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Expression of tumor-suppressor genes interferon regulatory factor 1 and death-associated protein kinase in primitive acute myelogenous leukemia cells
Abstract
Previous studies indicate that human acute myelogenous leukemia (AML) arises from a rare population of leukemic stem cells. Cells of this nature can initiate and maintain leukemic cell growth in both long-term cultures and nonobese diabetic/severe combined immune-deficient mice. To characterize the biology of primitive AML cells, gene expression screens were performed with 7 primary AML and 3 normal specimens. For each sample, stem cell populations (CD34+/CD38−) were isolated and used to synthesize radiolabeled complementary DNA (cDNA). AML vs normal probes were then hybridized to cDNA arrays containing genes related to cancer and apoptosis. Of approximately 1400 genes analyzed, 2 tumor-suppressor genes were identified that were overexpressed in all 7 of the AML CD34+/CD38−cell populations: death-associated protein kinase and interferon regulatory factor 1. Expression of each gene was confirmed by reverse-transcription polymerase chain reaction and immunoblot analysis. It is proposed that tumor-suppressor proteins play a role in the biology of primitive AML cells.
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“the transcription factor interferon regulatory factor-1 (IRF-1) is highly overexpressed in AML eventually leading to the upregulation of the IRF-1-dependent gene CD123 [29].”
From The haematopoietic GTPase RhoH modulates IL3 signalling through regulation of STAT activity and IL3 receptor expression (2010) · cites this paper as [29]
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Cited by
Gündogdu, M. S., Liu, H., Metzdorf, D., Hildebrand, D., Aigner, M., Aktories, K., Heeg, K., & Kubatzky, K. F. (2010) · Molecular Cancer · doi:10.1186/1476-4598-9-225 · Cited by 29
Metadata
- Authors
- Guzman, M. L., Upchurch, D., Grimes, B., Howard, D. S., Rizzieri, D. A., Luger, S. M., Phillips, G. L., & Jordan, C. T.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2001-04-01
- Volume
- 97
- Issue
- 7
- Pages
- 2177-2179
- ISSN
- 1528-0020
- 0006-4971
- Cited by
- 45
- References
- 1
- Language
- en
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