Loading
Life sciences · Journal article
Cancer Immunology Immunotherapy · September 20, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
Abstract Our previous work established that myeloid-derived suppressor cells (MDSCs) were abundant in human esophageal squamous cell carcinoma (ESCC) and correlated with adverse prognosis. Yet their direct, T cell-independent impact on tumor propagation remains undefined. Here, we show that MDSCs accelerate ESCC growth in both immunocompetent and T cell-deficient mice, indicating an intrinsic tumor-promoting program. Anti-Gr1-mediated MDSC depletion or IL-1β neutralization reduced intratumoral HNF1A expression, blunted CXCL1 promoter activity and down-regulated the stemness transcription factors Oct4, Nanog and Sox9. Deletion of HNF1A in tumor cells abolished MDSC-driven expansion of cancer stem cells (CSCs) and abrogated tumor initiation, whereas exogenous IL-1β reinstated CSC frequencies. Thus, MDSC-derived IL-1β licenses an HNF1A–CXCL1 axis that sustains CSC properties independently of adaptive immunity. Targeting this pathway may complement T cell-focused therapies in ESCC. Graphical abstract Myeloid-derived suppressor cells license stem-like properties in esophageal squamous cell carcinoma via HNF1A-driven CXCL1 signaling and predict poor prognosis.