Abstract
Antiviral and immunomodulatory effects of interferons (IFNs) are well-known. This communication lists arguments for explicit antiangiogenetic effects exerted by interferons. There is strong likelihood that IFNs α, β and γ inhibit the int family of genes whose gene product proteins are the acidic and basic fibroblast growth factors. Some of these growth factors promote the growth of vascular endothelial cells. IFN-α inhibits basic, and IFN-γ inhibits acidic fibroblast growth factors. Inhibition of Kaposi sarcoma cell growth is not due to immunological reconstitution of the host. As IFN-α induces clinical remissions but IFN-γ does not, basic and not acidic fibroblast growth factor should be implied as one of the proliferation-inducing factors of Kaposi sarcoma cells. lFNs may interfere with the growth promotional activity of the human immunodeficiency virus Tat protein on Kaposi sarcoma cells. The proliferation of certain melanoma cell populations requires fibroblast growth factors. If this mechanism is mediated through amplified int genes, IFNs may be active clinically in this subset of melanomas. Some breast carcinoma cells induce neovascularization and metastasize. If this activity is mediated through amplified int genes. IFNs may be active clinically in this subset of breast carcinomas.