P1.12-04 In Vivo Efficacy of AZD9592, an EGFR-cMET Bispecific ADC, in a Broad Panel of NSCLC Patient-Derived Xenograft Models

Molecular mechanisms of acquired resistance to targeted therapies, such as tyrosine kinase inhibitors (TKI), often manifest as both on-target and off-target aberrations. Such mechanisms include secondary mutations within the kinase domain of the targeted gene, amplifications and alterations in non-targeted genes, disruption of oncogene signalling cascades, and histological transformation. As a result, the molecular landscape of tumours treated with targeted therapies has become increasingly complex and heterogeneous.