Publication: An integrative analysis of genome-wide methylation and expression in ameloblastoma: A pilot study
Issued Date
2020-01-01
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ISSN
16010825
1354523X
1354523X
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2-s2.0-85097030068
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Mahidol University
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SCOPUS
Bibliographic Citation
Oral Diseases. (2020)
Suggested Citation
Monnat Pongpanich, Sirima Sanguansin, Sudaporn Kengkarn, Arkom Chaiwongkot, Boworn Klongnoi, Nakarin Kitkumthorn An integrative analysis of genome-wide methylation and expression in ameloblastoma: A pilot study. Oral Diseases. (2020). doi:10.1111/odi.13666 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/60458
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Title
An integrative analysis of genome-wide methylation and expression in ameloblastoma: A pilot study
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Abstract
© 2020 Wiley Periodicals LLC Objective: DNA methylation regulates the expression of various genes involved in tumorigenesis. Ameloblastoma is a benign odontogenic jaw tumor. It is locally aggressive with a high level of recurrence. A delay in treatment can lead to severe facial disfigurement. To the best of our knowledge, this is the first integrated analysis of DNA methylation and gene expression in ameloblastoma with the aim to identify genes that may be regulated by DNA methylation. Materials and Methods: We used an Infinium MethylationEPIC array to measure genome-wide methylation and the Illumina HiSeq platform to obtain gene expression data in ameloblastoma tissues from five patients and dental follicles from three healthy subjects. An integration analysis was performed using City of Hope CpG Island Analysis Pipeline software. Results: We identified 25,255 differentially methylated CpG sites and 17 differentially methylated CpG islands; six of the islands were negatively correlated with the expression of BAIAP2, DUSP6, FGFR2, FOXF2, NID2, and PAK6. Pyrosequencing and immunostaining techniques were further used to validate FGFR2, NID2, and PAK6. Conclusions: This analysis identifies a group of novel genes that may be regulated by DNA methylation and will possibly lead to new insights into the pathology and invasion mechanism of ameloblastoma.