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Pangaea Oncology Signs 1.1 Mln contract with In3BIO
July 8 (Reuters) – Pangaea Oncology SA: Source: https://uk.reuters.com/article/idUKL8N2EF4DZ
Anti-epidermal growth factor vaccine antibodies increase the antitumor activity of kinase inhibitors in ALK and RET rearranged lung cancer cells
Advanced NSCLC patients harboring EML4-ALK and CCDC6-RET rearrangements derive benefit from treatment with ALK and RET TKIs but not immune checkpoint inhibitors. New immunotherapeutic approaches,
Anti–Epidermal Growth Factor vaccine antibodies enhance the efficacy of tyrosine kinase inhibitors and delay the emergence of resistance in EGFR mutant lung cancer cells
Mutations in EGFR correlate with impaired response to immune checkpoint inhibitors and the development of novel immunotherapeutic approaches for EGFR mutant NSCLC is of particular interest.
Pathway Targeted Immunotherapy: Rationale and evidence of durable clinical responses with a novel, EGF-directed agent for advanced NSCLC
Around 85% of lung malignancies are NSCLCs.1 The most frequently encountered mutations are in EGFR and KRAS, and these mutations are mutually exclusive. In NSCLC, overexpression of EGFR has been associated with poor prognosis.
Anti-IN01 antibodies significantly improve the activity of RET, BRAF, MEK and PI3K kinase inhibitors in preclinical models
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.
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.
