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- Publisher Website: 10.1136/gut.2007.119859
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- PMID: 17483190
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Article: Risk for hepatocellular carcinoma with respect to hepatitis B virus genotypes B/C, specific mutations of enhancer II/core promoter/precore regions and HBV DNA levels
Title | Risk for hepatocellular carcinoma with respect to hepatitis B virus genotypes B/C, specific mutations of enhancer II/core promoter/precore regions and HBV DNA levels |
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Authors | |
Issue Date | 2008 |
Publisher | BMJ Publishing Group. The Journal's web site is located at http://gut.bmjjournals.com/ |
Citation | Gut, 2008, v. 57 n. 1, p. 98-102 How to Cite? |
Abstract | Background/aim: To examine the risks for hepatocellular carcinoma (HCC) with respect to hepatitis B virus (HBV) genotypes, specific viral mutations (MT), serum HBV DNA levels, and cirrhosis. Methods: HBV genotypes, 1653/1753/core promoter (CP)/precore MT and HBV DNA levels were determined in 248 HBV patients with HCC and 248 HBV controls. Results: Genotype C, CP-MT, T1653, HBV DNA levels ≥4 log 10 copies/ml and cirrhosis had a higher risk for HCC compared to patients with genotype B (p = 0.001, OR 1.9), CP wild-type (WT) (p<0.001, OR 4.1), C1653 (p = 0.028, OR 2.4), HBV DNA <4 log 10 copies/ml (p = 0.003, OR 2.1) and without cirrhosis (p<0.001, OR 4.0) respectively. Multivariate analysis showed that CP-MT, T1653, HBV DNA ≥4 log 10 copies/ml and cirrhosis were independent factors for HCC (all p<0.05). A receiver operating characteristics curve showed no cut-off HBV DNA level associated with minimal chance of HCC. Patients with CP-MT and cirrhosis had a 22.2-fold increased risk of HCC compared to patients with CP-WT and without cirrhosis. Patients with CP-MT and HBV DNA levels ≥4 log 10 copies/ml had a 7.2-fold increased risk of HCC compared to patients with CP-WT and HBV DNA levels <4 log 10 copies/ml. Patients with CP-MT and T1653 had a 9.9-fold increased risk of HCC compared to patients with wild-type for both regions. Conclusions: CP-MT, T1653, HBV DNA levels ≥4 log 10 copies/ml and cirrhosis are independent factors for development of HCC. The risks increased substantially in patients having these factors in combination. |
Persistent Identifier | http://hdl.handle.net/10722/57531 |
ISSN | 2023 Impact Factor: 23.0 2023 SCImago Journal Rankings: 8.052 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
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dc.contributor.author | Yuen, MF | en_HK |
dc.contributor.author | Tanaka, Y | en_HK |
dc.contributor.author | Shinkai, N | en_HK |
dc.contributor.author | Poon, RT | en_HK |
dc.contributor.author | But, DYK | en_HK |
dc.contributor.author | Fong, DYT | en_HK |
dc.contributor.author | Fung, J | en_HK |
dc.contributor.author | Wong, DKH | en_HK |
dc.contributor.author | Yuen, JCH | en_HK |
dc.contributor.author | Mizokami, M | en_HK |
dc.contributor.author | Lai, CL | en_HK |
dc.date.accessioned | 2010-04-12T01:39:15Z | - |
dc.date.available | 2010-04-12T01:39:15Z | - |
dc.date.issued | 2008 | en_HK |
dc.identifier.citation | Gut, 2008, v. 57 n. 1, p. 98-102 | en_HK |
dc.identifier.issn | 0017-5749 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/57531 | - |
dc.description.abstract | Background/aim: To examine the risks for hepatocellular carcinoma (HCC) with respect to hepatitis B virus (HBV) genotypes, specific viral mutations (MT), serum HBV DNA levels, and cirrhosis. Methods: HBV genotypes, 1653/1753/core promoter (CP)/precore MT and HBV DNA levels were determined in 248 HBV patients with HCC and 248 HBV controls. Results: Genotype C, CP-MT, T1653, HBV DNA levels ≥4 log 10 copies/ml and cirrhosis had a higher risk for HCC compared to patients with genotype B (p = 0.001, OR 1.9), CP wild-type (WT) (p<0.001, OR 4.1), C1653 (p = 0.028, OR 2.4), HBV DNA <4 log 10 copies/ml (p = 0.003, OR 2.1) and without cirrhosis (p<0.001, OR 4.0) respectively. Multivariate analysis showed that CP-MT, T1653, HBV DNA ≥4 log 10 copies/ml and cirrhosis were independent factors for HCC (all p<0.05). A receiver operating characteristics curve showed no cut-off HBV DNA level associated with minimal chance of HCC. Patients with CP-MT and cirrhosis had a 22.2-fold increased risk of HCC compared to patients with CP-WT and without cirrhosis. Patients with CP-MT and HBV DNA levels ≥4 log 10 copies/ml had a 7.2-fold increased risk of HCC compared to patients with CP-WT and HBV DNA levels <4 log 10 copies/ml. Patients with CP-MT and T1653 had a 9.9-fold increased risk of HCC compared to patients with wild-type for both regions. Conclusions: CP-MT, T1653, HBV DNA levels ≥4 log 10 copies/ml and cirrhosis are independent factors for development of HCC. The risks increased substantially in patients having these factors in combination. | en_HK |
dc.language | eng | en_HK |
dc.publisher | BMJ Publishing Group. The Journal's web site is located at http://gut.bmjjournals.com/ | en_HK |
dc.relation.ispartof | Gut | en_HK |
dc.rights | Gut. Copyright © B M J Publishing Group. | en_HK |
dc.subject.mesh | Carcinoma, Hepatocellular - virology | en_HK |
dc.subject.mesh | Enhancer Elements (Genetics) - genetics | en_HK |
dc.subject.mesh | Hepatitis B virus - genetics | en_HK |
dc.subject.mesh | Liver Neoplasms - virology | en_HK |
dc.subject.mesh | Promoter Regions (Genetics) - genetics | en_HK |
dc.title | Risk for hepatocellular carcinoma with respect to hepatitis B virus genotypes B/C, specific mutations of enhancer II/core promoter/precore regions and HBV DNA levels | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0017-5749&volume=57&issue=1&spage=98&epage=102&date=2008&atitle=Risk+for+hepatocellular+carcinoma+with+respect+to+hepatitis+B+virus+genotypes+B/C,+specific+mutations+of+enhancer+II/core+promoter/precore+regions+and+HBV+DNA+levels | en_HK |
dc.identifier.email | Yuen, MF: mfyuen@hku.hk | en_HK |
dc.identifier.email | Poon, RT: poontp@hku.hk | en_HK |
dc.identifier.email | Fong, DYT: dytfong@hku.hk | en_HK |
dc.identifier.email | Fung, J: jfung@sicklehut.com | en_HK |
dc.identifier.email | Wong, DKH: danywong@hku.hk | en_HK |
dc.identifier.email | Lai, CL: hrmelcl@hku.hk | en_HK |
dc.identifier.authority | Yuen, MF=rp00479 | en_HK |
dc.identifier.authority | Poon, RT=rp00446 | en_HK |
dc.identifier.authority | Fong, DYT=rp00253 | en_HK |
dc.identifier.authority | Fung, J=rp00518 | en_HK |
dc.identifier.authority | Wong, DKH=rp00492 | en_HK |
dc.identifier.authority | Lai, CL=rp00314 | en_HK |
dc.description.nature | published_or_final_version | en_HK |
dc.identifier.doi | 10.1136/gut.2007.119859 | en_HK |
dc.identifier.pmid | 17483190 | - |
dc.identifier.scopus | eid_2-s2.0-38349138512 | en_HK |
dc.identifier.hkuros | 130659 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-38349138512&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 57 | en_HK |
dc.identifier.issue | 1 | en_HK |
dc.identifier.spage | 98 | en_HK |
dc.identifier.epage | 102 | en_HK |
dc.identifier.isi | WOS:000251778400021 | - |
dc.publisher.place | United Kingdom | en_HK |
dc.identifier.scopusauthorid | Yuen, MF=7102031955 | en_HK |
dc.identifier.scopusauthorid | Tanaka, Y=7405315865 | en_HK |
dc.identifier.scopusauthorid | Shinkai, N=7003826116 | en_HK |
dc.identifier.scopusauthorid | Poon, RT=7103097223 | en_HK |
dc.identifier.scopusauthorid | But, DYK=24343113400 | en_HK |
dc.identifier.scopusauthorid | Fong, DYT=35261710300 | en_HK |
dc.identifier.scopusauthorid | Fung, J=23091109300 | en_HK |
dc.identifier.scopusauthorid | Wong, DKH=7401535819 | en_HK |
dc.identifier.scopusauthorid | Yuen, JCH=7102620480 | en_HK |
dc.identifier.scopusauthorid | Mizokami, M=7103318255 | en_HK |
dc.identifier.scopusauthorid | Lai, CL=7403086396 | en_HK |
dc.identifier.issnl | 0017-5749 | - |