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Lumican as a Novel Marker for Differential Diagnosis of Bowen Disease and Actinic Keratosis

Takayama, Ryoko MD*,†,‡; Ishiwata, Toshiyuki MD, PhD†,‡; Ansai, Shin-ichi MD, PhD*; Yamamoto, Tetsushi PhD†,‡; Matsuda, Yoko MD, PhD†,‡; Naito, Zenya MD, PhD†,‡; Kawana, Seiji MD, PhD*

American Journal of Dermatopathology: December 2013 - Volume 35 - Issue 8 - p 827–832
doi: 10.1097/DAD.0b013e31827c7f31
Original Study

Abstract: Lumican, a member of the small leucine-rich proteoglycan family, regulates the assembly and diameter of collagen fibers in the extracellular matrix of various tissues. Lumican expression correlates with pathological conditions, including skin fragility, corneal opacification, and corneal and cardiac wound healing. Lumican is overexpressed in tumor cells, including in the breast, colorectal, neuroendocrine cell, uterine cervical, and pancreatic cancers. Lumican expression also correlates with the growth and metastasis of various malignancies. For example, lumican expression is lower in the dermis of malignant melanoma cases than in early-stage melanomas. However, the expression patterns and roles of lumican in nonmelanoma skin cancer have not been elucidated. In this study, we used immunohistochemistry and in situ hybridization to examine the expression patterns of lumican in normal skin, Bowen disease, and actinic keratosis. In normal skin, lumican was expressed in the collagen fibers in the dermis, acrosyringium, follicular epithelium, and sebocytes but not in epidermal keratinocytes. In Bowen disease, lumican was expressed in 34 (91.8%) of 37 patients. Notably, all cases of actinic keratosis were negative for lumican. These findings suggest that lumican plays an important role in the pathogenesis of Bowen disease and actinic keratosis and might be useful as an adjunct to the diagnosis for subtypes of 2 diseases: bowenoid actinic keratosis and Bowen disease in sun-exposed areas.

*Department of Dermatology;

Department of Pathology; and

Department of Integrative Oncological Pathology, Nippon Medical School, Tokyo, Japan.

Reprints: Zenya Naito, MD, PhD, Departments of Pathology and Integrative Oncological Pathology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan, (e-mail: naito@nms.ac.jp).

Supported by a Grant-in-Aid for Young Scientists from the Japan Society for the Promotion of Science (B. 22790675 to T.Y.).

The authors declare that there are no conflicts of interest.

© 2013 by Lippincott Williams & Wilkins.