| Regulation of anchor cell invasion and uterine cell fates by the egl-43 Evi-1 proto-oncogene in Caenorhabditis elegans. | uterine, |
| Runx1 insufficiency suppresses oncogenic N-RAS-induced adverse effects (i.e., apoptosis, senescence, and differentiation) and disrupts the fail-safe mechanism normally active in stem/progenitor cells, thereby contributing to the development of leukemia. | leukemia, |
| Data suggest that Runx1 may act as a skin oncogene by directly promoting proliferation of the epithelial cells. | skin, |
| Runx1 directly promotes proliferation of hair follicle stem cells and epithelial tumor formation in mouse skin. | skin, |
| Control of EVI-1 oncogene expression in metastatic breast cancer cells through microRNA miR-22. | breast, |
| Downregulation of activated leukemic oncogenes AML1-ETO and RUNX1(K83N) expression with RNA-interference | leukemia, |
| [Downregulation of activated leukemic oncogenes AML1-ETO and RUNX1(K83N) expression with RNA-interference]. | leukemia, |
| data are indicative for a strong oncogenic potential of the RUNX1 gene in epithelial ovarian cancer progression | ovarian, |
| STAT3 mediates oncogenic addiction to TEL-AML1 in t(12;21) acute lymphoblastic leukemia. | leukemia, |
| Molecular genetic studies on 167 pediatric ALL patients from different areas of Pakistan confirm a low frequency of the favorable prognosis fusion oncogene TEL-AML1 (t 12; 21) in underdeveloped countries of the region. | pediatric, |
| The leukemia-associated RUNX1/ETO oncoprotein confers a mutator phenotype. | leukemia, |
| The study shows a low representation of ETV6-RUNX1 fusion oncogenes among pediatric acute lymphoblastic leukemia patients from King Abdulaziz Medical City, National Guard Health Affairs, Riyadh, Saudi Arabia. | leukemia,pediatric, |
| AML1-ETO as a single oncogenic hit in a non-mutated background blocks granulocytic differentiation, deregulates the gene program via altering the acetylome of the differentiating granulocytic cells, and induces t(8;21) AML associated leukemic characteristics. | leukemia, |
| Expression of the AML-1 oncogene shortens the G(1) phase of the cell cycle. | None |
| Oligomerization of RAR and AML1 transcription factors as a novel mechanism of oncogenic activation. | None |
| The E2A-HLF oncoprotein activates Groucho-related genes and suppresses Runx1. | None |
| the chromosomal translocation leads to formation of tel/aml1 fusion oncogene and is most common genetic aberration in childhood B-cell precursor ALL. | None |
| P/CAF and GCN5 acetylate the AML1/MDS1/EVI1 fusion oncoprotein. | None |
| Dominant negative effects of the AML1/ETO fusion oncoprotein. | None |
| Defining the oncogenic function of the TEL/AML1 (ETV6/RUNX1) fusion protein in a mouse model. | None |