Global DNA Methylation: Uncommon Event in Oral Lichenoid Disease
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE54211 | GEO | 2014/04/30
SECONDARY ACCESSION(S): PRJNA235902
REPOSITORIES: GEO
Similar Datasets
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2014-04-30 | E-GEOD-54211 | biostudies-arrayexpress
Project description:Purpose Accumulating evidence indicates aberrant DNA methylation is closely related to oral carcinogenesis, and it has been shown that methylation changes might be used as prognostic biomarker in oral squamous cell carcinoma. Oral lichenoid disease (OLD) is the most common oral potentially malignant disorder in our region. In this study, we have performed a wide DNA methylation study of a series of oral lichenoid disease in order to assess the relevance of DNA methylation changes in this premalignant disorder. Experimental Design Discovery phase utilized HumanMethylation27 DNA Analysis BeadChip assay in 18 OLD and 5 control samples. The differently methylated loci and the global DNA methylation surrogate LINE-, were further validated in an independent sample set consisting in 158 OLD and 65 controls. Results DNA methylation profile of the OLD showed only minor significant differences when compared to controls. MGC40178, ADORA1 and LINE-1 were slightly hypomethylated in 23, 40 and 43 % of the OLD samples respectively, while only in 13, 18 and 15% of the controls. Conclusions In summary, our data indicates that the frequency of aberrant DNA alteration is very low in OLD, which support the low rate of malignization of this oral potentially malignant disorder.
2014-04-30 | GSE50608 | GEO
Project description:Purpose: Accumulating evidence indicates aberrant DNA methylation is closely related to oral carcinogenesis, and it has been shown that methylation changes might be used as prognostic biomarker in oral squamous cell carcinoma. Oral lichenoid disease (OLD) is the most common oral potentially malignant disorder in our region. In this study, we have performed a wide DNA methylation study of a series of oral lichenoid disease in order to assess the relevance of DNA methylation changes in this premalignant disorder. Experimental Design: Discovery phase utilized the Illumina Golden Gate Cancer Panel I in 51 OLD and 6 control samples. The differently methylated loci and the global DNA methylation surrogate LINE-1, were further validated in an independent sample set consisting in 160 OLD and 65 controls. Results: DNA methylation profiles of the OLD showed only minor significant differences when compared to controls. Conclusions: In summary, our data indicates that the frequency of aberrant DNA alteration is very low in OLD, which support the low rate of malignization of this oral potentially malignant disorder.
2014-04-30 | GSE54210 | GEO
Project description:Purpose Accumulating evidence indicates aberrant DNA methylation is closely related to oral carcinogenesis, and it has been shown that methylation changes might be used as prognostic biomarker in oral squamous cell carcinoma. Oral lichenoid disease (OLD) is the most common oral potentially malignant disorder in our region. In this study, we have performed a wide DNA methylation study of a series of oral lichenoid disease in order to assess the relevance of DNA methylation changes in this premalignant disorder. Experimental Design Discovery phase utilized HumanMethylation27 DNA Analysis BeadChip assay in 18 OLD and 5 control samples. The differently methylated loci and the global DNA methylation surrogate LINE-, were further validated in an independent sample set consisting in 158 OLD and 65 controls. Results DNA methylation profile of the OLD showed only minor significant differences when compared to controls. MGC40178, ADORA1 and LINE-1 were slightly hypomethylated in 23, 40 and 43 % of the OLD samples respectively, while only in 13, 18 and 15% of the controls. Conclusions In summary, our data indicates that the frequency of aberrant DNA alteration is very low in OLD, which support the low rate of malignization of this oral potentially malignant disorder. Bisulphite converted DNA from the 17 Oral lichenoid samples and 5 control samples were hybridised to the Illumina Infinium 27k Human Methylation Beadchip v1.217
2014-04-30 | E-GEOD-50608 | biostudies-arrayexpress
Project description:Purpose: Accumulating evidence indicates aberrant DNA methylation is closely related to oral carcinogenesis, and it has been shown that methylation changes might be used as prognostic biomarker in oral squamous cell carcinoma. Oral lichenoid disease (OLD) is the most common oral potentially malignant disorder in our region. In this study, we have performed a wide DNA methylation study of a series of oral lichenoid disease in order to assess the relevance of DNA methylation changes in this premalignant disorder. Experimental Design: Discovery phase utilized the Illumina Golden Gate Cancer Panel I in 51 OLD and 6 control samples. The differently methylated loci and the global DNA methylation surrogate LINE-1, were further validated in an independent sample set consisting in 160 OLD and 65 controls. Results: DNA methylation profiles of the OLD showed only minor significant differences when compared to controls. Conclusions: In summary, our data indicates that the frequency of aberrant DNA alteration is very low in OLD, which support the low rate of malignization of this oral potentially malignant disorder. Bisulphite-converted DNA from the 51 oral lichenoid disease samples and 6 control samples were hybridised to the Illumina GoldenGate Methylation Cancer Panel I.
2014-04-30 | E-GEOD-54210 | biostudies-arrayexpress
Project description:Objectives: Earlier studies involving a priori gene selection have identified promoter regions deregulated by DNA methylation changes in oral squamous cell cancers (OSCCs) and precancers. Interrogation of global DNA methylation patterns for such specimens has not been reported, though such analyses are needed to uncover novel molecular factors driving disease. Materials and Methods: We evaluated global DNA methylation patterns for 30 biopsies obtained from 10 patients undergoing surgical removal of an OSCC or carcinoma in situ (CIS). From a disease field in each patient, we collected i) dysplastic, ii) CIS or OSCC, and iii) adjacent normal biopsies. DNA isolated from each biopsy was profiled for methylation status using the Illumina HumanMethylation27K platform. Results: Our data demonstrate that aberrant methylation of promoter CpG islands exists across oral precancer and OSCC genomes. Non-hierarchical clustering of all methylation data revealed distinct methylation patterns between the normal and the CIS/OSCC tissues (with results for dysplastic biopsies split between groups). Multiple genes exhibiting recurrent aberrant DNA methylation were found for both dysplastic and CIS/OSCC groups, and included enrichment for genes found in the WNT and MAPK signaling pathways. Conclusion: In identifying aberrant DNA methylation at the earliest stages of oral precancer and finding recurring epigenetic disruption of specific genes/pathways across our analyzed cohort, we conclude that CpG methylation changes are a hallmark of oral cancer progression and that global DNA methylation analyses are an essential component for wider studies seeking to derive biomarkers or potentially druggable targets for improving oral cancer outcomes.
2013-09-18 | GSE46802 | GEO
Project description:Objectives: Earlier studies involving a priori gene selection have identified promoter regions deregulated by DNA methylation changes in oral squamous cell cancers (OSCCs) and precancers. Interrogation of global DNA methylation patterns for such specimens has not been reported, though such analyses are needed to uncover novel molecular factors driving disease. Materials and Methods: We evaluated global DNA methylation patterns for 30 biopsies obtained from 10 patients undergoing surgical removal of an OSCC or carcinoma in situ (CIS). From a disease field in each patient, we collected i) dysplastic, ii) CIS or OSCC, and iii) adjacent normal biopsies. DNA isolated from each biopsy was profiled for methylation status using the Illumina HumanMethylation27K platform. Results: Our data demonstrate that aberrant methylation of promoter CpG islands exists across oral precancer and OSCC genomes. Non-hierarchical clustering of all methylation data revealed distinct methylation patterns between the normal and the CIS/OSCC tissues (with results for dysplastic biopsies split between groups). Multiple genes exhibiting recurrent aberrant DNA methylation were found for both dysplastic and CIS/OSCC groups, and included enrichment for genes found in the WNT and MAPK signaling pathways. Conclusion: In identifying aberrant DNA methylation at the earliest stages of oral precancer and finding recurring epigenetic disruption of specific genes/pathways across our analyzed cohort, we conclude that CpG methylation changes are a hallmark of oral cancer progression and that global DNA methylation analyses are an essential component for wider studies seeking to derive biomarkers or potentially druggable targets for improving oral cancer outcomes. Bisulphite converted DNA from the 30 samples were hybridised to the Illumina Infinium 27k Human Methylation BeadChip v1.2. Total RNA from 30 oral cancer samples were hybridized to Agilent 4x44k gene expression microarray.
| S-ECPF-GEOD-46802 | biostudies-other
Project description:This SuperSeries is composed of the SubSeries listed below.
2012-11-08 | GSE42119 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2012-12-19 | GSE32149 | GEO
Project description:DNA promoter methylation of tumor suppressor genes and global DNA hypomethylation are common features of head and neck cancers. Our goal was to identify early DNA methylation changes in oral premalignant lesions (OPL) that may serve as predictive markers of developing oral squamous cell carcinoma (OSCC). Using high-throughput DNA methylation profiles of 24 OPLs, we found that the top 86 genes differentially methylated between patients who did or did not develop OSCC were simultaneously hypermethylated, suggesting that a CpG island methylation phenotype may occur early during OSCC development. The vast majority of the 86 genes were nonmethylated in normal tissues and hypermethylated in OSCC versus normal mucosa. We used pyrosequencing in a validation cohort of 44 patients to evaluate the degree of methylation of AGTR1, FOXI2, and PENK promoters CpG sites that were included in the top 86 genes and of LINE1 repetitive element methylation, a surrogate of global DNA methylation. A methylation index was developed by averaging the percent methylation of AGTR1, FOXI2, and PENK promoters; patients with a high methylation index had a worse oral cancer-free survival (P = 0.0030). On the other hand, patients with low levels of LINE1 methylation had a significantly worse oral cancer-free survival (P = 0.0153). In conclusion, AGTR1, FOXI2, and PENK promoter methylation and LINE1 hypomethylation may be associated with an increased risk of OSCC development in patients with OPLs.
| S-EPMC4777304 | biostudies-literature