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Article: Recombinant human interferon alpha-2 and juvenile chronic myelogenous leukemia: Cell receptor binding, enzymatic induction, and growth suppression in vitro

TitleRecombinant human interferon alpha-2 and juvenile chronic myelogenous leukemia: Cell receptor binding, enzymatic induction, and growth suppression in vitro
Authors
Issue Date1987
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/exphem
Citation
Experimental Hematology, 1987, v. 15 n. 2, p. 127-132 How to Cite?
AbstractRecombinant human leukocyte interferon (HuIFN(α2)) was studied to determine its potential as a therapeutic agent for the lethal monocytic malignancy of infancy, juvenile chronic myelogenous leukemia (JCML). In sharp contrast to cell cultures of normal marrow, specimens from two patients with JCML yielded an excessive and rapid proliferation of monocyte-macrophage elements without growth factor in clonogenic assay and in liquid culture. Using IFN(α2) labeled with 125I, the characteristics of IFN binding to cultured JCML monocyte-macrophages and their receptor site numbers were determined. IFN binding to cells from both patients disclosed two components: a high-affinity of 120 and 430 sites/cell, and a lower affinity of 1230 and 2500 sites/cell, respectively. In control studies, normal blood mononuclear cells or tonsillar B-lymphocytes displayed only a high-affinity component. Brief exposure of JCML cells to IFN(α2) in vitro resulted in a sharp increase in the IFN-induced enzyme 2-5A synthetase, indicating the ability of JCML cells to respond metabolically. Dose-response studies performed in a clonogenic assay showed a dose-dependent growth inhibition of JCML monocyte-macrophage colonies using IFN(α2) at concentrations of 102-105 U/ml. These studies provide new information on the biological characteristics of JCML malignant cells, and suggest that IFN may be useful for treatment of this disorder.
Persistent Identifierhttp://hdl.handle.net/10722/170220
ISSN
2015 Impact Factor: 2.303
2015 SCImago Journal Rankings: 1.341
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorEstrov, Zen_US
dc.contributor.authorLau, ASen_US
dc.contributor.authorWilliams, BRGen_US
dc.contributor.authorFreedman, MHen_US
dc.date.accessioned2012-10-30T06:06:46Z-
dc.date.available2012-10-30T06:06:46Z-
dc.date.issued1987en_US
dc.identifier.citationExperimental Hematology, 1987, v. 15 n. 2, p. 127-132en_US
dc.identifier.issn0301-472Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/170220-
dc.description.abstractRecombinant human leukocyte interferon (HuIFN(α2)) was studied to determine its potential as a therapeutic agent for the lethal monocytic malignancy of infancy, juvenile chronic myelogenous leukemia (JCML). In sharp contrast to cell cultures of normal marrow, specimens from two patients with JCML yielded an excessive and rapid proliferation of monocyte-macrophage elements without growth factor in clonogenic assay and in liquid culture. Using IFN(α2) labeled with 125I, the characteristics of IFN binding to cultured JCML monocyte-macrophages and their receptor site numbers were determined. IFN binding to cells from both patients disclosed two components: a high-affinity of 120 and 430 sites/cell, and a lower affinity of 1230 and 2500 sites/cell, respectively. In control studies, normal blood mononuclear cells or tonsillar B-lymphocytes displayed only a high-affinity component. Brief exposure of JCML cells to IFN(α2) in vitro resulted in a sharp increase in the IFN-induced enzyme 2-5A synthetase, indicating the ability of JCML cells to respond metabolically. Dose-response studies performed in a clonogenic assay showed a dose-dependent growth inhibition of JCML monocyte-macrophage colonies using IFN(α2) at concentrations of 102-105 U/ml. These studies provide new information on the biological characteristics of JCML malignant cells, and suggest that IFN may be useful for treatment of this disorder.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/exphemen_US
dc.relation.ispartofExperimental Hematologyen_US
dc.subject.mesh2',5'-Oligoadenylate Synthetase - Biosynthesisen_US
dc.subject.meshCell Division - Drug Effectsen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshChilden_US
dc.subject.meshEnzyme Induction - Drug Effectsen_US
dc.subject.meshHumansen_US
dc.subject.meshInterferon-Gamma - Therapeutic Useen_US
dc.subject.meshLeukemia, Myeloid - Drug Therapy - Pathologyen_US
dc.subject.meshReceptors, Drug - Metabolismen_US
dc.subject.meshRecombinant Proteins - Therapeutic Useen_US
dc.titleRecombinant human interferon alpha-2 and juvenile chronic myelogenous leukemia: Cell receptor binding, enzymatic induction, and growth suppression in vitroen_US
dc.typeArticleen_US
dc.identifier.emailLau, AS:asylau@hku.hken_US
dc.identifier.authorityLau, AS=rp00474en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid3102273-
dc.identifier.scopuseid_2-s2.0-0023106432en_US
dc.identifier.volume15en_US
dc.identifier.issue2en_US
dc.identifier.spage127en_US
dc.identifier.epage132en_US
dc.identifier.isiWOS:A1987G257000004-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridEstrov, Z=7005487081en_US
dc.identifier.scopusauthoridLau, AS=7202626202en_US
dc.identifier.scopusauthoridWilliams, BRG=7404502964en_US
dc.identifier.scopusauthoridFreedman, MH=7203068454en_US

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