Abstract
Low levels of gene expression following systemic delivery have impaired the effectiveness of tumor suppressor gene replacement in treating metastases. We asked whether combined treatment with 2-methoxyestradiol (2-Me), which increases levels of wild-type p53 protein in cancer cells, and the systemic administration of an adenoviral vector expressing wild-type p53 (Ad-p53) would inhibit the growth of human metastatic lung cancer cells in vivo. The simultaneous administration of p53 and 2-Me resulted in a greater than additive reduction with the lung colony count reduced to 33% of its control value. These results suggest that the synergistic effect of 2-Me and Ad-p53 in combination treatment may have application in the systemic treatment of cancer.
Footnotes
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↵1 Partially supported by a Specialized Program of Research Excellence (SPORE) in Lung Cancer, NIH Grant P50-CA70907 (to J. A. R.); a Development Grant from National Cancer Institute for The University of Texas M. D. Anderson Cancer Center SPORE in Lung Cancer (to T. M.); gifts from Tenneco and Exxon for the Core Laboratory Facility (to the Division of Surgery and Anesthesiology); the University of Texas M. D. Anderson Cancer Center Support Core Grant CA16672 from National Cancer Institute; a grant from the Mathers Foundation; and a sponsored research agreement with Introgen Therapeutics, Inc. (Houston, Texas).
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↵2 To whom requests for reprints should be addressed, at Department of Thoracic and Cardiovascular Surgery, The University of Texas A. D. Anderson Cancer Center, Box 109, 1515 Holcombe Boulevard, Houston, TX 77030. Phone: (713) 792-6932; Fax: (713) 794-4901.
- Received June 3, 1998.
- Accepted September 17, 1998.
- ©1998 American Association for Cancer Research.
Volume 58, Issue 21
