What is it about?
The HGF-cMet signaling pathway is dysregulated in many cancers, which makes cMet an important target for novel therapeutic interventions. Oncolytic adenoviruses (Ads) have been used for the past three decades as a promising therapeutic approach for a wide array of neoplastic diseases. In the present study, we sought to test and validate a fiber-modified oncolytic Ad serotype 5 (Ad5) vector to retarget infection specificity to cancer cells that overexpress the cMet receptor. We hypothesized that this retargeting Ad5 would allow selective infection and killing of cMet expressing cancer cells.
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Why is it important?
The cMet oncogene is a cell surface receptor with tyrosine kinase activity. Activation of the cMet pathway in cancer has multiple effects on cell proliferation, motility, morphogenesis, and survival of tumor cells, as well as new blood vesssel formation. The cMet oncogene is dysregulated and activated in the majority of malignancies, including lung, breast, and hepatocellular carcinomas (HCCs), and is associated with poor outcome. The widespread involvement in cancer makes cMet a good target for novel therapeutic interventions.
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This page is a summary of: Characterization of an oncolytic adenovirus vector constructed to target the cMet receptor, Oncolytic Virotherapy, September 2015, Dove Medical Press,
DOI: 10.2147/ov.s87369.
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