AML1-ETO leukemia is the most common cytogenetic subtype of acute myeloid leukemia, defined by the presence of t(8;21). Remarkable progress has been achieved in understanding the molecular pathogenesis of AML1-ETO leukemia. Proteomic surveies have shown that AML-ETO forms a stable complex with ...
The significance of a permissive window is ironically best shown by a large number of failures in generating the animal model for acute myeloid leukemia (AML) with t(8;21). Over the decades, the RUNX1-ETO fusion gene created by t(8;21) has been introduced into various types of ...
The RUNX1/ETO (RE) fusion protein, which originates from the t(8;21) chromosomal rearrangement, is one of the most frequent translocation products found in de novo acute myeloid leukemia (AML). In RE leukemias, activated forms of the c-KIT tyrosine kinas
To elucidate mechanisms by which RUNX1–ETO, the common acute myeloid leukemia t(8;21) fusion protein, primes hematopoietic cells for oncogenic transformation, we previously carried out Affymetrix gene expression profiling of RUNX1–ETO-expressing human CD34+progenitor cells.1We identified the MYC tar...
This is an encouraging step forward in improving outcomes for leukemia patients.Luis Daniel Daniel Mata CasimiroManisha du Plessis PhDDennis UnthanHeyang ZhangMatthias Barz PhDRaymond M. Schiffelers PhDOlaf Heidenreich PhD
RUNX1T1 is a putative transcription factor which forms a heterodimer with CBFA2T3. Defects in RUNX1T1 have been associated with acute myeloid leukemia (AML-M2) and may be a cause of colorectal cancer. Anti-AML-ETO Antibody is ideal for research in Gene Expression and Cancer. ...
The t(8;21) translocation fuses the DNA-binding domain of the hematopoietic master regulator RUNX1 to the ETO protein. The resultant RUNX1/ETO fusion protein is a leukemia-initiating transcription factor that interferes with RUNX1 function. The result of this interference is a block in ...
Figure 3. RUNX1 Fusion Proteins Form Part of a Gene Regulatory Network Unique to Each Leukemia (A) UCSC genome browser screen shot of Spi1 showing ChIP-seq data of RUNX1 and RUNX1-EVI1 from t(3;21) SKH-1 cells, RUNX1 and RUNX1-ETO from t(8;21) Kasumi-1 cells, and RUNX1 from...
More recently, we have identified an alternatively spliced form of AML1-ETO, AML1-ETO9a, from t(8;21) acute myeloid leukemia (AML) patient samples. AML1-ETO9a lacks the C-terminal NHR3 and NHR4 domains of AML1-ETO and is highly leukemogenic in the mouse model. Here, we report ...
Large-scale chromosomal translocations are frequent oncogenic drivers in acute myeloid leukemia (AML). These translocations often occur in critical transcriptional/epigenetic regulators and contribute to malignant cell growth through alteration of normal gene expression. Despite this knowledge, the specific gen...