Mutations of the granulocyte-colony stimulating factor receptor in patients with severe congenital neutropenia are not required for transformation to acute myeloid leukaemia and may be a bystander phenomenon

1998 ◽  
Vol 101 (1) ◽  
pp. 141-149 ◽  
Author(s):  
Tanya Bernard ◽  
Rosemary E. Gale ◽  
Jane P. M. Evans ◽  
David C. Linch
Keyword(s):  
Acute Myeloid Leukaemia ◽  
Myeloid Leukaemia ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Severe Congenital Neutropenia ◽  
Congenital Neutropenia ◽  
Stimulating Factor ◽  
Acute Myeloid

scholarly journals From famine to feast: sending out the clones

Blood ◽  
2012 ◽  
Vol 119 (22) ◽  
pp. 5063-5064 ◽  
Author(s):  
Taly Glaubach ◽  
Seth J. Corey
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Compelling Evidence ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Severe Congenital Neutropenia ◽  
Congenital Neutropenia ◽  
Gain Of Function ◽  
Stimulating Factor ◽  
Acute Myeloid

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.1

Sign in / Sign up

Export Citation Format

Share Document