Project description:We analyzed, by last-generation high-resolution SNP arrays, colorectal adenocarcinoma samples and matched normal colonic tissues in order to determine the number of tumor-associated copy number abnormalities (CNAs) and copy neutral-loss of heterozygosity (CN-LOH) regions per patient and to identify possible recurring genomic abnormalities.
Project description:A core task to understand the consequences of non-coding single nucleotide polymorphisms (SNP) is to identify their genotype specific binding of transcription factor (TF). Here, we generate a large-scale TF-SNP interaction map for a selection of 116 colorectal cancer (CRC) risk loci and validated TF binding to 10 putatively functional SNPs. Our data further revealed TF binding complexity adjacent to the 116 risk loci, adding an additional layer of understanding to regulatory networks associated with CRC relevant loci.
Project description:The goal of this study is to investigate the secretion from human colorectal adenocarcinoma cell, which effect to peripheral blood mononuclear cell (PBMC). Genome wide DNA methylation profiling of co-cultured PBMC without human colorectal adenocarcinoma cell lines and co-cultured PBMC with human colorectal adenocarcinoma cell lines were generated datas by microarray technology. The Illumina Infinium MethylationEPIC BeadChip was used to obtain DNA methylation profiles across approximately 850,000 CpGs in enhancer regions, gene bodies, promoters and CpG islands. Samples included duplicate PBMC of female control, duplicate PBMC of male control, duplicate PBMC of female were co-cultured with HT29, and duplicate PBMC of male were co-cultured with SW480.
Project description:To identify genetic alterations involved in the pathogenesis of PETs, we have analysed a total of 32 PET samples (29 tissue specimens and 3 cell lines) using high-resolution single nucleotide polymorphism (SNP) arrays. Keywords: comparative genomic hybridisation
Project description:The genomic loci with copy number alterations are known to harbor cancer genes. We investigated a comprehensive panel of gastric cancer cell lines for their genome-wide copy number alterations. Eighteen gastric cancer cell lines were profiled using Affymetrix 500K SNP arrays. For copy number calculation, seven independent normal blood samples were profiled together. The copy numbers were calculated genome-wide, in these cell lines with high resolution and reveal the cell line specific amplification and copy number changes.
Project description:A core task to understand the consequences of non-coding single nucleotide polymorphisms (SNP) is to identify their genotype specific binding of transcription factor (TF). Here, we generate a large-scale TF-SNP interaction map for a selection of 116 colorectal cancer (CRC) risk loci and validated TF binding to 10 putatively functional SNPs. Our data further revealed TF binding complexity adjacent to the 116 risk loci, adding an additional layer of understanding to regulatory networks associated with CRC relevant loci.
Project description:To identify genomic abnormalities characteristic of pancreatic ductal adenocarcinoma (PDAC) in vivo, a panel of 27 microdissected PDAC specimens were analyzed using high-density microarrays representing ~116 000 single nucleotide polymorphism (SNP) loci. We detected frequent gains of 1q, 2, 3, 5, 7p, 8q, 11, 14q and 17q (>78% of cases), and losses of 1p, 3p, 6, 9p, 13q, 14q, 17p and 18q (>44%). Although the results were comparable with those from array CGH, regions of those genetic changes were defined more accurately by SNP arrays. Integrating the Ensembl public data, we have generated "gene" copy number indices that facilitate the search for novel candidates involved in pancreatic carcinogenesis. Copy numbers in a subset of the genes were validated using quantitative real-time PCR. The SKAP2/SCAP2 gene (7p15.2), which belongs to the src family kinases, was most frequently (63%) amplified in our sample set and its recurrent over-expression (67%) was confirmed by reverse transcription-PCR. Furthermore, fluorescence in situ hybridization and in situ RNA hybridization analyses for this gene have demonstrated a significant correlation between DNA copy number and mRNA expression level in an independent sample set (p<0.001). These findings indicate that the dysregulation of SKAP2/SCAP2, which is mostly caused by its increased gene copy number, is likely to be associated with the development of PDAC. Keywords: pancreatic cancer; tissue microdissection; SNP array; DNA copy number; LOH
Project description:Copy number profiling of 36 ovarian tumors on Affymetrix 100K SNP arrays Thirty-six ovarian tumors were profiled for copy-number alterations with the Affymetrix 100K Mapping Array. Copy number profiling of 36 ovarian tumors on Affymetrix 500K SNP arrays Sixteen ovary tumors were profiled for copy-number alterations with the high-resolution Affymetrix 500K Mapping Array.
