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Thyroid C-Cell Biology and Oncogenic Transformation.

Rozita Bagheri-Yarmand1, Elizabeth G Grubbs2, Marie-Claude Hofmann3

  • 1Department of Endocrine Neoplasia and Hormonal Disorders, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.

Recent Results in Cancer Research. Fortschritte Der Krebsforschung. Progres Dans Les Recherches Sur Le Cancer
|March 19, 2025
PubMed
Summary

Thyroid C-cells regulate calcium. Mutations in the RET gene drive medullary thyroid carcinoma by activating the RET-RAS-MAPK pathway, offering targets for new therapies.

Keywords:
Medullary thyroid carcinomaMouse modelsMulti-omicsParafollicular cellRASRETThyroid C-cell

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Area of Science:

  • Endocrinology
  • Oncology
  • Molecular Biology

Background:

  • Thyroid C-cells maintain serum calcium homeostasis through calcitonin secretion.
  • Thyroid C-cell oncogenic transformation involves hyperplasia and elevated calcitonin, a tumor biomarker.
  • Activating RET gene mutations cause Multiple Endocrine Neoplasia, type 2, highlighting the RET-RAS-MAPK pathway in medullary thyroid carcinoma.

Purpose of the Study:

  • To elucidate the role of the RET signaling pathway in thyroid C-cell oncogenesis.
  • To identify key molecular pathways involved in medullary thyroid carcinoma development.
  • To explore potential novel molecular targeted therapies for thyroid C-cell cancers.

Main Methods:

  • Analysis of RET gene mutations and their association with Multiple Endocrine Neoplasia, type 2.
  • Investigating the RET-RAS-MAPK signaling pathway in C-cell transformation.
  • Utilizing animal models and human tumor screening for candidate gene mutations (RAS, RB1).
  • Integrating multi-omics data to uncover novel oncogenic pathways.

Main Results:

  • RET gene mutations are a primary driver of medullary thyroid carcinoma.
  • The RET-RAS-MAPK pathway is crucial for C-cell initiation and progression.
  • Mutations in RAS family members and RB1 pathway inactivation also contribute to C-cell transformation.
  • Omics studies reveal new oncogenic pathways in thyroid C-cells.

Conclusions:

  • Understanding RET pathway interactions is key to C-cell function and oncogenesis.
  • Targeting the RET pathway and associated signaling networks holds promise for novel therapies.
  • Further research into multi-omics data will refine our understanding of medullary thyroid carcinoma.