ArticleClinical and experimental medicine2026
ITM2A promotes thyroid cancer differentiation through metabolic reprogramming and enhances PD-L1-dependent T-cell responses.
Article in Clinical and experimental medicine, 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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The differentiation status of thyroid cancer (THCA) is closely associated with prognosis; however, the underlying molecular regulatory mechanisms remain incompletely understood. This study aimed to identify hub genes associated with THCA differentiation based on progression-free interval (PFI)-related genes and to explore the underlying mechanisms. The common database datasets were integrated to identify differentially expressed genes, and univariate Cox regression analysis was performed to determine PFI-related genes. Molecular subtypes were constructed using consensus clustering based on PFI-related genes, and the differentiation status of different subtypes was evaluated. Hub genes were subsequently identified using least absolute shrinkage and selection operator (Lasso) regression and multivariate Cox regression analyses. In vitro experiments were conducted to validate the role of the hub gene in regulating dedifferentiation. Two PFI-related molecular subtypes were identified in this study. Cluster 2 exhibited a higher thyroid differentiation score (TDS), more favorable PFI outcomes, and metabolic features predominantly characterized by oxidative phosphorylation (OXPHOS) and fatty acid oxidation (FAO). ITM2A was identified as a hub gene. High expression of ITM2A promoted differentiation of THCA cells, suppressed malignant characteristics, and drove a metabolic shift from glycolysis toward FAO. In addition, ITM2A counteracted TGF-β-induced dedifferentiation and epithelial-mesenchymal transition, and enhanced antigen presentation as well as PD-L1-dependent T-cell responses. ITM2A maintained the differentiated state of THCA through metabolic reprogramming and shaped an immunologically favorable microenvironment, suggesting that it may serve as a potential biomarker for prognosis prediction and a therapeutic target for optimizing immunotherapy strategies.
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.