Cancer Research AACR Legacy  Genetics and Biology of Brain Cancer
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online

[Cancer Research 57, 2951-2955, July 15, 1997]
© 1997 American Association for Cancer Research

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wang, J.
Right arrow Articles by Liu, J. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wang, J.
Right arrow Articles by Liu, J. M.

Transformation Properties of the ETO Gene, Fusion Partner in t(8:21) Leukemias

Jianxiang Wang, Min Wang and Johnson M. Liu1

Hematology Branch, National Heart, Lung, and Blood Institute [J. W., J. M. L.], and Molecular Hematology Section, Laboratory of Chemical Biology, National Institute of Diabetes, Digestive and Kidney Diseases [M. W.], Bethesda, Maryland 20892

The (8;21)(q22;q22) translocation, reported in 40% of M2-subtype acute myeloid leukemias (AMLs), is the second-most frequently observed example of a nonrandom genetic alteration associated with AML. Juxtaposition of the AML1 gene on chromosome 21 to the ETO gene on chromosome 8 fuses the NH2-terminal portion of AML1 to near-full length ETO, creating AML1/ETO. Previous work has been focused on perturbation of AML1 gene function by the chimeric fusion protein as a mechanism of leukemogenesis. Here, we demonstrate that ETO itself has transforming properties. Ectopic ETO expression in NIH/3T3 cells led to foci of transformation and colony growth in soft agar. ETO-expressing cells grew to higher saturation densities and induced tumors following injection into irradiated and splenectomized nude mice. Our data suggests that ETO may play an important role in the leukemic transforming potential of the AML1/ETO fusion protein.

1 To whom requests for reprints should be addressed, at Hematology Branch, National Heart, Lung, and Blood Institute, NIH, 10/ACRF/7C103, Bethesda, MD 20892. Phone: (301) 496-5093; Fax: (301) 496-8396; E-mail: LiuJ@gwgate.nhlbi.nih.gov.

Received 5/ 3/96. Accepted 5/15/97.




This article has been cited by other articles:


Home page
BloodHome page
R. L. Redner, J. Wang, and J. M. Liu
Chromatin Remodeling and Leukemia: New Therapeutic Paradigms
Blood, July 15, 1999; 94(2): 417 - 428.
[Full Text] [PDF]


Home page
Proc. Natl. Acad. Sci. USAHome page
J. Wang, T. Hoshino, R. L. Redner, S. Kajigaya, and J. M. Liu
ETO, fusion partner in t(8;21) acute myeloid leukemia, represses transcription by interaction with the human N-CoR/mSin3/HDAC1 complex
PNAS, September 1, 1998; 95(18): 10860 - 10865.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1997 by the American Association for Cancer Research.