Journal
CELL CYCLE
Volume 7, Issue 5, Pages 586-591Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.7.5.5549
Keywords
HSCs; cell cycle; quiescence; leukemia; transcription; chromatin
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Funding
- NCI NIH HHS [R01 CA108056] Funding Source: Medline
- NHLBI NIH HHS [R01 HL090036, R01 HL090036-01A2] Funding Source: Medline
- NIAID NIH HHS [R01 AI051427, AI051427] Funding Source: Medline
- NIAMS NIH HHS [T32 AR07576, T32 AR007576] Funding Source: Medline
- NIDDK NIH HHS [K01 DK067119, DK067119, K01 DK067119-05] Funding Source: Medline
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Chromosomal translocations that disrupt transcriptional regulators are frequently involved in the etiology of leukemia. To gain an understanding of the normal and pathologic roles of these transcriptional regulators, both gain- and loss-of-function mutations have been examined in the context of steady-state hematopoiesis. These studies have identified a remarkable number of genes whose loss-of-function phenotype includes a perturbation of hematopoietic stem cell (HSC) proliferation. As more of these models are generated and analyzed using commonly available tools, the regulatory pathways that control HSC quiescence and proliferation are becoming clearer. An emerging theme is that leukemia-associated transcriptional regulators coordinate the balance of proliferation and quiescence within the HSC pool by modulating the number and frequency of cells transiting the cell cycle. Uncoupling proliferation from differentiation by the aberrant generation of chimeric oncogenes that retain some, but not all of the attributes of the original transcription factor is likely to be an important step during leukemogenesis.
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