Effect of interleukin-1 beta converting enzyme inhibitor on acute myelogenous leukemia progenitor proliferation.

@article{Estrov1995EffectOI,
  title={Effect of interleukin-1 beta converting enzyme inhibitor on acute myelogenous leukemia progenitor proliferation.},
  author={Zeev E Estrov and Roy A. Black and Paul R. Sleath and David M Harris and Quin Van and Ruth Lapushin and Elihu H Estey and Moshe Talpaz},
  journal={Blood},
  year={1995},
  volume={86 12},
  pages={
          4594-602
        }
}
Interleukin-1 beta (IL-1 beta) converting enzyme (ICE) is a cysteine protease that specifically cleaves precursor IL-1 beta to its biologically active form. Recent studies have also implicated ICE in the induction of apoptosis in vertebrate cells. Because IL-1 plays a major role in acute myelogenous leukemia (AML) blast proliferation, we sought to investigate the effect of ICE inhibition on AML progenitors. To do this, we used bocaspartyl (benzyl) chloromethylketone (BACMK) an inhibitor… 
View on PubMed
ashpublications.org
43 Citations
Background Citations
6
Methods Citations
2

Figures and Tables from this paper

43 Citations

Role of Interleukin-1β Converting Enzyme (ICE) in Acute Myelogenous Leukemia Cell Proliferation and Programmed Cell Death
TLDR
Recent data indicate that ICE is a member of an increasingly recognized family of cysteine proteases, in which IL-1b˜ acts as an autocrine growth factor, or induce apoptosis.
Phenylarsine oxide blocks interleukin-1beta-induced activation of the nuclear transcription factor NF-kappaB, inhibits proliferation, and induces apoptosis of acute myelogenous leukemia cells.
TLDR
The data showing that PAO is an effective in vitro inhibitor of AML cells suggest that this compound may have a role in future therapies for AML.
Resveratrol blocks interleukin-1beta-induced activation of the nuclear transcription factor NF-kappaB, inhibits proliferation, causes S-phase arrest, and induces apoptosis of acute myeloid leukemia cells.
TLDR
The data showing that resveratrol is an effective in vitro inhibitor of AML cells suggest that this compound may have a role in future therapies for AML.
1 , 25-Dihydroxyvitamin D 3 and its Analogues Inhibit Acute Myelogenous Leukemia Progenitor Proliferation by Suppressing Interleukin-1 b Production
TLDR
The results suggest that 1,25D 3 and its 20-epi analogues interrupt IL-1 b autocrine growth regulation by inhibiting IL- 1 b production and processing but not the response to IL-2 b.
for the Involvement of Mutated RAS 6 Production in Leukemia : Evidence β Autocrine Interleukin-1 Updated
TLDR
The observations suggest that mutatedRAS genes may mediate autocrine IL-1b production in some leukemias by stimulating signal transduction pathways that activate the IL- 1b promoter.
Autocrine interleukin-1beta production in leukemia: evidence for the involvement of mutated RAS.
TLDR
The observations suggest that mutated RAS genes may mediate autocrine IL-1beta production in some leukemias by stimulating signal transduction pathways that activate the IL- 1beta promoter.
In vitro and in vivo studies of ICE inhibitors
TLDR
Further optimization of the current generation of peptidyl ICE inhibitors will be required to produce agents suitable for administration in chronic inflammatory and neurodegenerative diseases.
Different Interleukin-1β Converting Enzyme (ICE) Family Protease Requirements for the Apoptotic Death of T Lymphocytes Triggered by Diverse Stimuli
TLDR
The data indicate that ICEfamily proteases comprise a common functional step in distinct T cell apoptotic death pathways, but suggest that different family members are likely to be critical in various differentiated T cell types, even when triggered by the same stimulus.
Interleukin-1--a major pleiotropic cytokine in tumor-host interactions.
[Cytokines in acute myeloid leukemia].
TLDR
The observed differences of concentrations may confirm the role of studied cytokines and P-selectin in the regulation of leukaemia cell proliferation and may additionally confirm the importance of immunoradiometric, immunoenzymatic and radioimmunologic kits.
...
...

References

SHOWING 1-10 OF 60 REFERENCES
Modulation of cell proliferation and cytokine production in acute myeloblastic leukemia by interleukin-1 receptor antagonist and lack of its expression by leukemic cells.
TLDR
Data show a role for IL-1 in the spontaneous proliferation and cytokine production of AML cells and suggest that an imbalanced synthesis ofIL-1 and of its natural receptor antagonist may contribute to the unrestricted growth ofAML cells.
Role of colony-stimulating factors in the biology of acute myelogenous leukemia.
TLDR
There is evidence for autonomous growth promotion of AML blast by constitutive production of growth factors active in an autocrine fashion and by recruitment of accessory cells to increase CSF supply via molecules such as interleukin 1 and TNF-alpha in a paracrine fashion.
Suppression of chronic myelogenous leukemia colony growth by interleukin-1 (IL-1) receptor antagonist and soluble IL-1 receptors: a novel application for inhibitors of IL-1 activity.
TLDR
Data implicate IL-1 beta in CML disease progression and suggest that the inhibitory effects of molecules such as sIL-1R and IL- 1RA could conceivably be the basis of a novel therapeutic strategy against this disorder.
Identification of a monocyte specific pre-interleukin 1 beta convertase activity.
TLDR
It is concluded that a protease activity found only in monocytes will specifically process IL-1 beta to an active form.
Inhibition of mature IL-1 beta production in murine macrophages and a murine model of inflammation by WIN 67694, an inhibitor of IL-1 beta converting enzyme.
TLDR
In activated murine peritoneal macrophages, WIN 67694 inhibited the release of mature IL-1 beta with an IC50 of 1.8 microM without any effect on therelease ofIL-1 alpha, IL-6, or TNF-alpha without affecting precursor protein synthesis.
Effects of an IL-1 receptor antagonist on acute myeloid leukemia cells.
TLDR
The effects of the IL-1ra on the clonogenicity of leukemia cells was observed even when the antagonist failed to inhibit DNA synthesis by the leukemia cell population as a whole, consistent with the concept that the administration of IL- 1ra subsequent to cytotoxic therapy has the potential of slowing the regrowth of leukemia Cells thereby potentiating the effects of chemotherapy.
Generation of biologically active interleukin-1 beta by proteolytic cleavage of the inactive precursor.
Interleukin-6 enhances growth factor-dependent proliferation of the blast cells of acute myeloblastic leukemia.
TLDR
IL-6 synergized with granulocyte macrophage colony-stimulating factor (GM-CSF) and interleukin-3 (IL-3) in the stimulation of AML blast colony formation and Responsiveness of blast progenitors to IL-6 was heterogeneous.
Induction of apoptosis in fibroblasts by IL-1β-converting enzyme, a mammalian homolog of the C. elegans cell death gene ced-3
Mice deficient in IL-1β-converting enzyme are defective in production of mature IL-1β and resistant to endotoxic shock
...
...