Overexpression of Cyclooxygenase-2 (COX-2) in transgenic mice leads to mammary tumorigenesis. The study used the murine mammary tumor virus (MMTV) promoter to drive human COX-2 expression in mammary glands. Transgenic mice showed increased COX-2 expression during pregnancy and lactation, leading to precocious mammary gland differentiation, hyperplasia, dysplasia, and metastatic tumors. Cox-2 overexpression reduced apoptosis in mammary epithelial cells, contributing to tumorigenesis. Tumor tissues had reduced levels of pro-apoptotic proteins Bax and Bcl-XL and increased levels of anti-apoptotic protein Bcl-2. These findings indicate that COX-2 overexpression is sufficient to induce mammary tumorigenesis. The study also shows that COX-2 is involved in prostanoid synthesis, which may contribute to mammary gland development and involution. The results suggest that COX-2 inhibition could be a chemopreventive strategy for carcinogenesis. The study highlights the role of COX-2 in tumorigenesis and provides a model to investigate its mechanisms. The findings support the idea that dysregulated COX-2 expression is a significant risk factor for breast cancer.Overexpression of Cyclooxygenase-2 (COX-2) in transgenic mice leads to mammary tumorigenesis. The study used the murine mammary tumor virus (MMTV) promoter to drive human COX-2 expression in mammary glands. Transgenic mice showed increased COX-2 expression during pregnancy and lactation, leading to precocious mammary gland differentiation, hyperplasia, dysplasia, and metastatic tumors. Cox-2 overexpression reduced apoptosis in mammary epithelial cells, contributing to tumorigenesis. Tumor tissues had reduced levels of pro-apoptotic proteins Bax and Bcl-XL and increased levels of anti-apoptotic protein Bcl-2. These findings indicate that COX-2 overexpression is sufficient to induce mammary tumorigenesis. The study also shows that COX-2 is involved in prostanoid synthesis, which may contribute to mammary gland development and involution. The results suggest that COX-2 inhibition could be a chemopreventive strategy for carcinogenesis. The study highlights the role of COX-2 in tumorigenesis and provides a model to investigate its mechanisms. The findings support the idea that dysregulated COX-2 expression is a significant risk factor for breast cancer.