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L ‐type amino acid transporter 1 (LAT1) is frequently expressed in thymic carcinomas but is absent in thymomas
Author(s) -
Kaira Kyoichi,
Oriuchi Noboru,
Imai Hisao,
Shimizu Kimihiro,
Yanagitani Noriko,
Sunaga Noriaki,
Hisada Takeshi,
Ishizuka Tamotsu,
Kanai Yoshikatsu,
Endou Hitoshi,
Nakajima Takashi,
Mori Masatomo
Publication year - 2009
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.21277
Subject(s) - immunohistochemistry , thymoma , thymic carcinoma , pathology , medicine , carcinoma , microvessel
Background L ‐type amino acid transporter 1 (LAT1) has been associated with tumor growth and is highly expressed in the primary human neoplasms. We investigated the significance of LAT1 expression to evaluate malignant potential in thymic epithelial tumors. Materials and Methods Immunohistochemical studies of 45 surgically resected thymic epithelial tumors [15 noninvasive thymomas (NT), 22 invasive thymomas (IT), and 8 thymic carcinomas (TC)] were conducted. LAT1, Ki‐67 labeling index (LI), vascular endothelial growth factor (VEGF), and microvessel density of the thymic epithelial tumors were analyzed. Results LAT1 expression for thymomas and thymic carcinomas were 0 (0%) of 37 and 6 (75%) of eight patients, respectively. Ki‐67 LI for NT, IT, and TC were 7.9 ± 2.8%, 16.1 ± 8.5%, and 50.6 ± 24.4%, respectively. VEGF expression in groups NT, IT, and TC was 0 (0%) of 15, 9 (41%) of 22, and 6 (75%) of eight patients, respectively. VEGF expression was statistically associated with microvessel count. The LAT1 expression was statistically associated with Ki‐67 LI, VEGF, and microvessel density in thymic carcinomas. Conclusion LAT1 is frequently expressed in thymic carcinomas but is absent in thymomas. Our results suggest that LAT1 expression might be an immunohistochemical marker for carcinomas, and could distinguish between thymomas and thymic carcinomas. J. Surg. Oncol. 2009;99:433–438. © 2009 Wiley‐Liss, Inc.