Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE4384
PROVIDER: PRJNA94565 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Collection of leukemia cell lines selected because they contain one of several recurrent chromosomal translocations commonly seen in acute lymphoblastic leukemia. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Computed
2005-12-20 | E-GEOD-3883 | biostudies-arrayexpress
Project description:Collection of leukemia cell lines selected because they contain one of several recurrent chromosomal translocations commonly seen in acute lymphoblastic leukemia. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set
2005-12-21 | GSE3883 | GEO
Project description:Chromosomal aneuploidy and translocations are hallmarks of acute lymphoblastic leukemia (ALL), but many patients lack a recurring chromosomal alteration. Here we report a recurring interstitial deletion of the pseudoautosomal region 1 of chromosomes X and Y in B-progenitor ALL that results in the expression of a novel fusion that juxtaposes the first non-coding exon of P2RY8 to the coding region of the CRLF2 (cytokine receptor like factor 2, or thymic stromal lymphopoietin receptor) gene. The P2RY8-CRLF2 fusion was identified in 7% of B-ALL cases, and was very common in ALL associated with Down syndrome (55% of cases) and was associated with the presence of JAK mutations. The P2RY8-CRLF2 fusion results in increased expression of CRLF2, a lymphoid signaling molecule that forms a heterodimeric complex with interleukin receptor 7 alpha. These findings identify a novel recurring chromosomal alteration in B-ALL, and suggest that perturbed CRLF2-mediated signaling is a key event in leukemogenesis in these cases. Profiling of tumor acquired DNA copy number alterations in 2 patients with Down syndrome associated B-progenitor acute lymphoblastic leukemia. Matched tumor and normal DNA was used for each array hybridization in each case.
2009-10-18 | E-GEOD-16724 | biostudies-arrayexpress
Project description:A recurrent chromosomal translocation detected in cannibalistic acute myeloid leukemia leads to the production of a ZMYND11-MBTD1 fusion protein.
- The ZMYND11-MBTD1 fusion protein is stably incorporated into the endogenous NuA4/TIP60 complex
- ZMYND11-MBTD1 leads to mistargeting of NuA4-TIP60 activity to the coding region of ZMYND11-target genes, altering gene expression and transcript isoforms.
- ZMYND11-MBTD1 binds the MYC gene leading to its upregulation, favoring growth and pluripotency while inhibiting differentiation markers.
2021-04-17 | MSV000087226 | MassIVE
Project description:Despite improved 5-year overall survival rates in B-cell acute lymphoblastic leukemia (B-ALL) due to therapy escalation, effective treatments for relapsed and treatment-resistant disease, especially in specific subtypes like those with TCF3 (formerly E2A) fusions, remain scarce. TCF3, a key regulator of B-cell development, is implicated in various chromosomal translocations linked to lymphoid malignancies, such as TCF3::PBX1 fusion (5% of pediatric B-ALL) and TCF3::HLF fusion (~0.5% of pediatric B-ALL). Current omics research predominantly relies on transcriptomics, but it's increasingly recognized that this may not adequately reflect protein expression, the main targets of drugs and functional entities in biological processes. This study comprehensively analyzed proteomic landscapes of TCF3::HLF+ (n=6) and TCF3::PBX1+ (n=5) B-ALL using primary patient-derived xenografts (PDX), liquid chromatography tandem mass spectrometry, and data-dependent acquisition.
2024-07-05 | PXD053677 | Pride
Project description:Acute Lymphoblastic Leukemia (ALL) in infants (<1 year) is characterized by a poor prognosis and a high incidence of MLL translocations. Several studies demonstrated the unique gene expression profile associated with MLL-rearranged ALL, but generally small cohorts were analyzed as uniform patient groups regardless of the type of MLL translocation, while the analysis of translocation-negative infant ALL remained unacknowledged. We generated and analyzed primary infant ALL expression profiles (n=73) typified by translocations t(4;11), t(11;19) and t(9;11), or the absence of MLL translocations, in order to study translocation-specific gene expression between the different genetic subtypes of infant ALL.
2009-12-15 | E-GEOD-19475 | biostudies-arrayexpress
Project description:Although the 5-year survival of childhood Acute Lymphoblastic Leukemia (ALL) exceeds 80%, a group of patients presents poor prognosis due to early relapse. To date, treatment strategies are defined by cytogenetically-based subtype categorization. However, ALL patients without chromosomal translocations associated with poor prognosis lack diagnostic markers to adjust specific therapies. DNA methylation alteration is a frequent event in cancer with high potential in diagnosis, prognosis and prediction of drug response. Hence, we aimed to characterize childhood B-ALLs without Philadelphia (BCR-ABL) and MLL translocations based on their DNA methylation profile of more than 450,000 CpG sites to improve accuracy in prognosis and treatment strategies.
2012-11-07 | GSE39141 | GEO
Project description:Acute Lymphoblastic Leukemia (ALL) in infants (<1 year) is characterized by a poor prognosis and a high incidence of MLL translocations. Several studies demonstrated the unique gene expression profile associated with MLL-rearranged ALL, but generally small cohorts were analyzed as uniform patient groups regardless of the type of MLL translocation, while the analysis of translocation-negative infant ALL remained unacknowledged.
2009-12-16 | GSE19475 | GEO
Project description:Background; The t(12;21)(p13;q22) translocation is found in 20 to 25% of cases of childhood B-lineage acute lymphoblastic leukemia (B-ALL). This rearrangement results in the fusion of ETV6 (TEL) and RUNX1 (AML1) genes and defines a relatively uniform category, although only some patients suffer very late relapse. TEL/AML1-positive patients are thus an interesting subgroup to study, and such studies should elucidate the biological processes underlying TEL/AML1 pathogenesis. We report an analysis of gene expression in 60 children with B-lineage ALL using Agilent whole genome oligo-chips (44K-G4112A) and/or real time RT-PCR. Results; We compared the leukemia cell gene expression profiles of 16 TEL/AML1-positive ALL patients to those of 44 TEL/AML1-negative patients, whose blast cells did not contain any additional recurrent translocation. Microarray analyses of 26 samples allowed the identification of genes differentially expressed between the TEL/AML1-positive and negative ALL groups. Gene enrichment analysis defined five enriched GO categories: cell differentiation, cell proliferation, apoptosis, cell motility and response to wounding, associated with 14 genes â??RUNX1, TCFL5, TNFRSF7, CBFA2T3, CD9, SCARB1, TP53INP1, ACVR1C, PIK3C3, EGFL7, SEMA6A, CTGF, LSP1, TFPIâ?? highlighting the biology of the TEL/AML1 sub-group. These results were first confirmed by the analysis of an additional microarray data-set (7 patient samples) and second by real-time RT-PCR quantification and clustering using an independent set (27 patient samples). Over-expression of RUNX1 (AML1) was further investigated and in one third of the patients correlated with cytogenetic findings. Conclusions; Gene expression analyses of leukemia cells from 60 children with TEL/AML1-positive and -negative B-lineage ALL led to the identification of five biological processes, associated with 14 validated genes characterizing and highlighting the biology of the TEL/AML1-positive ALL sub-group. Experiment Overall Design: We carried out a prospective multicentric study on childhood B-ALL leukemia to elucidate the molecular processes involved in TEL/AML1-positive leukemia. All the patients included in this study received treatment according to the French FRALLE 2000 trial. We used Agilent whole-genome oligo-chips (44K-G4112A) to compare the gene expression signatures of TEL/AML1-positive patients to those of TEL/AML1-negative patients with no recurrent chimeric products irrespective of their clinical risk category. Previous microarray gene expression studies had revealed the effect of chromosomal alteration on transcription profiles, so we excluded from our cohort those patients with other recurrent chromosomal translocations or fusion transcripts (BCR/ABL, E2A/PBX1, MLL rearrangements). We then searched for the biological pathways associated with genes differentially expressed in TEL/AML1-positive leukemia (ETV6/RUNX1).
2008-06-16 | E-GEOD-9170 | biostudies-arrayexpress
Project description:Large-scale chromosomal translocations are frequent oncogenic drivers in acute myeloid leukemia (AML). These translocations often occur in critical transcriptional/epigenetic regulators and contribute to malignant cell growth through alteration of normal gene expression. Despite this knowledge, the specific gene expression alterations that contribute to the development of leukemia remain incompletely understood. Here, through characterization of transcriptional regulation by the RUNX1-ETO fusion protein, we have identified Ras-association domain family member 2 (RASSF2) as a critical gene that is aberrantly transcriptionally repressed in t(8;21)-associated AML. Based on this, we performed molecular and functional characterization of RASSF2 in AML cells.
2019-11-27 | GSE141088 | GEO