Effect of heteronemin on gene expression profiles in chronic myelogenous K562 leukemia cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE16026 | GEO | 2009/10/14
SECONDARY ACCESSION(S): PRJNA115379
REPOSITORIES: GEO
Similar Datasets
Project description:Heteronemin is a sesterterpene first isolated from Hyrtios Erecta in 1976. In this study we decided to investigate the anti-cancer and anti-inflammatory potential of this marine natural compound at the transcriptomic level in chronic myelogenous K562 leukemia cells. Our results suggest that this sesterterpene has an impact on cell cycle, apoptosis, the MAP kinase signalling pathway and the NF-kappaB transcription factor. We used four experimental conditions : untreated cells, cells treated with heteronemin, cells treated with TNFalpha and cells co-treated with TNFalpha and heteronemin. Experiments were performed in three biological replicates including two technical replicates. Technical replicates were hybridized as dye-swaps. Dye-swap between replicates 1 and 2, 3 and 4, 5 and 6, respectively.
2009-10-14 | E-GEOD-16026 | biostudies-arrayexpress
Project description:We examined gene expression profiling in long-term chronic myelogenous leukemia (CML) stem cells isolated from Gdpd3+/+ and Gdpd3-/- CML mouse model by RNA sequence.
2020-08-18 | GSE149442 | GEO
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
Project description:Chronic myelogenous leukemia (CML) is a malignant stem cell disease characterized by a reciprocal translocation between chromosome 9 and 22. The selective bcr-abl tyrosine-kinase inhibitor Imatinib has become the therapy of choice for patients with newly diagnosed CML including those previously considered candidates for allogeneic haematopoietic stem cell transplantation. The tyrosine-kinase inhibitor Nilotinib is a derivate of Imatinib with higher potency. To examine the molecular and functional effects of Nilotinib and Imatinib in chronic myelogenous leukemia, we performed gene expression and functional analyses in K562 cells following treatment with the two tyrosine kinase inhibitors.
2009-12-19 | GSE19567 | GEO
Project description:Role of Gdpd3 in chronic myelogenous leukemia stem cells
| PRJNA628696 | ENA
Project description:This is a class prediction experiment, where the class is the response status to imatinib (also called Gleevec), a drug used to treat patients with chronic myelogenous leukemia (CML). There are two data sets, a training set (from Leipzig, 8 Responders and 5 Non-Responders) and a validation set (from Mannheim, 8 Responders and 7 Non-Responders). The objective is to identify differentially regulated genes between CML patients who respond and those who do not respond to imatinib and confirm the results in the validation data set. The samples from blood or bone marrow of CML patients were hybridized to Affymetrix HG-U95Av2 chip and RMA was used to generate the normalized signal values. Keywords = chronic myelogenous leukemia Keywords = imatinib Keywords = cytogenetic responses Keywords = Gleevec Keywords = Affymetrix Keywords: other
2005-04-18 | GSE2535 | GEO
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. 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.
2011-11-30 | E-GEOD-33243 | biostudies-arrayexpress
Project description:We show the molecular and functional characterization of a novel population of lineage-negative CD34-negative (Lin- CD34-) hematopoietic stem cells (HSCs) from chronic myelogenous leukemia (CML) patients at diagnosis. Molecular caryotyping and quantitative analysis of BCR/ABL transcript demonstrated that about one third of CD34- was leukemic. CML CD34- cells showed kinetic quiescence and limited clonogenic capacity. However, stroma-dependent cultures and cytokines induced CD34 expression on some HSCs, cell cycling, acquisition of clonogenic activity and increased expression of BCR/ABL transcript. CML CD34- cells showed an engraftment rate in immunodeficient mice similar to that of CD34+ cells. Gene expression profiling revealed the down-regulation of cell cycle arrest genes together with genes involved in antigen presentation and processing, while the expression of angiogenic factors was strongly up-regulated when compared to normal counterparts. Flow cytometry analysis confirmed the significant down-regulation of HLA class I and II molecules in CML CD34-cells. Increasing doses of imatinib mesilate (IM) did not affect fusion transcript levels, BCR-ABL kinase activity and the clonogenic efficiency of CML CD34- cells as compared to leukemic CD34+cells. Thus, we identified in CML a novel CD34- leukemic stem cell subset with peculiar molecular and functional characteristics which may be a potential target for CML therapeutics.
2010-01-05 | GSE11675 | GEO
Project description:We show the molecular and functional characterization of a novel population of lineage-negative CD34-negative (Lin- CD34-) hematopoietic stem cells (HSCs) from chronic myelogenous leukemia (CML) patients at diagnosis. Molecular caryotyping and quantitative analysis of BCR/ABL transcript demonstrated that about one third of CD34- was leukemic. CML CD34- cells showed kinetic quiescence and limited clonogenic capacity. However, stroma-dependent cultures and cytokines induced CD34 expression on some HSCs, cell cycling, acquisition of clonogenic activity and increased expression of BCR/ABL transcript. CML CD34- cells showed an engraftment rate in immunodeficient mice similar to that of CD34+ cells. Gene expression profiling revealed the down-regulation of cell cycle arrest genes together with genes involved in antigen presentation and processing, while the expression of angiogenic factors was strongly up-regulated when compared to normal counterparts. Flow cytometry analysis confirmed the significant down-regulation of HLA class I and II molecules in CML CD34-cells. Increasing doses of imatinib mesilate (IM) did not affect fusion transcript levels, BCR-ABL kinase activity and the clonogenic efficiency of CML CD34- cells as compared to leukemic CD34+cells. Thus, we identified in CML a novel CD34- leukemic stem cell subset with peculiar molecular and functional characteristics which may be a potential target for CML therapeutics. Leukemic cells were obtained from 12 chronic phase Ph+ CML patients at diagnosis and before treatment. Normal samples were leukapheresis products from 12 healthy stem cell donors receiving recombinant human granulocyte colony-stimulating factor (G-CSF; Lenograstim, Sanofi-Aventis, Milan, Italy). The protocol was approved by the ethical committee of the University Hospital and each patient/donor gave written informed consent. Hemopoietic stem/progenitor cell purification and phenotypic analyses were performed as previously described (Lemoli et al, Br J Haematol, 2003; Lemoli RM et al., Blood, 1997). Aliquots of sorted Lin-CD34-, Lin-CD34+ and Lin+CD34+ were reanalyzed by FacScan (Becton Dickinson, Franklin Lakes, NJ) to assess their purities. Total cellular RNA was extracted from 0.5x105 cells of each sample using RNeasy Micro kit (Qiagen, Valencia, CA) following the protocol supplied by the manufacturer. Disposable RNA chips (Agilent RNA 6000 Nano LabChip kit, Agilent Technologies, Waldbrunn, Germany) were used to determine the concentration and purity/integrity of RNA samples using Agilent 2100 Bioanalyzer. RNAs originating from 12 normal donors or from 12 CML patients were pooled in order to obtain at least 2 mg per sample. One-cycle target labeling assays, as well as the Affymetrix Human HG-U95Av2 GeneChip arrays hybridization, staining, and scanning, were performed, using Affymetrix standard protocols (Affymetrix, Santa Clara,CA).
2010-01-04 | E-GEOD-11675 | biostudies-arrayexpress
Project description:Purpose: This study was conducted to identify novel genes with importance to the biology of adult acute myelogenous leukemia (AML). Conclusions: NF1 null states are present in 7/95=7% of adult AML and delineate a disease subset that could be preferentially targeted by Ras or mTOR-directed therapeutics.
2010-12-02 | GSE21107 | GEO