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Spontaneous Murine Model of Anaplastic Thyroid Cancer
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Wnt/B-catenin Activation and TP53 Mutations Associate With Distinct Immune Profiles in Advanced Thyroid Cancer.

Sonia Moretti1, Martina Mandarano2, Elisa Menicali1

  • 1Section of Internal Medicine and Endocrine and Metabolic Sciences, Department of Medicine and Surgery, University of Perugia, Perugia 06132, Italy.

The Journal of Clinical Endocrinology and Metabolism
|September 27, 2024
PubMed
Summary

Anaplastic thyroid carcinomas (ATCs) with TP53 mutations show active immune responses, while poorly differentiated thyroid carcinomas (PDTCs) with Wnt/β-catenin pathway activation are immunologically inert. These findings highlight distinct immune profiles in thyroid cancers.

Keywords:
b-cateninimmune checkpoint inhibitorsimmunophenotypep53thyroid carcinoma

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Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Anaplastic thyroid carcinomas (ATCs) and poorly differentiated thyroid carcinomas (PDTCs) display contrasting immune profiles, with ATCs being immunologically active and PDTCs largely inert.
  • This divergence is linked to distinct immune-related gene expression patterns.

Purpose of the Study:

  • To investigate the mechanisms behind the differing immune phenotypes of ATCs and PDTCs.
  • Focus on the roles of the Wnt/β-catenin pathway and TP53 mutations in immune modulation.

Main Methods:

  • Analysis of TP53 mutation status and Wnt/β-catenin pathway activity in ATCs and PDTCs.
  • Correlation of these molecular alterations with immune cell infiltration and cytokine expression (e.g., CCL4).

Main Results:

  • ATCs frequently harbor TP53 mutations (83.3%), associated with a "hot" immune phenotype, high CCL4, and CD103+ dendritic cell recruitment.
  • PDTCs (12.5% TP53 mutation rate) often have a "cold" immune phenotype, linked to Wnt/β-catenin pathway activation and suppressed CCL4.
  • Loss of p53 function correlated inversely with β-catenin expression, promoting immune gene expression and infiltration.

Conclusions:

  • Wnt/β-catenin pathway activation may drive "cold" thyroid cancers via CCL4 suppression, while p53 mutations are linked to "hot" thyroid cancers.
  • These associations suggest distinct molecular drivers for thyroid cancer immunogenicity.
  • Further experimental studies are needed to confirm causality.