Project description:Data includes all available Affymetrix SNP data from a cohort of Pediatric malignant glioma samples, isolated from Formalin-fixed Paraffin embedded tissue. No clinical data is available. Copy number analysis of Affymetrix 250K Sty SNP arrays was performed for 28 pediatric malignant gliomas. The VN algorithm was used to generate the reference signal based on 48 Mapping 500k HapMap Trio Dataset template.
Project description:High-resolution genomic microarrays provides simultaneous detection of copy-number aberrations such as the known recurrent aberrations in Chronic Lymphocytic Leukemia_diagnostic sample_patient (del(11q), del(13q), del(17p) and trisomy 12), and copy-number neutral loss of heterozygosity. We screened 369 newly diagnosed Chronic Lymphocytic Leukemia_diagnostic sample_patient patient samples from a population-based cohort using 250K single nucleotide polymorphism-arrays.
Project description:Copy number analysis of 21 paediatric low-grade astrocytomas identified a discrete copy number gain of 1.9Mb in chromosome band 7q34. The gain was present in 12/14 cerebellar pilocytic astrocytomas. Subsequent analysis of tumour cDNA indentified a novel gene fusion between KIAA1549 and BRAF in these tumours. Copy number analysis of 21 paediatric low-grade astrocytomas using the Affymetrix GeneChip Human Mapping 250K Nsp Array. This study comprised 14 pilocytic astrocytomas, 4 diffuse astrocytomas, one pilomyxoid astrocytoma, one pilomyxoid glioma and one pleomorphic xanthoastrocytoma. Tumours were compared to the mean of two normal male DNA controls.
Project description:250k Sty, 250k Nsp, 250k Hind and 250k Xba Affymetrix SNP arrays for 50 leukemia remission samples used as controls for copy number analysis for GSE9109 and GSE9112. Keywords: Acute leukemia, BCR-ABL1, chronic myeloid leukemia, copy number analysis, loss-of-heterozygosity, genomics *** Due to privacy concerns, the primary SNP array data is no longer available with unrestricted access. Individuals wishing to obtain this data for research purposes may request access using the Web links below. ***
Project description:A novel method for detecting genome-wide ASM (allele-specific methylation) was developed by modification of the Affymetrix 250K StyI SNP arrays. Using this method, and the above mentioned samples, we consistently detected ASM in non-imprinted regions of the genome. Interestingly, ASM appears to be strongly correlated with the SNP sequences in cis.
Project description:In human, the 39 coding HOX genes and 18 referenced non-coding antisense transcripts are arranged in four genomic clusters named HOXA, B, C, and D. This highly conserved family belongs to the homeobox class of genes that encode transcription factors required for normal development. Therefore, HOX gene deregulation might contribute to the development of many cancer types. Here, we study HOX gene deregulation in adult glioma, a common type of primary brain tumor. We performed extensive molecular analysis of tumor samples, classified according to their isocitrate dehydrogenase (IDH1) gene mutation status, and of glioma stem cells. We found widespread expression of sense and antisense HOX transcripts only in aggressive (IDHwt) glioma samples, although the four HOX clusters displayed DNA hypermethylation. Integrative analysis of expression-, DNA methylation- and histone modification signatures along the clusters revealed that HOX gene upregulation relies on canonical and alternative bivalent CpG island promoters that escape hypermethylation. H3K27me3 loss at these promoters emerges as the main cause of widespread HOX gene upregulation in IDHwt glioma cell lines and tumors. Our study provides the first comprehensive description of the epigenetic changes at HOX clusters and their contribution to the transcriptional changes observed in adult glioma. It also identified putative "master" HOX proteins that might contribute to the tumorigenic potential of glioma stem cells.
Project description:A novel method for detecting genome-wide ASM (allele-specific methylation) was developed by modification of the Affymetrix 250K StyI SNP arrays. Using this method, and the above mentioned samples, we consistently detected ASM in non-imprinted regions of the genome. Interestingly, ASM appears to be strongly correlated with the SNP sequences in cis. DNA from various sources (6 normal blood, 2 normal bone marrow, 2 CD34+ bone marrow, and 3 placenta samples) was genotyped and ASM was scored as an allele call conversion from 'AB' (heterozygous) to 'AA' or 'BB' (homozygous) in the StyI+HpaII genomic representation, compared to the StyI-only representation. Each sample was subjected to 5 runs of genotyping on the 250K StyI array, including 2 StyI alone, 2 StyI+HpaII and 1 StyI+MspI.