Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA109599 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Genomic analysis of relapsed Acute Lymphoblastic Leukaemia in children
| PRJNA192670 | ENA
Project description:Genome-wide analysis of basal gene expression analysis of pediatric acute lymphoblastic leukaemia xenograft cells
| PRJNA269726 | ENA
Project description:Baseline glucocorticoid resistance profiles were measured in a panel of 15 paediatric T-Cell acute lymphoblastic leukaemia cell lines and correlated with Affymetrix Gene expression to identify genes and pathways associated with drug resistance in T-ALL. The cell lines' resistance to Methylprednisolone (MPRED) and Dexamethasone (DEX) was then tested using the MTT assay and IC50 values (drug concentration lethal to 50% of cells) for each drug were calculated.
2012-07-09 | E-MTAB-1208 | biostudies-arrayexpress
Project description:Stability of gene expression and epigenetic profiles highlights the utility of patient-derived paediatric acute lymphoblastic leukaemia xenografts for investigatoing molecular mechanisms of drug resistance (expression)
| PRJNA247370 | ENA
Project description:Acute myeloid leukaemia (AML) affects children and adults of all ages. AML remains one of the major causes of death in children with cancer and for children with AML relapse is the most common cause of death. By modelling AML in vivo we demonstrate that AML is discriminated by the age of the cell of origin. Young cells give rise to myeloid, lymphoid or mixed phenotype acute leukaemia, whereas adult cells give rise exclusively to AML, with a shorter latency. Unlike adult, young AML cells do not remodel the bone marrow stroma. Transcriptional analysis distinguishes young AML by the upregulation of immune pathways. Analysis of human paediatric AML samples recapitulates a paediatric immune cell interaction gene signature, highlighting two genes, RGS10 and FAM26F as prognostically significant. This work advances our understanding of paediatric AML biology, and provides murine models that offer the potential for developing paediatric specific therapeutic strategies.
2018-11-04 | GSE122066 | GEO
Project description:Acute myeloid leukaemia (AML) affects children and adults of all ages. AML remains one of the major causes of death in children with cancer and for children with AML relapse is the most common cause of death. Here, by modelling AML in vivo we demonstrate that AML is discriminated by the age of the cell of origin. Young cells give rise to myeloid, lymphoid or mixed phenotype acute leukaemia, whereas adult cells give rise exclusively to AML, with a shorter latency. Unlike adult, young AML cells do not remodel the bone marrow stroma. Transcriptional analysis distinguishes young AML by the upregulation of immune pathways. Analysis of human paediatric AML samples recapitulates a paediatric immune cell interaction gene signature, highlighting two genes, RGS10 and FAM26F as prognostically significant. This work advances our understanding of paediatric AML biology, and provides murine models that offer the potential for developing paediatric specific therapeutic strategies.
2018-06-14 | GSE107662 | GEO
Project description:Stability of gene expression and epigenetic profiles highlights the utility of patient-derived paediatric acute lymphoblastic leukaemia xenografts for investigatoing molecular mechanisms of drug resistance (methylation)
| PRJNA247373 | ENA
Project description:Distinctive genotypes in infants with T-cell acute lymphoblastic leukaemia
| PRJNA279398 | ENA
Project description:Characterisation of the genomic landscape of CRLF2 deregulated acute lymphoblastic leukaemia
| PRJNA325466 | ENA
Project description:Background: Patient-derived tumour xenografts are an attractive model for preclinical testing of anti-cancer drugs. Insights into tumour biology and biomarkers predictive of responses to chemotherapeutic drugs can also be gained from investigating xenograft models. As a first step towards examining the equivalence of epigenetic profiles between xenografts and primary tumours in paediatric leukaemia, we performed genome-scale DNA methylation and gene expression profiling on a panel of 10 paediatric B-cell precursor acute lymphoblastic leukaemia (BCP-ALL) tumours that were stratified by prednisolone response. Results: We found high correlations in DNA methylation and gene expression profiles between matching primary and xenograft tumour samples with Pearson’s correlation coefficients ranging between 0.85 and 0.98. In order to demonstrate the potential utility of epigenetic analyses in BCPALL xenografts, we identified DNA methylation biomarkers that correlated with prednisolone responsiveness of the original tumour samples. Differential methylation of CAPS2, ARHGAP21, ARX and HOXB6 were confirmed by locus specific analysis. We identified 20 genes showing an inverse relationship between DNA methylation and gene expression in association with prednisolone response. Pathway analysis of these genes implicated apoptosis, cell signalling and cell structure networks in prednisolone responsiveness. Conclusions: The findings of this study confirm the stability of epigenetic and gene expression profiles of paediatric BCP-ALL propagated in mouse xenograft models. Further, our preliminary investigation of prednisolone sensitivity highlights the utility of mouse xenograft models for preclinical development of novel drug regimens with parallel investigation of underlying gene expression and epigenetic responses associated with novel drug responses.
2014-05-14 | GSE57581 | GEO