Cited by 1,683Angiogenesis and VEGF in CancerCancer Cells and MetastasisMathematical Biology Tumor Growth

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Antiangiogenic therapy of experimental cancer does not induce acquired drug resistance

Boehm, Thomas, Folkman, Judah, Browder, Timothy, O'Reilly, Michael S.·1997·Nature

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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.

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Authors: Boehm, T., Folkman, J., Browder, T., & O'Reilly, M. S.
Affiliations: Harvard University (US)
Dana-Farber/Harvard Cancer Center (US)
Corresponding author: Boehm, Thomas
ORCID: Boehm, Thomas
Venue: Nature
Publisher: Springer Science and Business Media LLC
Published: 1997-11
Volume: 390
Issue: 6658
Pages: 404-407
ISSN: 0028-0836 (ISSN-L)
1476-4687
DOI: 10.1038/37126
OpenAlex: W1579297325
Cited by: 1,683
References: 12
Citations by year: 2026: 1 · 2025: 4 · 2024: 11 · 2023: 19 · 2022: 9 · 2021: 19 · 2020: 16 · 2019: 18 · 2018: 15 · 2017: 24 · 2016: 35 · 2015: 25 · 2014: 30 · 2013: 48 · 2012: 47
FWCI: 40.79
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature (publishedVersion)
PubMed (publishedVersion)
RePEc: Research Papers in Economics (submittedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
Physical Sciences › Mathematics › Modeling and Simulation › Mathematical Biology Tumor Growth
Keywords: anti-angiogenic therapy, acquired drug resistance, endostatin, angiogenesis inhibitors, tumor dormancy, Lewis lung carcinoma, B16F10 melanoma, tumor recurrence, endothelial cells, tumor heterogeneity
MeSH terms: Animals, Antineoplastic Agents, Collagen, Cyclophosphamide, Fibrosarcoma, Melanoma, Experimental, Mice, Inbred C57BL, Neoplasm Recurrence, Local, Neoplasm Transplantation, Neoplasms, Experimental, Neovascularization, Pathologic, Peptide Fragments, Carcinoma, Lewis Lung, Drug Resistance, Neoplasm, Endostatins, Mice

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Antiangiogenic therapy of experimental cancer does not induce acquired drug resistance

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