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Alpha ( 1,3)galactosyltransferase is the major xenoantigen associated with hyperacute rejection of xenotransplants. Tumor vaccines engineered to express this gene may show promise in breaking tumor tolerance. However there has been a lack of alternative tumor models to the highly published B16 with which to study the immunology associated with a(l,3) galactosyltransferase modified tumor vaccines. Moreover, limited in vivo models exist to study the basic biology of a(l,3) galactosyltransferase in xenotransplantation experiments. Therefore, we have developed a gastrointestinal stromal tumor, CA320M, derived from C57ZBL6 a(l,3)galactosyltransferase knock-out mice. Mice were subject to intraperitoneal injections of 9,10-dimethyl-1,2-benz-anthracene and 3-methylcholanthrene. Resultant tumors were harvested and characterized in vitro and in vivo. CA320M cells transduced with a herpes simplex virus amplicon vector (HE7agall) carrying the. murine a(l,3)GT gene resulted in significant agal epitope expression. CA320M cells expressing agal were incubated with normal human serum (NHS) or serum collected from a(l,3)GT KO mice immunized against agal (MS). Flow cytometric analysis of NHS exposed agal expressing cells demonstrated up to 97% complement lysis. Cells exposed to MS demonstrated up to 35% cell killing. The approach, however, is based in part on the sensitivity of tumor cells to the effects of complement. Tumors expressing complement resistance factors such as membrane cofactor (CD46), decay accelerating factor (CD55) and protectin (CD59) have been shown to be more resistant to complement lysis. Anchored to the membrane by a glycosylphosphotidylinositol moiety (GPI-anchored), CD55 and CD59 can be cleaved by Bacillus thuringiensis phosphatidylinositol-specific phospholipase C (PIPLC). The PIPLC

[alpha](1,3)galactosyltransferase mediated gene therapy for cancer: developing new models and improving on existing ones