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Year : 2017  |  Volume : 22  |  Issue : 1  |  Page : 117

Acquired tumor resistance to antiangiogenic therapy: Mechanisms at a glance

1 Department of Physiology, Applied Physiology Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
2 Department of Pharmacology, Isfahan Pharmaceutical Sciences Research Center, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran
3 Isfahan Cardiovascular Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran

Correspondence Address:
Shaghayegh Haghjooy Javanmard
Department of Physiology, Applied Physiology Research Center, Isfahan University of Medical Sciences, Isfahan
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jrms.JRMS_182_17

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Angiogenesis is critical for oxygen and nutrient delivery to proliferating tumor cells. Therefore, as angiogenesis is required and vital for the tumor growth and metastasis. Antiangiogenic therapy is considered to be beneficial for tumor growth prevention due to starvation of tumor of oxygen and nutrients, but in some cases, the benefits are not permanent. Tyrosine kinase inhibitors and many other agents often target angiogenesis through inhibition of the vascular endothelial growth factor (VEGF) pathway. Although preclinical studies showed satisfactory outcomes in tumor growth inhibition, antiangiogenic therapy in the clinical setting may not be effective.The resistance observed in several tumor types through alternative angiogenic “escape” pathways contributes to restoration of tumor growth and may induce progression, enhancement of invasion, and metastasis. Therefore, activation of major compensatory angiogenic pathways, sustaining tumor angiogenesis during VEGF blockade contributing to the recurrence of tumor growth overcome antiangiogenic strategies. In this review, we summarize the novel mechanisms involved in evasive resistance to antiangiogenic therapies and represent different cancer types which have the ability to adapt to VEGF inhibition achieving resistance to antiangiogenic therapy through these adaptive mechanisms.

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