May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
COX–2 Immunohistochemical Expression in Uveal Melanoma Animal Model
Author Affiliations & Notes
  • A.S. Sabrosa
    Ophthalmology, The Henry C. Witelson Ocular Pathology Laboratory, McGill University, Montreal, PQ, Canada
  • A.N. Odashiro
    Ophthalmology, The Henry C. Witelson Ocular Pathology Laboratory, McGill University, Montreal, PQ, Canada
  • A.B. Coutinho
    Ophthalmology, The Henry C. Witelson Ocular Pathology Laboratory, McGill University, Montreal, PQ, Canada
  • P.L. Blanco
    Ophthalmology, The Henry C. Witelson Ocular Pathology Laboratory, McGill University, Montreal, PQ, Canada
  • J.V. Burnier
    Ophthalmology, The Henry C. Witelson Ocular Pathology Laboratory, McGill University, Montreal, PQ, Canada
  • M.N. Burnier, Jr
    Ophthalmology, The Henry C. Witelson Ocular Pathology Laboratory, McGill University, Montreal, PQ, Canada
  • Footnotes
    Commercial Relationships  A.S. Sabrosa, None; A.N. Odashiro, None; A.B. Coutinho, None; P.L. Blanco, None; J.V. Burnier, None; M.N. Burnier, Jr., None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 3404. doi:
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      A.S. Sabrosa, A.N. Odashiro, A.B. Coutinho, P.L. Blanco, J.V. Burnier, M.N. Burnier, Jr; COX–2 Immunohistochemical Expression in Uveal Melanoma Animal Model . Invest. Ophthalmol. Vis. Sci. 2005;46(13):3404.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: Cyclooxygenase–2 (COX–2) is an enzyme responsible for the conversion of arachidonic acid to a variety of prostaglandins. Its expression occurs in 60 to 80% of human gastric cancers and is associated with poor prognosis in these tumors. COX–2 is involved in the process of invasion, growth and apoptosis in colorectal carcinoma. Recent studies have shown that COX–2 was expressed in 58% of uveal melanoma (UM) cases. In these studies COX–2 correlated with markers of poor prognosis such as the epithelioid cell type, presence of lymphocytic infiltration, vascular closed loops and cytomorphometry. The aim of this study is to determine COX–2 expression in an animal model of UM in both the intraocular tumor and the metastatic lesions. Methods: The UM animal model was performed as previously reported by The Henry C. Witelson Ocular Pathology Laboratory. Following the previously reported UM rabbit model, paraffin–embedded, formalin–fixed sections from 17 rabbits including primary ocular and metastatic lung tumors were retrieved. Immunostaining for COX–2 was performed using a standard avidin–biotin–peroxidase complex technique. Two pathologists analyzed all of the slides and the cases were classified as positive (low and high) or negative for COX–2 expression. Results: Of the 17 specimens of intraocular tumor, 88% (n=15) stained positively for COX–2, 20% of these (n= 3) had low positivity and 80% (n= 11) expressed high positivity. Lymphocytic infiltration was present in 1 of the negative intraocular specimens, 2 of the low positivity specimens and 7 of the high positivity specimens. Necrosis was present 2 of the negative cases, 3 of the low positivity cases, and 6 of the high positivity specimens. There was no statistically significant correlation between necrosis, lymphocytic infiltration and COX–2 expression. 82% (n=14) of the lung metastases were found to express COX–2. None of these cases were COX–2 negative in the intraocular and lung specimens. Conclusions: In this uveal melanoma animal model, COX–2 expression was found in most of the intraocular tumors and in a high proportion of lung metastases. These results suggest that COX–2 expression is preserved, at a high rate, during tumor progression from intraocular tumor to metastases. These results emphasize the need for further investigation regarding the possible use of COX–2 inhibitors as an adjuvant therapy option for patients with uveal melanoma.

Keywords: tumors • melanoma • immunohistochemistry 
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