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


Journal

Cancer medicine
ISSN: 2045-7634
Titre abrégé: Cancer Med
Pays: United States
ID NLM: 101595310

Informations de publication

Date de publication:
04 2022
Historique:
revised: 01 12 2021
received: 15 09 2021
accepted: 15 12 2021
pubmed: 18 2 2022
medline: 29 4 2022
entrez: 17 2 2022
Statut: ppublish

Résumé

The genomic characteristics of hepatocellular carcinoma (HCC) after a sustained virological response (SVR) and its differences according to whether an SVR was achieved by treatment with direct-acting antivirals (DAA) or interferon (IFN) are still not fully understood. Sixty-nine surgically resected HCCs from patients with hepatitis C virus infection were analyzed by gene expression profiling and whole-exome sequencing. Among the 69 HCC patients, 34 HCCs in which an SVR was not achieved at the time of surgery were classified as HCV-positive, and 35 HCCs in which an SVR was achieved at the time of surgery were classified as HCV-SVR. According to the HCV treatment, 35 HCV-SVR HCCs were classified into two groups: eight tumors with DAA (HCV-SVR-DAA) and 24 tumors with interferon (HCV-SVR-IFN). The frequency of samples with ARID2 mutations was significantly lower in HCV-SVR than in HCV-positive tumors (p = 0.048). In contrast, the frequency of samples with PREX2 mutations was significantly higher in HCV-SVR samples than in HCV-positive samples (p = 0.048). Among the patients with HCV-SVR, the frequency of samples with TP53 mutations was significantly higher in HCV-SVR-DAA tumors than in HCV-SVR-IFN tumors (p = 0.030). TP53 inactivation scores in HCV-SVR-DAA tumors were found to be significantly enhanced in comparison to HCV-SVR-IFN tumors (p = 0.022). In addition, chromosomal instability and PI3K/AKT/mTOR pathway signatures were enhanced in HCV-SVR-DAA tumors. HCV-SVR-DAA was significantly associated with portal vein invasion (p = 0.003) in comparison to HCV-SVR-IFN. 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.

Identifiants

pubmed: 35174643
doi: 10.1002/cam4.4571
pmc: PMC9041076
doi:

Substances chimiques

Antiviral Agents 0
TP53 protein, human 0
Tumor Suppressor Protein p53 0
Interferons 9008-11-1

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1769-1786

Informations de copyright

© 2022 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.

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Auteurs

Taisuke Imamura (T)

Division of Hepato-Biliary-Pancreatic Surgery, Shizuoka Cancer Center, Shizuoka, Japan.

Yukiyasu Okamura (Y)

Division of Hepato-Biliary-Pancreatic Surgery, Shizuoka Cancer Center, Shizuoka, Japan.
Department of Digestive Surgery, Nihon University School of Medicine, Tokyo, Japan.

Keiichi Ohshima (K)

Medical Genetics Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.

Katsuhiko Uesaka (K)

Division of Hepato-Biliary-Pancreatic Surgery, Shizuoka Cancer Center, Shizuoka, Japan.

Teiichi Sugiura (T)

Division of Hepato-Biliary-Pancreatic Surgery, Shizuoka Cancer Center, Shizuoka, Japan.

Takaaki Ito (T)

Division of Hepato-Biliary-Pancreatic Surgery, Shizuoka Cancer Center, Shizuoka, Japan.

Yusuke Yamamoto (Y)

Division of Hepato-Biliary-Pancreatic Surgery, Shizuoka Cancer Center, Shizuoka, Japan.

Ryo Ashida (R)

Division of Hepato-Biliary-Pancreatic Surgery, Shizuoka Cancer Center, Shizuoka, Japan.

Katsuhisa Ohgi (K)

Division of Hepato-Biliary-Pancreatic Surgery, Shizuoka Cancer Center, Shizuoka, Japan.

Shimpei Otsuka (S)

Division of Hepato-Biliary-Pancreatic Surgery, Shizuoka Cancer Center, Shizuoka, Japan.

Sumiko Ohnami (S)

Cancer Diagnostics Research Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.

Takeshi Nagashima (T)

Cancer Diagnostics Research Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.
SRL, Inc., Tokyo, Japan.

Keiichi Hatakeyama (K)

Medical Genetics Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.

Yuko Kakuda (Y)

Division of Pathology, Shizuoka Cancer Center, Shizuoka, Japan.

Takashi Sugino (T)

Division of Pathology, Shizuoka Cancer Center, Shizuoka, Japan.

Kenichi Urakami (K)

Cancer Diagnostics Research Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.

Yasuto Akiyama (Y)

Immunotherapy Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.

Ken Yamaguchi (K)

Shizuoka Cancer Center Hospital and Research Institute, Shizuoka, Japan.

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