Abstract | OBJECTIVE: METHODS: MNCs were cultured in liquid medium at the presence of IFN-alpha (200 U/ml) or IFN-alpha (200 U/ml) plus IL-6 (100 ng/ml). The viable cells were counted and the expression levels of beta-actin, bcr/abl, bcl-2 and c-myc genes were quantitatively detected by reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS: The cell growth was markedly inhibited by IFN-alpha, but the extent of the inhibition was slightly decreased when IFN-alpha combined with IL-6. The expression levels of bcr/abl and bcl-2 gene were reduced by IFN-alpha or IFN-alpha plus IL-6. The expression of c-myc gene was inhibited by IFN-alpha but promoted by IL-6. CONCLUSIONS: Both IFN-alpha and IFN-alpha plus IL-6 can inhibit the expression of anti-apoptosis genes, and modulate the expression of c-myc. It is the possible mechanism of IFN-alpha therapy for CGL in chronic phase.
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Authors | H Chen, L Tang, X Peng, Z Luo, S Luo, W Tan |
Journal | Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
(Zhonghua Xue Ye Xue Za Zhi)
Vol. 21
Issue 7
Pg. 341-4
(Jul 2000)
ISSN: 0253-2727 [Print] China |
PMID | 11877000
(Publication Type: English Abstract, Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Interferon-alpha
- Interleukin-6
- Proto-Oncogene Proteins c-bcl-2
- Proto-Oncogene Proteins c-myc
- RNA, Messenger
- Fusion Proteins, bcr-abl
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Topics |
- Adolescent
- Adult
- Apoptosis
(drug effects)
- Bone Marrow Cells
(drug effects, metabolism, pathology)
- Cell Count
- Cell Division
(drug effects)
- Drug Interactions
- Fusion Proteins, bcr-abl
(genetics)
- Gene Expression Regulation
(drug effects)
- Humans
- Interferon-alpha
(pharmacology)
- Interleukin-6
(pharmacology)
- Leukemia, Myelogenous, Chronic, BCR-ABL Positive
(blood, genetics, pathology)
- Middle Aged
- Proto-Oncogene Proteins c-bcl-2
(genetics)
- Proto-Oncogene Proteins c-myc
(genetics)
- RNA, Messenger
(drug effects, genetics, metabolism)
- Reverse Transcriptase Polymerase Chain Reaction
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