Nasopharyngeal angiofibroma with intracellular accumulation of SPARC - a hypothesis (SPARC in nasopharyngeal angiofibroma)

Nasopharyngeal angiofibroma is a histologically benign tumor composed of stroma and vessels. The vascular component of the lesion is prone to bleeding and responsible for its clinical "malignancy". Some nasopharyngeal angiofibromas are resistant to surgical therapy because of extensive growth and occasionally bone destruction. It has been shown that molecular factors supporting residual tissue after incomplete surgery might be targeted with pharmacotherapy as a cell based therapy. Because the cell of origin of nasopharyngeal angiofibroma is not recognized yet, it would be of interest to discuss molecule(s) relevant to all the cell components of the growth. Such molecule(s) may also regulate bone homing of the tumor. We propose that in nasopharyngeal angiofibroma the molecule responding to the cues mentioned above is SPARC (secreted protein acidic rich in cystein). We discuss SPARC-enabling formation of molecular complexes important for the angiogenic events and present nasopharyngeal angiofibroma as a hyperplastic angiogenic machinery or a "soil" without "seed". Therapeutic targeting of SPARC in nasopharyngeal angiofibroma would be targeting of a molecule at the roots of cooperation between stromatogenesis and angiogenesis, coexpressed with Ki67 in the vascular compartment. Considering the intracellular accumulation of SPARC, the benefit of (anti) SPARC therapy in nasopharyngeal angiofibroma is yet to be proved. (C) 2007 Elsevier Ltd. All rights reserved.