Evidence map›Paper›PMID 25337243›Full record

ArticleInternational journal of clinical and experimental pathology2014

Identification of hepatitis B virus X gene variants between hepatocellular carcinoma tissues and pericarcinoma liver tissues in Eastern China.

Dan Wang, Hao Cai, Wen-Bo Yu, Long Yu

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.3field-weighted citation impact, top 21% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Hepatitis B virus X protein in liver tumor microenvironment.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
  5. Article
  6. Article
  7. Review
  8. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Dan WangThe State Key Laboratory of Genetics Engineering, Fudan University Shanghai, 200433, P.R. China.
Hao CaiThe State Key Laboratory of Genetics Engineering, Fudan University Shanghai, 200433, P.R. China.
Wen-Bo YuThe State Key Laboratory of Genetics Engineering, Fudan University Shanghai, 200433, P.R. China.
Long YuThe State Key Laboratory of Genetics Engineering, Fudan University Shanghai, 200433, P.R. China.
Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelledHepatocellular carcinoma (HCC) is one of the most malignant tumors worldwide, especially in Eastern China where HBV infection confirmed as the most important pathological element. HBV X gene, extremely easy to mutate and integrate into hepatocytes, plays a significant role in HBV infection and HCC development. We deduced that mutations of integrated HBx gene make transformation more malignant. The aim of the study was to investigate whether there were different mutation patterns between the HCC tissues and the pericarcinoma liver tissues (PCLT) from patients with HCC in Eastern China.

methodsHBx genes extracted from 287 HCC tissue samples and 195 PCLT tissue samples were analyzed by sequence alignment and stratified analysis with the matched medical records.

resultsMutations occurred complicated and changeable in both HCC and PCLT. COOH-terminal truncation is more frequently found in HCC than PCLT (P < 0.05). There is no single site mutation of nucleic acid or amino acid makes distribution discrepancy between HCC and PCLT. Hydrophobic/hydrophilic character of amino acid of site 43, 47, 127, 131, 132 make distribution discrepancy between HCC and PCLT in men when stratified for gender (P < 0.05). Hydrophobic/hydrophilic character of amino acid of site 40 makes distribution discrepancy between HCC and PCLT in both male and female (P < 0.05). Hydrophobic/hydrophilic character of amino acid of site 47 and 127 make significant discrepancy among clinical stage I, II, III (P < 0.05).

conclusionsDuring the infection and replication of HBV, HBx mutates to adjust itself to the hepatocyte and increase the carcinogenesis. COOH-terminal truncated HBX may play a stimulative role in HBV-related HCC carcinogenesis as well as hydrophobic/hydrophilic character changes in some specific amino acid sites.

Indexed as

MutationAmino Acid SequenceCarcinoma, HepatocellularCell Transformation, ViralChinaDNA Mutational AnalysisDNA, ViralFemaleGenotypeHepatitis BHepatitis B virusHumansHydrophobic and Hydrophilic InteractionsLiverLiver NeoplasmsMaleDNA, Viralhepatitis B virus X proteinTrans-ActivatorsViral Regulatory and Accessory ProteinsHepatitis B virushepatocellular carcinomamutationpericarcinoma liver tissueX gene

Identifiers

PMID25337243
PMCPMC4203214
OpenAlexW902759758

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.