Introduction: cMET overexpression and/or activation have been implicated in
signaling pathways that promote cell proliferation, invasion, and survival. It has been
identified as an oncogenic driver in various malignancies and is currently being
investigated as a potential therapeutic target. The aim of this study is to provide insights
into the distribution of cMET expression by immunohistochemistry (IHC), amplification
by FISH, and mutation by next generation sequencing (NGS) across a variety of tumor
types. Also, we evaluate the correlation of cMET across technology platforms tested in a
CLIA-certified oncology reference laboratory.