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

The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.

Antiangiogenic therapy of experimental cancer does not induce acquired drug resistance

Boehm, Thomas, Folkman, Judah, Browder, Timothy, O'Reilly, Michael S.·1997·Nature
DOI 10.1038/37126
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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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Research works printed but not linked: 3

  1. Li, P. L., Schneider, J. A. & Kantor, A. F. in Cancer Medicine 3rd edn Vol. 1(eds Holland, J. F. et al.) 322–339 (Lea & Febiger, Philadelphia, (1993)).
  2. Morrow, C. S. & Cowan, K. H. in Cancer Medicine 3rd edn. Vol. 1(eds Holland, J. F. et al.) 618–630 (Lea & Febiger, Philadelphia, (1993)).
  3. Brem, H., Goto, F., Budson, A., Saunders, L. & Folkman, J. Minimal drug resistance after prolonged anti-angiogenic therapy with AGM-1470. Surg. Forum XLV, 674–677 (1994).

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Metadata

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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