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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Human acute myelogenous leukemia-initiating cells treated with fenretinide

ABSTRACT: Transcriptional profiling of human acute myelogenous leukemia (AML) CD34+ cells treated with 5 μM fenretinide. Two timepoints included are 6h, 12h, covering the apoptosis-induction time window of AML CD34+ cells responsing to the fenretinide treatment. We studied gene expression series in human AML CD34+ cells with or without 5 μM fenretinide treatment by cDNA microarray analysis. Several signal transduction pathways are involve, including stress response, NF-kappaB inhibition and p53 inhibition (p<0.05). These findings indicate fenretinide may represent a promising candidate for targeting AML-initiating cells. 6-condition experiment, untreated AML CD34+ cells vs. fenretinide-treated AML CD34+ cells,including 2 time points, for each point the untreated and 5 μM fenretinide treated, independently grown and harvested. Untreated was used to counteracting the background.

ORGANISM(S): Homo sapiens

SUBMITTER: Hui Zhang

PROVIDER: E-GEOD-33243 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Human acute myelogenous leukemia-initiating cells treated with fenretinide

Project description:Transcriptional profiling of human acute myelogenous leukemia (AML) CD34+ cells treated with 5 μM fenretinide. Two timepoints included are 6h, 12h, covering the apoptosis-induction time window of AML CD34+ cells responsing to the fenretinide treatment. We studied gene expression series in human AML CD34+ cells with or without 5 μM fenretinide treatment by cDNA microarray analysis. Several signal transduction pathways are involve, including stress response, NF-kappaB inhibition and p53 inhibition (p<0.05). These findings indicate fenretinide may represent a promising candidate for targeting AML-initiating cells.

2011-11-30 | GSE33243 | GEO

Transcription profiling of human untreated and fenretinide-treated CD34+ cells from 4 CML patients

Project description:Imatinib therapy is first-line treatment for chronic myeloid leukemia (CML), and its failure to target CML progenitor/stem cells may lead to an increased risk of relapse. We report here that fenretinide, a well-tolerated vitamin A derivative, is capable of eradicating primitive CML progenitor/stem cells and significantly enhances the efficacy of imatinib at physiologically achievable concentrations. As tested by colony forming cell assays, formation of various colonies derived primitive CML CD34+ cells was significantly suppressed by fenretinide, particularly with respect to the formation of colonies derived from erythroid progenitors and more primitive CML progenitor/stem cells. Also, fenretinide significantly enhanced the ability of imatinib to suppress the formation of the colonies. Moreover, fenretinide was able to induce apoptosis in primitive CML CD34+ cells while sparing the normal counterparts. In particular, primitive CML CD34+CD38- cells appeared to be most sensitive to fenretinide induced apoptosis. Through transcriptome analysis and molecular validation, we further showed that fenretinide induced apoptosis in CML CD34+ cells was probably mediated by a series of stress responsive events which were likely triggered by elevated levels of intracellular reactive oxygen species. Accordingly, the combination of fenretinide and imatinib may provide a potential solution for overcoming relapse and resistance in CML. Experiment Overall Design: Transcriptome profiles of CML CD34+ cells with and without fenretinide treatment were analyzed using whole genome expression arrays (Affymetrix HG-U133 Plus 2.0) in four CML patients (CML32, CML33, CML34 and CML35, see Table 1). To minimize potential data biases, both treated and untreated cell samples were maintained in culture for 48 hours before hybridization.

2009-12-05 | E-GEOD-17480 | biostudies-arrayexpress

Colon cancer shperes are sensitive to Fenretinide

Project description:Fenretinide has shown its antitumor activity in many tumor types with low cytotoxicity to normal cells. Recently, we have shown that fenretinide could eradicate chronic myeloid leukemia stem/progenitor cells and spheres from ovarian cancer. In this study, we investigate whether fenretinide could selectively target sphere cells of colon cancer. Using high-throughtput microarray system, we identified GO terms and pathway signatures enriched in fenretinide treated HT29 cells and HT29 derived sphere cells. Colon cancer cells HT29 were cultured in sphere formation conditions, HT29 cells and HT29 derived sphere cells were treated with fenretinide, and total RNA from those spheres and corresponding adhered cell was hybridized on Affymetrix U133 plus 2.0 genechip.

2016-04-03 | E-GEOD-66983 | biostudies-arrayexpress

Time-series transcriptome profilings of control and Fenretinide-treated human NB4 cells

Project description:Pharmacological intervention of redox balance in cancer cells often results in oxidative stress-mediated apoptosis, attracting much attention for the development of a new generation of targeted therapy in cancer. However, little is known about mechanisms underlying the conversion from oxidative signaling to downstream activities leading cells to death. We here report a systematic detection of transcriptome changes in response to oxidative signals generated in leukemia cells upon fenretinide treatment, implicating the occurrence of numerous stress-responsive events during the fenretinide induced apoptosis, such as redox response, endoplasmic reticulum stress/unfolded protein response, translational repression and proteasome activation. Moreover, the configuration of these relevant events is primarily orchestrated by stress responsive transcription factors, as typically highlighted by NF-E2-related factor-2 (NRF2) and heat shock factor 1 (HSF1). Several lines of evidence suggest that the coordinated regulation of these transcription factors and thus their downstream genes are involved in converting oxidative signaling into downstream stress-responsive events regulating pro-apoptotic and apoptotic activities at the temporal and spatial levels, typifying oxidative stress-mediated programmed death rather than survival in cancer cells. This study provides a roadmap for understanding oxidative stress-mediated apoptosis in cancer cells, which may be further developed into more sophisticated therapeutic protocols, as implicated by synergistic induction of cell apoptosis using proteasome inhibitors with fenretinide. Time-series experiment, fenretinide treated NB4 cells at 19 time points (i.e., 0.25, 0.5, 1, 2, 4, 6, 8, 10, 12, 15, 18, 21, 24, 30, 36, 42, 48, 54 and 60 hours) and untreated NB4 cells at 4 time points (i.e., 0, 8, 12 and 15 hours).

2010-05-05 | E-GEOD-16578 | biostudies-arrayexpress

Gene expression profiling in the leukemic stem cell-enriched CD34+ fraction identifies target genes that predict prognosis in normal karyotype AML

Project description:Mononuclear cells from AML patients (n=46) were sorted into CD34+ and CD34- subfractions and genome-wide expression analysis was performed using Illumina BeadChip Arrays (HT12 v3). Of 2 AML samples only the CD34+ fraction could be analyzed. AML CD34+ and CD34- gene expression was compared to a large group of normal CD34+ bone marrow cells (n=31). Mononuclear cells from AML patients (n=46) were sorted into CD34+ (46) and CD34- (44) subfractions and genome-wide expression analysis was performed using Illumina BeadChip Arrays (HT12 v3). AML CD34+ and CD34- gene expression was compared to a large group of normal CD34+ bone marrow cells (n=31).

2011-07-18 | E-GEOD-30029 | biostudies-arrayexpress

Transcriptome profiling of fenretinide-treated and untreated CD34+ cells from 4 CML patients

Project description:Imatinib, as the first-line agent of chronic myeloid leukemia (CML), is ineffective in eradicating CML stem/progenitor cells, thus unable to prevent late relapse. Here we present data indicating that fenretinide preferentially targets CD34+ CML cells and enhances the efficacy of imatinib in CML. As tested by colony forming cell assays, both number and size of total colonies derived from CD34+ CML cells were significantly reduced by fenretinide, and by combining fenretinide with imatinib. In particular, colonies derived from erythroid progenitors and those derived from more primitive pluripotent progenitor cells were highly sensitive to fenretinide/fenretinide plus immtinib. Further data showed that fenretinide was able to induce apoptosis in CD34+ CML cells which were refractory to imatinib. Through transcriptome analysis and followed by molecular validation, we further showed that apoptosis induced by fenretinide in CD34+ CML cells was mediated by complex mechanisms of stress responses, probably triggered by elevated levels of intracellular reactive oxygen species. Thus, fenretinide combines with imatinib may represent a new strategy for the treatment of CML, in which fenretinide targets primitive CD34+ CML cells whereas imatinib targets leukemic blasts. This strategy may eventually reduce the risk of relapse and probably resistant as well in CML patients.

2009-12-01 | GSE17480 | GEO

Gene expression change induced by TIM-3/galectin-9 interaction in primary AML

Project description:Analysis of gene expression change after galectin-9 stimulation in primary CD34+TIM-3+ AML cells Total RNA obtained from purified CD34+TIM-3+ primary AML cells with or without recombinant human galectin-9 stimulation (20hrs) was subjected to transcriptome analysis

2014-10-10 | E-GEOD-62223 | biostudies-arrayexpress

Label-free quantitative proteome of AML CD34+ and mobilized PB CD34+ cells

Project description:The label-free quantitative proteome was generated for 42 primary AML patient samples enriched for CD34+ cells (or mononuclear cells in the case of NPMcyt sameples) and as controls 6 mobilized peripheral blood CD34+ cells were included. Furthermore, 6 AML cell lines were included, and also primary mesenchymal stem cells grown under normaoxia or hypoxia were included.

2022-03-15 | PXD030463 | Pride

Integrated nuclear proteomics and transcriptomics identifies new high frequency dysregulated targets in acute myeloid leukemia

Project description:Acute myeloid leukemia (AML) is characterized by developmental arrest which is thought to arise from transcriptional dysregulation of myeloid development programs. Here, we have analyzed the transcriptome of AML blasts in comparison with normal human CD34+ cells using the HTA 2.0 gene chip. We have compared 18 minimally differentiated AML blasts with cord blood derived normal human CD34+ cells - this study is performed as a parallel analysis to compliment the nuclear proteomic studies.

2019-10-02 | E-MTAB-3873 | biostudies-arrayexpress

LAA expression profiles on LSC compared to other tissues

Project description:Leukemic stem cells (LSC) might be the source for leukemic disease self-renewal and account for disease relapse after treatment, which makes them a critical target for further therapeutic options. Leukemia associated antigens (LAA) might be suitable structures to be attacked by immunotherapeutic agents. We performed primary AML sample enrichment and microarray studies to define LAA expression levels in AML. We compared the LAA expression in the enriched CD34+CD38- AML fraction to that of enriched HSC of healthy donors and AML bulk cells (CD34+CD38+, CD34-CD38+ and CD34-CD38). Furthermore, we investigated the expression patterns of co-stimulatory molecules in LSC, bulk AML cells and enriched HSC, Conclusion: We demonstrated the differential expression of several LAA in LSC, and their suitability as target structures. We enriched primary AML samples using CD34 and CD38 as markers to compare LAA expression levels of LSC, HSC and AML bulk. LAA expression profiles comparing LSC, HSC and leukemic bulk AML citation: Leukemic progenitor cells are susceptible to targeting by stimulated cytotoxic T cells against immunogenic leukemia-associated antigens Vanessa Schneider, Lu Zhang, Markus Rojewski, Natalie Fekete, Hubert Schrezenmeier, Alexander Erle, Lars Bullinger, Susanne Hofmann, Marlies Götz, Konstanze Döhner, Susann Ihme, Hartmut Döhner, Christian Buske, Michaela Feuring-Buske, Jochen Greiner

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