ArticleGenomics, proteomics & bioinformatics2026
A Single-cell and Spatially Resolved Cell Atlas of Human Esophageal Squamous Cell Carcinoma.
Article in Genomics, proteomics & bioinformatics, 2026. 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.
- Cancer Heterogeneity and Cancer Cell Plasticity: Molecular Mechanisms and Precision Therapy.MedComm · 2026Review
- Single-cell Spatial Multiomics: Technologies, Methods, and Biological Applications.Genomics, proteomics & bioinformatics · 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
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor heterogeneity and the suppressive microenvironment are key challenges that limit the effectiveness of cancer treatment. In this study, we systematically elucidated the molecular characteristics and mechanisms underlying the suppressive immune microenvironment using a combination of single-cell RNA sequencing, spatial transcriptomics, and metabolomics for a series of human esophageal squamous cell carcinoma and matched non-tumor tissues. We found that COL17A1+ epithelial cells exhibited greater malignancy, characterized by the accumulation of triglycerides and phosphocholine. We also identified a tumor-specific POSTN+ fibroblast subgroup. We identified a unique epithelial-fibroblast niche with low infiltration of effector immune cells and substantial lipid enrichment, composed of POSTN+ fibroblasts and COL17A1+ epithelial cells, in which their crosstalk contributed to tumor progression. We confirmed that the INHBA/TP63 axis played a key role in mediating the regulation of COL17A1+ tumor cells by POSTN+ fibroblasts. Our findings provide new insights into the characteristics of the tumor microenvironment and the crosstalk between tumor cells and fibroblasts, offering valuable multi-omics data for elucidating tumor progression mechanisms.
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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.