ReviewFrontiers in immunology2026
Cancer-associated fibroblasts and immune remodeling in laryngeal squamous cell carcinoma: evidence and translational perspectives.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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
1 citing paper in PubMed.
- Testing immune priming failure in laryngeal squamous cell carcinoma: direct evidence, unresolved links, and a compartment-resolved framework.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Laryngeal squamous cell carcinoma (LSCC) remains a clinically challenging malignancy of the head and neck. Because organ preservation is a major therapeutic objective in LSCC, stromal biology is of particular clinical relevance. Stromal factors influence local disease control, functional outcomes, and treatment resistance. Cancer-associated fibroblasts (CAFs) are dynamic regulators of extracellular matrix remodeling, immune exclusion, angiogenesis, and therapeutic resistance. However, LSCC-specific evidence remains fragmented, and many mechanistic concepts are still extrapolated from head and neck squamous cell carcinoma (HNSCC) and hypopharyngeal squamous cell carcinoma (HPSCC). This review adopts an evidence-stratified framework that distinguishes direct LSCC evidence from translatable cross-site evidence and hypothesis-generating inferences. We propose a provisional five-state model for LSCC that includes myofibroblastic, inflammatory, antigen-presenting, extracellular matrix-remodeling, and putative immune-trapping CAF programs. Direct LSCC studies support the presence of early stromal activation along the leukoplakia-to-carcinoma continuum and the enrichment of
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