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• W2146993816 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." @default.
• W2146993816 created "2016-06-24" @default.
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• W2146993816 date "2014-01-06" @default.
• W2146993816 modified "2023-10-16" @default.
• W2146993816 title "C/EBPα: critical at the origin of leukemic transformation" @default.
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• W2146993816 doi "https://doi.org/10.1084/jem.20132530" @default.
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