[1896] Napsin A Expression in Neuroendocrine Tumors of the Lung

Philippe Joubert, Hangjun Wang, Mee Sook Roh, Maria C Pietanza, Inderpal Sarkaria, William D Travis, Natasha Rekhtman. Memorial Sloan-Kettering Cancer Center, New York, NY; College of Medicine, Dong-A University, Busan, Korea

Background: Napsin A is an aspartic proteinase involved in surfactant protein maturation, which is normally produced by type 2 pneumocytes. Recently, Napsin A has emerged as a useful supplement to TTF-1 as a marker of lung adenocarcinomas. A comparative study of Napsin A and TTF-1 expression in a large series of lung neuroendocrine tumors has not been performed.
Design: A total of 297 lung neuroendocrine tumors, including typical carcinoids (TC) n=89, atypical carcinoids (AC) n=89, small cell lung carcinomas (SCLC) n=37, and large cell neuroendocrine carcinomas (LCNEC) n=82, were evaluated for Napsin A (rabbit antibody, Ventana) and TTF-1 (8G7G3/1; DAKO) expression by immunohistochemistry on tissue microarray (TMA) sections, containing three representative cores per case. The percentage of positive tumor cells and intensity of staining (1+, 2+, 3+) were recorded.
Results: The staining results are summarized in the table below. Napsin A immunoreactivity was found in none of TCs, ACs, and SCLCs, whereas 8/82 (10%) of LCNECs showed a strong and diffuse labeling. TTF-1 reactivity was seen in 22% TCs, 40% ACs, 70% SCLCs and 46% LCNECs. When positive, TTF-1 labeling was typically strong and diffuse in SCLCs and LCNECs, while usually weak and focal in carcinoid tumors.

Conclusions: To our knowledge, this is the first report of Napsin A expression in a subset of LCNECs. Conversely, all other lung neuroendocrine tumors are consistently Napsin A-negative, which contrasts with the well-known expression of TTF-1 in all types of lung neuroendocrine tumors. Based on these data, we conclude that unlike TTF-1, Napsin A cannot be used as a marker of a lung origin for carcinoid tumors. Furthermore, Napsin A cannot be used to reliably differentiate lung adenocarcinomas from LCNECs, although Napsin A reactivity raises the possibility that a subset of LCNECs has a histogenetic relationship to adenocarcinomas.
Category: Pulmonary

Monday, March 4, 2013 1:00 PM

Poster Session II # 299, Monday Afternoon


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