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[Effect of hypoxia on the proliferation and hypoxia inducible factor-1α expression in human leukemia HL-60 cells].
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OBJECTIVE
To explore the effects of hypoxia on the proliferation of human leukemia HL-60 cells and the cellular expression of hypoxia inducible factor-1α (HIF-1α).
METHODS
Human acute myeloid leukemia HL-60 cells with exponential growth in routine culture were exposed to 50, 200, 400, 800 µmol/L
Hypoxia inducible factor (HIF)-2α accelerates disease progression in mouse models of leukemia and lymphoma but is not a poor prognosis factor in human AML.
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Hypoxia-inducible factor (HIF)-1α accumulation promotes hematopoietic stem cells' quiescence and is necessary to maintain their self-renewal. However, the role of HIF-2α in hematopoietic cells is less clear. We investigated the role of HIF-2α in leukemia and lymphoma cells. HIF-2α expression was
Hypoxia selects bortezomib-resistant stem cells of chronic myeloid leukemia.
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We previously demonstrated that severe hypoxia inhibits growth of Chronic Myeloid Leukemia (CML) cells and selects stem cells where BCR/Abl(protein) is suppressed, although mRNA is not, so that hypoxia-selected stem cells, while remaining leukemic, are independent of BCR/Abl signaling and thereby
[Effect of Hypoxia on the Proliferation and Hypoxia Inducible Factor-1α Expression in Human Leukemia K562 Cells].
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OBJECTIVE
To explore the effect of hypoxia on the cell proliferation and expression of hypoxia-inducible factor-1α(HIF-1α) of human leukemia K562 cells.
METHODS
The leukemia cells were divided into 2 groups: hypoxia-treated group and conventional oxygen group as control. The K562 cells in
Hypoxia increases HIF-1α expression and constitutive cytokine release by primary human acute myeloid leukaemia cells.
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BACKGROUND
Low oxygen tension is able to modulate the expression of several genes involved in physiological and pathological processes. A major regulator of gene expression is the heterodimeric transcription factor hypoxia inducible factor-1 (HIF-1), which also regulates angiogenesis-related genes,
Thyroid hormone induces hypoxia-inducible factor 1alpha gene expression through thyroid hormone receptor beta/retinoid x receptor alpha-dependent activation of hepatic leukemia factor.
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Thyroid hormones are important regulators of differentiation, growth, metabolism, and physiological function of virtually all tissues. Active thyroid hormone T(3) affects expression of genes that encode for angiogenic proteins like adrenomedullin or vascular endothelial growth factor and
Astrocyte-produced leukemia inhibitory factor expands the neural stem/progenitor pool following perinatal hypoxia-ischemia.
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Brain injuries, such as cerebral hypoxia-ischemia (H-I), induce a regenerative response from the neural stem/progenitors (NSPs) of the subventricular zone (SVZ); however, the mechanisms that regulate this expansion have not yet been fully elucidated. The Notch- Delta-Serrate-Lag2 (DSL) signaling
[Inhibitory effect of genistein on hypoxia-inducible factor-1alpha expression induced by cobalt chloride in leukemia cell line K562].
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This study was aimed to investigate the effect of genistein (gen) on the expression of hypoxia inducible factor-1alpha (HIF-1alpha) induced by cobalt chloride (CoCl(2)) in human leukemia cell line K562. The hypoxia condition was simulated by CoCl(2); the dose- and time-effect groups were prepared as
Hypoxia Up-regulates HIF Expression While Suppressing Cell Growth and NOTCH Activity in Leukaemia Cells.
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Fenretinide cytotoxicity is independent of both constitutive and pharmacologically modulated glutathione levels in pediatric acute lymphoblastic leukemia cells cultured at hypoxia.
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Fenretinide (4-HPR) cytotoxicity relative to glutathione levels in pediatric acute lymphoblastic leukemia cell lines cultured at bone marrow level hypoxia (5% O2) is evaluated. 4-HPR cytotoxicity correlated with reactive oxygen species generation (P < 0.001),but not with levels of intracellular
Activation of hypoxia-inducible factor 1 in human T-cell leukaemia virus type 1-infected cell lines and primary adult T-cell leukaemia cells.
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HTLV-1 (human T-cell leukaemia virus type 1) is the causative agent for ATL (adult T-cell leukaemia). HTLV-1 Tax can activate the PI3K (phosphoinositide 3-kinase)/Akt signalling pathway, which is responsible for survival of HTLV-1-infected T-cells. HIFs (hypoxia-inducible factors) are
Hypoxia-mediated fenretinide (4-HPR) resistance in childhood acute lymphoblastic leukemia cells.
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OBJECTIVE
N-(4-Hydroxyphenyl)-retinamide (4-HPR, Fenretinide) is a synthetic retinoid with cytotoxicity in acute lymphoblastic leukemia (ALL) cell lines. Since ALL is a disease of the bone marrow, a hypoxic tissue compartment, and it has been reported that there is an antagonistic effect of hypoxia
Induction of tumor arrest and differentiation with prolonged survival by intermittent hypoxia in a mouse model of acute myeloid leukemia.
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We showed previously that mild real hypoxia and hypoxia-mimetic agents induced in vitro cell differentiation of acute myeloid leukemia (AML). We here investigate the in vivo effects of intermittent hypoxia on syngenic grafts of leukemic blasts in a PML-RARalpha transgenic mouse model of AML. For
Effects of Hypoxia on Biology of Human Leukemia T-cell Line (MOLT-4 cells) Co-cultured with Bone Marrow Mesenchymal Stem Cells.
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UNASSIGNED
One of the most significant problems in the treatment of leukemia is the expansion of resistance to chemotherapeutic agents. Therefore, assessing the drug resistance and especially the drug resistance genes of leukemic cells is important in any treatment. The impact of Mesenchymal Stem
Hypoxia inhibits Moloney murine leukemia virus expression in activated macrophages.
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Hypoxia, a local decrease in oxygen tension, occurring in many pathological processes, modifies macrophage (Mphi) gene expression and function. Here, we provide the first evidence that hypoxia inhibits transgene expression driven by the Moloney murine leukemia virus-long terminal repeats (MoMLV-LTR)
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