File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
  • Find via Find It@HKUL
Supplementary

Conference Paper: High Rate of HBV DNA Integration in Hepatocellular Carcinoma Patients with Occult Hepatitis B Infection

TitleHigh Rate of HBV DNA Integration in Hepatocellular Carcinoma Patients with Occult Hepatitis B Infection
Authors
Issue Date2018
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/
Citation
The Liver Meeting 2018, American Association for the Study of Liver Diseases (AASLD), San Francisco, USA, 9-13 November 2018. Abstracts in Hepatology, 2018, v. 68 n. Suppl. 1, p. 331A How to Cite?
AbstractBackground: Hepatitis B surface antigen (HBsAg)-negative patients can have occult hepatitis B infection (OBI), which may cause hepatocellular carcinoma (HCC) (Wong et al. Hepatology 54:829-36). Integration of hepatitis B virus (HBV) DNA into host DNA can also lead to HCC. We aimed to examine the significance of OBI and HBV integration in HBsAg-negative HCC patients. Methods: Of the 90 HBsAg-negative HCC patients recruited, 84 had paired tumor and non-tumor tissues available, 3 had only tumor tissues and 3 had only non-tumor tissues available. OBI was detected in the liver DNA by nested PCR, with primers targeting the 4 HBV genomic regions. OBI was diagnosed when ≥2 positive PCR were detected in either tumor or non-tumor tissues. HBV integration was detected by Alu-PCR sequencing. Results: Of the 90 patients, 18 (21%) had alcoholic liver diseases (ALD), 14 (16%) had nonalcoholic fatty liver disease (NAFLD), 2 had primary biliary cholangitis (PBC), 2 had recurrent pyogenic cholangitis (RPC), 1 had autoimmune hepatitis (AIH), and the remaining 53 patients (60%) had unknown causes of (cryptogenic) HCC. OBI was found in 62/90 (69%) HCC patients, including 9/18 (50%) ALD, 9/14 (64%) NAFLD, 2 (100%) PBC, 2 (100%) RPC, and 40/53 (75%) patients with cryptogenic HCC. Unlike other forms of HCC, the majority (53/62; 85%) of OBI patients did not have liver cirrhosis histologically. Tumor-extracted DNA from 41 OBI patients (6 ALD, 6 NAFLD, 2 PBC, 2 RPC and 25 cryptogenic) were examined by Alu-PCR at the time of writing. Among these 41 OBI patients, 16 yielded amplifiable DNA, 12 (75%) of whom were found to have integrated HBV DNA at chromosomes 3 and 5 (3 cases each), chromosome 11 (2 cases), chromosomes 4, 10, 19 (1 case each), and at repetitive elements at various unidentifiable genomic sites (1 case). Integration was found at the preS/S (9 patients; 75%) and core region (3 patients; 25%). Only 1 patient with HBV integration had cirrhosis. One patient had HBV integration near the telomerase reverse transcriptase (TERT) promoter region, and 1 with integration at the intronic region of cyclin A2. Conclusion: 69% of HBsAg-negative HCC patients had OBI. 85% of HCC patients with OBI had no background of cirrhosis, and the oncogenic process might be explained by the high percentage (75%) of HBV integration detected. This suggests that HBV integration, especially those near apoptosis- or cell cycle-related genes such as TERT or cyclin A2, can be a likely cause of HCC in OBI patients.
DescriptionPoster Presentation - no. 553
Persistent Identifierhttp://hdl.handle.net/10722/269513
ISSN
2017 Impact Factor: 14.079
2015 SCImago Journal Rankings: 4.752

 

DC FieldValueLanguage
dc.contributor.authorWong, DKH-
dc.contributor.authorCheng, CYS-
dc.contributor.authorMak, LY-
dc.contributor.authorTo, WP-
dc.contributor.authorCheung, TT-
dc.contributor.authorSeto, WKW-
dc.contributor.authorFung, JYY-
dc.contributor.authorMan, K-
dc.contributor.authorLai, CL-
dc.contributor.authorYuen, RMF-
dc.date.accessioned2019-04-24T08:09:14Z-
dc.date.available2019-04-24T08:09:14Z-
dc.date.issued2018-
dc.identifier.citationThe Liver Meeting 2018, American Association for the Study of Liver Diseases (AASLD), San Francisco, USA, 9-13 November 2018. Abstracts in Hepatology, 2018, v. 68 n. Suppl. 1, p. 331A-
dc.identifier.issn0270-9139-
dc.identifier.urihttp://hdl.handle.net/10722/269513-
dc.descriptionPoster Presentation - no. 553-
dc.description.abstractBackground: Hepatitis B surface antigen (HBsAg)-negative patients can have occult hepatitis B infection (OBI), which may cause hepatocellular carcinoma (HCC) (Wong et al. Hepatology 54:829-36). Integration of hepatitis B virus (HBV) DNA into host DNA can also lead to HCC. We aimed to examine the significance of OBI and HBV integration in HBsAg-negative HCC patients. Methods: Of the 90 HBsAg-negative HCC patients recruited, 84 had paired tumor and non-tumor tissues available, 3 had only tumor tissues and 3 had only non-tumor tissues available. OBI was detected in the liver DNA by nested PCR, with primers targeting the 4 HBV genomic regions. OBI was diagnosed when ≥2 positive PCR were detected in either tumor or non-tumor tissues. HBV integration was detected by Alu-PCR sequencing. Results: Of the 90 patients, 18 (21%) had alcoholic liver diseases (ALD), 14 (16%) had nonalcoholic fatty liver disease (NAFLD), 2 had primary biliary cholangitis (PBC), 2 had recurrent pyogenic cholangitis (RPC), 1 had autoimmune hepatitis (AIH), and the remaining 53 patients (60%) had unknown causes of (cryptogenic) HCC. OBI was found in 62/90 (69%) HCC patients, including 9/18 (50%) ALD, 9/14 (64%) NAFLD, 2 (100%) PBC, 2 (100%) RPC, and 40/53 (75%) patients with cryptogenic HCC. Unlike other forms of HCC, the majority (53/62; 85%) of OBI patients did not have liver cirrhosis histologically. Tumor-extracted DNA from 41 OBI patients (6 ALD, 6 NAFLD, 2 PBC, 2 RPC and 25 cryptogenic) were examined by Alu-PCR at the time of writing. Among these 41 OBI patients, 16 yielded amplifiable DNA, 12 (75%) of whom were found to have integrated HBV DNA at chromosomes 3 and 5 (3 cases each), chromosome 11 (2 cases), chromosomes 4, 10, 19 (1 case each), and at repetitive elements at various unidentifiable genomic sites (1 case). Integration was found at the preS/S (9 patients; 75%) and core region (3 patients; 25%). Only 1 patient with HBV integration had cirrhosis. One patient had HBV integration near the telomerase reverse transcriptase (TERT) promoter region, and 1 with integration at the intronic region of cyclin A2. Conclusion: 69% of HBsAg-negative HCC patients had OBI. 85% of HCC patients with OBI had no background of cirrhosis, and the oncogenic process might be explained by the high percentage (75%) of HBV integration detected. This suggests that HBV integration, especially those near apoptosis- or cell cycle-related genes such as TERT or cyclin A2, can be a likely cause of HCC in OBI patients.-
dc.languageeng-
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/-
dc.relation.ispartofHepatology-
dc.relation.ispartofAmerican Association for the Study of Liver Diseases (AASLD): The Liver Meeting 2018-
dc.titleHigh Rate of HBV DNA Integration in Hepatocellular Carcinoma Patients with Occult Hepatitis B Infection-
dc.typeConference_Paper-
dc.identifier.emailWong, DKH: danywong@hku.hk-
dc.identifier.emailCheng, CYS: serenecy@hku.hk-
dc.identifier.emailCheung, TT: cheung68@hku.hk-
dc.identifier.emailSeto, WKW: wkseto@hku.hk-
dc.identifier.emailFung, JYY: jfung@hkucc.hku.hk-
dc.identifier.emailMan, K: kwanman@hku.hk-
dc.identifier.emailLai, CL: hrmelcl@hkucc.hku.hk-
dc.identifier.emailYuen, RMF: mfyuen@hku.hk-
dc.identifier.authorityWong, DKH=rp00492-
dc.identifier.authorityCheung, TT=rp02129-
dc.identifier.authoritySeto, WKW=rp01659-
dc.identifier.authorityFung, JYY=rp00518-
dc.identifier.authorityMan, K=rp00417-
dc.identifier.authorityLai, CL=rp00314-
dc.identifier.authorityYuen, RMF=rp00479-
dc.identifier.hkuros297389-
dc.identifier.volume68-
dc.identifier.issueSuppl. 1-
dc.identifier.spage331A-
dc.identifier.epage331A-
dc.publisher.placeUnited States-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats