Advances in Anti-EGFR Therapy of Metastatic Colorectal Cancer

Dear Colleagues,

The survival of patients affected by metastatic colorectal cancer (mCRC) has improved since 1) the introduction of biologic treatments and 2) the selection of patients on a genetic basis. In fact, it is well known that tumors bearing specific activating mutations in the KRAS (Kirsten Rat Sarcoma) oncogene do not respond to anti-EGFR (Epidermal Growth Factor Receptor) antibodies (panitumumab and cetuximab), which block and prevent growth factors from binding. In fact, in these cases, EGFR downstream signals work independently from the ligand engagement. However, panitumumab and cetuximab are two different drugs; the first is a fully humanized IgG2, the second a chimeric mouse–human IgG1. Recent data have shown that an immune-mediated mechanism could account for the anti-tumor activity of cetuximab being able to activate, much more effectively than panitumumab, the NK-mediated ADCC (Antibody Dependent Cellular Cytotoxicity) against tumor cells.

The aim of this Special Issue is to describe the innovative and less explored topics concerning the anti-EGFR treatment of mCRC, focusing on the following:

1. EGFR inhibition in mCRC—beyond the antibodies-based therapy;
2. Genetic profiling of the EGFR pathway—new approaches to ameliorate patient selection;
3. Links between anti-EGFR treatments and immune system activation.

One review on “where do we stand and where do we go” is also welcome.

Dr. Guglielmo Nasti
Guest Editor

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