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Conference Paper: Association of hepatitis B virus Pre-S mutations with the risk of hepatocellular carcinoma development

TitleAssociation of hepatitis B virus Pre-S mutations with the risk of hepatocellular carcinoma development
Authors
Issue Date2009
PublisherHong Kong Academy of Medicine.
Citation
The 14th Medical Research Conference (MRC 2009), Hong Kong, 10 January 2009. In Hong Kong Medical Journal, 2009, v. 15 suppl. 1, p. 38 How to Cite?
AbstractIntroduction: Recent studies suggest that hepatitis B virus (HBV) Pre-S/S mutations are associated with the development of hepatocellular carcinoma (HCC). However, in these case-control studies, the patients were not matched for age, gender and hepatitis B e-antigen (HBeAg) status. We aimed to investigate the association between PreS deletions and HCC using (1) a matched case-control approach and (2) a longitudinal approach. Methods: HBV PreS deletions were determined by DNA sequencing in sera collected from 105 HCC and 105 non-HCC patients matched with age, gender and HBeAg status, as well as in sera collected before the development of HCC. Results: PreS deletions were detected in 27 of 105 HCC cases (25.7%). At the time of writing, nucleotide sequence analysis in 68 HCC/non-HCC­–matched pairs showed that 20 HCC (29.4%) and 9 non-HCC (13.2%) patients acquired PreS2 deletions (P=0.035). In the longitudinal study, serum samples collected 1 to 7 years before HCC development were assessed in 12 HCC cases with PreS deletions. PreS deletions were absent in seven cases before HCC development (58.3%). Conclusion: The findings from this preliminary study suggested that PreS deletions, especially PreS2 deletions, were associated with HCC development. These results are being validated by our on-going studies with a larger number of patients.
Persistent Identifierhttp://hdl.handle.net/10722/62401
ISSN
2023 Impact Factor: 3.1
2023 SCImago Journal Rankings: 0.261

 

DC FieldValueLanguage
dc.contributor.authorYeung, Pen_HK
dc.contributor.authorWong, DKHen_HK
dc.contributor.authorFung, JYYen_HK
dc.contributor.authorYuen, JCHen_HK
dc.contributor.authorFung, FKCen_HK
dc.contributor.authorLai, CLen_HK
dc.contributor.authorYuen, RMFen_HK
dc.date.accessioned2010-07-13T04:00:27Z-
dc.date.available2010-07-13T04:00:27Z-
dc.date.issued2009en_HK
dc.identifier.citationThe 14th Medical Research Conference (MRC 2009), Hong Kong, 10 January 2009. In Hong Kong Medical Journal, 2009, v. 15 suppl. 1, p. 38-
dc.identifier.issn1024-2708-
dc.identifier.urihttp://hdl.handle.net/10722/62401-
dc.description.abstractIntroduction: Recent studies suggest that hepatitis B virus (HBV) Pre-S/S mutations are associated with the development of hepatocellular carcinoma (HCC). However, in these case-control studies, the patients were not matched for age, gender and hepatitis B e-antigen (HBeAg) status. We aimed to investigate the association between PreS deletions and HCC using (1) a matched case-control approach and (2) a longitudinal approach. Methods: HBV PreS deletions were determined by DNA sequencing in sera collected from 105 HCC and 105 non-HCC patients matched with age, gender and HBeAg status, as well as in sera collected before the development of HCC. Results: PreS deletions were detected in 27 of 105 HCC cases (25.7%). At the time of writing, nucleotide sequence analysis in 68 HCC/non-HCC­–matched pairs showed that 20 HCC (29.4%) and 9 non-HCC (13.2%) patients acquired PreS2 deletions (P=0.035). In the longitudinal study, serum samples collected 1 to 7 years before HCC development were assessed in 12 HCC cases with PreS deletions. PreS deletions were absent in seven cases before HCC development (58.3%). Conclusion: The findings from this preliminary study suggested that PreS deletions, especially PreS2 deletions, were associated with HCC development. These results are being validated by our on-going studies with a larger number of patients.-
dc.languageengen_HK
dc.publisherHong Kong Academy of Medicine.-
dc.relation.ispartofHong Kong Medical Journal-
dc.titleAssociation of hepatitis B virus Pre-S mutations with the risk of hepatocellular carcinoma developmenten_HK
dc.typeConference_Paperen_HK
dc.identifier.emailWong, DKH: danywong@hku.hken_HK
dc.identifier.emailFung, JYY: jfung@sicklehut.comen_HK
dc.identifier.emailYuen, JCH: jchyuen@HKUCC.hku.hken_HK
dc.identifier.emailFung, FKC: fredericfung@hotmail.comen_HK
dc.identifier.emailLai, CL: hrmelcl@hku.hken_HK
dc.identifier.emailYuen, RMF: mfyuen@hkucc.hku.hken_HK
dc.identifier.authorityWong, DKH=rp00492en_HK
dc.identifier.authorityFung, JYY=rp00518en_HK
dc.identifier.authorityLai, CL=rp00314en_HK
dc.identifier.authorityYuen, RMF=rp00479en_HK
dc.identifier.hkuros158496en_HK
dc.identifier.volume15-
dc.identifier.issuesuppl. 1-
dc.identifier.spage38-
dc.identifier.epage38-
dc.identifier.issnl1024-2708-

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