ArticleMolecular & cellular proteomics : MCP2026
Multiomics Profiling Reveals Distinct Immunosuppression and Metabolic Dysregulation in Aggressive Subtypes of Thyroid Cancer.
Article in Molecular & cellular proteomics : MCP, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Integrated Bioinformatics and Experimental Validation Reveal the Diagnostic and Prognostic Value of SMDT1 in Thyroid Carcinoma.Diagnostics (Basel, Switzerland) · 2026Article
- Cancer Stemness and Dedifferentiation in Anaplastic Thyroid Carcinoma: Insights into a Multigenic, Microenvironmental Network and the Role of CD44.Biomedicines · 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
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thyroid cancer comprises a heterogeneous group of malignancies with distinct clinical outcomes and molecular features, including papillary thyroid carcinoma (PTC), poorly differentiated thyroid carcinoma (PDTC), and anaplastic thyroid carcinoma (ATC). This study aimed to delineate the molecular and immune landscapes of these subtypes and identify potential biomarkers for the aggressive forms, ATC and PDTC. We assembled a well-annotated cohort of 120 formalin-fixed paraffin-embedded samples, including 35 ATC, 18 PDTC, 37 PTC cases, and 30 adjacent normal tissues (N) paired with PTC, collected over the past decade from multiple hospitals. To our knowledge, this represents the largest clinical ATC/PDTC cohort subjected to multiomics profiling and the first comprehensive proteomic analysis of these aggressive thyroid cancers. Using 4D-data-independent acquisition proteomics on 118 tumors (ATC 34, PDTC 18, PTC 36, and N 30), integrated with total RNA-seq on 69 samples (ATC 10, PDTC 5, PTC 31, and N 23), we revealed substantial molecular similarities between ATC and PDTC, both markedly distinct from PTC and adjacent normal tissues. ATC and PDTC exhibited significant enrichment in immune-related and metabolic pathways, with transcriptomic data indicating aggressive phenotypes and pronounced immunosuppression. Distinct immune landscapes of ATC and PDTC were revealed with neutrophil extracellular trap formation and M0 macrophage accumulation as key immunosuppressive mechanisms. Notably, Fc fragment of IgG receptor IIa (CD32) was identified as a promising biomarker for ATC, implicating a functional link between immune evasion and tumor aggressiveness. Our findings provide a comprehensive molecular and immunological characterization of thyroid cancer subtypes, offering novel insights into the pathogenesis of ATC and PDTC, and identifying potential targets for diagnosis and precision therapy.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.