Vascular endothelial growth factor secretion by tumor-infiltrating macrophages essentially supports tumor angiogenesis, and IgG immune complexes potentiate the process.

Tumor growth requires neoangiogenesis. Members of the vascular endothelial growth factor (VEGF) family play an important role as angiogenic promoters in malignant tumors. Tumor cells and stromal cells are sources of VEGF in the tumor.

IgG-recognizing shed tumor-associated antigens can promote tumor invasion and metastasis.

Tumors secreting glycoproteins that act as tumor-associated antigens have been described as highly invasive and metastatic. In this study, the consequences of the humoral immune response (HIR) against these antigens were investigated. Using an in vitro model of tumor cell invasion, results indicated that the invasiveness of tumor cells secreting antigenic secreted/shed tumor glycoproteins (STGP) increases in the presence of specific anti-STGP IgG, polymorphonuclear cells and monocytes.

Tumor cells express FcgammaRI which contributes to tumor cell growth and a metastatic phenotype.

High levels of circulating immune complexes containing tumor-associated antigens are associated with a poor prognosis for individuals with cancer. The ability of B cells, previously exposed to tumor-associated antigens, to promote both in vitro and in vivo tumor growth formed the rationale to evaluate the mechanism by which immune complexes may promote tumor growth. In elucidating this mechanism, FcgammaRI expression by tumor cells was characterized by flow cytometry, polymerase chain reaction, and sequence analysis.