Management of uveal melanomas: cycloxygenase-2 as a potential molecular target
KeywordsMelanoma Melanoma Cell Celecoxib Retinoblastoma Inhibit Tumor Growth
To The Editor
In a recent issue of International Ophthalmology, Ozdal et al.  wrote about cyclooxygenase-2 expression in human irradiated uveal melanomas. They reported that radiotherapy may actually decrease cycloxygenase-2 expression in uveal melanomas. This is of great clinical significance as almost 90 % of all uveal melanomas are immunoreactive for cycloxygenase-2 . In fact, increased cycloxygenase-2 expression by uveal melanomas is associated with a worse prognosis.
Cycloxygenase-2 inhibitors such as celecoxib have already been shown to inhibit tumor growth in cutaneous melanomas and cycloxygenase-2 may very well be an ideal target molecule to inhibit carcinogenesis in uveal melanomas . For instance, Marshall et al.  have recently demonstrated the effectiveness of a topical cycloxygenase inhibitor nepafenac in delaying tumor progression in animal models. Fernandes et al.  have also shown that amfenac (the active metabolite of nepafenac) increases the sensitivity of the tumor cells to radiotherapy. In fact, radiotherapy may very well have a synergistic effect with amfenac in inhibiting uveal melanoma cells. Interestingly, Souza et al.  have also reported increased cycloxygenase-2 expression in retinoblastomas.
Clearly, cycloxygenase-2 has a major role to play in the evolution and progression of ocular tumors. Given the massive potential that anti-cycloxygenase therapies such as nepafenac and radiotherapy have in the management of uveal melanomas, there is a clear and urgent need for further human studies to fully explore their potency and effectiveness in the management of these tumors.