| First Author | Elagib KE | Year | 2007 |
| Journal | Cancer Lett | Volume | 251 |
| Issue | 2 | Pages | 179-86 |
| PubMed ID | 17125917 | Mgi Jnum | J:121681 |
| Mgi Id | MGI:3710930 | Doi | 10.1016/j.canlet.2006.10.010 |
| Citation | Elagib KE, et al. (2007) Oncogenic pathways of AML1-ETO in acute myeloid leukemia: Multifaceted manipulation of marrow maturation. Cancer Lett 251(2):179-86 |
| abstractText | The leukemic fusion protein AML1-ETO occurs frequently in human acute myeloid leukemia (AML) and has received much attention over the past decade. An initial model for its pathogenetic effects emphasized the conversion of a hematopoietic transcriptional activator, RUNX1 (or AML1), into a leukemogenic repressor which blocked myeloid differentiation at the level of target gene regulation. This view has been absorbed into a larger picture of AML1-ETO pathogenesis, encompassing dysregulation of hematopoietic stem cell homeostasis at several mechanistic levels. Recent reports have highlighted a multifaceted capacity of AML1-ETO directly to inhibit key hematopoietic transcription factors that function as tumor suppressors at several nodal points during hematopoietic differentiation. A new model is presented in which AML1-ETO coordinates expansion of the stem cell compartment with diminished lineage commitment and with genome instability. |
