Evidence map›Paper›PMID 40445003›Full record

ArticleBriefings in bioinformatics2025

Multi-omics analysis of Helicobacter pylori-associated gastric cancer identifies hub genes as a novel therapeutic biomarker.

Sara H Mohamed, Mohamed Hamed, Hussain A Alamoudi, Zayd Jastaniah, Fadhl M Alakwaa, Asmaa Reda

Abstract read
In one paragraph

Article in Briefings in bioinformatics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Advances inOncology letters · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Impact ofInternational journal of molecular sciences · 2025
    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.

Sara H MohamedDepartment of Microbiology, Egyptian Drug Authority (EDA), formerly National Organization for Drug Control and Research (NODCAR), Giza 14281, Egypt.ORCID 0000-0003-1379-6493
Mohamed HamedInstitute for Biostatistics and Informatics in Medicine and Ageing Research (IBIMA), Rostock University Medical Center, Rostock 18057, Germany.ORCID 0000-0002-9102-8839
Hussain A AlamoudiRadiation Oncology Department, Oncology Center in East Jeddah Hospital (Jeddah First Health Cluster), Rabigh, Saudi Arabia.
Zayd JastaniahCenter of Nanotechnology, King Abdulaziz University, Jeddah 21589, Saudi Arabia.
Fadhl M AlakwaaDepartment of Internal Medicine, Division of Nephrology, University of Michigan, Ann Arbor, MI, United States.ORCID 0000-0001-5349-7960
Asmaa RedaCenter of Nanotechnology, King Abdulaziz University, Jeddah 21589, Saudi Arabia.ORCID 0000-0003-3887-8196

Funding

DAAD Ta'ziz project GJRC-IH: German-Jordanian Research Cluster in Intelligent Healthcare Informatics 57747902GARN-CLS: German Arab Research Network for Computational Life Science 57682181
6 · The paper itself

Abstract

Helicobacter pylori infection is one of the most common gastric pathogens; however, the molecular mechanisms driving its progression to gastric cancer remain poorly understood. This study aimed to identify the key transcriptomic drivers and therapeutic targets of H. pylori-associated gastric cancer through an integrative transcriptomic analysis. This analysis integrates microarray and RNA-seq datasets to identify significant differentially expressed genes (DEGs) involved in the progression of H. pylori-associated gastric cancer. In addition to independent analyses, data were integrated using ComBat to detect consistent expression patterns of hub genes. This approach revealed distinct clustering patterns and stage-specific transcriptional changes in common DEGs across disease progression, including H. pylori infection, gastritis, atrophy, and gastric cancer. Genes such as TPX2, MKI67, EXO1, and CTHRC1 exhibited progressive upregulation from infection to cancer, highlighting involvement in cell cycle regulation, DNA repair, and extracellular matrix remodeling. These findings provide insights into molecular shifts linking inflammation-driven infection to malignancy. Furthermore, network analysis identified hub genes, including CXCL1, CCL20, IL12B, and STAT4, which are enriched in immune pathways such as chemotaxis, leukocyte migration, and cytokine signaling. This emphasizes their role in immune dysregulation and tumor development. Expression profiling demonstrated the upregulation of hub genes in gastric cancer and stage-specific changes correlating with disease progression. Finally, drug-gene interaction analysis identified therapeutic opportunities, with hub genes interacting with approved drugs like abatacept and zoledronic acid, as well as developmental drugs such as adjuvant and relapladib. These findings highlight the key role of these hub genes as biomarkers and therapeutic targets, providing a foundation for advancing precision medicine in H. pylori-associated gastric cancer. Overall, this study paves the way for advancing precision medicine in H. pylori-associated gastric cancer by providing insights into the development of early detection biomarkers, risk stratification, and targeted therapies. This supports the clinical translation of precision medicine strategies in H. pylori-associated gastric cancer.

Indexed as

Biomarkers, TumorHelicobacter InfectionsHelicobacter pyloriStomach NeoplasmsGene Expression ProfilingGene Expression Regulation, NeoplasticGene Regulatory NetworksHumansMultiomicsTranscriptomeBiomarkers, TumorBiomarkers discoveryGastric cancerHelicobacter pyloriHub genesTherapeutic targetsTranscriptome analysis

Identifiers

PMID40445003
PMCPMC12123523

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.