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Related Experiment Video

Updated: Jun 10, 2026

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Published on: August 25, 2021

GNAq mutations are not identified in papillary thyroid carcinomas and hyperfunctioning thyroid nodules.

Clarissa A Cassol¹, Miao Guo, Shereen Ezzat

¹Department of Pathology, University of Toronto, Toronto, ON, Canada. clarissa.cassol@uhnres.utoronto.ca

Endocrine Pathology

|August 18, 2010

Summary

Activating GNAq mutations, common in uveal melanoma, were investigated in thyroid cancers. Researchers found no evidence of these mutations in thyroid papillary carcinomas or hyperfunctioning nodules.

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Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

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Published on: May 17, 2024

Area of Science:

Oncology
Molecular Biology
Genetics

Background:

Activating GNAq protein mutations at codon 209 are found in uveal melanomas.
Thyroid carcinomas and uveal melanomas share frequent MAP kinase pathway-activating mutations.
Activating GNAS1 mutations occur in thyroid adenomas, suggesting a potential role for GNAq in thyroid nodules.

Purpose of the Study:

To investigate the presence of GNAq mutations in exon 5, codon 209, within thyroid papillary carcinomas and hyperfunctioning thyroid nodules.
To determine if GNAq mutations contribute to the development of thyroid follicular neoplasms.
To explore the molecular basis of MAP-kinase pathway activation in thyroid carcinomas lacking RET-PTC, BRAF, or RAS mutations.

Main Methods:

Screening of 32 RET/PTC, BRAF, and RAS-negative thyroid papillary carcinomas for GNAq mutations.
Evaluation of 13 hyperfunctioning thyroid nodules for GNAq mutations.
Focus on exon 5, codon 209, a known hotspot for GNAq activating mutations.

Main Results:

No GNAq mutations were identified in any of the evaluated thyroid papillary carcinomas.
No GNAq mutations were detected in the examined hyperfunctioning thyroid nodules.
The study found no evidence supporting a role for GNAq mutations in thyroid follicular neoplasms.

Conclusions:

GNAq mutations do not appear to be a significant factor in the pathogenesis of thyroid papillary carcinomas or benign hyperfunctioning thyroid nodules.
The findings align with existing literature indicating a lack of GNAq hotspot mutations in thyroid cancers.
Further research is needed to elucidate the molecular mechanisms driving MAP-kinase pathway activation in thyroid carcinomas that are negative for common mutations (RET-PTC, BRAF, RAS).