838 related articles for article (PubMed ID: 8585955)
1. 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]
2. Rearrangements of the AML1/CBFA2 gene in myeloid leukemia with the 3;21 translocation: in vitro and in vivo studies.
Zent C; Rowley JD; Nucifora G
Leukemia; 1997 Apr; 11 Suppl 3():273-8. PubMed ID: 9209363
[TBL] [Abstract][Full Text] [Related]
3. The chimeric genes AML1/MDS1 and AML1/EAP inhibit AML1B activation at the CSF1R promoter, but only AML1/MDS1 has tumor-promoter properties.
Zent CS; Mathieu C; Claxton DF; Zhang DE; Tenen DG; Rowley JD; Nucifora G
Proc Natl Acad Sci U S A; 1996 Feb; 93(3):1044-8. PubMed ID: 8577711
[TBL] [Abstract][Full Text] [Related]
4. 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]
5. 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]
6. 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]
7. 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]
8. The AML1/ETO(MTG8) and AML1/Evi-1 leukemia-associated chimeric oncoproteins accumulate PEBP2beta(CBFbeta) in the nucleus more efficiently than wild-type AML1.
Tanaka K; Tanaka T; Kurokawa M; Imai Y; Ogawa S; Mitani K; Yazaki Y; Hirai H
Blood; 1998 Mar; 91(5):1688-99. PubMed ID: 9473235
[TBL] [Abstract][Full Text] [Related]
9. [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]
10. The EVI1 gene in myeloid leukemia.
Nucifora G
Leukemia; 1997 Dec; 11(12):2022-31. PubMed ID: 9447815
[TBL] [Abstract][Full Text] [Related]
11. The 3;21 translocation in myelodysplasia results in a fusion transcript between the AML1 gene and the gene for EAP, a highly conserved protein associated with the Epstein-Barr virus small RNA EBER 1.
Nucifora G; Begy CR; Erickson P; Drabkin HA; Rowley JD
Proc Natl Acad Sci U S A; 1993 Aug; 90(16):7784-8. PubMed ID: 8395054
[TBL] [Abstract][Full Text] [Related]
12. 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]
13. 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]
14. The leukemia-associated gene MDS1/EVI1 is a new type of GATA-binding transactivator.
Soderholm J; Kobayashi H; Mathieu C; Rowley JD; Nucifora G
Leukemia; 1997 Mar; 11(3):352-8. PubMed ID: 9067573
[TBL] [Abstract][Full Text] [Related]
15. t(3;21)(q26;q22) in myeloid leukemia: an aggressive syndrome of blast transformation associated with hydroxyurea or antimetabolite therapy.
Yin CC; Cortes J; Barkoh B; Hayes K; Kantarjian H; Jones D
Cancer; 2006 Apr; 106(8):1730-8. PubMed ID: 16532439
[TBL] [Abstract][Full Text] [Related]
16. CBFA2(AML1) translocations with novel partner chromosomes in myeloid leukemias: association with prior therapy.
Roulston D; Espinosa R; Nucifora G; Larson RA; Le Beau MM; Rowley JD
Blood; 1998 Oct; 92(8):2879-85. PubMed ID: 9763573
[TBL] [Abstract][Full Text] [Related]
17. AML1 fusion transcripts in t(3;21) positive leukemia: evidence of molecular heterogeneity and usage of splicing sites frequently involved in the generation of normal AML1 transcripts.
Sacchi N; Nisson PE; Watkins PC; Faustinella F; Wijsman J; Hagemeijer A
Genes Chromosomes Cancer; 1994 Dec; 11(4):226-36. PubMed ID: 7533526
[TBL] [Abstract][Full Text] [Related]
18. Human AML1/MDS1/EVI1 fusion protein induces an acute myelogenous leukemia (AML) in mice: a model for human AML.
Cuenco GM; Nucifora G; Ren R
Proc Natl Acad Sci U S A; 2000 Feb; 97(4):1760-5. PubMed ID: 10677531
[TBL] [Abstract][Full Text] [Related]
19. 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]
20. PEBP2 alpha B/mouse AML1 consists of multiple isoforms that possess differential transactivation potentials.
Bae SC; Ogawa E; Maruyama M; Oka H; Satake M; Shigesada K; Jenkins NA; Gilbert DJ; Copeland NG; Ito Y
Mol Cell Biol; 1994 May; 14(5):3242-52. PubMed ID: 8164679
[TBL] [Abstract][Full Text] [Related]
[Next] [New Search]
