[Histogenesis of pulmonary sclerosing hemangioma].
OBJECTIVE
To investigate the histogenesis of pulmonary sclerosing hemangioma (PSH).


METHODS
Tissue microarray and immunohistochemical technique were used to detect the expression of pan-cytokeratin, epithelial membrane antigen(EMA), vimentin, thyroid transcription factor (TTF)-1, napsin A, synaptophysin, chromogranin A, CD56, E-cadherin, β-catenin, CD117, CD68 and transforming growth factor(TGF)-β1 in 49 cases of PSH.


RESULTS
Immunohistochemistry revealed that all cuboidal surface cells expressed pan-cytokeratin, EMA, TTF-1 and napsin A. The polygonal cells expressed EMA, TTF-1, napsin A (positive rate 16.3%, 8/49), but not pan-cytokeratin. Both types of cells were negative for synaptophysin, chromogranin A and CD56. Strong positive staining for E-cadherin and β-catenin appeared on the membrane of cuboidal cells in all PSH, with cytoplasm staining for β-catenin as well. The expression levels of these adhesion molecules decreased in the polygonal cells, with the staining localized to the cytoplasm. E-cadherin staining was not detected or was weak. β-catenin staining was not detected on the cell membrane but partially in the cytoplasm. The polygonal cells stained strongly for vimentin, while only a few cuboidal cells were positive. CD117 and CD68 positive inflammatory cells were scattered between the polygonal cells, which was consistent with the distribution of TGF-β1 positive cells.


CONCLUSIONS
PSH originates from the primitive respiratory epithelium, and polygonal stromal cells may be derived from epithelial-mesenchymal transformation of the cuboidal cells. TGF-β1 may play an important role in the formation of sclerosing hemangioma.
Department of Pathology, Peking University School of Oncology, Beijing Cancer Hospital & Institute, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Beijing 100142, China.
Yu
Y
Sun
Li-xin
LX
Zhou
Min
M
Zhao
Xiang-hong
XH
Li
D000293:Adolescent; D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D016282:Aspartic Acid Endopeptidases / Q000378:metabolism; D015820:Cadherins / Q000378:metabolism; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007633:Keratins / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D018396:Mucin-1 / Q000378:metabolism; D009687:Nuclear Proteins / Q000378:metabolism; D011013:Pneumonectomy; D019009:Proto-Oncogene Proteins c-kit / Q000378:metabolism; D047868:Pulmonary Sclerosing Hemangioma / Q000378:metabolism / Q000473:pathology* / Q000601:surgery; D000074482:Thyroid Nuclear Factor 1; D014157:Transcription Factors / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000378:metabolism*; D014746:Vimentin / Q000378:metabolism; D055815:Young Adult; D051176:beta Catenin / Q000378:metabolism; D000097382:CD68 Molecule
D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D016282:Aspartic Acid Endopeptidases; D015820:Cadherins; D007633:Keratins; D018396:Mucin-1; D009687:Nuclear Proteins; D019009:Proto-Oncogene Proteins c-kit; D000074482:Thyroid Nuclear Factor 1; D014157:Transcription Factors; D053773:Transforming Growth Factor beta1; D014746:Vimentin; D051176:beta Catenin; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C513384:CDH1 protein, human; C495270:CTNNB1 protein, human; C000614412:NKX2-1 protein, human; C508960:TGFB1 protein, human; C498549:NAPSA protein, human