6635d9dc-1128-40b0-8d4f-317fad0d451f - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001009000 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Genomics of drug sensitivity in acute lymphoblastic leukemia
| EGAS00001006336 | EGA
Project description:Drug resistance remains a major obstacle to successful cancer treatment. Here we use a novel approach to identify rapamycin as a glucocorticoid resistance reversal agent. A database of drug-associated gene expression profiles was screened for molecules whose profile overlapped with a gene expression signature of glucocorticoid (GC) sensitivity/resistance in Acute Lymphoblastic Leukemia (ALL) cells. The screen indicated the mTOR inhibitor rapamycin profile matched the signature of GC-sensitivity. We thus tested the hypothesis that rapamycin would induce GC sensitivity in lymphoid malignancy cells, and found that it sensitized cells to glucocorticoid induced apoptosis via modulation of antiapoptotic MCL1. These data indicate that MCL1 is an important regulator of GC-induced apoptosis, and that the combination of rapamycin and glucocorticoids has potential utility in ALL. Furthermore this approach represents a novel strategy for identification of promising combination therapies for cancer. Experiment Overall Design: primary acute lymphoblastic leukemia samples were determined to be sensitive or resistant to in vitro treatment with glucocorticoids. Samples were then hybrized to affymetrix microarrays
2009-04-04 | E-GEOD-5820 | biostudies-arrayexpress
Project description:Single-cell RNA sequencing was performed on bone marrow mononuclear of a patient with acute myeloid leukemia with erythroid differentiation of the blasts and on peripheral blood mononuclear cells of a patient with acute myeloid leukemia with megakaryocytic differentiation of the blasts. Raw data for this dataset can be found at the EGA under accession EGAS00001006819.
2022-12-05 | E-MTAB-12607 | biostudies-arrayexpress
Project description:Arrested bone marrow (BM) lymphoid cell differentiation underlies the emergence of the most common childhood cancer, acute lymphoblastic leukemia (ALL). Recurrent genetic lesions often directly involve transcription factors (TFs), such as ETV6 and RUNX1 found in the most common ALL translocation. Here, we studied differential gene expression in ETV6-RUNX1 primary ALL samples and the REH cell line using single cell RNA-seq (scRNA-seq). Submitter declares that the raw data will be deposited in EGA due to patient privacy concerns. The raw data can be accessed at https://www.ebi.ac.uk/ega/studies/EGAS00001004374
2020-10-30 | GSE148218 | GEO
Project description:The development of a clinically relevant xenograft model of pediatric acute lymphoblastic leukemia, using a 4-drug treatment regimen designed to mimic pediatric remission induction therapy. Relapse and acquired drug resistance in T-cell acute lymphoblastic leukemia (T-ALL) remains a significant clinical problem. This study was designed to establish a preclinical model of resistance to induction therapy in childhood T-ALL to examine the emergence of drug resistance and identify novel therapies. We performed transcription profiling by array of human CD45-positive human lymphocytes from patients with acute pediatric lymphoblastic leukemia, and from xenografted NOD/SCID mice treated with vincristine, daunorubicin, dexamethasone and L-asparagine. Several different treatment regimes were used in this study (VLXD, VLXDR, VLXD2, VXL and VLXD2-ALL31) and are summarised in the protocols associated with this submission.
2013-11-01 | E-MEXP-3916 | biostudies-arrayexpress
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
2012-07-02 | E-GEOD-25117 | biostudies-arrayexpress
Project description:First evidence of a Cornelia de Lange Syndrome patient with a novel cohesin mutation and Acute Lymphoblastic Leukemia
2019-11-23 | GSE122859 | GEO
Project description:Drug resistance remains a major obstacle to successful cancer treatment. Here we use a novel approach to identify rapamycin as a glucocorticoid resistance reversal agent. A database of drug-associated gene expression profiles was screened for molecules whose profile overlapped with a gene expression signature of glucocorticoid (GC) sensitivity/resistance in Acute Lymphoblastic Leukemia (ALL) cells. The screen indicated the mTOR inhibitor rapamycin profile matched the signature of GC-sensitivity. We thus tested the hypothesis that rapamycin would induce GC sensitivity in lymphoid malignancy cells, and found that it sensitized cells to glucocorticoid induced apoptosis via modulation of antiapoptotic MCL1. These data indicate that MCL1 is an important regulator of GC-induced apoptosis, and that the combination of rapamycin and glucocorticoids has potential utility in ALL. Furthermore this approach represents a novel strategy for identification of promising combination therapies for cancer. This SuperSeries is composed of the following subset Series:; GSE5820: Gene expression-based chemical genomics identifies rapamycin as a modulator of MCL-1 and glucocorticoid resistance; GSE5821: Rapamycin treatment of CEM_C1 cells 24 hours; GSE5822: Rapamycin treated CEM-C1 cells 3 hours Experiment Overall Design: Refer to individual Series
2008-11-06 | E-GEOD-5824 | biostudies-arrayexpress
Project description:Genetic studies in T-cell acute lymphoblastic leukemia have uncovered a remarkable complexity of oncogenic and loss-of-function mutations. Amongst this plethora of genetic changes, NOTCH1 activating mutations stand out as the most frequently occurring genetic defect, identified in more than 50% of T-cell acute lymphoblastic leukemias, supporting an essential driver role for this gene in T-cell acute lymphoblastic leukemia oncogenesis. In this study, we aimed to establish a comprehensive compendium of the long non-coding RNA transcriptome under control of Notch signaling. For this purpose, we measured the transcriptional response of all protein coding genes and long non-coding RNAs upon pharmacological Notch inhibition in the human T-cell acute lymphoblastic leukemia cell line CUTLL1 using RNA-sequencing. Similar Notch dependent profiles were established for normal human CD34+ thymic T-cell progenitors exposed to Notch signaling activity in vivo. In addition, we generated long non-coding RNA expression profiles (array data) from GSI treated T-ALL cell lines, ex vivo isolated Notch active CD34+ and Notch inactive CD4+CD8+ thymocytes and from a primary cohort of 15 T-cell acute lymphoblastic leukemia patients with known NOTCH1 mutation status. Integration of these expression datasets with publically available Notch1 ChIP-sequencing data resulted in the identification of long non-coding RNAs directly regulated by Notch activity in normal and malignant T-cell context. Given the central role of Notch in T-cell acute lymphoblastic leukemia oncogenesis, these data pave the way towards development of novel therapeutic strategies that target hyperactive Notch1 signaling in human T-cell acute lymphoblastic leukemia.
2014-10-27 | GSE61866 | GEO
Project description:High levels of branched-chain amino acid (BCAA) transaminase 1 (Bcat1) have been associated with adverse prognosis and drug resistance in several cancer types. However, the mechanistic role of Bcat1 in T-cell acute lymphoblastic leukemia (T-ALL) development is ill defined.We determined the effects of BCAT1 depletion on cellular sensitivity to DNA damaging agents (etoposide).
2025-01-02 | GSE275161 | GEO