Posters

Anti-EGF antibodies generated by vaccination significantly improve the activity of kinase inhibitors in preclinical models

Epidermal Growth Factor Receptor (EGFR) signaling system is frequently unbalanced in cancer and the ligand Epidermal Growth Factor (EGF) could be an attractive target. KRAS mutated and EML4-ALK fusion tumors are treated with several compounds but resistance invariably appears. Previously we described the biological effects of EGFR antibodies raised by a “cancer vaccine” against human EGF in EGFR mutated NSCLC cells(1,2).

Anti-EGF antibodies increase the effect of ALK and MEK inhibitors in ALK and KRAS NSCLC and CRC cell lines

Epidermal Growth Factor Receptor (EGFR) signaling is frequently unbalanced in non-small-cell lung cancer (NSCLC) and the ligand Epidermal Growth Factor (EGF) could be an attractive target. A “cancer vaccine” against human EGF has demonstrated efficacy in a phase III trial including unselected NSCLC patients, but little was known about the mechanisms involved in the effects of the anti- EGF antibodies generated by vaccination (anti-EGF VacAbs) or their activity in tumor cells with different genetic backgrounds (1-3)

Antitumor effects of anti-EGF antibodies generated by vaccination in NSCLC tumor cells

Epidermal unbalanced in non-small-cell lung cancer (NSCLC) and the ligand Epidermal Growth Factor (EGF) could be an attractive target. A “cancer vaccine” against human EGF has demonstrated efficacy in a phase III trial including unselected NSCLC patients, but little was known about the mechanisms involved in the effects of the anti-EGF antibodies generated by vaccination (anti-EGF VacAbs) or their activity in tumor cells with different genetic backgrounds (1-3)

The effect of EGF-Pathway Targeted Immunization (EGF-PTI) on STAT3 and cancer stem cells in EGFR mutant NSCLC cells

The Epidermal Growth Factor Receptor (EGFR) signaling system is frequently unbalanced in non-small-cell lung cancer (NSCLC) and the ligand Epidermal Growth Factor (EGF) could be an attractive target. EGFR tyrosine kinase inhibitors (TKI) are a standard treatment in EGFR mutated tumors but resistance invariably appears due to various mechanisms, such as the secondary mutation p.T790M or the activation of alternative pathways (MET, AXL). We have assayed the antibodies raised by a “cancer vaccine” against human EGF that block EGF-EGFR interaction. This “cancer vaccine“ has been tested successfully in an unselected population in a Phase III clinical trial.