Jae Won Chang

TL;DR: It was found that mutated cancer genes were associated with cellular response to most currently available cancer drugs, and systematic pharmacogenomic profiling in cancer cell lines provides a powerful biomarker discovery platform to guide rational cancer therapeutic strategies.

TL;DR: It is found that Torin1, a highly potent and selective ATP-competitive mTOR inhibitor that directly inhibits both complexes, impairs cell growth and proliferation to a far greater degree than rapamycin.

TL;DR: A label-free proteomic workflow is developed to analyse as few as 5,000 formalin-fixed, paraffin-embedded cells microdissected from each compartment and finds that stromal methyltransferase nicotinamide N-methyltransferase (NNMT) regulates the transition of normal fibroblasts to cancer-associated fibro Blasts through histone methylation and promotes ovarian cancer growth and metastasis.

TL;DR: It is shown that MAGL is elevated in androgen-independent versus androgens-dependent human prostate cancer cell lines, and that pharmacological or RNA-interference disruption of this enzyme impairs prostate cancer aggressiveness, and a role for this enzyme in protumorigenic metabolism that, for prostate cancer, involves the dual control of endocannabinoid and fatty acid pathways is supported.

TL;DR: It is demonstrated that Torin1 is a useful probe of mTOR-dependent phenomena and that benzonaphthridinones represent a promising scaffold for the further development of m TOR-specific inhibitors with the potential for clinical utility.