EGFR and KRAS mutations do not enrich for the activation of IL-6, JAK1 or phosphorylated STAT3 in resected lung adenocarcinoma
Timothy D Clay, Prudence A Russell, Hongdo Do, Vijaya Sundararajan, Matthew Conron, Gavin M Wright, Benjamin Solomon, Alexander Dobrovic, Sue-Anne McLachlan, Melissa M Moore
MEDICAL ONCOLOGY | HUMANA PRESS INC | Published : 2017
Resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) against EGFR mutant lung adenocarcinoma develops after a median of nine to thirteen months. Upregulation of the interleukin-6 (IL-6)/Janus kinase (JAK)/signal transducers and activators of transcription (STAT) pathway may be a potential source of resistance to EGFR TKIs. We undertook a detailed assessment of the IL-6/JAK1/phosphorylated STAT3 (pSTAT3) pathway in resected lung adenocarcinoma specimens, with special interest in whether the presence of an EGFR mutation enriched for pSTAT3 positivity. Tumours from 143 patients with resected lung adenocarcinoma were assessed. EGFR and KRAS mutation status were..View full abstract
Funding for this study was provided by St. Vincent's Hospital research endowment fund. Dr Clay was supported by Australian Postgraduate Award from the University of Melbourne.