Project description:Little has been known about the genome-wide methylation frameworks of the chemo-resistant cells of SCLC currently, which might provide prospective layouts to discover the genes and the signal pathways related with chemo-resistance of SCLC. Thus, this research reported for the first time the genome-wide abnormal methylation pattern of chemo-resistant H446/DDP cells of human SCLC induced by the cisplatin
Project description:We found that ERY974 shows only moderate antitumor efficacy in NCI-H446 non-inflamed tumor in huNOG mice. We also observed that ERY974 + cisplatin increases antitumour efficacy in non-inflamed NCI-H446 tumours. To identify a mechanism of combination effect, we compared RNA expression of NCI-H446 tumors treated with ERY974, cisplatin, or combination.
Project description:We found that ERY974 shows only moderate antitumor efficacy in NCI-H446 non-inflamed tumor in huNOG mice. We also observed that ERY974 + paclitaxel increases antitumour efficacy in non-inflamed NCI-H446 tumours. To identify a mechanism of combination effect, we compared RNA expression of NCI-H446 tumors treated with ERY974, cisplatin, or combination.
Project description:This is a comparative study. This study is to compare the diagnostic sensitivity between circulating tumor DNA methylation and carcinoembryonic antigen in detecting colorectal cancer. There are two steps in this study. Firstly, the diagnostic model is established based on tumor-specific plasma circulating tumor DNA methylation markers. Secondly, the sensitivity, specificity and accuracy of plasma circulating tumor DNA methylation are compared with that of carcinoembryonic antigen in detecting colorectal cancer.
Project description:Physiological and pathological stimuli result in distinct anatomic forms of cardiac hypertrophy, but the head-to-head comparison of molecular regulation between physiological and pathological cardiac hypertrophy is less well understood, especially at the DNA methylation level. We conducted an in vitro study using human cardiomyocyte cell line AC16 exposed to angiotensin II (AngII) and insulin-like growth factor 1 (IGF-1) to mimic pathologically and physiologically hypertrophic heart models, respectively. Whole genome DNA methylation patterns were profiled by the Infinium human MethylationEPIC platform with >850K DNA methylation loci. We detected 194 loci that are significantly differentially methylated after AngII treatment (vs control) with 50.0% hypermethylated, and 206 significant loci after IGF-1 treatment (vs control) with 45.1% hypermethylated (Adjusted P < 0.05). Mapping the significant loci to genes, we identified 158 genes corresponding to AngII treatment and 175 genes to IGF-1 treatment, with 67 genes overlapping between AngII and IGF-1.
Project description:Using the Illumina Infinium Human Methylation27 BeadChip, we performed a genome-wide analysis of DNA methylation in right coronary artery in the area of advanced atherosclerotic plaques, atherosclerotic-resistant internal mammary arteries, and great saphenous veins obtained from same patients with coronary heart disease. The resulting DNA methylation patterns were markedly different between all the vascular tissues. The genes hypomethylated in athero-prone arteries to compare with atherosclerotic-resistant arteries were predominately involved in regulation of inflammation and immune processes, as well as development. The great saphenous veins exhibited an increase of the DNA methylation age in comparison to the internal mammary arteries. Gene ontology analysis for genes harboring hypermethylated CpG-sites in veins revealed the enrichment for biological processes associated with the development. Four CpG-sites located within the MIR10B gene sequence and about 1 Kb upstream of the HOXD4 gene were also confirmed as hypomethylated in the independent dataset of right coronary arteries in the area of advanced atherosclerotic plaques in comparison with the other vascular tissues.
Project description:Using the Illumina Infinium Human Methylation27 BeadChip, we performed a genome-wide analysis of DNA methylation in right coronary artery in the area of advanced atherosclerotic plaques, atherosclerotic-resistant internal mammary arteries, and great saphenous veins obtained from same patients with coronary heart disease. The resulting DNA methylation patterns were markedly different between all the vascular tissues. The genes hypomethylated in athero-prone arteries to compare with atherosclerotic-resistant arteries were predominately involved in regulation of inflammation and immune processes, as well as development. The great saphenous veins exhibited an increase of the DNA methylation age in comparison to the internal mammary arteries. Gene ontology analysis for genes harboring hypermethylated CpG-sites in veins revealed the enrichment for biological processes associated with the development. Four CpG-sites located within the MIR10B gene sequence and about 1 Kb upstream of the HOXD4 gene were also confirmed as hypomethylated in the independent dataset of right coronary arteries in the area of advanced atherosclerotic plaques in comparison with the other vascular tissues. Bisulfite converted genomic DNA from 24 samples was denatured, whole-genome amplified, fragmented and subsequently hybridized to the Illumina Infinium 27k Human Methylation Beadchip.