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Hepatocellular carcinoma after a sustained virological response by direct-acting antivirals harbors TP53 inactivation.

Taisuke ImamuraYukiyasu OkamuraKeiichi OhshimaKatsuhiko UesakaTeiichi SugiuraTakaaki ItoYusuke YamamotoRyo AshidaKatsuhisa OhgiShimpei OtsukaSumiko OhnamiTakeshi NagashimaKeiichi HatakeyamaYuko KakudaTakashi SuginoKenichi UrakamiYasuto AkiyamaKen Yamaguchi
Published in: Cancer medicine (2022)
Our dataset potentially serves as a fundamental resource for the genomic characteristics of HCV-SVR-DAA tumors. Our comprehensive genetic profiling by WES revealed significant differences in the mutation rate of several driver genes between HCV-positive tumors and HCV-SVR tumors. Furthermore, it was revealed that the frequency of samples with mutations in TP53 was significantly higher in HCV-SVR-DAA tumors than in HCV-SVR-IFN tumors.
Keyphrases
  • hepatitis c virus
  • human immunodeficiency virus
  • single cell
  • genome wide
  • copy number
  • immune response
  • hiv infected
  • antiretroviral therapy