Napsin A Is Differentially Expressed in Sclerosing Hemangiomas of the Lung

2012 ◽  
Vol 136 (12) ◽  
pp. 1580-1584 ◽  
Author(s):  
Lindsay A. Schmidt ◽  
Jeffrey L. Myers ◽  
Jonathan B. McHugh
Keyword(s):  
Transcription Factor ◽  
Respiratory Epithelium ◽  
Type Ii ◽  
Cell Of Origin ◽  
Ultrastructural Studies ◽  
Thyroid Transcription Factor 1 ◽  
Thyroid Transcription Factor ◽  
Napsin A ◽  
Type Ii Pneumocytes ◽  
Transcription Factor 1

Context.—Sclerosing hemangiomas (SH) are lung tumors characterized by surface cuboidal cells and round stromal cells. The cell of origin remains controversial, though immunohistochemical and ultrastructural studies suggest primitive respiratory epithelium. Napsin A, a human aspartic proteinase found primarily in type II pneumocytes and alveolar macrophages, is emerging as a helpful immunohistochemical marker in characterizing the origin of lung neoplasms, and may be of use in evaluating SH. Objective.—To evaluate napsin A immunohistochemical staining in SH to further characterize the cell of origin. Design.—Six cases of SH were stained for napsin A, as well as thyroid transcription factor 1 and cytokeratin in selected cases. Results.—Surface and round cells were positive for thyroid transcription factor 1 in all cases stained with this marker. Cytokeratins were positive in surface cells in all cases stained with this marker; 2 cases had focal cytokeratin staining in round cells. Round cells had focal napsin A staining in 1 case (17%); surface cells were napsin positive in all cases. Conclusions.—The observation of thyroid transcription factor 1 positivity in both surface and round cells in all SH suggests primitive respiratory epithelium as the cell of origin of SH. Our napsin A findings support this, with positivity in surface cells of all tumors (100%), and focal round cell staining in only 1 (17%). In fact, surface cells may represent entrapped type II pneumocytes, which normally express napsin A in a granular cytoplasmic pattern, similar to surface cells. The coexpression of thyroid transcription factor 1 and napsin A also introduces a caveat in differentiating primary pulmonary adenocarcinomas from SH in small biopsy specimens.

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

2005 ◽  
Vol 129 (7) ◽  
pp. 915-919 ◽  
Author(s):  
Seong Ho Yoo ◽  
Kyeong Cheon Jung ◽  
Joo Hyun Kim ◽  
Sook Whan Sung ◽  
Jin-Haeng Chung ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Lung Tissue ◽  
Epithelial Membrane Antigen ◽  
Fetal Lung ◽  
Type Ii ◽  
Sclerosing Hemangioma ◽  
Thyroid Transcription Factor 1 ◽  
Thyroid Transcription Factor ◽  
Type Ii Pneumocytes ◽  
Transcription Factor 1

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.

Prostatakarzinom imitiert metastasiertes Bronchialkarzinom – Ein Fallbericht

2017 ◽  
Vol 38 (09) ◽  
pp. 586-588
Author(s):  
Konstantinos Drosos ◽  
Klaus Höfner
Keyword(s):  
Transcription Factor ◽  
Thyroid Transcription Factor 1 ◽  
Thyroid Transcription Factor ◽  
Napsin A ◽  
Transcription Factor 1

ZusammenfassungEs wird über den Fall eines PSA-negativen und lokal fortgeschrittenen azinären Prostatakarzinoms berichtet, das bei thyroid transcription factor-1 (TTF-1) Expression eine Metastase eines bereits behandelten Bronchialkarzinoms imitierte. Unseres Wissens ist ein TTF-1 positiv azinäres Prostatakarzinom bisher nur ein Mal in der Literatur dokumentiert. Die Bestimmung des Immunophänotyps des Karzinoms mit Napsin A, CK7 und CK20 in Kombination mit der Beurteilung des gesamten Krankheitsverhaltens waren für die definitive Diagnose eines primären Prostatakarzinoms entscheidend.

Congenital diaphragmatic hernia, tracheal occlusion, thyroid transcription factor-1, and fetal pulmonary epithelial maturation

2005 ◽  
Vol 289 (1) ◽  
pp. L44-L52 ◽  
Author(s):  
Cheryl J. Chapin ◽  
Robert Ertsey ◽  
Jyoji Yoshizawa ◽  
Akihiko Hara ◽  
Lourenco Sbragia ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Dna Content ◽  
Pulmonary Hypoplasia ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii ◽  
Lung Growth ◽  
Thyroid Transcription Factor 1 ◽  
Thyroid Transcription Factor ◽  
Transcription Factor 1

Congenital diaphragmatic hernia (CDH) occurs in ∼1:2,500 human births and has high morbidity and mortality rates, primarily due to pulmonary hypoplasia and pulmonary hypertension. Tracheal occlusion (TO), in experimental animals, distends lungs and increases lung growth and alveolar type I cell maturation but decreases surfactant components and reduces alveolar type II cell density. We examined effects of CDH and CDH+TO on lung growth and maturation in fetal rats. To induce CDH, we administered nitrofen (100 mg) to dams at 9.5 days of gestation. We compared lungs from fetuses with CDH, CDH+TO, and those exposed to nitrofen without CDH. CDH decreased lung wet weight bilaterally ( P < 0.0001) and DNA content in lung ipsilateral to CDH ( P < 0.05). CDH+TO significantly increased lung wet weights bilaterally; DNA content was intermediate between CDH and NC. To evaluate effects on the distal pulmonary epithelium, we examined surfactant mRNA and protein levels, type I and II cell-specific markers (RTI40 and RTII70, respectively), and transcriptional regulator thyroid transcription factor-1 (TTF-1). Decreased lung distension (due to CDH) increased SP-C mRNA and TTF-1 protein expression and reduced RTI40 ( P < 0.05 for all). Increased lung distension (due to CDH+TO) reduced expression of SP mRNAs and pro-SP-C and TTF-1 proteins and enhanced expression of RTI40 (mRNA and protein; P < 0.05 for all). We conclude that CDH+TO partially reverses effects of CDH; it corrects the pulmonary hypoplasia and restores type I cell differentiation but adversely affects SP expression in type II cells. These effects may be mediated through changes in TTF-1 expression.

Tissue-Preserving Antibody Cocktails to Differentiate Primary Squamous Cell Carcinoma, Adenocarcinoma, and Small Cell Carcinoma of Lung

2013 ◽  
Vol 137 (9) ◽  
pp. 1274-1281 ◽  
Author(s):  
Alan F. Brown ◽  
Deepika Sirohi ◽  
Junya Fukuoka ◽  
Philip T. Cagle ◽  
Maria Policarpio-Nicolas ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cell Carcinoma ◽  
Small Cell ◽  
Lung Cancers ◽  
Thyroid Transcription Factor 1 ◽  
Thyroid Transcription Factor ◽  
Napsin A ◽  
Cytokeratin 5 ◽  
Transcription Factor 1 ◽  
Desmoglein 3

Context.—With the availability of cell type–specific therapies, differentiating primary lung squamous cell carcinomas (SCCs) and adenocarcinomas (ACAs) has become important. The limitations of small sample size and the need to conserve tissue for additional molecular studies necessitate the use of sensitive and specific marker panels on a single slide. Objective.—To distinguish SCC from ACA and small cell carcinoma (SmCC) of lung using 2 novel tissue-conserving cocktails. Design.—We compared two antibody cocktails, desmoglein 3 + cytokeratin 5/napsin A and p40/thyroid transcription factor 1 (Biocare Medical, Concord, California) in diagnosing SCC and ACA of the lung on tissue microarray, cytology, and surgical specimens. Both lung and nonlung tissue were evaluated on an 1150-core tissue microarray that contained 200 lung cancers. A microarray of 35 SmCCs and 5 small cell SCCs was also evaluated. Results.—A cocktail of desmoglein 3 + cytokeratin 5/napsin A provided diagnostic accuracy in lung cancers with a sensitivity and specificity of 100% in SCCs and a sensitivity of 86% and a specificity of 100% in ACAs. A p40/thyroid transcription factor 1 cocktail showed p40 to have a specificity of 92% and a sensitivity of 93% in SCCs, whereas thyroid transcription factor 1 had a specificity of 100% and a sensitivity of 77% in ACAs. Cell blocks of fine-needle aspiration cytology compared with corresponding surgical (n = 20) specimens displayed similar findings. The p40 was useful in differentiating bladder from prostate carcinoma with 88% sensitivity. Isolated carcinomas from nonlung tissues were desmoglein 3 + cytokeratin 5 positive. Napsin A was positive in 22% of renal tumors as previously observed. Both cocktails were excellent in differentiating SmCCs and small cell SCCs because none of the SmCCs stained with p40. Conclusions.—Both antibody cocktails are excellent in differentiating primary lung ACA from SCC, as well as excluding SmCC and ACAs from all other sites on small specimens. A cocktail of desmoglein 3 + cytokeratin 5/napsin A is slightly superior compared with p40/thyroid transcription factor 1 cocktail.

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