12 VEGF autocrine survival signalling is mediated via neuropilin 1 receptor in NSCLC cells

Abstract

Methods: Data on all tested patients was prospectively collected from the inauguration of the EGFR genetic service. There were three specific aims in the study. First, did the outcomes in an off-trial population with an often poor socio-economic status match those reported in a clinical trial population? Second, did the Scottish prevalence of common EGFR mutations reflect what has been described internationally? Finally, were there any interesting EGFR genetic variants and what was their potential response to erlotinib? Results: Between July 2012 and June 2013, 49 EGFR mutations were detected from 488 patients tested (10.04%) who had a new diagnosis of first line metastatic non-squamous NSCLC. Of those mutated cancers, 34 had a tyrosine kinase inhibitor (TKI) sensitising variant, 4 patients had a TKI resistance variant, 4 had both a TKI sensitising and resistance mutation, and 7 had mutations of uncharacterised clinical significance. One patient with a c.2543C>T; p.Pro848Leu mutation demonstrated a clinical response after two months of erlotinib treatment, a genetic variant with no prior description of benefit from EGFR inhibition. Conclusions: Interesting genetic EGFR variants have been identified in the west of Scotland NSCLC population, one of which has demonstrated a previously uncharacterised clinical response to erlotinib. To date, prevalence of EGFR mutation and response to TKI treatment in the west of Scotland has reflected that reported in an international trial population.