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MEK inhibition as a strategy for targeting residual breast cancer cells with low DUSP4 expression

Sven Rottenberg1 and Jos Jonkers2

Author Affiliations

1 Division of Molecular Oncology, Plesmanlaan 121, The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands

2 Division of Molecular Pathology, Plesmanlaan 121, The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands

Breast Cancer Research 2012, 14:324  doi:10.1186/bcr3327

Published: 5 November 2012

Abstract

Lack of eradication of disseminated breast cancer by chemotherapy is a central clinical problem. Even tumors that show substantial shrinkage after drug treatment frequently relapse and eventually become refractory to all drugs available. The mechanisms underlying this lack of eradication are largely undefined and it is therefore difficult to develop curative strategies using systemic anti-cancer therapy. In a recent article low DUSP4 expression was reported to activate RAS-ERK signaling in residual breast cancer after neoadjuvant chemotherapy. This may be a druggable characteristic because MEK inhibition increases docetaxel sensitivity in a xenograft model.