<i>TSC1/2</i> mutations define a molecular subset of HCC with aggressive behaviour and treatment implication

Abstract

Taken together, our findings suggest the significance of previously undocumented mutation-dependent mTOR hyperactivation and frequent <i>TSC1/2</i> mutations in HBV-associated HCCs. They define a molecular subset of HCC having genetic aberrations in mTOR signalling, with potential significance of effective specific drug therapy.