Abstract

Abstract Due to the importance and incidence of prostatic carcinoma in man, some animals are being used as a model in the investigation of the pathogenesis and development of this lesion. Similarly to men, the dog presents a spontaneous development of prostate cancer, which is locally invasive and can develop bone metastasis. Proliferative inflammatory atrophy (PIA) is considered a pre-neoplastic lesion in men. Overexpression of COX-2 has been associated with PIA, PIN and prostatic carcinoma playing a role in angiogenesis, apoptosis inhibition, increasing of invasive capacity, metastasis and inflammation in different prostatic affections. The aim of this study was to assess the protein and gene expression of COX-2 in laser capture microdissected stroma and epithelial cells of PIA foci in canine prostate by immunohistochemistry (IHC) and qRT-PCR. For IHC, 38 PIA lesions arranged in a tissue microarray were evaluated. Frozen fragments from 17 PIA and 3 normal prostatic tissues were used for COX2 gene expression. Our results showed increased COX2 gene expression in stromal cells compared to epithelial cells. High level of COX-2 protein expression was observed in 87% of PIA lesions, despite epithelial or stromal compartment. The In the present study, the stroma presented an important role, since the COX-2 gene expression in canine PIA lesions was increased in this cell compartment. To the best of our knowledge, this is the first report of COX2 gene expression in canine PIA. Since high levels of COX-2 have been associated to the risk of developing of prostate cancer in man, dog can be used as a natural model for this disease. The stroma can act as paracrine way in the epithelial cells, stimulating epithelial proliferation, reducing the apoptosis of this compartment and promoting angiogenesis in the microenvironment, factor that contribute to prostatic carcinogenesis and that the protein expression is increased in this lesion. Sponcer: Fapesp (Fundação de Apoio a Pesqusia do Estado de São Paulo) Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2406. doi:10.1158/1538-7445.AM2011-2406

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