Evidence map›Paper›PMID 40854652›Full record

ArticleJournal, genetic engineering & biotechnology2025

cfDNA Key genomic markers in HCV-Induced hepatocellular carcinoma in Egyptian patients.

Mohamed Khalifa, Ahmed A Hmed, Khaled S Elfeky, Sayed Bakry, Manal El Hamshary, Ahmed R Sofy

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In one paragraph

Article in Journal, genetic engineering & biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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

1 citing paper in PubMed.

  1. Article
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

6 authors.

Mohamed KhalifaZoology Department, Faculty of Science, Al-Azhar University, Nasr City, Cairo 11884, Egypt; Molecular Pathology Laboratory, Children Cancer Hospital, 57357 Cairo, Egypt. Electronic address: mohamedkamal96@hotmail.com.
Ahmed A HmedBotany and Microbiology Department, Faculty of Science, Al-Azhar University, Nasr City, Cairo 11884, Egypt.
Khaled S ElfekyZoology Department, Faculty of Science, Al-Azhar University, Nasr City, Cairo 11884, Egypt.
Sayed BakryCenter for Genetic Engineering- Al-Azhar University, Nasr City, Cairo 11884, Egypt.
Manal El HamsharyMolecular Genetics and Molecular Diagnostics, Molecular Diagnostics and Therapeutics Department, Genetic Engineering and Biotechnology Research Institute, University of Sadat City, Menofia, Egypt.
Ahmed R SofyBotany and Microbiology Department, Faculty of Science, Al-Azhar University, Nasr City, Cairo 11884, Egypt.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMalignant liver disease is among the highest in the world, with hepatocellular carcinoma (HCC) accounting for up to 90 % of all cases. In Egypt, HCC poses a significant public-health concern, representing 47.17 % of cancer cases. The high incidence of hepatitis C virus (HCV) in the Egypt was a major predisposing factor for HCC. MATERIAL: This study included 63 Egyptian HCC patients, 55 % of whom had a history of HCV infection.

methodsUsing a paired sampling strategy, approximately 2800 COSMIC mutations from 50 oncogenes and tumor-suppressor genes were NGS sequenced.

resultsTotal of 381 somatic mutations were identified, 91 mutations detected in the HCC group and 291 in the HCV-related HCC group. The top 10 mutated genes in the non-HCV group were TP53, ATM, EGFR, CDH1, FGFR1, MET, SMAD4, ERBB2, FLT3, and FBXW7, while in the HCV-related HCC group, genes were KIT, ATM, TP53, APC, FBXW7, KDR, RB1, SMAD4, EGFR, and PIK3CA.

conclusionThe present study represents the first comprehensive somatic mutation profile in HCC Egyptian patients. This finding suggests that HCV viral infection played a direct and indirect role in increasing the somatic mutation burden in HCV-related HCC patients and opens new promises of targeted therapies for those patients.

Indexed as

cfDNAHCCHCVNGSSomatic mutationTumor signature

Identifiers

PMID40854652
PMCPMC12301743

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