Inhibition of BRAF and BRAF+MEK drives a metastatic switch in melanoma.
Recent analyses by our group and others showed that the majority of melanoma patients who fail BRAF inhibitor therapy do so at new disease sites. Using phosphoproteomics we showed that BRAF inhibition mediates a switch to an aggressive/metastatic melanoma phenotype that is driven by ligand-independent erythropoietin-producing hepatocellular receptor A2 (EphA2) signaling.
Department of Tumor Biology; The Moffitt Cancer Center & Research Institute; Tampa, FL, USA; Department of Cutaneous Oncology; The Moffitt Cancer Center & Research Institute; Tampa, FL, USA.
Keiran Sm
KS
Smalley
Department of Tumor Biology; The Moffitt Cancer Center & Research Institute ; Tampa, FL, USA.
Inna V
IV
Fedorenko
BRAF; ephrin; melanoma; metastasis; resistance