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Blood, Vol. 93 No. 2 (January 15), 1999:
pp. 440-446
RAPID COMMUNICATION
Deletion of a Critical Internalization Domain in the G-CSFR in Acute
Myelogenous Leukemia Preceded by Severe Congenital Neutropenia
Melissa G. Hunter and
Belinda R. Avalos
From the Molecular, Cellular, and Developmental Biology Program, Bone
Marrow Transplantation Program, The Ohio State University, Arthur G. James Cancer Hospital and Research Institute, Columbus, OH.
Acquired mutations in the granulocyte colony-stimulating factor
receptor (G-CSFR) occur in a subset of patients with severe congenital
neutropenia (SCN) who develop acute myelogenous leukemia (AML). These
mutations affect one allele and result in hyperproliferative responses
to G-CSF, presumably through a dominant-negative mechanism. Here we
show that a critical domain in the G-CSFR that mediates ligand
internalization is deleted in mutant G-CSFR forms from patients with
SCN/AML. Deletion of this domain results in impaired ligand
internalization, defective receptor downmodulation, and enhanced growth
signaling. These results explain the molecular basis for G-CSFR
mutations in the pathogenesis of the dominant-negative phenotype and
hypersensitivity to G-CSF in SCN/AML.
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