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 |
|---|---|
| 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 1 |
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All Science Journal Classification (ASJC) codes
- Immunology
- Immunology and Allergy
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C/EBPα : Critical at the origin of leukemic transformation. / Roe, Jae-Seok; Vakoc, Christopher R.
In: Journal of Experimental Medicine, Vol. 211, No. 1, 01.01.2014, p. 1-4.Research output: Contribution to journal › Short survey
TY - JOUR
T1 - C/EBPα
T2 - Critical at the origin of leukemic transformation
AU - Roe, Jae-Seok
AU - Vakoc, Christopher R.
PY - 2014/1/1
Y1 - 2014/1/1
N2 - 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.
AB - 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.
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UR - http://www.scopus.com/inward/citedby.url?scp=84892550999&partnerID=8YFLogxK
U2 - 10.1084/jem.20132530
DO - 10.1084/jem.20132530
M3 - Short survey
VL - 211
SP - 1
EP - 4
JO - Journal of Experimental Medicine
JF - Journal of Experimental Medicine
SN - 0022-1007
IS - 1
ER -