Dr. Kwan Ho Tang
Research Scientist, New York University School of Medicine, USA

Date: Thursday, 19-September-2019
Time: 2:30 p.m.
Venue: Seminar Room 4, G/F, Laboratory Block, Faculty of Medicine Building
21 Sassoon Road, Pokfulam, Hong Kong​

Summary:
KRAS is one of the most altered genes in solid tumors: nearly all pancreas, ~50% of colon, and 30% of non-small cell lung cancer have mutant KRAS. Majority of the mutant KRAS had long been considered to be “undruggable”. Attempts have also been made to target KRAS-mutant tumors by inhibiting downstream pathways (e.g., MEK-inhibitors). Unfortunately, adaptive resistance to the inhibitors inevitably lead to lack of efficacy and progression. Adaptive resistance to MEK inhibitors typically occurs via induction of genes for different receptor tyrosine kinases (RTK) and/or their ligands. SHP2 is required for RAS/ERK pathway activation by most RTKs and might provide a common resistance node. Dr. Tang’s group found that combining SHP2 inhibitor with MEK inhibitors can effectively target KRAS-mutant cancers, as well as other cancers that show aberrant activation of RAS/ERK pathway. Importantly, in addition to its tumor cell-autonomous effect, Dr. Tang also found that SHP2 inhibition can significant modulate the tumor microenvironment. Understand the non-cell autonomous effects of SHP2 inhibition on the tumor-associated immune microenvironment would allow us to design more effective, rational treatment combinations that can overcome intrinsic drug resistance, as well as to harness the beneficial immune modulating properties of such inhibition.

ALL ARE WELCOME