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Updated: Jan 29, 2026

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
Published on: April 17, 2013
Integrated Bioinformatics Analysis of Hub Genes and Pathways in Anaplastic Thyroid Carcinomas
Xueren Gao1, Jianguo Wang1, Shulong Zhang2
1Department of Pediatric Endocrinology/Genetics, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200092, China.
Abstract:
Anaplastic thyroid carcinoma (ATC) is a very rare malignancy; the pathogenesis of which is still not fully understood. The aim of the present study was to identify hub genes and pathways in ATC by microarray expression profiling. Two independent datasets (GSE27155 and GSE53072) were downloaded from GEO database. The differentially expressed genes (DEGs) between ATC tissues and normal thyroid tissues were screened out by the limma package and then enriched by gene ontology (GO) and KEGG pathway analysis. The hub genes were selected by protein-protein interaction (PPI) analysis. A total of 141 common upregulated and 87 common downregulated genes were screened out. These DEGs were significantly enriched in the phagosome and NF-kappa B signaling pathway. Through PPI analysis, TOP2A, TYMS, CCNB1, RACGAP1, FEN1, PRC1, and UBE2C were selected as hub genes, which were highly expressed in ATC tissues. TCGA data suggested that the expression levels of TOP2A, TYMS, FEN1, and PRC1 genes were also upregulated in other histological subtypes of thyroid carcinoma. High expression of TOP2A, TYMS, FEN1, PRC1, or UBE2C gene significantly decreased disease-free survival of patients with other thyroid carcinomas. In conclusion, the present study identified several hub genes and pathways, which will contribute to elucidating the pathogenesis of ATC and providing therapeutic targets for ATC.
Insights
This study identifies key genes and pathways in anaplastic thyroid carcinoma (ATC). Researchers found that genes like TOP2A and TYMS are highly expressed in ATC and linked to poorer survival, offering potential therapeutic targets.
Area of Science:
- Oncology
- Genetics
- Molecular Biology
Background:
- Anaplastic thyroid carcinoma (ATC) is a rare and aggressive thyroid malignancy with poorly understood pathogenesis.
- Identifying specific molecular markers and pathways is crucial for understanding ATC development and finding new treatments.
Purpose of the Study:
- To identify key genes (hub genes) and signaling pathways involved in the pathogenesis of anaplastic thyroid carcinoma (ATC).
- To explore the potential of these identified genes as therapeutic targets for ATC.
Main Methods:
- Utilized microarray expression profiling from two independent datasets (GSE27155 and GSE53072) from the GEO database.
- Applied the limma package to identify differentially expressed genes (DEGs) between ATC and normal thyroid tissues.
- Performed Gene Ontology (GO) and KEGG pathway analysis for enrichment, and protein-protein interaction (PPI) analysis to identify hub genes.
Main Results:
- Identified 141 common upregulated and 87 common downregulated genes in ATC tissues compared to normal tissues.
- Enriched pathways included phagosome and NF-kappa B signaling.
- Selected hub genes (TOP2A, TYMS, CCNB1, RACGAP1, FEN1, PRC1, UBE2C) showed high expression in ATC and were linked to decreased disease-free survival in other thyroid cancer subtypes.
Conclusions:
- The study successfully identified significant hub genes and enriched pathways crucial for understanding ATC pathogenesis.
- The identified genes, particularly TOP2A, TYMS, FEN1, PRC1, and UBE2C, represent potential therapeutic targets for anaplastic thyroid carcinoma.
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