AML1 and the AML1-ETO fusion protein in the pathogenesis of t(8;21) AML
نویسندگان
چکیده
منابع مشابه
E protein silencing by the leukemogenic AML1-ETO fusion protein.
The AML1-ETO fusion protein, generated by the t(8;21) chromosomal translocation, is causally involved in nearly 15% of acute myeloid leukemia (AML) cases. This study shows that AML1-ETO, as well as ETO, inhibits transcriptional activation by E proteins through stable interactions that preclude recruitment of p300/CREB-binding protein (CBP) coactivators. These interactions are mediated by a cons...
متن کاملThe AML1/ETO fusion protein activates transcription of BCL-2.
The AML1 gene, located on chromosome 21, is involved in several distinct chromosomal translocations in human leukemia. In t(8;21) acute myelogenous leukemia (AML), the AML1 gene is juxtaposed to the ETO gene located on chromosome 8, generating an AML1/ETO fusion protein. Both AML1/ETO and the AML1 proteins recognize the same consensus DNA-binding motif (TGT/CGGT), which is found in the promoter...
متن کاملGeographic Heterogeneity of the AML1-ETO Fusion Gene in Iranian Patients with Acute Myeloid Leukemia
Background: The human AML1 gene, located on chromosome 21, can be fused to the AML1- eight-twenty-one (ETO) oncoprotein on chromosome eight, resulting in a t(8;21)(q22;q22) translocation. Acute myeloid leukemia (AML) associated with this translocation is considered a distinct AML with a favorable prognosis. Due to the various incidences of the translocation, which is associated with geographic ...
متن کاملMEIS2 Is an Oncogenic Partner in AML1-ETO-Positive AML.
Homeobox genes are known to be key factors in leukemogenesis. Although the TALE family homeodomain factor Meis1 has been linked to malignancy, a role for MEIS2 is less clear. Here, we demonstrate that MEIS2 is expressed at high levels in patients with AML1-ETO-positive acute myeloid leukemia and that growth of AML1-ETO-positive leukemia depends on MEIS2 expression. In mice, MEIS2 collaborates w...
متن کاملDominant negative effects of the AML1/ETO fusion oncoprotein.
The t(8;21)(q22;q22) translocation, present in 10-15% of acute myeloid leukemia (AML) cases results in the production of the AML1/ETO fusion protein. Expression of AML1/ETO in patients or mouse models is not sufficient to induce AML. Despite convincing evidence that AML1/ETO is directly involved in the pathogenesis of AML, the underlying mechanism is not well understood. Genetic and biochemical...
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ژورنال
عنوان ژورنال: Oncogene
سال: 2001
ISSN: 0950-9232,1476-5594
DOI: 10.1038/sj.onc.1204593