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Spontaneous Murine Model of Anaplastic Thyroid Cancer
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High Local and Systemic Expression of Pentraxin-3 in Anaplastic Thyroid Cancer
Andreea Bojoga1,2, Pepijn van Houten2, Martin Jaeger2
1Faculty of Medicine, Carol Davila University of Medicine and Pharmacy, 020021 Bucharest, Romania.
International Journal of Molecular Sciences
|December 11, 2025
Summary
Long pentraxin 3 (PTX3) shows higher levels in aggressive thyroid cancers (TC), particularly anaplastic (ATC) and poorly differentiated (PDTC) types. PTX3 tissue expression is also elevated in ATC, suggesting a role in aggressive tumor progression.
Area of Science:
- Oncology
- Immunology
- Biochemistry
Background:
- Chronic inflammation is a known driver of cancer development.
- Aggressive thyroid cancers (TC) exhibit immune infiltration and systemic inflammation.
- Long pentraxin 3 (PTX3), an inflammatory protein, is linked to tumor progression.
Purpose of the Study:
- To evaluate plasma levels of PTX3 in non-medullary thyroid cancer (TC) patients versus benign thyroid disease.
- To investigate PTX3 tissue expression in different thyroid cancer subtypes.
- To explore the association between PTX3 and aggressive thyroid cancer characteristics.
Main Methods:
- Prospective study of 55 TC patients (papillary, follicular, oncocytic, anaplastic, poorly differentiated) and 32 controls with benign thyroid disease.
- Plasma PTX3 concentrations measured using ELISA.
- Tissue expression of PTX3 and CD68 analyzed via immunohistochemistry.
Main Results:
- PTX3 plasma levels did not differ significantly between overall TC and controls.
- Markedly higher PTX3 plasma concentrations were observed in poorly differentiated (PDTC) and anaplastic (ATC) thyroid cancer patients.
- Strong PTX3 tissue expression was found in most ATC cases, with minimal staining in benign and differentiated thyroid tissues.
- CD68 expression indicated tumor-associated macrophage infiltration in ATC.
Conclusions:
- PTX3 may be associated with aggressive thyroid cancer, especially ATC.
- Elevated PTX3 levels and tissue expression in ATC warrant further investigation.
- The cellular origin and functional role of PTX3 in aggressive TC require elucidation.

