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Comment
. 2012 May 31;119(22):5063-4.
doi: 10.1182/blood-2012-04-417287.

From famine to feast: sending out the clones

Taly Glaubach  1 , Seth J Corey
Affiliations
Comment

From famine to feast: sending out the clones

Taly Glaubach et al. Blood. .

Abstract

In this issue of Blood, Beekman et al provide compelling evidence for the multistep evolution of acute myeloid leukemia (AML) from severe congenital neutropenia (SCN) over a 17-year period. Moreover, they found that 5 different gain-of-function mutations in the granulocyte colony-stimulating factor receptor (GCSFR) arose during this transformation, suggesting that 2 mutations behaved as drivers for clonal outgrowth, while 3 others did not.

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Conflict of interest statement

Conflict-of-interest disclosure: The authors declare no competing financial interests. ■

Figures

None
Natural selection of clones. Mutations involving granulocyte colony-stimulating factor receptor (GCSFR) emerge during the course of severe congenital neutropenia (SCN) treated by recombinant human G-CSF. However, some mutations thrive and persist, while others die off. Professional illustration by Debra T. Dartez adapted from Figure 4 in Beekman et al, which begins on page 5071.
See this image and copyright information in PMC

Comment on

References

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