| abstract |
Increased expression of a secreted FGF-binding protein (FGF-BP) occurs in certain autoimmune and malignant disease conditions. It is found, for example, that tumor secretions of FGF-BP results in mobilization and activation of locally-stored FGFs that can serve as an angiogenic switch molecule. Furthermore, it has been found that in an animal model of multiple sclerosis (MS), the exacerbation of the disease is accompanied by increased FGF-BP. Using ribozymes, it is possible to cause cleavage of the FGF-BP mRNA. Hence, administration of ribozymes which cleave the FGF-BP mRNA in sufficient amounts to inhibit disease processes triggered by FGF-BP is appropriate. |