MET in Cancer

Dear Colleagues,

This Special Issue invites investigators to contribute original research reports as well as review articles that describe studies on the MET oncogene.

The MET oncogene encodes the tyrosine kinase receptor for hepatocyte growth factor (HGF). MET signaling triggers pro-mitogenic and anti-apoptotic pathways that sustain tumor growth and progression in several cancer settings. Accordingly, relentless activation of MET due to protein overexpression or gain-of-function genetic abnormalities is a hallmark of several malignancies and correlates with aggressive disease. Recent drug development efforts have led to the characterization of several MET-blocking reagents, including monoclonal antibodies and small molecule inhibitors, some of which have entered clinical trials. The challenge now is to leverage what is known about MET genetics, signals and functions for molecularly-based stratification of patients potentially responsive to MET inhibition.

Tentative topics include, but are not limited to:

• Insights into the signaling mechanisms of MET activity: receptor recycling, degradation, and signal compartmentalization.
• Predictive biomarkers of response and resistance to MET inhibitors
• Tumor settings that might benefit from rational treatment with MET inhibitors
• MET activation and resistance to targeted therapies
• MET in the tumor microenvironment

Prof. Dr. Livio Trusolino
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

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