FcR may function as a progression factor of nonlymphoid tumors.

Tumor progression is a multistep process involving genetic and epigenetic changes in a transformed clone. Some of these changes may be induced by host factors which may also select for transformed cellular variants with a high ability to survive and propagate. In this article we review studies showing that receptors for the Fc portion of IgG may be expressed on cells from human or animal tumors of nonlymphoid origin. We also review data demonstrating that at least with respect to cells transformed in vitro with Polyoma virus, transformation per se is not sufficient for the induction of Fc receptor expression. We also summarize preliminary data showing that Fc receptor expression is causally involved in conferring a high malignancy phenotype upon transformed cells. Possible mechanisms to explain these observations are discussed.