Retinoids induce rapid dynamic changes in the non-coding RNAs and epigenetic profiles of murine Hox clusters (ChIP-chip)
ABSTRACT: Physiologically relevant concentrations of retinoic acid are added to Mouse ES cells and a time course (0-72 hours) is examined with tiling array ChIP-chip and RNA-seq to characterize the early dynamics of expression of coding and non-coding RNAs and epigenetics in and around the Hox clusters. Expression, epigenetics, and RARs are examined at various timepoints (0-24hrs) after retinoic acid induced neuronal differentiation
Project description:ChIP microarrays were used to investigate whether dibutylphthalate (DBP)-mediated repression of SF1-regulated genes was associated with changes in transcription factor binding to genes involved in DBP-induced testicular maldevelopment. The repressive effect of DBP on SF1 regulated gene expression in fetal testes correlates with inhibition of SF1 binding to steroidogenic gene promoters. Comparison of control- and DBP- in utero 500mg/Kg treated fetal rat testes
Project description:T-ALL Xenograft Histone Modification at ERG locus: The cells used are human T-acute lymphoblastic leukaemia cells that have been propagated in NOD/SCID mice. T-ALL8,T-ALL16, T-ALL27, T-ALL29, T-ALL30 and T-ALL31 are cells from six different patients. Normalized data files containing chromosome 21 data are available on the FTP site for this experiment in the E-MTAB-431.additional.zip archive.
Project description:B-ALL Xenograft Histone Modification at BIM locus<br>The cells used are human B- acute lymphoblastic leukaemia cells that have been propagated in<br>NOD/SCID mice. B-ALL2 and B-ALL3 are cells from two different patients.<br><br>Normalized data files containing chromosome 2 data are available on the FTP site for this experiment in the E-MEXP-2814.additional.zip archive.
Project description:Chip-on-chip experiment with NT2 wildtype cells untreated (0 h) or treated with Retinoic Acid (1h and 3 h) at 0.01 µM. The goal was to determine the genome-wide occupancy of ZRF1 at gene promoters in undifferentiated cells and at the onset of differentiation. Three-condition experiment. Biological replicates: NT2 cells were treated with or without RA on three different days from cycling NT2 cells (0h, 1h and 3h of RA). Chromatin was prepared and a triplicate of IPs was performed with specific ZRF1 antibodies for every condition. A triplicate of control IPs was performed with IgGs.
Project description:Multiple carcinogenesis is one of the major characteristics of human hepatocellular carcinoma (HCC). The history of multiple tumors, i.e., whether they are derived from a common precancerous or cancerous ancestor or individually from hepatocytes, is a major issue. Multiple HCC is clinically classified into intratumor metastasis (IM) and multicentric carcinogenesis (MC). Molecular markers differentiating IM and MC are of interest to clinical practitioners because clinical diagnosis of IM and MC often leads to different therapies. We analyzed multiple HCCs for somatic mutations of cancer-related genes, chromosomal aberrations, and promoter methylation of tumor suppressor genes, using techniques such as high-resolution melting, array-comparative genomic hybridization (CGH), and quantitative methylation-specific PCR. Comparative genomic hybridizaion experiments. A total of 20 tumor samples: ten pairs of HCC (from ten patients).
Project description:Genome-wide methylation analysis was performed by methylated DNA immunoprecipitation (MeDIP)-CpG island (CGI) microarray analysis to identify candidate CGIs specifically methylated in mouse colon tumors associated with colitis. We sucessfully identified 23 candidate CGIs methylated in tumors. Two samples were analyzed by MeDIP-CGI microarray. One is a pool of two AOM/DSS-induced colon tumors in BALB/c mice and another is a pool of two normal colonic epithelial cell samples obtained from untreated BALB/c mice by the crypt isolation technique. The pool of normal colonic epithelial cell samples was used as reference. Dye-swaps were not perfromed. The methylation statuses of CGIs identified by microarray were confirmed by another method, methylation-specific PCR.