de Farias CB, Schwartsmann G and Roesler R
Acquired resistance to anti-epidermal growth factor receptor (EGFR) monoclonal antibodies such as cetuximab and panitumumab represents an important limitation to the treatment of colorectal cancer (CRC), and research efforts have increasingly been directed towards understanding molecular mechanisms of resistance. We propose that neurotrophin signaling mediated by brain-derived neurotrophic factor (BDNF) and its receptor, tropomyosinrelated kinase B (TrkB), might be a compensatory mechanism contributing to decreased response to anti-EGFR therapy in CRC. The combined targeting of EGFR and TrkB is a novel strategy worth of further investigation.
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