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International Ophthalmology

, Volume 32, Issue 4, pp 305–305 | Cite as

Management of uveal melanomas: cycloxygenase-2 as a potential molecular target

  • Shailendra Kapoor
Letter to the Editor
  • 376 Downloads

Keywords

Melanoma Melanoma Cell Celecoxib Retinoblastoma Inhibit Tumor Growth 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

To The Editor

In a recent issue of International Ophthalmology, Ozdal et al. [1] 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 [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 [3]. For instance, Marshall et al. [4] have recently demonstrated the effectiveness of a topical cycloxygenase inhibitor nepafenac in delaying tumor progression in animal models. Fernandes et al. [5] 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. [6] 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.

References

  1. 1.
    Ozdal PC, Callejo S, Caissie AL, Edelstein C, Bakalian S, Vianna RN et al (2008) Cyclooxygenase-2 expression in human irradiated uveal melanomas. Int Ophthalmol 28:1–6PubMedCrossRefGoogle Scholar
  2. 2.
    Cryan LM, Paraoan L, Hiscott P, Damato BE, Grierson I, Gray D et al (2008) Expression of COX-2 and prognostic outcome in uveal melanoma. Curr Eye Res 33:177–184PubMedCrossRefGoogle Scholar
  3. 3.
    Wilson KS (2006) Clinical activity of celecoxib in metastatic malignant melanoma. Cancer Invest 24:740–746PubMedCrossRefGoogle Scholar
  4. 4.
    Marshall JC, Fernandes BF, Di Cesare S, Maloney SC, Logan PT, Antecka E et al (2007) The use of a cyclooxygenase-2 inhibitor (nepafenac) in an ocular and metastatic animal model of uveal melanoma. Carcinogenesis 28:2053–2058PubMedCrossRefGoogle Scholar
  5. 5.
    Fernandes BF, Marshall JC, Di Cesare S, Logan P, Maloney S, Burnier MN Jr (2008) Amfenac increases the radiosensitivity of uveal melanoma cell lines. Eye 22:701–706PubMedCrossRefGoogle Scholar
  6. 6.
    Souza Filho JP, Martins MC, Correa ZM, Odashiro AN, Antecka E, Coutinho AB et al (2006) The expression of cyclooxygenase 2 in retinoblastoma: primary enucleated eyes and enucleation after conservative treatment. Am J Ophthalmol 142:625–631PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media B.V. 2012

Authors and Affiliations

  1. 1.University of Illinois at ChicagoChicagoUSA

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