Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Gene expression profiles of ALL cells

ABSTRACT: Using using ATLAS cDNA expression arrays, we performed gene expression profiling of primary leukemia cells from 31 infants and 30 non-infant children (pediatric patients) with ALL to determine if any of these signature genes are differentially expressed in infant ALL vs. pediatric ALL. Reduced expression levels of 6 of the 9 CD22E12 signature genes that were represented on the human cDNA arrays, including TP53 and APC as well as MDM2, SATB1, CCNG1 and GNB2 discriminated infant BPL from non-infant BPL. Total RNA was extracted from primary ALL cells and human ATLAS c DNA expression arrays were used for gene expression profiling.

ORGANISM(S): Homo sapiens

SUBMITTER: Sanjive Qazi

PROVIDER: E-GEOD-24000 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

CD22 EXON 12 deletion as a pathogenic mechanism of human B-precursor leukemia.

Uckun Fatih M FM Goodman Patricia P Ma Hong H Dibirdik Ilker I Qazi Sanjive S

Proceedings of the National Academy of Sciences of the United States of America 20100914 39

Here, we report that primary leukemic cells from infants with newly diagnosed B-precursor leukemia express a truncated and functionally defective CD22 coreceptor protein that is unable to transmit apoptotic signals because it lacks most of the intracellular domain, including the key regulatory signal transduction elements and all of the cytoplasmic tyrosine residues. Expression of this structurally and functionally abnormal CD22 protein is associated with a very aggressive in vivo growth of pati ...[more]

PMID: 20841423

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Project description:Extensive molecular and prognostic characterization of wild-type MLL infant ALL. Background: Approximately 20% of all infant ALL cases carry wild-type (or germline) MLL genes. To date, wild-type MLL infant ALL patients are generally regarded as young pediatric precursor B-ALL patients, but extensive characterization of this specific patient group largely remains unacknowledged. Methods: We here studied a relatively large cohort of 78 wild-type MLL infant ALL samples, using clinical parameters, array-comparative genomic hybridization analysis, gene expression profiling, multiplex ligation-dependent probe amplification, and conventional sequencing. Findings: Wild-type MLL infant ALL patients are generally characterized by a lower incidence of favourable prognostic factors than pediatric (non-infant) B-ALL patients, and patients at high risk of therapy failure typically display an immature pro-B immunophenotype or respond poorly to prednisone. Using gene expression profiling, we found MEIS1 expression to additionally be highly predictive for clinical outcome in wild-type MLL infant ALL with a favourable prognosis in the wild-type MLL infants with low MEIS1 expression (DFS 88%% versus 50%, p=0•01). Overall the incidence of DNA copy number variations and genetic abnormalities in genes involved in B-cell differentiation is lower in wild-type MLL infant ALL patients as compared with pediatric precursor B-ALL patients. Interpretation: Wild-type MLL infant ALL represents a highly heterogeneous patient group, which cannot be unified by one or a few known recurrent genomic aberrations. High-level MEIS1 expression and an immature pro-B immunophenotype in high-risk wild-type MLL infant ALL patients shows parallel with the unfavourable prognosis of MLL-rearranged infant ALL patients. In contrast, wild-type MLL infant ALL patients expressing lower levels of MEIS1 and displaying more differentiated (pre-B or common) phenotypes may well be more related to pediatric precursor B-ALL patients older than 1 year of age. We advocate that a treatment strategy in wild-type MLL infant ALL based on MEIS1 expression could be beneficial for improving survival. Gene expression profiling of wild-type MLL infant ALL. Additional wild-type MLL infant ALL patient samples (n=17) to the earlier samples published under GSE19475 (GSM485309 to GSM485322).

Dataset Information

Gene expression profiles of ALL cells

Publications

CD22 EXON 12 deletion as a pathogenic mechanism of human B-precursor leukemia.

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