Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA238316 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gene expression analysis in primary blasts of AML patients and CD34+normal progenitors after 6 hours of HDACi treatment.
| PRJNA238128 | ENA
Project description:AML cell lines (K562, U937 and NB4) were treated with MS27-275 (MS) and SAHA for 6 hours and the gene expression analysis revealed commonly regulated genes by the 2 HDACi. AML blasts were treated with SAHA for 6 hours and gene expression profiles were compared to commonly regulated genes by MS and SAHA in AML cell lines. The analysis revealed commonly regulated genes in these systems by SAHA.
2017-03-01 | GSE54871 | GEO
Project description:AML blasts and CD34+ normal progenitors were treated with SAHA, and gene expression profiles were compared to 6-hours treatments. The analysis revealed commonly regulated genes in these systems by HDACi.
2017-03-01 | GSE54873 | GEO
Project description:K562, U937 and NB4 AML cell lines were treated with 2 HDACi, MS-275 and SAHA, and gene expression profiles were analysed to 6-hours treatments. The analysis revealed commonly regulated genes in the 3 cell lines and by 2 HDACi.
2017-03-01 | GSE54869 | GEO
Project description:PURPOSE: Inhibitors of histone deacetylases (HDACIs) like valproic acid (VPA) display activity in murine leukemia models, and induce tumor-selective cytoxicity against blasts from patients with acute myeloid leukemia (AML). However, despite of the existing knowledge of the potential function of HDACIs, there remain many unsolved questions especially regarding the factors that determine whether a cancer cell undergoes cell cycle arrest, differentiation, or death in response to HDACIs. Furthermore, there is still limited data on HDACIs effects in vivo, as well as HDACIs function in combination with standard induction chemotherapy, as most studies evaluated HDACIs as single agent in vitro. Thus, our first goal was to determine a VPA response signature in different myeloid leukemia cell lines in vitro, followed by an in vivo analysis of VPA effects in blasts from adult de novo AML patients entered within two randomized multicenter treatment trials of the German-Austrian AML Study Group. PATIENTS AND METHODS: To define a VPA in vitro response signature we profiled gene expression in myeloid leukemia cell lines (HL60, NB4, HEL, and K-562) following 48 hours of VPA treatment by using DNA Microarray technology. Next, we evaluated the VPA effects on gene expression in AML samples collected within the AMLSG 07-04 trial for younger (age<60yrs) and within the AMLSG 06-04 trial for older adults (age>60yrs), in which patients are randomized to receive standard induction chemotherapy (idarubicine, cytarabine, and etoposide = ICE) with or without concomitant VPA. We profiled gene expression in diagnostic AML blasts and following 48 hours of treatment with ICE or ICE/VPA. cDNA microarrays from the Stanford Functional Genomics Facility were used to perform mRNA transcript profiling of 4 leukemia cell lines treated with 1mM VPA for 48 hours in comparison to untreated cell lines, and to perform mRNA transcript profiling of freshly-frozen, from matched acute myeloid leukemia peripheral blood specimens collected from 14 AML patients at diagnosis and following 48 hours of treatment with either chemotherapy +/- VPA.
2012-09-19 | E-GEOD-32240 | biostudies-arrayexpress
Project description:Primary human AML cells (newly diagnosed, prior to treatment initation) was obtained from donor after consent and AML blasts were isolated by standard Ficoll centrifugation. Cells were treated ex vivo with DMSO vehicle control or 10 nM FLT3 inhibitors quizartinib, crenolanib, gilteritinib for 6 hours in SILAC medium and processed for LC/MS.
2022-08-25 | PXD034081 | Pride
Project description:Gene expression analysis in AML cells lines, AML primary blasts and in CD34+ normal progenitors after 6-hour exposure to HDACi
| PRJNA238649 | ENA
Project description:PURPOSE: Inhibitors of histone deacetylases (HDACIs) like valproic acid (VPA) display activity in murine leukemia models, and induce tumor-selective cytoxicity against blasts from patients with acute myeloid leukemia (AML). However, despite of the existing knowledge of the potential function of HDACIs, there remain many unsolved questions especially regarding the factors that determine whether a cancer cell undergoes cell cycle arrest, differentiation, or death in response to HDACIs. Furthermore, there is still limited data on HDACIs effects in vivo, as well as HDACIs function in combination with standard induction chemotherapy, as most studies evaluated HDACIs as single agent in vitro. Thus, our first goal was to determine a VPA response signature in different myeloid leukemia cell lines in vitro, followed by an in vivo analysis of VPA effects in blasts from adult de novo AML patients entered within two randomized multicenter treatment trials of the German-Austrian AML Study Group. PATIENTS AND METHODS: To define a VPA in vitro response signature we profiled gene expression in myeloid leukemia cell lines (HL60, NB4, HEL, and K-562) following 48 hours of VPA treatment by using DNA Microarray technology. Next, we evaluated the VPA effects on gene expression in AML samples collected within the AMLSG 07-04 trial for younger (age<60yrs) and within the AMLSG 06-04 trial for older adults (age>60yrs), in which patients are randomized to receive standard induction chemotherapy (idarubicine, cytarabine, and etoposide = ICE) with or without concomitant VPA. We profiled gene expression in diagnostic AML blasts and following 48 hours of treatment with ICE or ICE/VPA.
2012-09-19 | GSE32240 | GEO
Project description:Chip-chip data from primary human AML patient blasts, normal CD34+ HSCs, normal neutrophils and normal T cells with H3K9 and H3K27 antibodies. Gene expression profiling from primary human AML patient blasts and CD34+ normal cells. Analysis of the chromatin landscape of the ERG locus using H3K9 and H3K27 as markers of euchromatin and heterochromatin respectively. Analysis of ERG expression in AML patients with normal CD34+ HSCs as control. Correlation of the activity of a stem cell enhancer at the ERG locus in AML primary patient blasts with their transcriptome and clinical outcome data.
2013-04-04 | E-GEOD-38865 | biostudies-arrayexpress
Project description:RAS mutations are frequently found among AML patients, generating a constitutively active signaling protein changing cellular proliferation, differentiation and apoptosis. We previously showed that treatment of AML patients with high-dose cytarabine (HDAC) is preferentially beneficial for those with an oncogenic RAS mutation. By applying a murine AML model, we could ascribe this effect to a RAS-driven, p53-dependent induction of differentiation. Here, we sought to confirm the correlation between RAS status and differentiation of blasts obtained from AML patients. The expression signature of primary AML blasts expressing oncogenic RAS where compared to blasts with wtRAS. Blasts where obtained from peripheral blood or bone marrow samples from patients with CBFbeta-MYH11 translocations and with or without an additional NRAS point mutation. As a reference, the Kasumi-1 acute myeloid leukemia cell line was used.
2015-11-20 | E-MTAB-2090 | biostudies-arrayexpress