En esta ocasión traemos un artículo interesante con relación a la genética:
Global methylation profiling to identify epigenetic signature of gallbladder cancer and gallstone disease (Perfilación global de la metilación para identificar la firma epigenética de cáncer de vesícula biliar y enfermedad biliar)
Resumen: Promoter methylation in various tumor suppressor genes is reported to influence gallbladder carcinogenesis. Here, we aimed to identify methylation status in gallbladder cancer (GBC) by performing a comprehensive genome-wide DNA methylation profiling. The methylation status of 485,577 CpG sites were investigated using Illumina’s Infinium Human Methylation 450 BeadChip array in 24 tissues (eight each of tumor, adjacent non-tumor, and gallstone). About 33,443 differentially methylated sites (DMRs) were obtained in the whole human genome, of which 24,188 (72 %) were hypermethylated and 9255 (28 %) were hypomethylated. The data also revealed that majority of the DMRs are localized on the proximal promoter region [Transcription start sites (TSS200, TSS1500) and 5′ untranslated region (5′UTR)] and first exon. Exclusion of first exon detected a total of 10,123 (79 %) hypermethylated and 2703 (21 %) hypomethylated sites. Comparative analysis of the later with our differential proteomics data resulted in identification of 7 hypermethylated or down-regulated (e.g., FBN1, LPP, and SOD3) and 61 hypomethylated or up-regulated markers (e.g., HBE1, SNRPF, TPD52) for GBC. These genes could be further validated on the basis of their methylation/ expression status in order to identify their utility to be used as biomarker/s for early diagnosis and management of GBC.
Puede revisar el artículo en el link: Perfilación global de la metilación para identificar la firma epigenética de cáncer de vesícula biliar y la enfermedad biliar
Global methylation profiling to identify epigenetic signature of gallbladder cancer and gallstone disease (Perfilación global de la metilación para identificar la firma epigenética de cáncer de vesícula biliar y enfermedad biliar)
Resumen: Promoter methylation in various tumor suppressor genes is reported to influence gallbladder carcinogenesis. Here, we aimed to identify methylation status in gallbladder cancer (GBC) by performing a comprehensive genome-wide DNA methylation profiling. The methylation status of 485,577 CpG sites were investigated using Illumina’s Infinium Human Methylation 450 BeadChip array in 24 tissues (eight each of tumor, adjacent non-tumor, and gallstone). About 33,443 differentially methylated sites (DMRs) were obtained in the whole human genome, of which 24,188 (72 %) were hypermethylated and 9255 (28 %) were hypomethylated. The data also revealed that majority of the DMRs are localized on the proximal promoter region [Transcription start sites (TSS200, TSS1500) and 5′ untranslated region (5′UTR)] and first exon. Exclusion of first exon detected a total of 10,123 (79 %) hypermethylated and 2703 (21 %) hypomethylated sites. Comparative analysis of the later with our differential proteomics data resulted in identification of 7 hypermethylated or down-regulated (e.g., FBN1, LPP, and SOD3) and 61 hypomethylated or up-regulated markers (e.g., HBE1, SNRPF, TPD52) for GBC. These genes could be further validated on the basis of their methylation/ expression status in order to identify their utility to be used as biomarker/s for early diagnosis and management of GBC.
Puede revisar el artículo en el link: Perfilación global de la metilación para identificar la firma epigenética de cáncer de vesícula biliar y la enfermedad biliar
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