Evidence map›Paper›PMID 31630500›Full record

ArticleClinical and molecular hepatology2020

Influence of some methylated hepatocarcinogenesis-related genes on the response to antiviral therapy and development of fibrosis in chronic hepatitis C patients.

Waleed Seif Eldin Mohamed Mostafa, Mohammed Hassan Saiem Al-Dahr, Dalia Abdel Hamid Omran, Zeinab Fathy Abdullah, Suzan Hamdy Elmasry, Mohamed Nabil Ibrahim

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical and molecular hepatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

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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

3 citing papers in PubMed, 5 citations in OpenAlex.

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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Waleed Seif Eldin Mohamed MostafaVirology and Immunology Unit, Department of Cancer Biology, National Cancer Institute, Cairo University, Cairo, Egypt.
Mohammed Hassan Saiem Al-DahrDepartment of Clinical Laboratory Sciences, College of Applied Medical Sciences, Jouf University, Al-Qurayyate, Kingdom of Saudi Arabia.
Dalia Abdel Hamid OmranDepartment of Endemic Medicine and Hepatogastroenterology, Faculty of Medicine, Cairo University, Cairo, Egypt.
Zeinab Fathy AbdullahVirology and Immunology Unit, Department of Cancer Biology, National Cancer Institute, Cairo University, Cairo, Egypt.
Suzan Hamdy ElmasryDepartment of Biochemistry, Ibn Sina National College for Medical Studies, Jeddah, Kingdom of Saudi Arabia.
Mohamed Nabil IbrahimDepartment of Clinical Laboratory Sciences, College of Applied Medical Sciences, Jouf University, Al-Qurayyate, Kingdom of Saudi Arabia.
Al Jouf University · SACairo University · EGIbn Sina National College for Medical Studies · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetics involved in multiple normal cellular processes. Previous research have revealed the role of hepatitis C virus infection in accelerating methylation process and affecting response to treatment in chronic hepatitis patients. This work aimed to elucidate the role of promoter methylation (PM) in response to antiviral therapy, and its contribution to the development of fibrosis through hepatocarcinogenesis-related genes. A total of 159 chronic hepatitis Egyptian patients versus 100 healthy control group were included. The methylation profile of a panel 9 genes (SFRP1, p14, p73, APC, DAPK, RASSF1A, LINE1, O6MGMT, and p16) was detected in patients' plasma using methylation-specific polymerase chain reaction (MSP). Clinical and laboratory findings were gathered for patients with combined pegylated interferon and ribavirin antiviral therapy. Regarding the patients' response to antiviral therapy, the percentage of non-responders for APC, O6MGMT, RASSF1A, SFRP1, and p16 methylated genes were significantly higher versus responders (P<0.05). Of the 159 included patients, the most frequent methylated genes were SFRP1 (102/159), followed by p16 (100/159), RASSF1A (98/159), then LINE1 (81/159), P73 (81/159), APC (78/159), DAPK (66/159), O6MGMT (66/159), and p14 (54/159). A total of 67/98 (68.4%) cases of RASSF1A methylated gene (P=0.0.024), and 62/100 (62%) cases of P16 methylated gene (P=0.03) were associated with mild-degree fibrosis. To recapitulate, the PM of SFRP1, APC, RASSF1A, O6MGMT, and p16 genes increases in chronic hepatitis C patients, and can affect patients' response to antiviral therapy. The RASSF1A and P16 genes might have a role in the distinction between mild and marked fibrosis.

Indexed as

DNA MethylationAdultAntiviral AgentsCase-Control StudiesDeoxyribonuclease IEgyptFemaleGenotypeHepacivirusHepatitis C, ChronicHumansIntercellular Signaling Peptides and ProteinsLiver CirrhosisMaleMembrane ProteinsMiddle AgedAntiviral AgentsDeoxyribonuclease IIntercellular Signaling Peptides and ProteinsLINE-1 endonuclease, humanMembrane ProteinsRASSF1 protein, humanSecreted Frizzled-Related ProteinsSFRP1 protein, humanTumor Suppressor ProteinsFibrosisHepatitis C, ChronicPeginterferon alfa-2bRibavirin

Identifiers

PMID31630500
PMCPMC6940485
OpenAlexW2981442625

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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.