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Spatial Transcriptomics Reveals Transcriptomic and Immune Microenvironment Reprogramming during Thyroid Carcinoma

Kang Ning1,2,3, Bu Zou1,2,3, Yongchao Yu1,2,3

  • 1Department of Head and Neck Surgery, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|September 5, 2025
PubMed
Summary
This summary is machine-generated.

Anaplastic thyroid carcinoma (ATC) evolves from differentiated thyroid carcinoma (DTC) via genomic changes and immune suppression. Loss of PDCD4 drives tumor-associated macrophage infiltration, crucial for ATC progression.

Keywords:
M2 macrophagePDCD4anaplastic thyroid carcinomadifferentiated thyroid carcinomaspatial transcriptomics

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Area of Science:

  • Oncology
  • Genomics
  • Immunology

Background:

  • Anaplastic thyroid carcinoma (ATC) is a highly lethal malignancy.
  • ATC often arises from differentiated thyroid carcinoma (DTC) through a poorly understood dedifferentiation process.

Purpose of the Study:

  • To elucidate the molecular mechanisms driving the transition from DTC to ATC.
  • To identify key regulators and cellular players in thyroid cancer dedifferentiation.

Main Methods:

  • Spatial transcriptomic sequencing (spRNAseq) on coexisting DTC and ATC regions.
  • Whole-exome sequencing and inferCNV analysis.
  • Trajectory analysis and mechanistic experiments.

Main Results:

  • ATC exhibits upregulated immune suppression, angiogenesis, and ECM remodeling genes.
  • Adjacent DTC regions show early genomic alterations priming for dedifferentiation.
  • PDCD4 and TYMP are key regulators of thyroid cancer dedifferentiation.
  • TYMP+ tumor-associated macrophages (TAMs) are enriched in ATC, promoting immunosuppression.
  • Loss of PDCD4 promotes TAM infiltration via eIF4A-dependent pathways.

Conclusions:

  • DTC with ATC-like genomic alterations undergoes transcriptomic and immune reprogramming to become ATC.
  • PDCD4 loss-induced TAM formation is critical for ATC development and progression.