Project description:Pediatric patients with de novo acute myeloid leukemia. To define genomic architecture, we performed genome-wide copy number abberation analysis in 460 paired diagnostic-remission bone marrow aspirates. Illumina SNP arrays were performed according to the manufacturer's directions on DNA extracted from cryopreserved diagnostic and remission bone marrow samples.
Project description:Copy number and LOH analysis was performed for 56 chronic myeloid leukemia cases obtained from 23 CML cases obtained atchronic phase, accelerated phase, blast crisis, or remission. All caseswere genotyped with Affymetrix 250k Sty and Nsp arrays. 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: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:Pediatric patients with de novo acute myeloid leukemia. To define genomic architecture, we performed genome-wide copy number abberation analysis in 460 paired diagnostic-remission bone marrow aspirates.
Project description:We recently identified recurrent mutations of cohesin complex in myeloid neoplasms through whole-exome sequencing analysis. In this study, we performed SNP array analysis to detect abnormal copy number of the cohesin genes.
Project description:Copy number and LOH analysis was performed for 36 acute leukemia cell lines. All cases were genotyped with Affymetrix 250k Sty and Nsp arrays. Keywords: Acute leukemia, BCR-ABL1, cell lines, 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:We recently identified recurrent mutations of cohesin complex in myeloid neoplasms through whole-exome sequencing analysis. In this study, we performed SNP array analysis to detect abnormal copy number of the cohesin genes. Copy number analysis by Affymetrix 50K or 250K SNP arrays was performed for 93 AML and 70 MDS tumor samples.
Project description:BCR-ABL1 lymphoblastic leukaemia is characterized by the deletion of Ikaros. The Philadelphia chromosome, encoding BCR-ABL1, is the defining lesion of chronic myelogenous leukemia (CML) and a subset of acute lymphoblastic leukemia (ALL) cases. To define oncogenic lesions that cooperate with BCR-ABL1 to induce ALL, we performed genome-wide analysis of leukemic samples from 23 CML cases and 304 ALL cases, including 43 BCR-ABL1 B-ALL cases. IKZF1 (encoding the transcription factor Ikaros) was deleted in 83.7% of BCR-ABL1 B-ALL cases, but not in chronic phase CML. Deletion of IKZF1 was also identified as an acquired lesion in lymphoid blast crisis of CML. The IKZF1 deletions resulted in haploinsufficiency, expression of a dominant negative Ikaros isoform or the complete loss of Ikaros expression. Sequencing of IKZF1 deletion breakpoints suggested that aberrant V(D)J recombination is responsible for the deletions. These findings suggest that genetic lesions resulting in the loss of Ikaros function are a key event in the development of BCR-ABL1 ALL. *** 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. *** This SuperSeries is composed of the SubSeries listed below.