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20 in total

1. Deletion of an AML1-ETO C-terminal NcoR/SMRT-interacting region strongly induces leukemia development.

Authors: Ming Yan; Sebastien A Burel; Luke F Peterson; Eiki Kanbe; Hiromi Iwasaki; Anita Boyapati; Robert Hines; Koichi Akashi; Dong-Er Zhang
Journal: Proc Natl Acad Sci U S A Date: 2004-11-29 Impact factor: 11.205

2. Expression of a knocked-in AML1-ETO leukemia gene inhibits the establishment of normal definitive hematopoiesis and directly generates dysplastic hematopoietic progenitors.

Authors: T Okuda; Z Cai; S Yang; N Lenny; C J Lyu; J M van Deursen; H Harada; J R Downing
Journal: Blood Date: 1998-05-01 Impact factor: 22.113

3. Dichotomy of AML1-ETO functions: growth arrest versus block of differentiation.

Authors: S A Burel; N Harakawa; L Zhou; T Pabst; D G Tenen; D E Zhang
Journal: Mol Cell Biol Date: 2001-08 Impact factor: 4.272

4. AML1-ETO expression is directly involved in the development of acute myeloid leukemia in the presence of additional mutations.

Authors: Y Yuan; L Zhou; T Miyamoto; H Iwasaki; N Harakawa; C J Hetherington; S A Burel; E Lagasse; I L Weissman; K Akashi; D E Zhang
Journal: Proc Natl Acad Sci U S A Date: 2001-08-28 Impact factor: 11.205

5. Analysis of the role of AML1-ETO in leukemogenesis, using an inducible transgenic mouse model.

Authors: K L Rhoades; C J Hetherington; N Harakawa; D A Yergeau; L Zhou; L Q Liu; M T Little; D G Tenen; D E Zhang
Journal: Blood Date: 2000-09-15 Impact factor: 22.113

6. Exogenous cdk4 overcomes reduced cdk4 RNA and inhibition of G1 progression in hematopoietic cells expressing a dominant-negative CBF - a model for overcoming inhibition of proliferation by CBF oncoproteins.

Authors: J Lou; W Cao; F Bernardin; K Ayyanathan; F J RauscherIII; A D Friedman
Journal: Oncogene Date: 2000-05-18 Impact factor: 9.867

7. ETO, a target of t(8;21) in acute leukemia, makes distinct contacts with multiple histone deacetylases and binds mSin3A through its oligomerization domain.

Authors: J M Amann; J Nip; D K Strom; B Lutterbach; H Harada; N Lenny; J R Downing; S Meyers; S W Hiebert
Journal: Mol Cell Biol Date: 2001-10 Impact factor: 4.272

8. Expression of a conditional AML1-ETO oncogene bypasses embryonic lethality and establishes a murine model of human t(8;21) acute myeloid leukemia.

Authors: Masakazu Higuchi; Darin O'Brien; Parasakthy Kumaravelu; Noel Lenny; Eng-Juh Yeoh; James R Downing
Journal: Cancer Cell Date: 2002-02 Impact factor: 31.743

Fusion-protein truncation provides new insights into leukemogenesis.

1. Deletion of an AML1-ETO C-terminal NcoR/SMRT-interacting region strongly induces leukemia development.

2. Expression of a knocked-in AML1-ETO leukemia gene inhibits the establishment of normal definitive hematopoiesis and directly generates dysplastic hematopoietic progenitors.

3. Dichotomy of AML1-ETO functions: growth arrest versus block of differentiation.

4. AML1-ETO expression is directly involved in the development of acute myeloid leukemia in the presence of additional mutations.

5. Analysis of the role of AML1-ETO in leukemogenesis, using an inducible transgenic mouse model.

6. Exogenous cdk4 overcomes reduced cdk4 RNA and inhibition of G1 progression in hematopoietic cells expressing a dominant-negative CBF - a model for overcoming inhibition of proliferation by CBF oncoproteins.

7. ETO, a target of t(8;21) in acute leukemia, makes distinct contacts with multiple histone deacetylases and binds mSin3A through its oligomerization domain.

8. Expression of a conditional AML1-ETO oncogene bypasses embryonic lethality and establishes a murine model of human t(8;21) acute myeloid leukemia.

9. ETO, a target of t(8;21) in acute leukemia, interacts with the N-CoR and mSin3 corepressors.

10. Structure and expression of the human MTG8/ETO gene.

1. New insights into transcriptional and leukemogenic mechanisms of AML1-ETO and E2A fusion proteins.

Review 2. Effect of transcription-factor concentrations on leukemic stem cells.

Review 3. Targeting genetic alterations in protein methyltransferases for personalized cancer therapeutics.