Abstract

Tumour Protein 53 (TP53) plays a role in angiogenesis by regulating vascular endothelial growth factor A (VEGFA) and VEGF receptor 2 (VEGFR2). In patients (pts) with EGFR+ NSCLC, TP53 mutations, notably on exon 8, are associated with poorer outcomes of EGFR tyrosine kinase inhibitor treatment and may be involved in primary resistance. We evaluated the relationship between TP53 status and outcomes in RELAY.

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