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Review

Escaping Antiangiogenic Therapy: Strategies Employed by Cancer Cells

by
Mauricio P. Pinto
1,*,
Paula Sotomayor
2,
Gonzalo Carrasco-Avino
3,
Alejandro H. Corvalan
4,5 and
Gareth I. Owen
1,5,6,7,8
1
Department of Physiology, Faculty of Biological Sciences, Pontificia Universidad Católica de Chile, Santiago 8331150, Chile
2
Center for Integrative Medicine and Innovative Science, Facultad de Medicina, Universidad Andrés Bello, Santiago 8370071, Chile
3
Department of Pathology, Faculty of Medicine, Universidad de Chile, Santiago 8380456, Chile
4
Department of Hematology-Oncology, Faculty of Medicine, Pontificia Universidad Católica de Chile, Santiago 8330032, Chile
5
Center UC Investigation in Oncology (CITO), Pontificia Universidad Católica de Chile, Santiago 8330023, Chile
6
Biomedical Research Consortium of Chile, Santiago 8331150, Chile
7
Millennium Institute on Immunology & Immunotherapy, Santiago 8331150, Chile
8
Advanced Center for Chronic Diseases (ACCDiS), Universidad de Chile, Santiago 8380492, Chile
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2016, 17(9), 1489; https://doi.org/10.3390/ijms17091489
Submission received: 10 July 2016 / Revised: 22 August 2016 / Accepted: 30 August 2016 / Published: 6 September 2016
(This article belongs to the Special Issue Vascular Biology and Therapeutics)
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Abstract

Tumor angiogenesis is widely recognized as one of the “hallmarks of cancer”. Consequently, during the last decades the development and testing of commercial angiogenic inhibitors has been a central focus for both basic and clinical cancer research. While antiangiogenic drugs are now incorporated into standard clinical practice, as with all cancer therapies, tumors can eventually become resistant by employing a variety of strategies to receive nutrients and oxygen in the event of therapeutic assault. Herein, we concentrate and review in detail three of the principal mechanisms of antiangiogenic therapy escape: (1) upregulation of compensatory/alternative pathways for angiogenesis; (2) vasculogenic mimicry; and (3) vessel co-option. We suggest that an understanding of how a cancer cell adapts to antiangiogenic therapy may also parallel the mechanisms employed in the bourgeoning tumor and isolated metastatic cells delivering responsible for residual disease. Finally, we speculate on strategies to adapt antiangiogenic therapy for future clinical uses.
Keywords: vasculogenic mimicry; vascular co-option; cancer dormancy; residual disease vasculogenic mimicry; vascular co-option; cancer dormancy; residual disease

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MDPI and ACS Style

Pinto, M.P.; Sotomayor, P.; Carrasco-Avino, G.; Corvalan, A.H.; Owen, G.I. Escaping Antiangiogenic Therapy: Strategies Employed by Cancer Cells. Int. J. Mol. Sci. 2016, 17, 1489. https://doi.org/10.3390/ijms17091489

AMA Style

Pinto MP, Sotomayor P, Carrasco-Avino G, Corvalan AH, Owen GI. Escaping Antiangiogenic Therapy: Strategies Employed by Cancer Cells. International Journal of Molecular Sciences. 2016; 17(9):1489. https://doi.org/10.3390/ijms17091489

Chicago/Turabian Style

Pinto, Mauricio P., Paula Sotomayor, Gonzalo Carrasco-Avino, Alejandro H. Corvalan, and Gareth I. Owen. 2016. "Escaping Antiangiogenic Therapy: Strategies Employed by Cancer Cells" International Journal of Molecular Sciences 17, no. 9: 1489. https://doi.org/10.3390/ijms17091489

APA Style

Pinto, M. P., Sotomayor, P., Carrasco-Avino, G., Corvalan, A. H., & Owen, G. I. (2016). Escaping Antiangiogenic Therapy: Strategies Employed by Cancer Cells. International Journal of Molecular Sciences, 17(9), 1489. https://doi.org/10.3390/ijms17091489

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