Acute myeloid leukemia (AML) is often initiated by genetic alterations of machineries that regulate chromatin and transcription, thereby blocking cell differentiation. Such mechanisms may also render leukemia cells vulnerable to perturbations of transcriptional regulators, which includes small molecules targeting the coactivator protein BRD4. Numerous studies have validated BRD4 as a therapeutic target in diverse subtypes of AML; however, the vital function of BRD4 in this disease is only beginning to be understood. Here we discuss the recent progress in elucidating the transcriptional function of BRD4 in AML cells, with an emphasis on the desirable attributes, but also the inherent limitations, of targeting general coactivator proteins as cancer therapy.
|Number of pages||6|
|Journal||Cold Spring Harbor Symposia on Quantitative Biology|
|Publication status||Published - 2016|
Bibliographical noteFunding Information:
C.R.V. is supported by the Leukemia and Lymphoma Society, the Burroughs-Wellcome Fund, the Pershing Square Sohn Cancer Research Alliance, the Starr Cancer Consortium, and the National Institutes of Health (NIH)/National Cancer Institute (NCI) grants RO1 CA174793 and 5P01CA013106.
© 2016 Roe and Vakoc.
All Science Journal Classification (ASJC) codes
- Molecular Biology