No association for Chinese HBV-related hepatocellular carcinoma susceptibility SNP in other East Asian populations

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Abstract

Background

A recent genome-wide association study (GWAS) using chronic HBV (hepatitis B virus) carriers with and without hepatocellular carcinoma (HCC) in five independent Chinese populations found that one SNP (rs17401966) in KIF1B was associated with susceptibility to HCC. In the present study, a total of 580 HBV-derived HCC cases and 1351 individuals with chronic hepatitis B (CHB) or asymptomatic carrier (ASC) were used for replication studies in order to evaluate the reported association with HBV-derived HCC in other East Asian populations.

Results

We did not detect any associations between rs17401966 and HCC in the Japanese cohorts (replication 1: OR = 1.09, 95 % CI = 0.82-1.43; replication 2: OR = 0.79, 95 % CI = 0.54-1.15), in the Korean cohort (replication 3: OR = 0.95, 95 % CI = 0.66-1.36), or in the Hong Kong Chinese cohort (replication 4: OR = 1.17, 95 % CI = 0.79-1.75). Meta-analysis using these cohorts also did not show any associations with P = 0.97.

Conclusions

None of the replication cohorts showed associations between rs17401966 and HBV-derived HCC. This may be due to differences in the genetic diversity among the Japanese, Korean and Chinese populations. Other reasons could be the high complexity of multivariate interactions between the genomic information and the phenotype that is manifesting. A much wider range of investigations is needed in order to elucidate the differences in HCC susceptibility among these Asian populations.

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Global cancer statistics in the year 2000.

D M Parkin (2001)

Estimation of the burden of cancer in terms of incidence, mortality, and prevalence is a first step to appreciating appropriate control measures in a global context. The latest results of such an exercise, based on the most recent available international data, show that there were 10 million new cases, 6 million deaths, and 22 million people living with cancer in 2000. The most common cancers in terms of new cases were lung (1.2 million), breast (1.05 million), colorectal (945,000), stomach (876,000), and liver (564,000). The profile varies greatly in different populations, and the evidence suggests that this variation is mainly a consequence of different lifestyle and environmental factors, which should be amenable to preventive interventions. World population growth and ageing imply a progressive increase in the cancer burden--15 million new cases and 10 million new deaths are expected in 2020, even if current rates remain unchanged.

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Associations Between Hepatitis B Virus Genotype and Mutants and the Risk of Hepatocellular Carcinoma

Hwai-I Yang, Shiou-Hwei Yeh, Pei-Jer Chen … (2008)

Background The risk of hepatocellular carcinoma (HCC) increases with increasing level of hepatitis B virus (HBV) in serum (viral load). However, it is unclear whether genetic characteristics of HBV, including HBV genotype and specific genetic mutations, contribute to the risk of HCC. We examined the HCC risk associated with HBV genotypes and common variants in the precore and basal core promoter (BCP) regions. Methods From January 5, 1991, to December 21, 1992, baseline blood samples were collected from 2762 Taiwanese men and women who were seropositive for HBV surface antigen but had not been diagnosed with HCC; the samples were tested for HBV viral load by real-time polymerase chain reaction and genotyped by melting curve analysis. Participants who had a baseline serum HBV DNA level greater than 104 copies/mL (n = 1526) were tested for the precore G1896A and BCP A1762T/G1764A mutants by direct sequencing. Incident cases of HCC were ascertained through follow-up examinations and computerized linkage to the National Cancer Registry and death certification profiles. A Cox proportional hazards model was used to estimate the risk of HCC associated with HBV genotype and precore and BCP mutants after adjustment for other risk factors. All statistical tests were two-sided. Results A total of 153 HCC cases occurred during 33 847 person-years of follow-up. The HCC incidence rates per 100 000 person-years for participants infected with HBV genotype B or C were 305.6 (95% confidence interval [CI] = 236.9 to 388.1) and 785.8 (95% CI = 626.8 to 972.9), respectively. Among participants with a baseline HBV DNA level of at least 104 copies/mL, HCC incidence per 100 000 person-years was higher for those with the precore G1896 (wild-type) variant than for those with the G1896A variant (955.5 [95% CI = 749.0 to 1201.4] vs 269.4 [95% CI = 172.6 to 400.9]) and for those with the BCP A1762T/G1764A double mutant than for those with BCP A1762/G1764 (wild-type) variant (1149.2 [95% CI = 872.6 to 1485.6] vs 358.7 [95% CI = 255.1 to 490.4]). The multivariable-adjusted hazard ratio of developing HCC was 1.76 (95% CI = 1.19 to 2.61) for genotype C vs genotype B, 0.34 (95% CI = 0.21 to 0.57) for precore G1896A vs wild type, and 1.73 (95% CI = 1.13 to 2.67) for BCP A1762T/G1764A vs wild type. Risk was highest among participants infected with genotype C HBV and wild type for the precore 1896 variant and mutant for the BCP 1762/1764 variant (adjusted hazard ratio = 2.99, 95% CI = 1.57 to 5.70, P < .001). Conclusions HBV genotype C and specific alleles of BCP and precore were associated with risk of HCC. These associations were independent of serum HBV DNA level.

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Hepatocellular carcinoma: epidemiology, surveillance, and diagnosis.

Morris Sherman (2010)

Hepatocellular carcinoma (HCC) is increasing in incidence in many countries, and is the most common cause of death in patients with cirrhosis. With regular surveillance, small early HCC lesions can be identified. An algorithm has been developed that allows for diagnosis of these lesions. Very early HCC lesions have high cure rates with appropriate treatment. If all these factors are in place most HCCs can be cured.

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Author and article information

Journal

Journal ID (nlm-ta): BMC Med Genet

Journal ID (iso-abbrev): BMC Med. Genet

Title: BMC Medical Genetics

Publisher: BioMed Central

ISSN (Electronic): 1471-2350

Publication date Collection: 2012

Publication date (Electronic): 19 June 2012

Volume: 13

Page: 47

Affiliations

[1 ]Department of Human Genetics, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan

[2 ]The Research Center for Hepatitis and Immunology, National Center for Global Health and Medicine, Ichikawa, Japan

[3 ]Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan

[4 ]Department of Internal Medicine, Hokkaido University Graduate School of Medicine, Sapporo, Japan

[5 ]Department of Internal Medicine, Teine Keijinkai Hospital, Sapporo, Japan

[6 ]First Department of Internal Medicine, Iwate Medical University, Iwate, Japan

[7 ]Division of Gastroenterology and Hepatology, Internal Medicine, Saitama Medical University, Saitama, Japan

[8 ]Department of Gastroenterology, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan

[9 ]Division of Gastroenterology and Hepatology, Musashino Red Cross Hospital, Tokyo, Japan

[10 ]Department of Gastroenterology, Kanazawa University Graduate School of Medicine, Kanazawa, Japan

[11 ]Department of Medicine, Shinshu University School of Medicine, Matsumoto, Japan

[12 ]Department of Clinical Molecular Informative Medicine, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan

[13 ]Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, Kyoto, Japan

[14 ]National Hospital Organization Osaka National Hospital, Osaka, Japan

[15 ]Division of Hepatology and Pancreatology, Kawasaki Medical College, Kurashiki, Japan

[16 ]Second department of Internal Medicine, Faculty of Medicine, Tottori University, Yonago, Japan

[17 ]Department of Gastroenterology and Metabology, Ehime University Graduate School of Medicine, Ehime, Japan

[18 ]Division of Gastroenterology, Department of Medicine, Kurume University School of Medicine, Fukuoka, Japan

[19 ]Department of International Medicine, Yonsei University College of Medicine, Seoul, Korea

[20 ]Department of Medicine, the University of Hong Kong, Queen Mary Hospital, Hong Kong, China

Article

Publisher ID: 1471-2350-13-47

DOI: 10.1186/1471-2350-13-47

PMC ID: 3407509

PubMed ID: 22712471

SO-VID: 27be7858-9276-4051-b66f-5366304dbcd9

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

No association for Chinese HBV-related hepatocellular carcinoma susceptibility SNP in other East Asian populations

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Abstract

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Results

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G3: Genes|Genomes|Genetics

Most cited references 10

Global cancer statistics in the year 2000.

Associations Between Hepatitis B Virus Genotype and Mutants and the Risk of Hepatocellular Carcinoma

Hepatocellular carcinoma: epidemiology, surveillance, and diagnosis.

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