Examination of the role of CSF-1 independence in myc retrovirus induced monocyte tumorigenesis.

摘要: These studies were initiated as an attempt to estimate the number and nature of genetic changes that are required in addition c-myc deregulation during monocyte tumorigenesis, determine whether oncogenic can be created vitro resemble actual occur vivo. We found superinfecting myc-immortalized monocytes with a colony stimulating factor-1 (CSF-1) expressing retrovirus strongly promoted whereas granulocyte/macrophage-CSF (GM-CSF) v-fms retroviruses, or spontaneous acquisition CSF-1 independence did so only moderately. In myc-infected isolated from mice at stage prior tumor formation more tumorigenic than monocytes, but they still largely dependent, not reinnoculated cells. simplest model two activations for monocyte/macrophage transformation, immortalization cells gene. However, all mechanisms result loss dependence lead full tumorigenicity, suggesting vivo tumorigenesis may involve multiple secondary events including growth factor independence.