Paul R. Gavine

TL;DR: The findings show that AZD4547 is a novel selective small-molecule inhibitor of FGFR with potent antitumor activity against FGFR-deregulated tumors in preclinical models and is under clinical investigation for the treatment ofFGFR-dependent tumors.

TL;DR: The data support therapeutic intervention with FGFR inhibitors, such as AZD4547, in patients with gastric cancer carrying FGFR2 gene amplification, and enhancement of in vivo antitumor efficacy using AZD 4547 in combination with chemotherapeutic agents.

TL;DR: A similar incidence of FGFR2 amplification was found in Asian and UK GCs and was associated with lymphatic invasion and poor prognosis, and it is shown that HER2 andFGFR2 amplifications are mostly exclusive.

TL;DR: The translational science presented here provides a strong rationale for investigation of AZD4547 as a therapeutic option for patients with squamous NSCLC tumors harboring amplification ofFGFR1 and extends the clinical significance of this finding by using multiple FGFR1-amplified squamous lung cancer PDTX models to show tumor stasis or regression effects using a specific FGFR inhibitor (AZD454547).

TL;DR: To investigate the incidence of cMET gene copy number changes and protein overexpression in Chinese gastric cancer and to preclinically test the hypothesis that the novel, potent and selective cMET small‐molecule inhibitor volitinib, will deliver potent anti‐tumor activity in cMET‐dysregulated GC patient‐derived tumor xenograft (PDX) models.