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Abstract

Our ability to therapeutically manage breast tumors has been revolutionized by the use of drugs targeting the activity of the estrogen and HER2 receptors. However, the efficacy of these treatments is restricted to tumors expressing/overexpressing these receptors, leaving the 18% of patients that lack ER and HER2 receptor expression minimal options for therapy. In particular, triple negative (TN) breast cancer patients are limited to a small set of chemotherapeutics for treatment options. Many small molecule kinase inhibitors are currently under clinical investigation for treatment of TN tumors, but despite targeting pathways shown to be commonly upregulated in this subtype, clinical success with these single agent targeted therapies has been poor. In this work we attempt to better understand the resistance mechanisms underlying the innate resistance of TN tumors to targeted kinase inhibitors.

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