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Updated: Apr 15, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
[Molecular pathogenesis of thyroid tumors]
Vera Tiedje1, Denise Zwanziger1, Saskia Ting2
1Klinik für Endokrinologie und Stoffwechselerkrankungen, Universitätsklinikum Essen.
Abstract:
The molecular pathogenesis of thyroid tumors has been an evolving field in the past years. The constitutive activation of intracellular tyrosine kinases has been identified as a hallmark of thyroid cancer. The activation of MAPK and PI3K pathways through somatic gene mutations or gene rearrangements seem to play a pivotal role in the pathogenesis of follicular-cell-derived tumors. In poorly differentiated tumors and anaplastic tumors often an accumulation of genetic alterations from differentiated thyroid cancer but also novel gene mutations can be observed. The C-cell-derived medullary thyroid cancer evolves through the constitutive activation of the RET kinase, either through germline RET mutations or somatic RET and RAS mutations. The better knowledge of the molecular pathogenesis allowed the development of targeted therapies in thyroid cancer patients. The identification of molecular response markers to tyrosine kinase inhibitor therapy is desirable.
Insights
Thyroid cancer pathogenesis involves activated tyrosine kinases, driving tumor growth through MAPK, PI3K, and RET pathways. Understanding these molecular drivers aids targeted therapy development.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Context:
- Thyroid tumors exhibit complex molecular alterations.
- Intracellular tyrosine kinase activation is a key feature.
- Understanding these pathways is crucial for effective treatment.
Purpose:
- To review the molecular pathogenesis of thyroid tumors.
- To highlight the role of specific signaling pathways (MAPK, PI3K, RET).
- To discuss the implications for targeted therapy.
Summary:
- Follicular-cell-derived tumors are driven by MAPK and PI3K pathway activation via mutations/rearrangements.
- Poorly differentiated and anaplastic thyroid cancers show accumulated genetic alterations.
- Medullary thyroid cancer arises from constitutive RET kinase activation.
Impact:
- Advances in understanding molecular pathogenesis have enabled targeted therapies.
- Identifying molecular response markers for tyrosine kinase inhibitors is a critical next step.
- This knowledge facilitates personalized treatment strategies for thyroid cancer patients.
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