The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Analysis of the role of AML1-ETO in leukemogenesis, using an inducible transgenic mouse model
Abstract
As reported previously, AML1-ETO knock-in mice were generated to investigate the role of AML1-ETO in leukemogenesis and to mimic the progression of t(8;21) leukemia. These knock-in mice died in midgestation because of hemorrhaging in the central nervous system and a block of definitive hematopoiesis during embryogenesis. Therefore, they are not a good model system for the development of acute myeloid leukemia. Therefore, mice were generated in which the expression of AML1-ETO is under the control of a tetracycline-inducible system. Multiple lines of transgenic mice have been produced with the AML1-ETO complementary DNA controlled by a tetracycline-responsive element. In the absence of the antibiotic tetracycline, AML1-ETO is strongly expressed in the bone marrow of AML1-ETO and tet-controlled transcriptional activator double-positive transgenic mice. Furthermore, the addition of tetracycline reduces AML1-ETO expression in double-positive mice to nondetectable levels. Throughout the normal murine lifespan of 24 months, mice expressing AML1-ETO have not developed leukemia. In spite of this, abnormal maturation and proliferation of progenitor cells have been observed from these animals. These results demonstrate that AML1-ETO has a very restricted capacity to transform cells. Either the introduction of additional genetic changes or the expression of AML1-ETO at a particular stage of hematopoietic cell differentiation will be necessary to develop a model for studying the pathogenesis of t(8;21).
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Cites
Tight control of gene expression in mammalian cells by tetracycline-responsive promoters.
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Cited by
Huntly, B. J. P., Shigematsu, H., Deguchi, K., Lee, B. H., Mizuno, S., Duclos, N., Rowan, R., Amaral, S., Curley, D., Williams, I. R., et al. (2004) · Cancer Cell · doi:10.1016/j.ccr.2004.10.015 · Cited by 697
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AML1–ETO downregulates the granulocytic differentiation factor C/EBPα in t(8;21) myeloid leukemia
Pabst, T., Mueller, B. U., Harakawa, N., Schoch, C., Haferlach, T., Behre, G., Hiddemann, W., Zhang, D.-E., & Tenen, D. G. (2001) · Nature Medicine · doi:10.1038/86515 · Cited by 463
Self-citationSurvival of acute myeloid leukemia cells requires PI3 kinase activation
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Metadata
- Authors
- Rhoades, K. L., Hetherington, C. J., Harakawa, N., Yergeau, D. A., Zhou, L., Liu, L.-Q., Little, M.-T., Tenen, D. G., & Zhang, D.-E.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2000-09-15
- Volume
- 96
- Issue
- 6
- Pages
- 2108-2115
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W201291539
- Cited by
- 257
- References
- 7
- FWCI
- 11.87
- Type
- journal article
- Language
- en
- Open access
- closed
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