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Fibroblast and hematopoietic cell transformation by the fms oncogene (CSF‐1 receptor)
Author(s) -
Sherr Charles J.
Publication year - 1987
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041330416
Subject(s) - biology , receptor tyrosine kinase , oncogene , haematopoiesis , microbiology and biotechnology , receptor , cancer research , stem cell factor , ror1 , tyrosine kinase , signal transduction , gene , platelet derived growth factor receptor , cell cycle , genetics , growth factor , stem cell
The c‐ fms proto‐oncogene encodes the receptor for the mononuclear phagocyte colony stimulating factor, CSF‐1. Although the tyrosine kinase activity of the CSF‐1 receptor is stimulated by its ligand, the viral oncogene, v‐ fms , encodes a constitutive receptor kinase that can transform both fibroblasts and hematopoietic cells by a nonautocrine mechanism. Mutations in the c‐ fms gene as well as a critical alteration of the distal 3′ coding sequences appear to be responsible for fully activating its latent transforming potential. The v‐ fms gene can convert CSF‐1 or IL‐3 dependent hematopoietic cell lines to factor independence and render them tumorigenic. Expression of the v‐ fms gene product does not transmodulate the normal receptors for CSF‐1 or IL‐3 and affects neither their affinity, number, nor potential to be independently down‐regulated by their ligands or by phorbol esters. The ability of v‐ fms to transform hematopoietic target cells suggests that critical alterations in the c‐ fms proto‐oncogene might similarly contribute to leukemia.