Antiangiogenic therapy of experimental cancer does not induce acquired drug resistance View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1997-11

AUTHORS

Thomas Boehm, Judah Folkman, Timothy Browder, Michael S. O'Reilly

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 States, 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 cells. In contrast, endothelial cells are genetically stable, homogeneous 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. Endostatin, 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. More... »

PAGES

404-407

Journal

TITLE

Nature

ISSUE

6658

VOLUME

390

Author Affiliations

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/37126

    DOI

    http://dx.doi.org/10.1038/37126

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1038226830

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/9389480


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