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Overexpression of GATA1 confers resistance to chemotherapy in acute megakaryocytic leukemia

ABSTRACT: Gene expression study of shRNA knockdown of GATA1 in the megakaryoblastic cell line Meg01.

ORGANISM(S): Homo sapiens

PROVIDER: GSE42879 | GEO | 2013/07/01

SECONDARY ACCESSION(S): PRJNA183697

REPOSITORIES: GEO

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Overexpression of GATA1 confers resistance to chemotherapy in acute megakaryocytic leukemia

Project description:Gene expression study of shRNA knockdown of GATA1 in the megakaryoblastic cell line Meg01. Cell culture samples from two Meg01 clones (GATA1 4-14 and GATA1 5-13) were compared against a negative control infection sample (GATA1-neg). Two dye-swap microarrays were completed for each clone.

2013-07-01 | E-GEOD-42879 | biostudies-arrayexpress

Identification of GATA1 transcriptional regulation in the megakaryoblastic cell line Meg01

Project description:chIP-on-chip analysis of GATA1 in the megakaryoblastic cell line Meg01.

2013-07-01 | GSE43018 | GEO

Overexpression of GATA1 confers resistance to chemotherapy in acute megakaryocytic Leukemia.

Project description: Not available

| S-EPMC3707876 | biostudies-literature

Identification of GATA1 transcriptional regulation in the megakaryoblastic cell line Meg01

Project description:chIP-on-chip analysis of GATA1 in the megakaryoblastic cell line Meg01. The IP was obtained with a GATA1 C-terminus antibody. The control sample was a normal goat IgG pull down done side by side with the GATA1 (C-20) antibody using the same soluble chromatin sample from non-treated Meg-01 cells. A 2-chip microarray set (Agilent 240K) was used for the chIP-on-chip analysis.

2013-07-01 | E-GEOD-43018 | biostudies-arrayexpress

Homo sapiens

Project description:Identification of GATA1 transcriptional regulation in the megakaryoblastic cell line Meg01

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Inducible Gata1 Suppression Expands Erythro-Megakaryocytic Progenitors from Embryonic Stem Cells

Project description:Embryonic stem (ES) and induced pluripotent stem (iPS) cells represent a potential source of megakaryocytes and platelets for transfusion therapies. However, most current ES/iPS cell differentiation protocols are limited by low yields of hematopoietic progeny. Mutations in the mouse and human genes encoding transcription factor GATA1 cause accumulation of proliferating, developmentally arrested megakaryocytes. To exploit this clinical observation, we engineered wildtype (WT) murine ES cells to express doxycycline (dox)-regulated Gata1 short hairpin (sh) RNAs. In vitro differentiation with dox and thrombopoietin (Tpo) resulted in approximately 1013-fold expansion of immature hematopoietic progenitors. Upon dox withdrawal with multilineage cytokines, GATA1 expression was restored and the cells differentiated into erythroblasts and megakaryocytes. With Tpo alone, dox-deprived progenitors formed mainly mature megakaryocytes that generated functional platelets in vivo. Our findings provide a novel, readily reproducible strategy to expand ES-cell derived megakaryocyte-erythroid progenitors and direct their differentiation into megakaryocytes producing functional platelets in clinically relevant numbers.

2015-12-09 | GSE66479 | GEO

Inducible Gata1 Suppression Expands Erythro-Megakaryocytic Progenitors from Embryonic Stem Cells

2015-12-09 | E-GEOD-66479 | biostudies-arrayexpress

The unique role of GATA1s in Down syndrome acute megakaryocytic leukemia biology and therapy

Project description:Microarray gene expression profiling of lentivirus shRNA knockdown of the GATA1 gene in a DS AMkL cell line, CMK (harbors a mutated GATA1 gene and only expresses GATA1s).

2012-06-01 | GSE32388 | GEO

Gene expression signature of MYB-GATA overexpression plus GATA1 down regulation in undifferentiated or differentiated UT7 cells

Project description:Acute basophilic leukemia is a rare subtype of acute myeloblastic leukemia. We recently described a recurrent t(X;6)(p11;q23) translocation occurring in male infants with acute basophilic leukemia, generating a MYB-GATA1 fusion gene. To better understand the role of MYB-GATA1 in the leukemogenesis of acute basophilic leukemias, we expressed this chimeric transcription factor in the UT-7 cell line under normal or differentiating conditions. A gene expression analysis revealed 9 genes deregulated by both MYB-GATA1 and the basophilic differentiation. Three of these genes (CCL23, IL1RL1 and NTRK1) were also increased by MYB-GATA1 in CD34-positive cells, as indicated by quantitative RT-PCR. Two independant experiments (A and S) were performed. For each experiment, UT7 cells were transduced with two lentivirus: a lentivirus carrying the MYB-GATA1 (or a control) coding sequence, and a lentivirus carrying a GATA1 (or control) shRNA. Cells transduced with both lentiviruses were selected, and kept in culture under standard or differentiating conditions for 7 days before RNA extraction.

2016-09-01 | E-GEOD-72913 | biostudies-arrayexpress

Erythroid/megakaryocytic differentiation confers BCL-XL dependency and venetoclax resistance in acute myeloid leukemia

Project description:Myeloid neoplasms with erythroid or megakaryocytic differentiation include pure erythroid leukemia (PEL), myelodysplastic syndrome (MDS) with erythroid features, and acute megakaryoblastic leukemia (FAB M7) and are characterized by poor prognosis and limited treatment options. Here, we investigate the drug sensitivity landscape of these rare malignancies. We show that acute myeloid leukemia (AML) cells with erythroid or megakaryocytic differentiation depend on the anti-apoptotic protein BCL-XL, rather than BCL-2, using combined ex vivo drug sensitivity testing, genetic perturbation, and transcriptomic profiling. Single-cell and bulk transcriptomics of patient samples with erythroid and megakaryoblastic leukemias identified high BCL2L1 expression compared to other subtypes of AML and other hematological malignancies, where BCL2 and MCL1 were more prominent. Our results suggest targeting BCL-XL as a potential therapy option in erythroid/megakaryoblastic leukemias and highlight an AML subgroup with potentially reduced sensitivity to venetoclax-based treatments.

| EGAS00001006819 | EGA

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