphy
, positivity reported in this study was solely based on IHC scores greater than the 25th percentile ( Skliris et al . 2009 ). Relapse-free survival (RFS) was defined as the time from initial surgery to the date of clinically documented local or distant disease
Yuji Ikeda, Kazuma Kiyotani, Poh Yin Yew, Taigo Kato, Kenji Tamura, Kai Lee Yap, Sarah M Nielsen, Jessica L Mester, Charis Eng, Yusuke Nakamura, and Raymon H Grogan
knockdown on the proliferation of HCC1143 cells. (d) Kaplan–Meier analysis of relapse-free survival and overall survival in 4142 patients with breast cancer patients (from GEO, EGA, and TCGA datasets) according to the expression of PARP4 . High and low
Z Culig, H Steiner, G Bartsch, and A Hobisch
incubation with androgen, it was sufficient for induction of the stimulation of growth of the androgen-ablated subline in vitro and in vivo. In a recently published study in which tissues from patients with relapsed cancer were obtained, AR mean optical
L-A Martin, S Pancholi, C M W Chan, I Farmer, C Kimberley, M Dowsett, and S R D Johnston
Introduction Most patients with oestrogen receptor (ER)-positive advanced breast cancer who have relapsed on tamoxifen (TAM) are prescribed aromatase inhibitors. Unlike TAM, which competes with oestrogen for the ER, aromatase
Emmanuelle Fleurot, Caroline Goudin, Vincent Hanoux, Pierre-Jacques Bonnamy, and Jérôme Levallet
al. 2011 ). Although antiestrogens are used to treat BCs, they are not effective inhibitors of the proliferation of all ER(+) tumor cells. Thus, de novo or acquired resistance leads to the relapse of approximately 20–30% of patients. The triple