| FLT3 K663Q is a novel AML-associated oncogenic kinase: Determination of biochemical properties and sensitivity to Sunitinib (SU11248). | None |
| Targeted degradation of the AML1/MDS1/EVI1 oncoprotein by arsenic trioxide. | None |
| Runx1 protects hematopoietic stem/progenitor cells from oncogenic insult. | None |
| Epigenetic silencing of the myelopoiesis regulator microRNA-223 by the AML1/ETO oncoprotein. | None |
| AML1/ETO oncoprotein is directed to AML1 binding regions and co-localizes with AML1 and HEB on its targets. | None |
| Findings indicate a role for replication-independent pathways in RUNX and RUNX1-ETO senescence, and show that the context-specific oncogenic activity of RUNX1 fusion proteins is mirrored in their distinctive interactions with fail-safe responses. | None |
| RUNX1 and its fusion oncoprotein derivative, RUNX1-ETO, induce senescence-like growth arrest independently of replicative stress. | None |
| EVI-1 oncogene expression predicts survival in chronic-phase CML patients resistant to imatinib treated with second-generation tyrosine kinase inhibitors. | None |
| High EVI-1 oncogene expression is associated with chronic-phase CML patients resistant to imatinib treated with second-generation tyrosine kinase inhibitors. | None |
| Reverse engineering of TLX oncogenic transcriptional networks identifies RUNX1 as tumor suppressor in T-ALL. | None |
| Epigenetic silencing of Bcl-2, CEBPA and p14(ARF) by the AML1-ETO oncoprotein contributing to growth arrest and differentiation block in the U937 cell line. | None |
| Activating c-KIT mutations confer oncogenic cooperativity and rescue RUNX1/ETO-induced DNA damage and apoptosis in human primary CD34+ hematopoietic progenitors. | None |
| Data suggest that RUNX1 functions in stem cells regulating cell differentiation; cancer cells appear to have corrupted this function of RUNX1 into promotion of oncogenesis. [REVIEW] | None |
| RUNX1 functions as an oncogene to facilitate metastasis and EMT in CRC by directly interacting with beta-catenin and activating KIT transcription to enhance the Wnt/beta-catenin signalling pathway | None |
| Overexpression of the AML1 proto-oncoprotein in NIH3T3 cells leads to neoplastic transformation depending on the DNA-binding and transactivational potencies. | None |