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Expression profiling of CD4+and CD8+ T cells in peripheral blood (PB) of AML patients who were treated with induction chemotherapy plus pomalidomide

ABSTRACT: Transcriptional profiles of highly purified (≥ 98%) PB CD4+ or CD8+ T cells at early lymphocyte recovery (ELR) from newly diagnosed AML patients, who were treated with standard induction chemotherapy plus pomalidomide were compared to age-matched AML controls, who received standard induction chemotherapy only.

ORGANISM(S): Homo sapiens

PROVIDER: GSE130753 | GEO | 2022/05/05

REPOSITORIES: GEO

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Expression profiling of CD8+ T-cells in peripheral blood (PB) of AML patients

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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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Gene expression alterations in transporters with Pb (lead) exposure in mice tissues

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Alox5 mediates survival of LSCs, and chemoresistance in AML via LTB4-BLTR signaling

Project description:Acute myeloid leukemia (AML) is characterized by poor clinical outcomes due to high rates of relapse following induction chemotherapy. While many pathogenic drivers have been described in AML, our understanding of the molecular mechanisms mediating chemotherapy resistance remains poor, and initial management of AML continues to rely on standard induction chemotherapy for many patients. Given the importance of identifying new approaches to improve the efficiency of induction therapy in AML, we sought to identify resistance genes to induction therapy in AML and identified ALOX5 is a novel mediator of resistance to anthracycline based therapy. ALOX5 mRNA is expressed at high levels in AML patient blasts in comparison to normal hematopoietic stem/progenitor cells (HSPCs) and ALOX5 mRNA and protein expression is increased in response to induction therapy. Genetic and pharmacologic perturbations of ALOX5 function in vitro and in vivo confirm that ALOX5 positively regulates the leukemogenic potential of AML LSCs, while ALOX5 loss does not significantly affect the function of normal HSPCs. ALOX5 mediates resistance to daunorubicin (DNR) and promotes AML cell survival and maintenance through its leukotriene (LT) synthetic capacity. Specifically, the ALOX5 dependent resistance phenotype depends on its ability to synthesize LTB4 and bind to the LTB receptor (BLTR). Overall, our studies reveal a previously unrecognized role of LT’s in AML pathogenesis and chemoresistance, and provide a potential novel strategy to enhance the therapeutic efficacy of induction chemotherapy in AML.

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