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Combination therapy with IL-2 and wild-type p53 expressed by Ad-vectors induces tumor regression in vivo without cytokine related toxicity.
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Transformation-defective E1A-products of the Ad12-non-oncogenic host range mutant CS-1 are able to disrupt E2F-containing complexes and to transactivate E2F-motif containing promoters.
Interleukin-12 and B7-1 costimulatory molecule expressed by an adenovirus vector act synergistically to facilitate tumor regression.