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A point mutation in the granulocyte colony-stimulating factor receptor
(G-CSF-R) gene in a case of acute myeloid leukemia results in the
overexpression of a novel G-CSF-R isoform
F Dong, M van Paassen, C van Buitenen, LH Hoefsloot, B Lowenberg and IP Touw
Department of Hematology, Dr. Daniel den Hoed Cancer Center, Rotterdam, The
Netherlands.
A novel human granulocyte colony-stimulating factor (G-CSF) receptor
isoform, designated SD, has been identified in which the distal C- terminal
cytoplasmic region, previously shown to be essential for maturation
signalling, is substituted by an altered C-terminus. The SD receptor has a
high affinity for G-CSF and retains the membrane- proximal cytoplasmic
region known to be sufficient for proliferative signalling. Nonetheless,
the SD isoform lacks the ability to transduce growth signals in murine BAF3
cells and, in contrast to the wild-type G- CSF receptor, is scarcely
capable of activating JAK2 kinase. Expression of SD receptor was found to
be low in normal granulocytes, but was significantly increased in a patient
with acute myeloid leukemia (AML). The leukemic cells of this patient
harbour a point mutation in the SD splice donor site of the G-CSF receptor
gene. These findings provide the first evidence that mutations in the G-CSF
receptor gene can occur in certain cases of clinical de novo AML. The
possible contribution of defective G-CSF receptor signalling to
leukemogenesis is discussed.
Volume 85,
Issue 4,
pp. 902-911,
02/15/1995
Copyright © 1995 by The American Society of Hematology
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