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Homo sapiens

ABSTRACT: Treatment of primary acute myelogenous leukemia (AML) specimens with parthenolide (PTL)

OTHER RELATED OMICS DATASETS IN: E-GEOD-7538

PROVIDER: PRJNA99367 | ENA |

REPOSITORIES: ENA

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Transcription profiling of human primary CD34+ acute myelogenous leukemia specimens obtained from 12 patients treated with 7.5 micromolar parthenolide (PTL)

Project description:The effects of 7.5 micromolar parthenolide (PTL) were assessed on primary CD34+ acute myelogenous leukemia specimens obtained from 12 patients. Experiment Overall Design: Acute myelogenous leukemia (AML) specimens were obtained from 12 patients and CD34+ cells were isolated. For each patient, cells were cultured in vitro and exposed to either 7.5 micromolar parthenolide (PTL) or left untreated (UT) for 6 h. Total RNA was then harvested for global gene expression analysis.

2008-04-07 | E-GEOD-7538 | biostudies-arrayexpress

Treatment of primary acute myelogenous leukemia (AML) specimens with parthenolide (PTL)

Project description:The effects of 7.5 micromolar parthenolide (PTL) were assessed on primary CD34+ acute myelogenous leukemia specimens obtained from 12 patients. Keywords: drug response, gene expression search agent

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E-GEOD-7538

Project description:Transcription profiling of human primary CD34+ acute myelogenous leukemia specimens obtained from 12 patients treated with 7.5 micromolar parthenolide (PTL)

2015-07-27 | E-GEOD-7538 | ExpressionAtlas

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Project description:Mutant RAS oncoproteins activate signaling molecules that drive oncogenesis in multiple human tumors including acute myelogenous leukemia (AML). However, the specific function of these pathways in AML is unclear. To elucidate the downstream functions of activated NRAS in AML, we employed a murine model of AML harboring Mll-AF9 and NRASG12V. We found that NRASG12V enforced leukemia self-renewal gene expression signatures and was required to maintain an MLL-AF9 and MYB-dependent gene expression program. In a multiplexed analysis of RAS-dependent signaling intermediates, the leukemia stem cell compartment was preferentially sensitive to RAS withdrawal. Use of RAS-pathway inhibitors showed that NRASG12V maintained leukemia self-renewal through mTOR and MEK pathway activation, implicating these pathways as potential targets for cancer stem cell-specific therapies. Mice harboring NRASG12V/Mll-AF9 AML were treated with doxycyline to abolish NRASG12V expression. Leukemia samples were harvested at 24 hour intervals after doxycyline treatment.

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