scholarly journals Myeloid leukemia cell differentiation protein (MCL-1); tumor necrosis factor–related apoptosis-inducing ligand (TRAIL)

2010 ◽  
Vol 3 (14) ◽  
pp. 429-429
Keyword(s):  
Cell Differentiation ◽  
Tumor Necrosis Factor ◽  
Myeloid Leukemia ◽  
Tumor Necrosis ◽  
Leukemia Cell ◽  
Necrosis Factor ◽  
Myeloid Leukemia Cell

scholarly journals In vitro action of tumor necrosis factor on myeloid leukemia cells

Blood ◽  
1987 ◽  
Vol 69 (4) ◽  
pp. 1102-1108 ◽  
Author(s):  
R Munker ◽  
P Koeffler
Keyword(s):  
Tumor Necrosis Factor ◽  
Myeloid Leukemia ◽  
Tumor Necrosis ◽  
Leukemia Cell ◽  
Leukemia Cells ◽  
Necrosis Factor Alpha ◽  
Gm Csf ◽  
Necrosis Factor ◽  
Clonogenic Cells

Abstract We investigated the in vitro action of recombinant tumor necrosis factor alpha (TNF) on the clonal growth of normal and malignant myeloid cells. Clonogenic cells from six of nine myeloid leukemia cell lines were very sensitive to the effects of TNF with 50% of the colonies inhibited (ED50) by concentrations of TNF that ranged between 6 and 150 U/mL. A decrease in DNA, RNA, and protein synthesis and in cloning efficiency occurred within three hours of exposure of HL-60 promyelocytes to TNF. The TNF in combination with recombinant interferons produced an additive or synergistic inhibition of colony formation of HL-60 and THP-1 myelomonoblasts. Normal human CFU-GM are sensitive to TNF (ED50 between 100 and 50,000 U/mL), but their sensitivity to TNF depends on the source of colony stimulating factor (CSF) with T lymphocyte derived GM-CSF (recombinant or natural) partially protecting the CFU-GM from the suppression exerted by TNF (and interferons). In eight of 15 cases the clonogenic myeloid leukemia cells from patients with acute or chronic myeloid leukemia were more sensitive than normal CFU-GM using GM-CSF as a source of colony stimulating activity. Further studies showed that the action of TNF on myeloid leukemia cells probably can be only partially explained by differentiation. Our finding of a possible selective cytotoxicity to leukemic clonogenic cells by TNF suggests that TNF may have value in the therapy of some patients with myeloid leukemia.

scholarly journals In vitro action of tumor necrosis factor on myeloid leukemia cells

Blood ◽  
1987 ◽  
Vol 69 (4) ◽  
pp. 1102-1108 ◽  
Author(s):  
R Munker ◽  
P Koeffler
Keyword(s):  
Tumor Necrosis Factor ◽  
Myeloid Leukemia ◽  
Tumor Necrosis ◽  
Leukemia Cell ◽  
Leukemia Cells ◽  
Necrosis Factor Alpha ◽  
Gm Csf ◽  
Necrosis Factor ◽  
Clonogenic Cells

We investigated the in vitro action of recombinant tumor necrosis factor alpha (TNF) on the clonal growth of normal and malignant myeloid cells. Clonogenic cells from six of nine myeloid leukemia cell lines were very sensitive to the effects of TNF with 50% of the colonies inhibited (ED50) by concentrations of TNF that ranged between 6 and 150 U/mL. A decrease in DNA, RNA, and protein synthesis and in cloning efficiency occurred within three hours of exposure of HL-60 promyelocytes to TNF. The TNF in combination with recombinant interferons produced an additive or synergistic inhibition of colony formation of HL-60 and THP-1 myelomonoblasts. Normal human CFU-GM are sensitive to TNF (ED50 between 100 and 50,000 U/mL), but their sensitivity to TNF depends on the source of colony stimulating factor (CSF) with T lymphocyte derived GM-CSF (recombinant or natural) partially protecting the CFU-GM from the suppression exerted by TNF (and interferons). In eight of 15 cases the clonogenic myeloid leukemia cells from patients with acute or chronic myeloid leukemia were more sensitive than normal CFU-GM using GM-CSF as a source of colony stimulating activity. Further studies showed that the action of TNF on myeloid leukemia cells probably can be only partially explained by differentiation. Our finding of a possible selective cytotoxicity to leukemic clonogenic cells by TNF suggests that TNF may have value in the therapy of some patients with myeloid leukemia.

Oroxylin a Heightens Tumor Necrosis Factor a-Induced Differentiation Effects on Acute Myeloid Leukemia Cells Via Modulation on AKT and NF-Kb Pathways Involving RXRa

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 4840-4840
Author(s):  
Jingyan Xu ◽  
Jian Ouyang ◽  
Hui Hui
Keyword(s):  
Acute Myeloid Leukemia ◽  
Tumor Necrosis Factor ◽  
Myeloid Leukemia ◽  
Tumor Necrosis ◽  
Conflicts Of Interest ◽  
Combination Group ◽  
Oroxylin A ◽  
Necrosis Factor ◽  
Acute Myeloid ◽  
Resistant Cells

Abstract Tumor necrosis factor alpha (TNFα) is a complicated cytokine which could induce differentiation of acute myeloid leukemia (AML) cells. We have found that Oroxylin A, a natural compound isolated from Scutellariae radix, markedly enhanced TNFα-induced NBT reduction and CD11b/CD14 expression of AML cells. Besides, Giemsa staining also displayed that the combination group induced U937-MDR cells to differentiate into monocyte-like cells yet NB4 and HL-60-resistant cells to granulocytic-like cells. Further study showed that TNFα induced PI3K subunit p85α binding to N-terminal truncated nuclear receptor RXRα (tRXRα) proteins and activating AKT. On the contrary, these could be inhibited by Oroxylin A through inhibiting interaction between tRXRα and p85α in NB4 and HL-60-resistant cells. Moreover, Oroxylin A inhibited the activation of NF-κB signaling and the DNA binding activity by TNFα proved by EMSA in these two AML cells. All these suggested that Oroxylin A was able to inhibit NF-κB signaling and RXRα-dependent AKT signaling, the negative effects of TNFα for AML therapy, suggesting that combination of Oroxylin A and TNFα might be a novel candidate for differentiation therapy for AML cells and required further investigation. Disclosures No relevant conflicts of interest to declare.

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