Table 1

Multi-omics research on gastric inflammation-induced tumorigenesis

Omics levelOmics conductedSample categoriesStudy designHighlighted findingsRefs
PhenotypePhenomicsClinical follow-up informationLongitudinalAssociation between smoking and IM progression47
PhenotypePhenomicsTissue samples and PBMCLongitudinalAssociation between serum biomarkers and gastric precancerous progression48
CellularSingle-cell transcriptomicsTissue samplesCross-sectionalSingle-cell atlas, cell cluster marker, GC signatures33
CellularSingle-cell transcriptomicsTissue samples and PBMCCross-sectionalTME components, receptor‒ligand network34
CellularSingle-cell transcriptomicsTissue samplesCross-sectionalHeterogeneous cell population, epithelial-myofibroblast transition49
CellularSingle-cell transcriptomics, spatial transcriptomicsTissue samples, in vitro and in vivo modelsCross-sectionalLineage states across GC subtypes35
CellularSingle-cell transcriptomicsAscites samplesCross-sectionalDiversity in tumor cell lineage composition, intertumoral heterogeneity36
MolecularGenomicsTissue samplesCross-sectionalGenomic amplification in GC37
MolecularGenomicsCell linesCross-sectionalTranscription factors and their role in tumorigenesis38
MolecularGenomicsTissue samplesCross-sectionalMolecular subtypes of GC39
MolecularGenomicsTissue samplesCross-sectionalAssociation between genetic instability and HP infection40
MolecularGenomics, epigenomicsTissue samplesLongitudinalMolecular features of IM progression50
MolecularMicrobiomicsTongue-coating samplesCross-sectionalAssociation between the variation in tongue-coating microbiota and development of gastritis20