Abstract
Purpose :
Degenerative changes in dermal elastic tissue, and consequent tumor formation, may occur secondary to ultraviolet light damage. Normal skin exposed to UV radiation over-expresses elafin, which binds to elastin-rich elastic fibers. It is believed that a progressive loss of elafin expression could facilitate invasive growth of basal cell carcinoma (BCC), and result in the more infiltrative type of BCC, so called sclerosing or morphea-type. The purpose of this study is to assess if the expression of elafin in BCC of the eyelid is related to the tumor type (morphea-type vs. nodular) and if it could represent a protective system against tumor invasiveness and aggressiveness.
Methods :
Fifty formalin-fixed paraffin-embedded specimens from histopathologically confirmed BCC of the eyelid (25 nodular and 25 morphea-type) were retrieved from the MUHC-McGill University Ocular Pathology & Translational Research Laboratory database. The tumors were sent for routine histo-processing and 5um sections were obtained. Immunohistochemistry was performed using a monoclonal antibody against elafin and a polyclonal antibody against elastin in a Ventana automated system (Tucson, AZ). The intensity of the elafin and elastin staining was scored as 0 (no staining), 1 (mild intensity), and 2 (high intensity). Non-parametric statistical analysis was performed using the Mann-Whitney test (SPSS, IBM).
Results :
In morphea-type tumors elafin was absent in 32% (n=8), mild in 64% (n=16) and high in 4% (n=1) of the cases. In nodular tumors elafin was absent in 20% (n=1), mild in 76% (n=19) and high in 4% (n=5) of the cases. Nodular BCCs showed a significant increased expression of elafin in comparison to morphea-type BCCs (p=0.005), whereas no significant difference was observed for elastin.
Conclusions :
Basal cell carcinomas with infiltrative properties (morphea-type) tend to have lower levels of elafin and no change in elastin, when compared to non-infiltrative tumors (nodular type). Our findings suggest a potential protective effect from elafin. We hypothesize that the elafin–elastin complex may protect elastic fibers from degradation by elastase. Whilst both tumor subtypes show accumulation of damaged elastic fibers, as shown by the elastin stain, it appears that elafin could be an important factor determining tumor aggressiveness.
This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.