[448] Epidermal Hyperplasia: A Role for Growth Factor Ligand and Receptor Mediated Induction?
BC Dickson, KG Danielson, MA Young, JS Brooks. Pennsylvania Hospital, Philadelphia, PA
Background: Epidermal hyperplasia (EH) is a benign process characterized by increased thickness of squamous epithelium in a number of clinical entities, including dermatofibroma (DF). Our hypothesis was that one or more growth factor ligands and receptors may be expressed in neoplasms with and without EH.
Design: We tested 15 cases of DF, comparing them to 5 cases of dermatofibrosarcoma protuberans (DFSP). Immunohistochemistry (IHC) was performed on FFPE sections using a panel of antibodies for various markers, including: FGF-2 (1:400; sc-79; Santa Cruz, CA), FGF-3 (1:10; sc-80034; Santa Cruz) and IGF-1 (1:10; sc-9013; Santa Cruz); Bek (1:100; sc-122; Santa Cruz), FGFR-3 (1:100; sc-123; Santa Cruz) and IGFR-1 (1:100; sc-81167; Santa Cruz). Cytoplasmic staining was quantified based on the percentage of cells showing immunoreactivity (0-5) for the epidermis (E), neoplasm (N) and dermal fibroblasts (F).
Results: IHC for each of the markers revealed appreciable intra- and inter- group differences in staining. From the summarized scores no consistent relationship with overexpression emerged (Table). Analysis of variance (ANOVA) comparing DF with DFSP demonstrated significantly greater IGFR-1 expression within the epidermis (P<0.005), neoplasm (P<0.005) and dermal fibroblasts (P<0.05) of DF compared to DFSP. There was significantly greater IGF-1 expression within the epidermis of DF compared to DFSP (P<0.05). Finally, there was significantly more FGF-3 produced within the neoplastic cells of DF compared to DFSP (P<0.05).
| Lesion | Location | FGF-2 | FGF-3 | IGF-1 | BEK | FGFR-3 | IGFR-1 |
| DF | E | 2.2 | 3.4 | 4.4 | 1.2 | 1.8 | 2.0 |
| N | 3.4 | 4.0 | 3.9 | 2.1 | 1.4 | 1.8 | |
| F | 3.8 | 3.2 | 3.8 | 2.1 | 2.0 | 2.0 | |
| DFSP | E | 2.3 | 3.3 | 3.3 | 1.3 | 2.0 | 1.3 |
| N | 3.8 | 3.0 | 3.8 | 1.8 | 1.2 | 1.2 | |
| F | 3.8 | 2.3 | 3.3 | 1.8 | 2.0 | 1.5 |
Conclusions: Our analysis of several common growth factors and receptors failed to identify a definitive mechanism responsible for EH in DF. Nevertheless, there is greater IGFR-1 expression in the epidermis, neoplastic cells and fibroblasts of DF compared to DFSP. Why IGF-1 expression is greater in the epidermis is somewhat counterintuitive, but may suggest a possible contribution to EH. It is interesting that statistical significance was also achieved with FGF-3 expression in the neoplastic cells of DF; however, its receptor is not increased in the epidermis, making the relevance of this observation unclear. Thus, EH is likely the result of a complex and interdependant epidermis
neoplasm relationship.Category: Dermatopathology
Tuesday, March 10, 2009 1:00 PM
Poster Session IV # 75, Tuesday Afternoon