Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA358590 | ENA |
REPOSITORIES: ENA
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Project description:Acute myeloid leukemia remodels the bone marrow non-hematopoietic microenvironment which disrupts niche archiecture and normal hematopoiesis The precise interactions underlying this process are not well understood We used microarrays to detail the global programme of gene expression underlying the interactions between healthy mesenchymal stroma cells and normal hematopoietic progenitors/stem cells (HSPCs) and AML
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Project description:Antibody-based therapy for cancer is now one of the most successful and important strategies for treating patients with hematological malignancies. However, the lack of efficient tumor-associated antigens restricts the targeting therapy of myeloid leukemia. Analysis of the gene expression proï¬les of primary bone marrow samples from human acute myeloid leukemia (AML) patients or healthy donors was to identify and expand novel targets for the treatment of myeloid leukemias. we found that epithelial cell adhesion molecule (EpCAM) is overexpressed in patients with AML. we analyzed the gene expression proï¬les of bone marrow mononuclear cells from 2 human acute myeloid leukemia (AML) patients and 2 healthy donors using an oligonucleotide microarray, to identify up-regulated genes in AML samples comparing with healthy tissues.
2016-05-14 | E-GEOD-79605 | biostudies-arrayexpress
Project description:Acute myeloid (AML) is characterized by frequent relapse, which is driven by resistant leukemic stem cells (LSC)1, highlighting the necessity to target the malignant stem-cell pool for disease control. Here, we report a tumor suppressive mechanism that can be harnessed to clear LSC while promoting healthy hematopoiesis. We discovered that genetic deletion of homotrimeric lymphotoxin alpha (LTα3) blocks cell death and accelerates leukemogenesis in a murine model of FLT3-ITD+ AML. Accordingly, exposure of primary murine or human AML cells to exogenous recombinant LTα3 stimulates cell death and myeloid differentiation. In leukemia-bearing mice and AML patient-derived xenografts, recombinant LTα3 induces deep and lasting remissions even in PDX samples with adverse genetic profiles. Mechanistically, LTα3 represses leukemia by depleting TNFR-associated factor 2 (TRAF2) via TNF receptor (TNFR)1 and TNFR2. In contrast to most AML therapies, LTα3 exerts little to no toxicity on healthy hematopoiesis but rather boosts healthy hematopoietic progenitor cells thereby effectively uncoupling leukemia treatment from unwanted BM suppression. Leveraging this endogenous TRAF2-dependent negative feedback loop in leukemia, our data suggest that recombinant LTα3 represents a therapeutic opportunity for AML eradication.
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Project description:Targeting of DNMT3A hotspot mutations in Clonal Hematopoiesis and Acute Myeloid Leukemia
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Project description:we show that YBX1 is specifically required for maintaining myeloid leukemia cell survival but is dispensable for normal hematopoiesis. We found that expression of YBX1 is significantly upregulated in myeloid leukemia cells, and deletion of YBX1 significantly induces apoptosis, coupled with reduced proliferation and impaired leukemic capacity of primary human and mouse acute myeloid leukemia (AML) cells in vitro and in vivo. Loss of YBX1 does not obviously affect normal hematopoiesis. Mechanistically, YBX1 interacts with IGF2BPs and stabilizes m6A-tagged RNA. Moreover, YBX1 deficiency promotes mRNA decay in an m6A-dependent manner, which contributes to the defective survival due to YBX1 deletion. Thus, our findings uncover a selective and critical role of YBX1 in maintaining myeloid leukemia survival that might provide a rationale for the therapeutic targeting of YBX1 in myeloid leukemia.
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Project description:we show that YBX1 is specifically required for maintaining myeloid leukemia cell survival but is dispensable for normal hematopoiesis. We found that expression of YBX1 is significantly upregulated in myeloid leukemia cells, and deletion of YBX1 significantly induces apoptosis, coupled with reduced proliferation and impaired leukemic capacity of primary human and mouse acute myeloid leukemia (AML) cells in vitro and in vivo. Loss of YBX1 does not obviously affect normal hematopoiesis. Mechanistically, YBX1 interacts with IGF2BPs and stabilizes m6A-tagged RNA. Moreover, YBX1 deficiency promotes mRNA decay in an m6A-dependent manner, which contributes to the defective survival due to YBX1 deletion. Thus, our findings uncover a selective and critical role of YBX1 in maintaining myeloid leukemia survival that might provide a rationale for the therapeutic targeting of YBX1 in myeloid leukemia.
2021-04-01 | GSE159152 | GEO
Project description:Epigenomic and transcriptomic studies of human hematopoiesis and acute myeloid leukemia
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Project description:we show that YBX1 is specifically required for maintaining myeloid leukemia cell survival but is dispensable for normal hematopoiesis. We found that expression of YBX1 is significantly upregulated in myeloid leukemia cells, and deletion of YBX1 significantly induces apoptosis, coupled with reduced proliferation and impaired leukemic capacity of primary human and mouse acute myeloid leukemia (AML) cells in vitro and in vivo. Loss of YBX1 does not obviously affect normal hematopoiesis. Mechanistically, YBX1 interacts with IGF2BPs and stabilizes m6A-tagged RNA. Moreover, YBX1 deficiency promotes mRNA decay of MYC and BCL2 in an m6A-dependent manner, which contributes to the defective survival due to YBX1 deletion. Thus, our findings uncover a selective and critical role of YBX1 in maintaining myeloid leukemia survival that might provide a rationale for the therapeutic targeting of YBX1 in myeloid leukemia.
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