Evidence map›Paper›PMID 34165682›Full record

ArticleMolecular and cellular biochemistry2021

Association of interleukin-18 genotypes (-607C > A) and (-137 G > C) with the hepatitis B virus disease progression to hepatocellular carcinoma.

Taqveema Ali, Roli Saxena, Isha Rani, Renuka Sharma, Deepti More, Rajendra Ola, Stuti Agarwal, Yogesh Kumar Chawla, Jyotdeep Kaur

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Article in Molecular and cellular biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 49% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

Taqveema AliDepartment of Biochemistry, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.
Roli SaxenaDepartment of Biochemistry, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.
Isha RaniDepartment of Biochemistry, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.
Renuka SharmaDepartment of Biochemistry, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.
Deepti MoreDepartment of Biochemistry, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.
Rajendra OlaDepartment of Biochemistry, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.
Stuti AgarwalDepartment of Biochemistry, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.
Yogesh Kumar ChawlaDepartment of Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.
Jyotdeep KaurDepartment of Biochemistry, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India. jyotdeep2001@yahoo.co.in.ORCID http://orcid.org/0000-0003-0284-4517
Post Graduate Institute of Medical Education and Research · IN

Funding

Department of Science and Technology, Ministry of Science and Technology SR/S0/HS-0043/2012
6 · The paper itself

Abstract

Chronic infection with HBV has been reported to be associated with the development of HCC. The inflammation mounted by cytokine-mediated immune system plays an important role in the pathogenesis of HBV-associated HCC. IL-18 is a pro-inflammatory cytokine whose role in the development of HBV-associated chronic to malignant disease state has not been much studied. The present study was conceived to determine the role of genetic polymorphisms in IL-18, serum levels of IL-18, and expression level of its signal transducers in the HBV disease progression. A total of 403 subjects were enrolled for this study including 102 healthy subjects and 301 patients with HBV infection in different diseased categories. Polymorphism was determined using PCR-RFLP. Genotypic distributions between the groups were compared using odd's ratio and 95% CI were calculated to express the relative risk. Circulating IL-18 levels were determined by ELISA. Expression levels of pSTAT-1 and pNFƙB was determined by western blotting. In case of IL-18(- 607C > A), the heterozygous genotype (CA) was found to be a protective factor while in case of IL-18(- 137G > C) the heterozygous genotype (GC) acted as a risk factor for disease progression from HBV to HCC. Moreover, serum IL-18 levels were significantly increased during HBV disease progression to HCC as compared to controls. Also the levels of activated signal transducers (pSTAT-1 and pNF-κB) of IL-18 in stimulated PBMCs were significantly increased during HBV to HCC disease progression. These findings suggest that IL-18 has the potential to act as a biomarker of HBV-related disease progression to HCC.

Indexed as

AdultCarcinoma, HepatocellularCase-Control StudiesDisease ProgressionFemaleGenetic Predisposition to DiseaseHepatitis B, ChronicHepatitis B virusHumansInterleukin-18Liver NeoplasmsMalePolymorphism, Single NucleotideIL18 protein, humanInterleukin-18GenotypeHCCHepatitis B virusIL-18SNPs

Identifiers

PMID34165682
OpenAlexW3130898330

What OpenQuestion holds

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Registered trials

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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.