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In dogs with MMTs, level of MMP-9 expression by stromal cells was related to factors of poor prognosis and shorter overall survival times and disease-free intervals. These results suggested that MMP-9 produced by tumor-adjacent stromal cells contributed to MMT progression in female dogs and that assessment of MMP-9 expression may be a valuable prognostic factor.

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Placental cadherin (P-cadherin) is a classical cadherin [1] expressed by myoepithelial cells of the human mammary gland [2,3]. Changes to P-cadherin expression have been observed and implicated in human breast carcinogenesis [4][5][6]. Feline mammary tumours show similarities with the women tumours concerning many histological characteristics and clinical evolution, being proposed as good animal model to study mammary carcinogenesis [7].To study P-cadherin expression in feline mammary gland an immunohistochemistry assay was performed in 61 samples of normal (n = 4), hyperplastic (n = 12), benign (n = 6) and malignant (n = 39) feline mammary tissues and the immunostaining assessment was based on the estimated percentage of luminal epithelial cells labeling (aberrant expression).In normal mammary gland, mammary hyperplasia and benign tumours, P-cadherin immunolabelling was restricted to myoepithelial cells. Nevertheless, in malignant tumours there was an aberrant epithelial Pcadherin immunoexpression in 64,1% (n = 25) of the cases, with a membranar and/or cytoplasmic pattern of cellular distribution. Consequently, P-cadherin expression in feline mammary lesions was not exclusive of myoepithelial cells.It was possible to observe a significant statistical correlation between P-cadherin expression intensity and feline mammary lesions (p = 0.0001). In malignant mammary tumors a statistical correlation between P-cadherin immunoexpression intensity and histological grade was observed (p = 0.0132). Aberrant epithelial P-cadherin expression seems to be correlated with tumor malignancy in feline mammary gland.

Background: Experimental studies have shown that cyclo-oxygenase-2 (Cox2) is related to the development and progression of tumors, since this enzyme is induced and expressed by cells such as macrophages, osteoblasts, "activated" endothelial cells, and tumor cells. The activity in tumors includes proliferation, cell transformation, tumor growth, invasion and metastasis and may play an important role in carcinogenesis of the canine osteosarcoma, since it has high expression in tissue fragments. The combination of selective Cox2 inhibitors and other treatment modalities is the basis for a new anti-cancer therapy strategy. This in vitro study exposed primary cells of five different canine osteosarcoma cultures to selective Cox2 inhibitor at increasing concentrations and times. Results: For Cox2 negative cultures, despite the absence of differences, greater sensitivity of cells to treatment was observed. For Cox2 positive cultures, a higher number of necrotic cells were observed (P ≤ 0.05), when compared with negative cultures. For exposure times with Celecoxib doses, no difference (P > 0.05) was found between the three times analyzed for living, apoptotic and apoptotic/necrotic cells. There are similarities in the values of 24 h and 48 h, with slight reduction of living cells, increasing those undergoing apoptosis and apoptosis/necrosis. There was significance for necrosis (P ≤ 0.05). In 72 hours, a significant difference was observed between the other two previous values (P ≤ 0.05). It was found for the group of 100 µM·L −1, that there was a numerically greater signaling for apoptosis and lower (P = 0.08) for necrosis, and this point was the onset of the pharmacodynamic phenomenon, with drop in the values for living cells and increased number of necrotic cells, with a tendency (P = 0.08) for reducing the percentage of necrotic cells for the group of 100 µM·L