Cambridge Journals Online

Review Article

Pathogenesis of infantile haemangioma: new molecular and cellular insights

Matthew R. Rittera1, Ross A. Butscheka1, Martin Friedlandera1 and Sheila F. Friedlandera1a2 c1 a1 The Scripps Research Institute, Department of Cell Biology, La Jolla, CA, USA. a2 Departments of Pediatrics and Medicine (Dermatology), University of California San Diego, and Department of Pediatric Dermatology, Children's Hospital San Diego, CA, USA.

Article author query ritter mr   butschek ra   friedlander m   friedlander sf

Abstract

Infantile haemangioma is the most common tumour of infancy, yet the origin of these lesions remains controversial and the predictable life cycle is poorly understood. Much new information on infantile haemangiomas has emerged over the past decade, but experts continue to debate fundamental features, including cell of origin, nonrandom distribution, and mechanisms regulating the sometimes explosive growth and slow involution. The development of useful laboratory models has been difficult, in turn restricting the development of treatment options available to the clinician. Despite this, new research and creative thinking has spawned several hypotheses on the origin of these tumours and their interesting clinical behaviour, including suggestions of an intrinsic defect in local endothelial cells, a contribution of circulating endothelial progenitors or haemangioblasts, embolisation of shed placental cells and developmental field defects. While no single hypothesis seems to describe all features of infantile haemangioma, continued research seeks to integrate these ideas, create a better understanding of these important tumours and bring new treatments to the clinic.

Correspondence:

^c1 Corresponding author: Sheila F. Friedlander, UCSD Division of Pediatric Dermatology, Rady Children's Hospital San Diego, 8010 Frost Street, Suite 602, San Diego, CA 92123, USA. Tel: +1 858 966 6795; Fax: +1 858 576 9260; E-mail: sfriedlander@rchsd.org