| The data suggest that the tumor suppressor activity of both RUNX1t1 and TFF1 are mechanistically connected to CEBPB and that cross-regulation between CEBPB-RUNX1t1-TFF1 plays an important role in gastric carcinogenesis. | gastric, |
| Sensitivity of acute myeloid leukemia Kasumi-1 cells to binase toxic action depends on the expression of KIT and capital A, CyrillicML1-ETO oncogenes. | leukemia, |
| increased FOXO1 represents a critical mechanism driving aberrant self-renewal in preleukemic cells expressing the t(8;21)-associated oncogene AML1-ETO. | leukemia, |
| 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, |
| Nuclear import and subnuclear localization of the proto-oncoprotein ETO (MTG8). | None |
| MTG8 proto-oncoprotein interacts with the regulatory subunit of type II cyclic AMP-dependent protein kinase in lymphocytes. | 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 |
| The cooperative effect of the expression of mutated KIT and AML1-ETO oncogenes is crucial for selective toxic action of binase on malignant cells. | None |
| Subcellular localization of the oncoprotein MTG8 (CDR/ETO) in neural cells. | None |