Signaling pathways in the development of infantile hemangiomaReport as inadecuate

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Journal of Hematology and Oncology

, 7:13

First Online: 31 January 2014Received: 05 December 2013Accepted: 28 January 2014DOI: 10.1186-1756-8722-7-13

Cite this article as: Ji, Y., Chen, S., Li, K. et al. J Hematol Oncol 2014 7: 13. doi:10.1186-1756-8722-7-13


Infantile hemangioma IH, which is the most common tumor in infants, is a benign vascular neoplasm resulting from the abnormal proliferation of endothelial cells and pericytes. For nearly a century, researchers have noted that IH exhibits diverse and often dramatic clinical behaviors. On the one hand, most lesions pose no threat or potential for complication and resolve spontaneously without concern in most children with IH. On the other hand, approximately 10% of IHs are destructive, disfiguring and even vision- or life-threatening. Recent studies have provided some insight into the pathogenesis of these vascular tumors, leading to a better understanding of the biological features of IH and, in particular, indicating that during hemangioma neovascularization, two main pathogenic mechanisms prevail, angiogenesis and vasculogenesis. Both mechanisms have been linked to alterations in several important cellular signaling pathways. These pathways are of interest from a therapeutic perspective because targeting them may help to reverse, delay or prevent hemangioma neovascularization. In this review, we explore some of the major pathways implicated in IH, including the VEGF-VEGFR, Notch, β-adrenergic, Tie2-angiopoietins, PI3K-AKT-mTOR, HIF-α-mediated and PDGF-PDGF-R-β pathways. We focus on the role of these pathways in the pathogenesis of IH, how they are altered and the consequences of these abnormalities. In addition, we review the latest preclinical and clinical data on the rationally designed targeted agents that are now being directed against some of these pathways.

KeywordsInfantile hemangioma Neovascularization Angiogenesis Vasculogenesis Electronic supplementary materialThe online version of this article doi:10.1186-1756-8722-7-13 contains supplementary material, which is available to authorized users.

Yi Ji, Siyuan Chen contributed equally to this work.

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Author: Yi Ji - Siyuan Chen - Kai Li - Li Li - Chang Xu - Bo Xiang


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