Project description:To shed light on the molecular bases of B-lineage acute lymphoblastic leukemia lacking known rearrangements (B-NEG ALL) and the differences between children and adults, we analyzed 168 B-NEG ALLs - including children, adolescents/young adults (AYA) and adults by genome-wide technologies, namely Next-generation sequencing and copy number aberration (CNA). Affymetrix SNP array analysis was performed according to the manufacturer's directions on DNA extracted from bone marrow sampled at diagnosis and paired germline DNA extracted from peripheral blood/bone marrow at complete remission or saliva.
Project description:Development of B-acute lymphoblastic leukemia accompanies with multiple variable mutations. Beside the structural and chromosomal alterations, especially mutations in the regulators of B cell differentiation are common. Around 60% of the B-ALL show deletions of these genes. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from cryopreserved diagnostic bone marrow or peripheral blood samples. Copy number analysis of Affymetrix SNP 6.0 arrays was performed for 20 pediatric B-ALL samples and intraindividually matching remission samples which were used as references.
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.
Project description:This SuperSeries is composed of the following subset Series: GSE25102: Illumina SNP-array data for 2 ETV6/RUNX1-positive Acute Lymphoblastic Leukemia samples and corresponding normal samples GSE25116: Affymetrix SNP-array data for 2 ETV6/RUNX1-positive Acute Lymphoblastic Leukemia samples and corresponding normal samples Refer to individual Series
Project description:We performed single nucleotide polymorphism (SNP) array profiling on 9 early T-cell precursor lymphoblastic lymphoma and 15 non-early T-cell precursor lymphoblastic lymphoma cases. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from unstained slides.
Project description:Childhood T-cell malignancies include T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma (T-LBL). T-ALL and T-LBL share common morphologic and immunophenotypic features and are treated with similar therapeutic approaches. Nonetheless, they show distinct clinical presentations suggesting that they may represent two different biological entities. In order to investigate the common and unique genetic aberrations of T-LBL and T-ALL, copy number alteration (CNA) analysis was performed on a subset of the samples analyzed by GEP Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from diagnostic bone marrow aspirates or tumor tissue samples. Copy number analysis of Affymetrix 100K SNP arrays was performed for 9 T-ALL and 9 T-LBL pediatric samples. The samples from leukemia/lymphoma remission were used as references for copy number inference.