FGFR1 was recently shown to be activated as part of a compensatory response to prolonged
treatment with the MEK inhibitor trametinib in several KRAS-mutant lung and pancreatic …

KRAS, an oncogene mutated in nearly one third of human cancers, remains a
pharmacologic challenge for direct inhibition except for recent advances in selective …

Adaptive resistance to MEK inhibitors (MEKi) typically occurs via induction of genes for
different receptor tyrosine kinases (RTK) and/or their ligands, even in tumors of the same …

RAS is one of the most frequently altered oncogenes, yet RAS-driven tumors are largely
refractory to anticancer therapies. Fedele and colleagues demonstrate that SHP2 inhibitors …

KRAS is the most frequently mutated human oncogene, and KRAS inhibition has been a
longtime goal. Recently, inhibitors were developed that bind KRASG12C-GDP and react …

Protein tyrosine phosphatase SHP2 mediates RAS-driven MAPK signaling and has
emerged in recent years as a target of interest in oncology, both for treating with a single …

The ubiquitously expressed non-receptor protein tyrosine phosphatase SHP2, encoded by
PTPN11, is involved in signal transduction downstream of multiple growth factor, cytokine …

Cancer cells bearing distinct KRAS mutations exhibit variable sensitivity to SHP2 inhibitors
(SHP2i). Here we show that cells harboring KRAS Q61H are uniquely resistant to SHP2i …

Abstract KRAS G12C inhibitors have shown promise in KRAS G12C–mutant lung cancer but
intrinsic and acquired resistance are common. Cotreatment with inhibitors of the protein …

Purpose: Although KRAS represents the most commonly mutated oncogene, it has long
been considered an “undruggable” target. Novel covalent inhibitors selective for the …