ArticleFrontiers in pharmacology2025
Identification of novel germline and somatic mutations associated with hepatocellular carcinoma by next-generation sequencing.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Inhibition of PERK signaling suppresses tumor progression and blocks GP73-GRP78-dependent stromal activation in hepatocellular carcinoma.Neoplasia (New York, N.Y.) · 2026Article
- Identification of Somatic and Germline Mutations Influencing Treatment Outcomes and Disease Susceptibility in Tunisian Triple-Negative Breast Cancer Using Next-Generation Sequencing.British journal of biomedical science · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Hepatocellular carcinoma (HCC) is the third leading cause of cancer-associated deaths worldwide with an estimated of 900,000 new cases annually. HCC typically arises in patients with chronic liver disease, including hepatitis, cirrhosis, and non-alcoholic fatty liver diseases. Identifying of the main driver genetic alterations in oncogenic genes is essential for understanding HCC pathogenesis and defining prognostic biomarkers in high-risk patients. This study aimed to identify both germline and somatic mutations associated with HCC in a Tunisian patient's cohort. Methods: Forty HCC patients with different etiologies were included in this study. Peripheral blood samples were collected from 24 patients with advanced-stage HCC. Paired tumor and adjacent non-tumoral liver tissue samples were obtained from 16 early-stage HCC patients undergoing hepatic resection, including 10 fresh-frozen samples and 6 FFPE samples. DNA was extracted using the MagCore® Plus II system. Targeted next-generation sequencing was performed using Results: A total of 35 germline mutations were identified across 25 genes. Recurrently altered genes included FGFR3 (100%), PDGFRA (100%), RET (98%), APC (92%), TP53 (88%), and EGFR (75%). In addition, 14 somatic mutations were detected in 13 genes, with frequent alterations observed in APC (100%), ALK (94%), HNF1A (56%), CDKN2A (50%), and HRAS (50%). Conclusion: This study offers the first comprehensive overview of novel germline and somatic mutations in Tunisian HCC patients, representing a North African cohort, and highlights key molecular drivers of hepatocarcinogenesis. These findings support the integration of genetic profiling into clinical practice to enhance early diagnosis and guide personalized therapies.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.