ArticleScientific reports2026
Visualizing malignant progression: in situ CD109-based spatial immunofluorescence assay delineates papillary to anaplastic thyroid carcinoma transformation within the tumor microenvironment.
Article in Scientific reports, 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
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
1 citing paper in PubMed.
- Cell-state transitions and microenvironmental remodeling in thyroid cancer progression revealed by single-cell and spatial transcriptomics.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
11 authors.
Funding
Abstract
Anaplastic thyroid carcinoma (ATC) is the rarest and most aggressive subtype of thyroid cancer, and considered to arise from differentiated thyroid carcinoma, however, the underlying molecular processes remain largely unknown. Using CD109 as a malignant marker, we analyzed an ATC case containing a papillary thyroid carcinoma (PTC) component. Our newly developed spatial immunofluorescence (SPI) assay, which enabled the differential expression of CD109 and CK8/18, a PTC marker, demonstrated gradual and completely opposed changes at the boundary between ATC and PTC components. Similar specific expression patterns were observed in E-cadherin, vimentin, PCNA, αSMA, Iba-1, collagen (COL) III/VI, TGFβ1-induced (TGFBI), active Yes-associated protein, periostin, and S100. The zonal and reciprocal transitions between PTC and ATC markers suggested that anaplastic transformation was not merely the result of clonal expansion, but rather it was executed by ATC-specific tumor microenvironment (ATC-TME) that recruited more Iba-1- and S100-positive macrophages, along with unique ATC-cancer-associated fibroblasts (CAFs), which deposited more COL III/VI and TGFBI. We proposed that expansion of ATC-CAFs caused extracellular matrix stiffening and compromised PTC cells, thereby inducing necroptosis and S100 release. This process simultaneously promoted the epithelial-mesenchymal transition in PTC cells and selected pre-existing PTC cells harboring additional gene mutations sufficient for anaplastic transformation.
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.