ArticleCell death & disease2026
The PLAU-ITGB1-TGF-β axis orchestrates spatiotemporal reprogramming of fibroblasts at the invasive front to drive dual immunosuppressive niche and immunotherapy resistance in oral squamous cell carcinoma.
Article in Cell death & disease, 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
9 authors.
Funding
Abstract
The initiation and progression of cancer are driven by the dynamic interplay between somatic mutations and the tumor microenvironment. Identifying core cell populations driving malignant transformation and understanding the intercellular interactions within the tumor microenvironment are, therefore, crucial for early diagnosis and effective treatment. Here, we construct a spatiotemporal atlas of oral squamous cell carcinoma (OSCC) progression by integrating multi-omics approaches. Our analysis reveals that the critical driver gene PLAU activates the TGF-β pathway via ITGB1, thereby promoting the conversion of fibroblasts into the COL11A1⁺ fibroblast (COL11A1⁺ Fib). These specialized fibroblasts remodel the extracellular matrix (ECM), collectively establishing an immunosuppressive niche composed of malignant epithelial cells, COL11A1
Indexed as
Identifiers
What Socratic 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 Socratic graph.