Int. J. Dev. Biol. 55: 563 - 567 (2011)
doi: 10.1387/ijdb.103231rh
© UPV/EHU Press

Escape mechanisms after antiangiogenic treatment, or why are the tumors growing again?

Ruslan Hlushchuk1, Andrew N. Makanya1,2 and Valentin Djonov*,1,3

1Department of Medicine, University of Fribourg, Fribourg, Switzerland, 2Department of Vet Anatomy and Physiology, University of Nairobi, Nairobi, Kenya and 3Institute of Anatomy, University of Bern, Bern, Switzerland

ABSTRACT Inhibitors of angiogenesis and radiation induce compensatory changes in the tumor vasculature both during and after cessation of treatment. In numerous preclinical studies, angiogenesis inhibitors were shown to be efficient in the treatment of many pathological conditions, including solid cancers. In most clinical trials, however, this approach turned out to have no significant effect, especially if applied as monotherapy. Recovery of tumors after therapy is a major problem in the management of cancer patients. The mechanisms underlying tumor recovery (or therapy resistance) have not yet been explicitly elucidated. This review deals with the transient switch from sprouting to intussusceptive angiogenesis, which may be an adaptive response of tumor vasculature to cancer therapy that allows the vasculature to maintain its functional properties. Potential candidates for molecular targeting of this angioadaptive mechanism are yet to be elucidated in order to improve the currently poor efficacy of contemporary antiangiogenic therapies.


antiangiogenic therapy, anticancer therapy, protein tyrosine kinase inhibitor, tumor recovery, intussusceptive angiogenesis, escape mechanism

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