Cytoplasmic overexpression of β-catenin was observed in the majority of the cases of SbCC of eyelid, and this correlated significantly with tumour size. The authors therefore hypothesise that β-catenin overexpression in SbCC of eyelid may be a result of Wnt/β-catenin pathway dysregulation. However, its role both in the development of sebaceous cell carcinoma of the eyelid as well as its prognosis needs to be explored further.

Epigenetic inactivation of the E-cadherin gene causes loss of membrane-bound E-cadherin and could contribute to the reduced disease-free survival in eyelid sebaceous gland carcinoma. Mutations in the β-catenin gene do not seem to be involved in the pathogenesis of eyelid sebaceous gland carcinoma.

812 Research letter forms of LEF1 mRNA. This mutation may be involved in the pathogenesis of eyelid SGC by causing dysregulation of Wnt/bcatenin signalling in eyelid sebaceous carcinoma. Our data add to the existing body of literature implicating an altered b-catenin signalling pathway playing a major role in SGC progression.

No abstract