ArticleOncology2026
Unique Stroma of Higher-Grade Pancreatic Intraepithelial Neoplasia: Fibroblastic Cluster Formation and CD36 Downregulation.
Article in Oncology, 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionIdentifying pathological markers to differentiate between high- and low-grade pancreatic intraepithelial neoplasia (PanIN) remains an unmet clinical need. Recent studies suggest that the tumor microenvironment undergoes dynamic changes during PanIN progression. To establish objective pathological markers, this study investigated histological, immunohistochemical, and molecular alterations in PanIN-associated stroma across different grades.
methodsFibroblastic cluster (FC) was defined and characterized using immunohistochemistry (IHC) for SMA, CD31, and CD34, and their frequency was assessed according to PanIN grade in 202 PanIN lesions and 58 normal ducts. To identify molecular differences among PanIN types, multiple gene expression analysis (MGEA) was performed for six normal ducts and for three PanIN1, three PanIN2, and six PanIN3 lesions. IHC and fluorescent dual IHC for CD31 and CD36 were performed to quantify CD36-positive stromal vessels. RNA scope for PPARγ and IHC for thrombospondin-1 (TSP-1) and forkhead box O1 (FOXO-1) were performed to explore the molecular basis of CD36 downregulation.
resultsFCs were identified in 86.6% of PanIN3 stroma and were significantly more frequent than in lower-grade PanINs. MGEA revealed downregulation of CD36 in PanIN2-3 compared with PanIN1, and CD36-positive vessels were significantly fewer in higher-grade PanIN stroma. PPARγ signals were present in low-grade but absent in high-grade PanIN stroma. TSP-1 expression paralleled CD36 expression. These findings suggest that the possible relationship between the repression of CD36 in the stromal vasculature of high-grade PanIN and reduced PPARγ and TSP-1 signaling.
conclusionsHigher-grade PanINs harbor a unique stroma characterized by FC formation and an increased proportion of CD36-negative vessels.
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.