title: The correlation of hepatitis B virus pre-S mutation with cellular oxidative DNA damage in hepatocellular carcinoma.
abstract: OBJECTIVE
  Recent research has proposed a role for HBV pre-S mutation in the development of HCC. Although the mechanism is not clear, pre-S mutant-induced endoplasmic reticulum (ER) stress and oxidative DNA damage may participate in this process. Therefore, we investigated the correlation of HBV pre-S mutation with ER stress and cellular oxidative DNA damage in HBV-related HCC patients.
  
  
  METHODS
  Thirty HBV-related HCC patients and 8 control patients were included. HBV DNA was extracted from sera and the HBV S coding region was analyzed by PCR and sequencing. Immunohistochemical staining for 8-oxoG and OGG1 were performed in HCC and non-neoplastic tissues.
  
  
  RESULTS
  Study subjects were categorized into three groups: the pre-S mutant HBV-infected HCC patients (group 1, n=20), wild-type HBV-infected HCC patients (group 2, n=10) and HBV non-infected patients (group 3, n=8). The expression level of 8-oxoG and OGG1 in non-neoplastic tissue was higher in group 1/2 than in group 3; however, there was no significant difference between group 1 and 2. There was no significant difference in 8-oxoG/OGG1 expressions between HCC and non-neoplastic tissues.
  
  
  CONCLUSIONS
  The present study did not support a pathophysiologic role for HBV pre-S mutation, related to ER stress and oxidative DNA damage, in hepatocarcinogenesis.
authors.affiliation: Department of Medicine and Digestive Disease Research Center, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
authors.forename: Geum-Youn
authors.initials: GY
authors.lastname: Gwak
authors.forename: Dong Ho
authors.initials: DH
authors.lastname: Lee
authors.forename: Tae Gun
authors.initials: TG
authors.lastname: Moon
authors.forename: Moon Seok
authors.initials: MS
authors.lastname: Choi
authors.forename: Joon Hyeok
authors.initials: JH
authors.lastname: Lee
authors.forename: Kwang Cheol
authors.initials: KC
authors.lastname: Koh
authors.forename: Seung Woon
authors.initials: SW
authors.lastname: Paik
authors.forename: Cheol Keun
authors.initials: CK
authors.lastname: Park
authors.forename: Jae-Won
authors.initials: JW
authors.lastname: Joh
authors.forename: Byung Chul
authors.initials: BC
authors.lastname: Yoo
mesh_terms: D000368:Aged; D006528:Carcinoma, Hepatocellular / Q000235:genetics* / Q000821:virology; D004249:DNA Damage / Q000235:genetics*; D045647:DNA Glycosylases / Q000378:metabolism; D004721:Endoplasmic Reticulum; D005260:Female; D006514:Hepatitis B Surface Antigens / Q000235:genetics*; D006515:Hepatitis B virus / Q000235:genetics*; D006801:Humans; D007150:Immunohistochemistry; D008099:Liver / Q000821:virology; D008113:Liver Neoplasms / Q000235:genetics* / Q000821:virology; D008297:Male; D008875:Middle Aged; D009154:Mutation / Q000235:genetics; D018384:Oxidative Stress / Q000235:genetics*; D011498:Protein Precursors / Q000235:genetics*; D014759:Viral Envelope Proteins / Q000235:genetics*
chemical_list: D006514:Hepatitis B Surface Antigens; D011498:Protein Precursors; D014759:Viral Envelope Proteins; C050806:presurface protein 1, hepatitis B surface antigen; D045647:DNA Glycosylases; C479058:oxoguanine glycosylase 1, human