182 related articles for article (PubMed ID: 15914564)
1. Dysplastic definitive hematopoiesis in AML1/EVI1 knock-in embryos.
Maki K; Yamagata T; Asai T; Yamazaki I; Oda H; Hirai H; Mitani K
Blood; 2005 Sep; 106(6):2147-55. PubMed ID: 15914564
[TBL] [Abstract][Full Text] [Related]
2. Expression of a knocked-in AML1-ETO leukemia gene inhibits the establishment of normal definitive hematopoiesis and directly generates dysplastic hematopoietic progenitors.
Okuda T; Cai Z; Yang S; Lenny N; Lyu CJ; van Deursen JM; Harada H; Downing JR
Blood; 1998 May; 91(9):3134-43. PubMed ID: 9558367
[TBL] [Abstract][Full Text] [Related]
3. [Study of genes involved in chronic myeloid leukemia with t (3; 21) (q26; q22) in blastic crisis].
Liu XP; Zhang MR; Dai Y; Zhang L; Li R; Hao YS; Xiao ZJ
Zhonghua Xue Ye Xue Za Zhi; 2006 May; 27(5):310-3. PubMed ID: 16875579
[TBL] [Abstract][Full Text] [Related]
4. Both AML1 and EVI1 oncogenic components are required for the cooperation of AML1/MDS1/EVI1 with BCR/ABL in the induction of acute myelogenous leukemia in mice.
Cuenco GM; Ren R
Oncogene; 2004 Jan; 23(2):569-79. PubMed ID: 14724585
[TBL] [Abstract][Full Text] [Related]
5. Rearrangement of the AML1/CBFA2 gene in myeloid leukemia with the 3;21 translocation: expression of co-existing multiple chimeric genes with similar functions as transcriptional repressors, but with opposite tumorigenic properties.
Zent C; Kim N; Hiebert S; Zhang DE; Tenen DG; Rowley JD; Nucifora G
Curr Top Microbiol Immunol; 1996; 211():243-52. PubMed ID: 8585955
[TBL] [Abstract][Full Text] [Related]
6. AML1, the target of multiple chromosomal translocations in human leukemia, is essential for normal fetal liver hematopoiesis.
Okuda T; van Deursen J; Hiebert SW; Grosveld G; Downing JR
Cell; 1996 Jan; 84(2):321-30. PubMed ID: 8565077
[TBL] [Abstract][Full Text] [Related]
7. MDS1/EVI1 enhances TGF-beta1 signaling and strengthens its growth-inhibitory effect but the leukemia-associated fusion protein AML1/MDS1/EVI1, product of the t(3;21), abrogates growth-inhibition in response to TGF-beta1.
Sood R; Talwar-Trikha A; Chakrabarti SR; Nucifora G
Leukemia; 1999 Mar; 13(3):348-57. PubMed ID: 10086725
[TBL] [Abstract][Full Text] [Related]
8. RUNX1-EVI1 induces dysplastic hematopoiesis and acute leukemia of the megakaryocytic lineage in mice.
Nakamura Y; Ichikawa M; Oda H; Yamazaki I; Sasaki K; Mitani K
Leuk Res; 2018 Nov; 74():14-20. PubMed ID: 30278283
[TBL] [Abstract][Full Text] [Related]
9. Intergenic splicing of MDS1 and EVI1 occurs in normal tissues as well as in myeloid leukemia and produces a new member of the PR domain family.
Fears S; Mathieu C; Zeleznik-Le N; Huang S; Rowley JD; Nucifora G
Proc Natl Acad Sci U S A; 1996 Feb; 93(4):1642-7. PubMed ID: 8643684
[TBL] [Abstract][Full Text] [Related]
10. Generation of the AML1-EVI-1 fusion gene in the t(3;21)(q26;q22) causes blastic crisis in chronic myelocytic leukemia.
Mitani K; Ogawa S; Tanaka T; Miyoshi H; Kurokawa M; Mano H; Yazaki Y; Ohki M; Hirai H
EMBO J; 1994 Feb; 13(3):504-10. PubMed ID: 8313895
[TBL] [Abstract][Full Text] [Related]
11. The t(3;21) fusion product, AML1/Evi-1, interacts with Smad3 and blocks transforming growth factor-beta-mediated growth inhibition of myeloid cells.
Kurokawa M; Mitani K; Imai Y; Ogawa S; Yazaki Y; Hirai H
Blood; 1998 Dec; 92(11):4003-12. PubMed ID: 9834202
[TBL] [Abstract][Full Text] [Related]
12. The AML1 gene: a transcription factor involved in the pathogenesis of myeloid and lymphoid leukemias.
Lo Coco F; Pisegna S; Diverio D
Haematologica; 1997; 82(3):364-70. PubMed ID: 9234595
[TBL] [Abstract][Full Text] [Related]
13. Dual functions of the AML1/Evi-1 chimeric protein in the mechanism of leukemogenesis in t(3;21) leukemias.
Tanaka T; Mitani K; Kurokawa M; Ogawa S; Tanaka K; Nishida J; Yazaki Y; Shibata Y; Hirai H
Mol Cell Biol; 1995 May; 15(5):2383-92. PubMed ID: 7739522
[TBL] [Abstract][Full Text] [Related]
14. Consistent intergenic splicing and production of multiple transcripts between AML1 at 21q22 and unrelated genes at 3q26 in (3;21)(q26;q22) translocations.
Nucifora G; Begy CR; Kobayashi H; Roulston D; Claxton D; Pedersen-Bjergaard J; Parganas E; Ihle JN; Rowley JD
Proc Natl Acad Sci U S A; 1994 Apr; 91(9):4004-8. PubMed ID: 8171026
[TBL] [Abstract][Full Text] [Related]
15. Cooperation of BCR-ABL and AML1/MDS1/EVI1 in blocking myeloid differentiation and rapid induction of an acute myelogenous leukemia.
Cuenco GM; Ren R
Oncogene; 2001 Dec; 20(57):8236-48. PubMed ID: 11781838
[TBL] [Abstract][Full Text] [Related]
16. Repression of RUNX1 activity by EVI1: a new role of EVI1 in leukemogenesis.
Senyuk V; Sinha KK; Li D; Rinaldi CR; Yanamandra S; Nucifora G
Cancer Res; 2007 Jun; 67(12):5658-66. PubMed ID: 17575132
[TBL] [Abstract][Full Text] [Related]
17. The leukemia-associated transcription repressor AML1/MDS1/EVI1 requires CtBP to induce abnormal growth and differentiation of murine hematopoietic cells.
Senyuk V; Chakraborty S; Mikhail FM; Zhao R; Chi Y; Nucifora G
Oncogene; 2002 May; 21(20):3232-40. PubMed ID: 12082639
[TBL] [Abstract][Full Text] [Related]
18. The distal zinc finger domain of AML1/MDS1/EVI1 is an oligomerization domain involved in induction of hematopoietic differentiation defects in primary cells in vitro.
Senyuk V; Li D; Zakharov A; Mikhail FM; Nucifora G
Cancer Res; 2005 Sep; 65(17):7603-11. PubMed ID: 16140925
[TBL] [Abstract][Full Text] [Related]
19. Evi1 is essential for hematopoietic stem cell self-renewal, and its expression marks hematopoietic cells with long-term multilineage repopulating activity.
Kataoka K; Sato T; Yoshimi A; Goyama S; Tsuruta T; Kobayashi H; Shimabe M; Arai S; Nakagawa M; Imai Y; Kumano K; Kumagai K; Kubota N; Kadowaki T; Kurokawa M
J Exp Med; 2011 Nov; 208(12):2403-16. PubMed ID: 22084405
[TBL] [Abstract][Full Text] [Related]
20. Targeted degradation of the AML1/MDS1/EVI1 oncoprotein by arsenic trioxide.
Shackelford D; Kenific C; Blusztajn A; Waxman S; Ren R
Cancer Res; 2006 Dec; 66(23):11360-9. PubMed ID: 17145882
[TBL] [Abstract][Full Text] [Related]
[Next] [New Search]
