Evidence map›Paper›PMID 24829649›Full record

ArticleMiddle East journal of digestive diseases2012

Hepatitis B virus genome asymmetry in hepatocellular carcinoma.

Zahra Shokrgozar, Sirous Tayebi, Zarrin Minucheher, Ashraf Mohamadkhani

Abstract read
In one paragraph

Article in Middle East journal of digestive diseases, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Zahra ShokrgozarResearcher,University of Mohaghegh Ardabili, Ardabil, Iran.
Sirous TayebiDigestive Disease Research Center, Shariati Hospital, Tehran University of Medical Science, Tehran, Iran.
Zarrin MinucheherNational Institute of Genetic Engineering and Biotechnology, NIGEB, Tehran, Iran.
Ashraf MohamadkhaniDigestive Disease Research Center, Shariati Hospital, Tehran University of Medical Science, Tehran, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe association between hepatitis B virus (HBV) mutations and hepatocarcinogenesis were reported in the literature. Preference for G over C in the leading DNA strand has been reported to account for the asymmetry in nucleotide (nt) composition. The aim of this study was to analyze the complete genome sequence and compositional asymmetry of HBV in different stages of hepatitis B.

methodsFull genome sequencing of 24 patients with chronic hepatitis B, some of whom also had cirrhosis and hepatocellular carcinoma (HCC) was performed. Mutations analysis was implemented in a comparison with a HBV genotype D reference from an international DNA database. CpGProD, a web-based application, was used to evaluate CG content and predict CpG islands.

resultsAll strains were 3182 base pairs (bp) in length, except for two cases of HCC in which 9 and 21 nt, respectively, were deleted in preS2. The genetic relatedness of these isolates was 97%-100%. There were common CpG-rich regions in all 24 isolated full genome sequences, however a strong negative GC skew for forming a CpG island in the minus strand were exhibited in overlap with enhancer I in three HCC patients, a cirrhotic patient and three with chronic hepatitis.

conclusionThe high percentage of sequence identity between HBV isolates in our patients demonstrates that genomic factors, except for genotype, are involved in hepatocarcinogenesis. Variations in GC content which were caused by a different spectrum of mutations may affect DNA compositional asymmetry and epigenetic modification of HBV DNA in HCC.

Indexed as

HBV genome CpGHepatitis B virus (HBV)Hepatocellular carcinoma (HCC)

Identifiers

PMID24829649
PMCPMC3990121

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