Abstract
Acute myeloid leukemia (AML) is a hematopoietic malignancy characterized by clonal expansion of myeloid progenitor cells. A major mechanistic theme in AML biology is the extensive collaboration among fusion oncoproteins, transcription factors, and chromatin regulators to initiate and sustain a transformed cellular state. A new study in this issue describes how the C/EBPα transcription factor is crucial for the initiation of AML induced by MLL fusion oncoproteins, but is entirely dispensable for the maintenance of established disease. These observations provide a unique glimpse into the pioneer round of regulatory events that are critical at the origin of AML formation. Furthermore, this study implies the existence of oncogene-induced positive feedback loops capable of bypassing the continuous need for certain regulators to propagate disease.
Original language | English |
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Pages (from-to) | 1-4 |
Number of pages | 4 |
Journal | Journal of Experimental Medicine |
Volume | 211 |
Issue number | 1 |
DOIs | |
Publication status | Published - 2014 Jan |
All Science Journal Classification (ASJC) codes
- Immunology and Allergy
- Immunology