Immunohistochemistry staining showed that VEGFR-3 remained unchanged between nonrecurrent and recurrent lymphangiomas (<i>p</i> > 0.05), and VEGF-C and Nrp2 were significantly increased in recurrent lymphangioma compared with nonrecurrent lymphangioma (<i>p</i> < 0.05).
Vascular endothelial growth factor (VEGF) and its receptor act as a major contributor to lymphangioma, but their role on nonrecurrent and recurrent lymphangiomas remain unclear.
To extend the molecular basis of the pathogenesis of lymphangioma, we have characterized the expression of vascular endothelial growth factor (VEGF) and VEGF receptors (VEGFR) in 29 cases of lymphangioma by RNA in situ hybridization.
Endothelial cells of lymphangioma co-express transcripts of VEGF-C and its receptors VEGFR-3 (Flt4) and VEGFR-2 (Flk1), which are not detectable in the adjacent connective tissue.
Endothelial cells of lymphangioma co-express transcripts of VEGF-C and its receptors VEGFR-3 (Flt4) and VEGFR-2 (Flk1), which are not detectable in the adjacent connective tissue.
Immunohistochemistry staining showed that VEGFR-3 remained unchanged between nonrecurrent and recurrent lymphangiomas (<i>p</i> > 0.05), and VEGF-C and Nrp2 were significantly increased in recurrent lymphangioma compared with nonrecurrent lymphangioma (<i>p</i> < 0.05).
Although fluid collection might be an alternative explanation for this increase in size, this lymphangioma might harbor a neoplastic nature related to the recently discovered PIK3CA mutation.