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Effect of depletion or overexpression of CaSR on gene expression in BM-derived Lineage negative AML cells

ABSTRACT: Effect of depletion or overexpression of CaSR on gene expression in BM-derived Lineage negative AML cells

PROVIDER: PRJNA858833 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20210821_1.fastq.gz	Fastqsanger.gz
	SRR20210821_2.fastq.gz	Fastqsanger.gz
	SRR20210822_1.fastq.gz	Fastqsanger.gz
	SRR20210822_2.fastq.gz	Fastqsanger.gz
	SRR20210823_1.fastq.gz	Fastqsanger.gz

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Effect of depletion or overexpression of CaSR on gene expression in BM-derived Lineage negative AML cells

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Expression data from human AML blasts and healthy CD34+ bone marrow cells

Project description:Treatment for acute myeloid leukemia (AML) remains suboptimal and many patients remain refractory or relapse upon standard chemotherapy based on nucleoside analogs plus anthracyclines. The crosstalk between AML cells and the bone marrow (BM) stroma is a major mechanism underlying therapy resistance in AML. Lenalidomide and pomalidomide, a new generation immunomodulatory drugs (IMiDs), possess pleiotropic anti-leukemic properties including potent immune-modulating effects and are commonly used in hematological malignances associated with intrinsic dysfunctional BM such as myelodysplastic syndromes and multiple myeloma. Whether IMiDs may improve the efficacy of current standard treatment in AML remains understudied. Here, we have exploited in vitro and in vivo preclinical AML models to analyze whether IMiDs potentiate the efficacy of AraC/Iradubicin (standard AML chemotherapy) by interfering with the BM stroma-mediated chemoresistance. We report that lenalidomide and pomalidomide have cytotoxic effects on neither AML cells nor BM-MSCs, but they increase the immunosuppressive/immunomodulatory properties of BM-MSCs. When combined with AraC and Idarubicin, IMiDs fail to circumvent BM stroma-mediated resistance of AML cells in vitro and in vivo but induce robust extramedullary mobilization of AML cells. When administered as a single agent, lenalidomide highly mobilizes AML cells, but not healthy CD34+ cells, to peripheral blood (PB) likely through specific downregulation of CXCR4 in AML blasts. Global gene expression profiling supports a migratory/mobilization gene signature in lenalidomide-treated AML blasts but not in CD34+ cells. Collectively, IMiDs mobilize AML blasts to PB through downregulation of CXCR4 but do not improve AraC/Idarubicin activity in a preclinical model of AML.

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