Related Experiment Video
Updated: Aug 6, 2026
05:39
Spontaneous Murine Model of Anaplastic Thyroid Cancer
Published on: February 3, 2023
Cell-state transitions and microenvironmental remodeling in thyroid cancer progression revealed by single-cell and
Xin Wang1, Deshuang Tao2, Jinming Xu3
1Department of General Surgery, First Affiliated Hospital of Jiamusi University, Jiamusi, Heilongjiang, China.
Frontiers in Immunology
|July 23, 2026
Summary
Thyroid cancer progression involves dynamic changes in malignant cell states, tumor microenvironment, and immune cell patterns. Understanding these shifts offers new therapeutic strategies for various thyroid cancer types.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Thyroid cancer encompasses a spectrum from indolent to aggressive forms.
- Current classifications lack resolution for cellular states and spatial heterogeneity during progression.
- Differentiated thyroid cancer (DTC), poorly differentiated thyroid carcinoma (PDTC), and anaplastic thyroid carcinoma (ATC) represent distinct disease stages.
Purpose of the Study:
- To integrate multi-omic single-cell and spatial transcriptomic data across thyroid cancer progression.
- To elucidate changes in malignant epithelial cells, stromal components, and immune infiltrates.
- To identify potential therapeutic targets and hypotheses based on cell-cell interactions.
Main Methods:
- Review and integration of single-cell RNA sequencing and spatial transcriptomics studies.
- Analysis of localized papillary thyroid carcinoma (PTC), metastatic/refractory DTC, PDTC, and ATC.
- Examination of epithelial plasticity, stromal remodeling, and immune microenvironment.
Main Results:
- Thyroid cancer progression is associated with epithelial dedifferentiation and EMT-like states.
- Stromal changes include invasive borders and CAF/ECM-rich regions.
- Distinct immune patterns characterize different thyroid cancer subtypes, with myeloid-rich ATC observed.
- Candidate signaling pathways (e.g., POSTN-IL-4, CCL20/CXCL5, SIGLEC15) identified.
Conclusions:
- Epithelial plasticity, genomic context, stromal, and immune interactions drive thyroid cancer progression.
- Identified mechanisms and cell-cell interactions provide a basis for therapeutic hypothesis generation.
- Further functional and clinical validation is required for proposed therapeutic strategies.
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