Comparison of Oncostatin M Expression in Keratoacanthoma and Squamous Cell Carcinoma

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 OSMlabeled 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.

Oncostatin-M Expression in Oral Squamous Cell Carcinoma.

“…Comparable results were observed by Tran et al, they explained this indirectly proportional relationship by the possibility of presence of negative feedback mechanism between the tumor cells and the surrounding infiltrative macrophages (22). Inefficient OSM protein expression in neoplastic cells was also explained by Radtke et al who suggested the presence of abnormalities in various stages of OSMRβ production and activation (17) , furthermore, Lacreusetteet al, 2007 in their study on melanoma, identified epigenetic modifications in the OSMRβ promoter as histone deacetylation (14) .…”

“…, in OSCC (22) , in prostate carcinoma (19) , in breast cancer (7), in esophageal SCC (12) and lastly in OSCC Chuerduangphui et al suggested that keratinocyte growth factor can stimulate OSM expression in tumor cells (2) .…”

Effect of human papillomavirus 16 oncoproteins on oncostatin M upregulation in oral squamous cell carcinoma

“…Tran et al suggested that OSM overexpression in tumor cells was found in keratoacanthoma (a low-grade tumor) and in dermal squamous cell carcinoma, relative to normal tonsillar controls [18]. By contrast, Ryan et al could not demonstrate OSM expression in colon cancer cells, but strong expression in tumorinfiltrating neutrophils, indicating that these neutrophils were the main source of OSM secreted in this cancer [8].…”

VCAM (CD-106) and ICAM (CD-54) Adhesion Molecules Distinguish Keratoacanthomas from Cutaneous Squamous Cell Carcinomas

“…Although the biologic behavior of keratoacanthoma is usually characterized by rapidly growing neoplasia, with regression in several months, there are cases of metastases (3). This has led to the controversy over whether keratoacanthoma are a distinct entity or a variant of cutaneous squamous cell carcinoma (16,17). In this study we have looked at two adhesion molecules in an attempt to explain the biologic behavior and pathogenesis of keratoacanthoma.…”