Antiangiogenic therapy of experimental cancer does not induce acquired drug resistance

Thomas Boehm (), Judah Folkman, Timothy Browder and Michael S. O'Reilly
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Thomas Boehm: Dana Farber Cancer Center
Judah Folkman: Dana Farber Cancer Center
Timothy Browder: Dana Farber Cancer Center
Michael S. O'Reilly: Dana Farber Cancer Center

Nature, 1997, vol. 390, issue 6658, 404-407

Abstract: Abstract Acquired drug resistance is a major problem in the treatment of cancer. Of the more than 500,000 annual deaths from cancer in the United States1, many follow the development of resistance to chemotherapy. The emergence of resistance depends in part on the genetic instability, heterogeneity and high mutational rate of tumour cells2. In contrast, endothelial cells are genetically stable, homogenous and have a low mutational rate. Therefore, antiangiogenic therapy directed against a tumour's endothelial cells should, in principle, induce little or no drug resistance. Endostatin3, a potent angiogenesis inhibitor, was administered to mice bearing Lewis lung carcinoma, T241 fibrosarcoma or B16F10 melanoma. Treatment was stopped when tumours had regressed. Tumours were then allowed to re-grow and endostatin therapy was resumed. After 6, 4 or 2 treatment cycles, respectively, no tumours recurred after discontinuation of therapy. These experiments show that drug resistance does not develop in three tumour types treated with a potent angiogenesis inhibitor. An unexpected finding is that repeated cycles of antiangiogenic therapy are followed by prolonged tumour dormancy without further therapy.

Date: 1997
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DOI: 10.1038/37126

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