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A mutation of the common receptor subunit for interleukin-3 (IL-3),
granulocyte-macrophage colony-stimulating factor, and IL-5 that leads to
ligand independence and tumorigenicity
R D'Andrea, J Rayner, P Moretti, A Lopez, GJ Goodall, TJ Gonda and M Vadas
Hanson Centre for Cancer Research, Institute of Medical and Veterinary
Science, Adelaide, Australia.
The cytokines interleukin-3, interleukin-5, and granulocyte-macrophage
colony-stimulating factor bind with high affinity to a receptor complex
that contains a ligand-specific alpha-chain and a common beta-chain, h beta
c. We report here the isolation of a mutant form of h beta c, from growth
factor-independent cells, that arose spontaneously after infection of a
murine factor-dependent hematopoietic cell line (FDC-P1) with a retroviral
h beta c expression construct. Analysis of this h beta c mutation shows
that a small (37 amino acid) duplication of extracellular sequence that
includes two conserved sequence motifs is sufficient to confer
ligand-independent growth on these cells and lead to tumourigenicity.
Because this is a conserved region in the cytokine receptor superfamily,
our results suggest that the large family of cytokine receptors has the
capacity to become oncogenically active.
Volume 83,
Issue 10,
pp. 2802-2808,
05/15/1994
Copyright © 1994 by The American Society of Hematology
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