Related Experiment Video

Updated: Jun 26, 2026

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
07:49

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods

Published on: July 17, 2019

Oncogenic activation of MAP kinase by BRAF pseudogene in thyroid tumors

Minjing Zou1, Essa Y Baitei, Ali S Alzahrani

  • 1Department of Genetics, King Faisal Specialist Hospital and Research Centre, Riyadh 11211, Saudi Arabia.

Neoplasia (New York, N.Y.)
|December 25, 2008
PubMed

Insights

BRAF pseudogene activation may contribute to thyroid tumor development, particularly in tumors lacking BRAF mutations. This pseudogene can activate signaling pathways and promote tumor growth.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Activating BRAF mutations are common in papillary thyroid carcinomas (PTCs).
  • The role of the BRAF pseudogene in thyroid tumorigenesis remains uninvestigated.

Purpose of the Study:

  • To investigate BRAF pseudogene expression and its functional role in thyroid tumors.
  • To determine the correlation between BRAF pseudogene expression and BRAF mutations in thyroid cancer.

Main Methods:

  • Analysis of BRAF pseudogene expression in 68 thyroid tumors (goiters, PTCs, anaplastic carcinomas).
  • Functional studies including Western blots, soft agar assays, and in vivo tumorigenesis in nude mice.
  • Correlation analysis between pseudogene expression and BRAF mutation status.

Main Results:

  • BRAF pseudogene expression was detected in various thyroid tumors, including multinodular goiters and PTCs.
  • An inverse correlation was observed between BRAF pseudogene expression and BRAF mutations.
  • Pseudogene expression activated the MAP kinase pathway, transformed NIH3T3 cells, and induced tumors in mice.

Conclusions:

  • BRAF pseudogene activation may play a significant role in thyroid tumor development.
  • The pseudogene might represent an alternative oncogenic mechanism in BRAF-wildtype thyroid tumors.

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