Abstract |
The mechanism of responsiveness of chronic myelogenous leukemia (CML) cells to interferon (IFN)-alpha was examined by using two subclones of CML cell line KT-1 which exhibited significantly different sensitivities to the antiproliferative and apoptosis-inducing effects of IFN-alpha. IFN-stimulated gene factor 3 (ISGF3) formation by IFN-alpha was reduced in the IFN-alpha-resistant subclone compared to the IFN-alpha-sensitive subclone. We conclude that the level of ISGF3 formation is responsible for the difference in IFN-alpha responses between these subclones.
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Authors | H Yamauchi, I Sakai, H Narumi, S Soga, S Fujita |
Journal | Acta haematologica
(Acta Haematol)
Vol. 104
Issue 1
Pg. 1-9
( 2000)
ISSN: 0001-5792 [Print] Switzerland |
PMID | 11111114
(Publication Type: Comparative Study, Journal Article)
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Copyright | Copyright 2000 S. Karger AG, Basel |
Chemical References |
- Antineoplastic Agents
- DNA-Binding Proteins
- IRF9 protein, human
- Interferon-Stimulated Gene Factor 3
- Interferon-Stimulated Gene Factor 3, gamma Subunit
- Interferon-alpha
- Protein Subunits
- RNA, Messenger
- STAT1 Transcription Factor
- STAT1 protein, human
- STAT2 Transcription Factor
- Trans-Activators
- Transcription Factors
- Protein-Tyrosine Kinases
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Topics |
- Antineoplastic Agents
(pharmacology)
- Apoptosis
(drug effects)
- Blotting, Western
- Cell Division
(drug effects)
- Clone Cells
(drug effects)
- DNA Fragmentation
- DNA-Binding Proteins
(drug effects, genetics, metabolism, pharmacology, physiology)
- Electrophoresis, Agar Gel
- Flow Cytometry
- Humans
- Interferon-Stimulated Gene Factor 3
- Interferon-Stimulated Gene Factor 3, gamma Subunit
- Interferon-alpha
(genetics, pharmacology, physiology)
- Leukemia, Myelogenous, Chronic, BCR-ABL Positive
(pathology)
- Promoter Regions, Genetic
(drug effects)
- Protein Binding
(physiology)
- Protein Subunits
- Protein-Tyrosine Kinases
(physiology)
- RNA, Messenger
(biosynthesis, drug effects)
- Response Elements
(drug effects)
- STAT1 Transcription Factor
- STAT2 Transcription Factor
- Signal Transduction
(drug effects)
- Time Factors
- Trans-Activators
(drug effects, metabolism, physiology)
- Transcription Factors
(drug effects, genetics, metabolism, pharmacology)
- Tumor Cells, Cultured
(drug effects)
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