ArticleHereditas2026
Multi-omics mapping of TIMP1-associated stromal-myeloid remodeling in autoimmune gastritis and gastric cancer.
Article in Hereditas, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
backgroundAutoimmune gastritis (AIG) is a chronic immune-mediated atrophic disease that can induce cancer-related epithelial remodeling, although its association with gastric adenocarcinoma depends on histological and clinical modifiers. Gastric cancer (GC) progression is shaped by the tumor microenvironment (TME), including cancer-associated fibroblasts (CAFs), myeloid cells, and extracellular matrix (ECM) remodeling. Whether AIG-related mucosal remodeling shares stromal programs with GC-associated stromal-myeloid niches remains unclear.
methodsWe integrated one AIG bulk-transcriptomic cohort and three GC cohorts to identify shared differentially expressed genes (DEGs), followed by LASSO, random forest and protein-protein interaction (PPI) analyses. TIMP1 was evaluated using tissue transcriptomic cohorts, serum RT-qPCR, survival analysis, immune infiltration profiling, scRNA-seq, inferCNV-based epithelial classification, CellChat ligand-receptor inference and spatial transcriptomics.
resultsA total of 51 shared DEGs were identified between AIG and GC. TIMP1 was the only candidate supported by both machine-learning screening and PPI hub-gene analysis. TIMP1 was upregulated in GC tissues and serum and showed an exploratory tumor-normal ROC AUC of 0.941 in the TCGA_STAD cohort, while higher TIMP1 expression was associated with poorer overall survival. Functional analyses linked TIMP1-high GC to ECM organization, integrin binding, epithelial-mesenchymal transition (EMT), transforming growth factor-β signaling and immune infiltration. scRNA-seq of 160,812 GC cells localized TIMP1 mainly to CAF and myeloid compartments. In AIG, TIMP1-high fibroblasts displayed enhanced CAF-associated stromal and inflammatory transcriptional programs. CellChat and spatial transcriptomics further linked TIMP1-associated stromal and myeloid states to ECM-dominant communication and fibroblast-rich, myeloid-associated remodeling regions.
conclusionsTIMP1 may mark related stromal-myeloid remodeling states across AIG-associated mucosal remodeling and GC, providing a hypothesis-generating framework potentially relevant to inflammation-associated gastric tumorigenesis.
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.