Posters

We have recently shown that anti-IN01 antibodies having functionality to recognize EGF potentiate the effects of tyrosine kinase inhibitors (TKIs) in epidermal growth factor receptor mutant (EGFR-mut) cell lines (1). As a result, a Phase I/II clinical trial of anti-IN01 antibodies in combination with afatinib has been initiated.

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).

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)

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 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.