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Updated: Jun 21, 2026

Spontaneous Murine Model of Anaplastic Thyroid Cancer
05:39

Spontaneous Murine Model of Anaplastic Thyroid Cancer

Published on: February 3, 2023

Aggressive inherited and sporadic medullary thyroid carcinomas display similar oncogenic pathways

Nabahet Ameur1, Ludovic Lacroix, Sophie Roucan

  • 1CNRS FRE 2939, Institut de Cancérologie Gustave-Roussy, Villejuif, France.

Endocrine-Related Cancer
|August 14, 2009
PubMed

Insights

Familial and sporadic medullary thyroid carcinomas (MTC) share similar oncogenic pathways. Gene expression analysis revealed distinct MTC subtypes, with some sporadic tumors mirroring inherited RET mutations and showing increased metastasis-associated gene expression.

Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • RET oncogene mutations are prevalent in familial and some sporadic medullary thyroid carcinomas (MTC).
  • The oncogenic mechanisms driving non-RET mutated sporadic MTC are not fully understood.

Purpose of the Study:

  • To investigate gene expression alterations in both inherited and sporadic MTC.
  • To identify molecular differences and similarities between MTC subtypes.

Main Methods:

  • Pangenomic DNA microarrays analyzed the transcriptome of 13 MTC samples (4 familial, 9 sporadic).
  • Differential gene expression was identified using ANOVA, with validation by real-time quantitative PCR and immunohistochemistry.
  • MTC cell lines were used to assess the effect of RET gene silencing on PTN expression.

Main Results:

  • A subset of 173 differentially expressed genes was identified.
  • Sporadic MTCs were classified into two groups based on gene expression profiles, with one group resembling inherited RET634 tumors.
  • The second sporadic MTC group, similar to inherited RET918 tumors, showed overexpression of proliferation, invasion, and matrix remodeling genes (e.g., PTN, ESM1, CEACAM6, COL1A1, COL1A2, FAP).
  • RET918 tumors overexpressed pleiotrophin (PTN), a gene linked to metastasis. Silencing RET inhibited PTN expression.

Conclusions:

  • Familial and sporadic MTC may activate similar oncogenic pathways.
  • Distinct molecular subtypes of MTC exist, potentially correlating with clinical outcomes and metastatic potential.
  • PTN may play a significant role in MTC progression and metastasis, particularly in RET-mutated tumors.

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