Expression Patterns of Markers for Type II Pneumocytes in Pulmonary Sclerosing Hemangiomas and Fetal Lung Tissues

Abstract

Abstract Context.—Although the histogenesis of sclerosing hemangioma is currently not well understood, the tumor has been characterized by its 2 histologically different types of cells, namely, surface and polygonal cells. Objective.—To elucidate the origin of these cells, we analyzed samples from 15 cases of sclerosing hemangioma and 15 specimens of fetal lung tissue. Design.—We immunostained specimens from 15 cases of sclerosing hemangioma and 15 samples of fetal lung tissue using antibodies against thyroid transcription factor 1, MUC1, Thomsen-Friedenreich antigen, and CD44v6, known as markers for type II pneumocytes, and a panel of antibodies against cytokeratin, epithelial membrane antigen, synaptophysin, CD56, estrogen receptor, and progesterone receptor. Results.—In fetal lung tissue, MUC1 and thyroid transcription factor 1 were expressed throughout all developmental stages of airway epithelium, whereas Thomsen-Friedenreich antigen and CD44v6 were expressed by type II pneumocytes of saccular and alveolar origin. Thomsen-Friedenreich antigen was expressed in the bronchial bud of the pseudoglandular stage. MUC1, thyroid transcription factor 1, and epithelial membrane antigen were observed in both surface and polygonal cells of sclerosing hemangioma. Only the surface cells in all cases of sclerosing hemangioma showed positivity for cytokeratin and CD44v6. Thomsen-Friedenreich antigen was expressed in the surface cells of 11 of 15 cases of sclerosing hemangioma. Epithelial membrane antigen was expressed in both types of tumor cells, whereas cytokeratin was not detected on polygonal cells, but was reactive with surface cells. Conclusions.—Our results suggest that the 2 types of cells in sclerosing hemangioma may derive from a common precursor cell through divergent differentiation toward the type II pneumocyte during tumorigenesis.