Pathways Deregulation in Oral Squamous Cell Carcinoma using Methylation Profiling

Introduction: Analyses based on methylation profiling offers an understanding in the mechanisms of carcinogenesis. Single gene analysis is insufficient to describe the complex perturbations responsible for cancer onset, progression and invasion.Objective: To identify gene pathways of highly hypermet...

Full description

Bibliographic Details
Main Authors: Thong, Kwai Lin, Khor, G.H., Zain, R.B.
Format: Article
Published: 2011
Subjects:
_version_ 1825719127196565504
author Thong, Kwai Lin
Khor, G.H.
Zain, R.B.
author_facet Thong, Kwai Lin
Khor, G.H.
Zain, R.B.
author_sort Thong, Kwai Lin
collection UM
description Introduction: Analyses based on methylation profiling offers an understanding in the mechanisms of carcinogenesis. Single gene analysis is insufficient to describe the complex perturbations responsible for cancer onset, progression and invasion.Objective: To identify gene pathways of highly hypermethylated genes in oral squamous cell carcinoma (OSCC) using DNA microarray-based methylation profiling. The study focused on the deregulation of gene sets or pathways rather than on individual genes involved in carcinogenesis mechanisms. Methods: DNA methylation assay was carried out on bisulfite-converted DNA extracted from frozen section tissues of 3 normal subjects and 20 patients of OSCC, using Illumina Infinium Methylation assay. 20620 genes of raw data obtained were normalized and analyzed using Genome Studio software. Significant methylated genes were generated by Gene Set Enrichment Analysis (GSEA), with less than 25% false discovery rate and 0.05 of nominal p-value were applied in gene pathway analysis. Results: High quality bisulfite-converted DNA was obtained and the methylation array was successfully run on all samples. In unsupervised cluster analysis, the normal subject samples were cluster differently from OSCC cases with false discovery rate in p-value of less than 0.05 and fold change more than 2.0. 113 hypermethylated genes were generated by GSEA where 18 hypermethylated genes are involved in pancreatic cancer, 42 in cell cycle, 20 in apoptosis, 15 in chronic myeloid leukemia, 7 in bladder cancer and 9 in non-small cell lung cancer. Conclusions: Based on the data analysis, the hypermethylated genes found on these pathways are related the cancer-causing mechanisms.
first_indexed 2024-03-06T05:14:55Z
format Article
id um.eprints-5661
institution Universiti Malaya
last_indexed 2024-03-06T05:14:55Z
publishDate 2011
record_format dspace
spelling um.eprints-56612018-10-15T04:26:37Z http://eprints.um.edu.my/5661/ Pathways Deregulation in Oral Squamous Cell Carcinoma using Methylation Profiling Thong, Kwai Lin Khor, G.H. Zain, R.B. Q Science (General) QR Microbiology Introduction: Analyses based on methylation profiling offers an understanding in the mechanisms of carcinogenesis. Single gene analysis is insufficient to describe the complex perturbations responsible for cancer onset, progression and invasion.Objective: To identify gene pathways of highly hypermethylated genes in oral squamous cell carcinoma (OSCC) using DNA microarray-based methylation profiling. The study focused on the deregulation of gene sets or pathways rather than on individual genes involved in carcinogenesis mechanisms. Methods: DNA methylation assay was carried out on bisulfite-converted DNA extracted from frozen section tissues of 3 normal subjects and 20 patients of OSCC, using Illumina Infinium Methylation assay. 20620 genes of raw data obtained were normalized and analyzed using Genome Studio software. Significant methylated genes were generated by Gene Set Enrichment Analysis (GSEA), with less than 25% false discovery rate and 0.05 of nominal p-value were applied in gene pathway analysis. Results: High quality bisulfite-converted DNA was obtained and the methylation array was successfully run on all samples. In unsupervised cluster analysis, the normal subject samples were cluster differently from OSCC cases with false discovery rate in p-value of less than 0.05 and fold change more than 2.0. 113 hypermethylated genes were generated by GSEA where 18 hypermethylated genes are involved in pancreatic cancer, 42 in cell cycle, 20 in apoptosis, 15 in chronic myeloid leukemia, 7 in bladder cancer and 9 in non-small cell lung cancer. Conclusions: Based on the data analysis, the hypermethylated genes found on these pathways are related the cancer-causing mechanisms. 2011 Article PeerReviewed Thong, Kwai Lin and Khor, G.H. and Zain, R.B. (2011) Pathways Deregulation in Oral Squamous Cell Carcinoma using Methylation Profiling. Journal Dental Research.
spellingShingle Q Science (General)
QR Microbiology
Thong, Kwai Lin
Khor, G.H.
Zain, R.B.
Pathways Deregulation in Oral Squamous Cell Carcinoma using Methylation Profiling
title Pathways Deregulation in Oral Squamous Cell Carcinoma using Methylation Profiling
title_full Pathways Deregulation in Oral Squamous Cell Carcinoma using Methylation Profiling
title_fullStr Pathways Deregulation in Oral Squamous Cell Carcinoma using Methylation Profiling
title_full_unstemmed Pathways Deregulation in Oral Squamous Cell Carcinoma using Methylation Profiling
title_short Pathways Deregulation in Oral Squamous Cell Carcinoma using Methylation Profiling
title_sort pathways deregulation in oral squamous cell carcinoma using methylation profiling
topic Q Science (General)
QR Microbiology
work_keys_str_mv AT thongkwailin pathwaysderegulationinoralsquamouscellcarcinomausingmethylationprofiling
AT khorgh pathwaysderegulationinoralsquamouscellcarcinomausingmethylationprofiling
AT zainrb pathwaysderegulationinoralsquamouscellcarcinomausingmethylationprofiling