The ECM of astrocytic tumors promotes and modulates a variety of cell functions, such as cell attachment, migration, proliferation, survival, and signaling. Recent studies indicate that there are extensive and complex interactions among ECM molecules and that these can modify the function of the participating molecules, interactions between the proteoglycan, phosphacan, and the ECM protein, tenascin, being an example (63). In addition, on nonastrocytic cell types it has been shown that an integrin receptor and the cell surface proteoglycan CD44 recognize the same ECM ligand osteopontin, and thus modulate each others function (77, 86). Thus, interacting components in the ECM and cell surface receptors likely cooperate in regulating cell function and tumor invasion (59, 77, 80, 85-87, 95). As tumor cells are capable of remodeling their ECM through synthesis of ECM proteins and proteoglycans, as well as upregulating integrin receptors and proteoglycans on their cell surface, tumor cells are capable of controlling their own destiny. ECM molecules which are concentrated in blood vessels of malignant astrocytomas, such as tenascin-C and the 250-kDa CSPG (NG2), are potentially therapeutic targets.