( SOUTH SAN FRANCISCO Calif. June 04 ...)Cell Genesys Reports Additional Data From Phase 2 Clinical Trial of,GVAX Immunotherapy for Pancreatic Cancer,Health

SOUTH SAN FRANCISCO, Calif., June 04, 2007 /PRNewswire-FirstCall/ -- Cell Genesys, Inc. today announced follow-up data from a Phase 2 clinical trial of GVAX immunotherapy for pancreatic cancer which was conducted by the Johns Hopkins Sidney Kimmel Cancer Center. The trial enrolled 60 patients with operable pancreatic cancer who received GVAX after surgical resection of their tumor and adjuvant radiation and chemotherapy.

The median overall survival for these patients was previously reported to be 26.8 months, a result which compares favorably to the 17 to 22 months median survival results published from multiple studies in patients undergoing pancreatic cancer surgery and adjuvant therapy. Of note, 53 of the 60 patients were considered high risk, based on the unfavorable finding that their cancer had spread to regional lymph nodes. The new data reported today included a median disease-free survival of approximately 16 months which compares favorably to the 13 months disease-free survival recently reported for gemcitabine adjuvant therapy.

Moreover, a comparison of the median overall survival of 60 patients from this trial with patients at Johns Hopkins with operable pancreatic cancer who underwent surgery and adjuvant therapy without receiving GVAX indicated that the median overall survival of the latter group was approximately 21 months or nearly six months shorter than the patients in the Phase 2 trial. The analysis of survival data further showed that the potential additive benefit of GVAX following surgery and adjuvant therapy was present during the first three years of the study although GVAX dosing did not continue beyond 18 months, suggesting that ongoing booster administrations of GVAX should be evaluated. Immunologic findings showed that there was an association between disease-free survival and treatment-associated antitumor immunity as measured by the induction of T cell responses to the pancreatic cancer-associated antigen, m
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