AbstractRetrovirally expressed human CSF-1 receptor can induce CSF-1-dependent growth of IL-3-dependent hemopoietic cells FDC-P1. Here we show that expression of the human CSF-1 receptor also allowed FDC-P1 cells to grow in response to Insulin-like Growth Factor-1 (IGF-I). The authentic receptor for IGF-I was identified by affinity cross-linking and binding analysis on both control (infected with aneovector) and CSF-1 receptor expressing FDC-P1 cells. DNA and RNA analysis of these cells and of five clones of IGF-I responsive cells demonstrated that the IGF-I receptor gene was not rearranged nor was it abnormally expressed in IGF-I responsive cells. These results suggest that myeloid cells over-expressing CSF-1R (c-fmsprotooncogene product) might have a proliferative advantage over normal myeloid cells in a physiological situation, independently of the presence of CSF-1 or the capacity of the cells to respond to CSF-1. This would indicate a possible role forc-fmsin human neoplasia.