¹Division of Dermatopathology, Department of Pathology and Laboratory Medicine, Albany Medical College, Albany, New York

Correspondence: J. Andrew Carlson, M.D., Department of Pathology and Laboratory Medicine, Albany Medical College, MC-81, 47 New Scotland Avenue, Albany, NY 12208; e-mail: carlsoa@mail.amc.edu; fax: 518-252-6251.

Accepted 27 September 1999.

Abstract

Oncostatin M (OSM) is a 28-kDa glycoprotein, produced by stimulated macrophages and T lymphocytes, that inhibits the proliferation and induces differentiation of a number of different cell lines derived from solid tumors. To determine whether keratoacanthoma (KA) is unique or a variant of squamous cell carcinoma (SCC), we compared the immunohistochemical expression of OSM in the tumor cells and peri- and intratumoral macrophages of 21 mature KAs, 7 regressing KAs, and 27 SCCs. An inverse correlation was identified between OSM tumor labeling and the density of OSM-labeled tumor-associated macrophages for KAs (r = -.4; P =.09). OSM tumor expression was significantly more frequent and more intense in KAs than in SCCs (95% versus 63%; P <.01). In contrast, the density of OSM-labeled macrophages was significantly higher in SCCs compared with mature KAs (7/3 high power fields versus 4/3 high power fields; P =.02). These OSM-positive macrophages were predominantly located at the advancing, infiltrative margins of both neoplasms. Regressing KAs demonstrated a decreased level of OSM tumor expression compared with mature KAs (53% versus 95%; P =.001), but there was no difference in density of OSM-labeled macrophages. Both the above differences and the overlapping patterns of OSM expression suggest that KAs are a variant of SCC where OSM, possibly as an autocrine factor, may mediate KA's overwhelming but not absolute tendency to involute.