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

Daniel Wai-Hung HoLo K ChanYung T ChiuIris M J XuRonnie T P PoonTan T CheungChung N TangVictor W L TangIrene L O LoPolly W Y LamDerek T W YauMiao X LiChun M WongIrene O L Ng
Published in: Gut (2016)
Taken together, our findings suggest the significance of previously undocumented mutation-dependent mTOR hyperactivation and frequent TSC1/2 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.
Keyphrases
  • cell proliferation
  • hepatitis b virus
  • copy number
  • single molecule
  • genome wide
  • gene expression
  • stem cells
  • mesenchymal stem cells
  • dna methylation
  • bone marrow
  • human health
  • drug induced
  • electronic health record