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Oral Surg Oral Med Oral Pathol Oral Radiol. 2018 Feb;125(2):172-178. doi: 10.1016/j.oooo.2017.10.004. Epub 2017 Nov 24.

The Wnt/β-catenin pathway is deregulated in cemento-ossifying fibromas.

Author information

1
Department of Oral Surgery and Pathology, School of Dentistry, Universidade Federal de Minas Gerais, Minas Gerais, Brazil.
2
Department of Pathology, Biological Sciences Institute, Universidade Federal de Minas Gerais, Minas Gerais, Brazil.
3
Genomics Multi-user Laboratory, Biological Sciences Institute, Universidade Federal de Minas Gerais, Minas Gerais, Brazil.
4
Department of Oral Surgery and Pathology, School of Dentistry, Universidade Federal de Minas Gerais, Minas Gerais, Brazil. Electronic address: Rsgomez@ufmg.br.

Abstract

OBJECTIVE:

The molecular pathogenesis of cemento ossifying fibroma (COF) is unclear. The purpose of this study was to investigate mutations in 50 oncogenes and tumor suppressor genes, including APC and CTNNB1, in which mutations in COF have been previously reported. In addition, we assessed the transcriptional levels of the Wnt/β-catenin pathway genes in COF.

STUDY DESIGN:

We used a quantitative polymerase chain reaction array to evaluate the transcriptional levels of 44 Wnt/β-catenin pathway genes in 6 COF samples, in comparison with 6 samples of healthy jaws. By using next-generation sequencing (NGS) in 7 COF samples, we investigated approximately 2800 mutations in 50 genes.

RESULTS:

The expression assay revealed 12 differentially expressed Wnt/β-catenin pathway genes in COF, including the upregulation of CTNNB1, TCF7, NKD1, and WNT5 A, and downregulation of CTNNBIP1, FRZB, FZD6, RHOU, SFRP4, WNT10 A, WNT3 A, and WNT4, suggesting activation of the Wnt/β-catenin signaling pathway. NGS revealed 5 single nucleotide variants: TP53 (rs1042522), PIK3 CA (rs2230461), MET (rs33917957), KIT (rs3822214), and APC (rs33974176), but none of them was pathogenic.

CONCLUSIONS:

Although NGS detected no oncogenic mutation, deregulation of key Wnt/β-catenin signaling pathway genes appears to be relevant to the molecular pathogenesis of COF.

PMID:
29239811
DOI:
10.1016/j.oooo.2017.10.004
[Indexed for MEDLINE]

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