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Gene expression in pediatric cALL

ABSTRACT: Common ALL (cALL) is the most frequent entity of childhood ALL and carries an early pre-B cell phenotype. Expression patterns of 25 pediatric cALL samples were analyzed by use of high-density DNA microarrays HG-U133A. Leukemic patients’ bone marrow samples were compared to sorted B cells from cord blood of healthy donors expressing CD19 and CD10 surface antigens. Differential gene expression profiling of pediatric cALL versus non-malignant tissues enabled the identification of aberrantly expressed genes in malignant cells, facilitating discrimination of leukemic from normal cells and possibly revealing specific disease mechanisms. Principal component analysis clearly distinguished leukemia samples from normal controls. Significance analysis of microarrays revealed 487 genes significantly up-regulated, and 572 down-regulated genes in leukemic cells. A comparison to previous publications investigating genetically defined subsets of cALL revealed 465 genes previously not associated with cALL. Interestingly, terminal deoxynucleotidyl-transferase (DNTT) as well as in the context of cALL unknown genes, were found to be the strongest predictive genes for the malignant phenotype signifying the diagnostic value of our approach.

ORGANISM(S): Homo sapiens

PROVIDER: GSE34670 | GEO | 2012/06/30

SECONDARY ACCESSION(S): PRJNA150327

REPOSITORIES: GEO

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Gene expression in pediatric cALL

Project description:Common ALL (cALL) is the most frequent entity of childhood ALL and carries an early pre-B cell phenotype. Expression patterns of 25 pediatric cALL samples were analyzed by use of high-density DNA microarrays HG-U133A. Leukemic patientsâ bone marrow samples were compared to sorted B cells from cord blood of healthy donors expressing CD19 and CD10 surface antigens. Differential gene expression profiling of pediatric cALL versus non-malignant tissues enabled the identification of aberrantly expressed genes in malignant cells, facilitating discrimination of leukemic from normal cells and possibly revealing specific disease mechanisms. Principal component analysis clearly distinguished leukemia samples from normal controls. Significance analysis of microarrays revealed 487 genes significantly up-regulated, and 572 down-regulated genes in leukemic cells. A comparison to previous publications investigating genetically defined subsets of cALL revealed 465 genes previously not associated with cALL. Interestingly, terminal deoxynucleotidyl-transferase (DNTT) as well as in the context of cALL unknown genes, were found to be the strongest predictive genes for the malignant phenotype signifying the diagnostic value of our approach. RNA was extracted from bone marrow or peripheral blood samples form pediatric cALL patients, leukemia cell lines, and purified fetal B cells and hybridized with Affymetrix HG_U133A microarrays.

2012-06-29 | E-GEOD-34670 | biostudies-arrayexpress

Homo sapiens

Project description:Gene expression in pediatric cALL

| PRJNA150327 | ENA

MondoA mediates in vivo aggressiveness of common ALL and may serve as a T cell immunotherapy target

Project description:Oncogene addiction provides ideal targets for immunotherapy. We previously showed that the high expression of the conserved transcription factor MondoA mediates glucose consumption and stemness of a cALL cell line. We now report the expression of MondoA (MLXIP) in cALL compared to other malignancies, its role in malignancy of cALL in vivo, downstream pathways and correlation with relapse risk. Given the non-accessibility of transcription factors by drugs or chimeric antigen receptor transgenic T cells, we assessed the targetability of MondoA by allo-restricted, peptide-specific T cells. We found MondoA to be most highly expressed in pediatric cALL. MondoA knock down (KD) in cALL cell lines and their subsequent analysis in xenograft mice reduced the number of leukemic blasts in blood, marrow and spleen. Spleen size and weight normalized in mice after MondoA KD. Consistent with these data, MondoA overexpression correlated with relapse risk in cALL patients, as its expression was 63% higher in the very high-risk group relative to the non-high-risk group. Transcriptomic profiling of cALL cell lines after MondoA KD revealed an induction of aerobic glycolysis switch genes and hypoxia-response by MondoA. Indeed, MondoA appeared to be required for HIF1A protein stabilization. Therapeutically, MondoA-derived peptide antigens and HLA-A*02:01+ cALL lines were successfully recognized and killed by specific, allo-restricted CD8+ T cells. In conclusion, our findings demonstrate that MondoA maintains leukemic burden and aggressiveness of cALL in vivo possibly by modulating metabolic and hypoxia stress response. Moreover, we identified MondoA as a promising target for immunotherapy of cALL.

2016-04-30 | GSE76277 | GEO

pediatric AML and normal bone marrow

Project description:This series represents leukemic samples obtained from pediatric AML patients at diagnosis and control normal bone marrow samples. Keywords: other

2005-01-28 | GSE2191 | GEO

E-GEOD-34670

Project description:Gene expression in pediatric cALL

2015-09-22 | E-GEOD-34670 | ExpressionAtlas

Homo sapiens

Project description:Affymetrix SNP array data for Pediatric malignant glioma samples

| PRJNA134227 | ENA

Transcription profiling of human pediatric acute myeloid leukemia samples

Project description:This series represents leukemic samples obtained from pediatric AML patients at diagnosis and control normal bone marrow samples.

2007-08-25 | E-GEOD-2191 | biostudies-arrayexpress

Engraftment of limited numbers of pediatric leukemia into NOD/SCID/IL2Rcg-null mice enables surrogate markers for clinical outcome

Project description:Cultured immortalized cell lines have been extensively used to study the characteristics of various malignant stem cell clones and to optimize new treatment strategies. Nonetheless, the usefulness of such in vitro systems to recapitulate primary disease proved to be limited. Therefore, the design of more meaningful pre-clinical in vivo models ideally utilizing primary patient-derived material is of critical importance. In this context, the recently described NOD.Cg-Prkdcscid IL2rgtmWjl/Sz (NSG) mouse strain has been reported to sustain superior engraftment rates of patient-derived acute lymphatic and myeloid leukemic samples. However, limited data exist whether NSG-derived blasts retain their leukemogenecity over successive mouse generations and whether characteristics of this mouse model will indeed allow correlation to clinical parameters. In the present study, we thus engrafted NSG mice with 18 different pediatric B cell precursor ALL, AML and T-ALL samples and could demonstrate that NSG-derived blasts retained their leukemogenic profile with respect to immune-phenotype, chromosomal aberrations, transcriptome, flowcytometric- and PCR-minimal residual disease (MRD) marker expression. Moreover, the extent of leukemic engraftment and the overall survival of NSG mice highly correlated with the individual prognosis of pediatric B cell precursor ALL, AML and T-ALL patients. Thus, we here report on a complex in vivo model that provides a valuable tool for studying the heterogeneity of leukemic disease and for improving patient-tailored leukemia-targeting strategies . In the present study, we thus engrafted NSG mice with 18 different pediatric B cell precursor ALL, AML and T-ALL samples and could demonstrate that NSG-derived blasts retained their leukemogenic profile with respect to immune-phenotype, chromosomal aberrations, transcriptome, flowcytometric- and PCR-minimal residual disease (MRD) marker expression.

2012-03-31 | E-GEOD-35504 | biostudies-arrayexpress

Engraftment of limited numbers of pediatric leukemia into NOD/SCID/IL2Rcg-null mice enables surrogate markers for clinical outcome

2012-04-01 | GSE35504 | GEO

Affymetrix SNP array data for Pediatric malignant glioma samples

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.

2011-11-23 | E-GEOD-25589 | biostudies-arrayexpress

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