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understood, histopathologic and cell surface marker studies have improved our
understanding of this entity. Genetic factors have been investigated, with twin
studies suggesting that heredity does not play a large role. This is consistent
with observations that IH usually occur sporadically. Others, however, have
speculated a genetic contribution as evidenced by a doubling of risk if present in
a family member,17 while the racial predilection in Caucasians compared to
non-whites also suggests some genetic component.
Examination of molecular markers expressed by in vivo IH cells, cultured
IH endothelial cells (HemEC), and hemangioma-derived stem cells (HemSC)
have shed considerable light on possible mechanisms. Both angiogenesis (i.e.,
proliferation or migration from preexisting vessels) and vasculogenesis (i.e., de
novo formation of vessels from progenitor cells) have been implicated in the
pathogenesis of IH. In vivo IH cells express endothelial cell and immature
vascular markers.18 Further study of expression patterns of cultured IH
endothelial cells (HemEC) have discovered upregulated glucose transporter
protein type-1 (GLUT-1), vascular endothelial growth factor (VEGF), basic
fibroblast growth factor (bFGF), among others, with downregulation of other
markers, such as CD146.2,17 GLUT-1 is a particularly useful cell surface
marker in the diagnosis of these lesions as they are found exclusively in IH.19
This research on HemEC expression patterns suggests a clonal proliferation of