IndraLab
Statements
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"Conclusions: Our results indicate that carrying the minor allele of the MAFK polymorphisms, particularly when they are located in the 3'-UTR, has a high risk for the severity of gastric mucosal atrophy; furthermore, CDKN2A CpG methylation may develop in subjects with homozygous minor allele of these polymorphisms."
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"CpG methylation of the p16INK4a, RASSF1A, E cadherin, and GSTP1 genes was correlated to the reduction of mRNA levels in the cell lines, and mRNA expression of these 4 genes were indeed restored by low concentrations (2-6 micromol/L) of As2O3 through demethylation, as well as 1 micromol/L of 5-aza-2'-deoxycytidine."
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"Because 5'CpG islands methylation of p16 and p15 genes might be an early event in HCC xref - xref , and because the gene expression due to extensive CpG island methylation had accepted as the main cause of inactivation of the p16 gene xref , the risk of p16 methylation directly response to the pathogenesis of HCC."
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"In human PGL samples, promoter CpG methylation of the p16 INK4A gene alone as well as promoter methylation of at least 3 of the following genes RASSF1A , NORE1A ,p16 INK4A , RARB , DCR2 , CDH1 and APC (i.e. CpG island methylator phenotype (CIMP)) but notp14 ARF has been shown to correlate with aggressive tumor behavior xref , xref ."
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"ORNi-PCR with ORN_p16_U and ORN_p16_M strongly suppressed the amplification of the target CDKN2A (p16) sequence from bisulfite-treated unmethylated and CpG-methylated human gDNA, respectively, as shown in xref A. Amplification from bisulfite-treated HCT116 gDNA was moderately suppressed by each ORN, probably due to the hemi-allelic CpG methylation of CDKN2A (p16) ."
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"A group of researchers in Bangladesh evaluated prenatal exposure to As and its association with DNA methylation [ xref ], finding higher methylation in some of the CpG sites of the p16 gene, which is involved in cell regulation, and also codifies a tumor suppressor protein [ xref ]."
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"To this end, we mixed gDNA of HCT116 (one copy of each CpG-methylated and unmethylated CDKN2A (p16) ) and 293T (two copies of unmethylated CDKN2A (p16) ), so that the CpG-methylated CDKN2A (p16) accounted for 5–0.05% of total CDKN2A (p16) , and then subjected them to bisulfite treatment."
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"Significant correlation between folates and methylation at specific CpG sites of p16 and MLH1 were different from those linked to arsenic exposure; in this study, we found correlations with methylation of p16 sites 3 and 5 and MLH1 site 4, compared with sites 1 both in p16 and MLH1 associated with arsenic exposure."
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"Many studies have investigated the potential role of expression genes for prognostic use, and unsurprisingly most of them are similar to those with a high potential for diagnostic use; in example, promoter CpG methylation of HLTF and CDKN2A is used with prognostic and diagnostic functions in tumours [ xref , xref ]."