## Abstract __AML1__ is among the most frequent targets of chromosomal rearrangements in human leukemias. We report here the molecular analysis of a t(4;21)(q28;q22) that has disrupted __AML1__ in a patient with de novo Tβcell acute lymphoblastic leukemia. By using 3β²βRACE analysis, we show that th
Secondary acute myeloblastic leukemia with t(16;21)(q24;q22) involving the AML1 gene
β Scribed by R. Berger; M. Le Coniat; S. P. Romana; P. Jonveaux
- Publisher
- Springer
- Year
- 1996
- Tongue
- English
- Weight
- 139 KB
- Volume
- 38
- Category
- Article
- ISSN
- 1269-3286
No coin nor oath required. For personal study only.
π SIMILAR VOLUMES
## Abstract The t(1;21)(p36;q22) is a recurrent chromosome abnormality associated with therapyβrelated acute myeloid leukemia (AML). Although involvement of __RUNX1__ has been detected by fluorescence in situ hybridization analysis, the partner gene has not been reported previously. We identified a
## Abstract The __AML1__ gene (also known as __RUNX1__) at 21q22 codes for core binding factor (CBF) Ξ±, which forms a heterodimer with CBF Ξ² that acts as a transcriptional activating factor. CBF is a critical regulator in the generation and differentiation of definitive hematopoietic stem cells and
We report on a novel chromosomal aberration, inv(8)(p11q24), in an M5 acute myeloid leukemia. We show by fluorescence in situ hybridization and Southern blot analyses that a t(8;16)(p11;p13) is masked by this inversion. The translocation targets the MOZ gene from the 8p11 and the CBP gene from the 1
## Abstract __RUNX1__ (previously __AML1__) is involved in multiple recurrent chromosomal rearrangements in hematological malignances. Recently, we identified a novel fusion between __RUNX1__ and __LPXN__ from an acute myeloid leukemia (AML) patient with t(11;21)(q12;q22). This translocation genera