Abstract:  Abstract　Objective: To preliminarily investigate the mechanism underlying the occurrence and progression of human pregnancy-associated breast cancer by detecting the effect of pregnancy environment on growth of breast cancer growth in Tientsin Albino 2 ( TA2 ) mice. Methods: A total of 84 TA2 mice with spontaneous breast cancers were collected, and the behavior, histology, and immune phenotypes of the tumors were observed. Breast cancer cells were grafted into the mammary glands of pregnant TA2 mice (n = 20) and virgin mice ( n = 10 ). The growth of tumors during pregnancy was detected, and the tumor size was calculated to construct a tumor growth curve. Peripheral blood was collected from the two groups, and serum estradiol and progestin were tested using electrochemistry. Real-time polymerase chain reaction was used to determine estrogen receptor alpha ( ERα ) and progesterone receptor ( PR ) mRNA expression in the mammary glands and tumors in the pregnant group. Immunohistochemistry was performed to detect the expression of ERα, PR, p53 proliferating cell nuclear antigen ( PCNA ), and cluster of differentiation 31 ( CD31 ) in tumors in the pregnant group and the control. Results: All spontaneous breast cancers in TA2 mice were found during pregnancy or lactation. The tumor in the TA2 mice favors metastasis to the visceral organs, including the lungs, liver, and spleen. These tumors were poorly differentiated and were negative for ER and PR, and positive for p53. Compared with the virgin group, the breast tumor in the pregnancy group grew quickly, and the average tumor weight was higher in the pregnant group than that in the control group ( t = 4.142, 3.173, P = 0.000, and 0.004, respectively ). The serum estradiol and progestin levels in the pregnant mice increased dramatically ( t = -1.568, -8.927, P = 0.168, and 0.000, respectively ), whereas ERα and PR mRNA were significantly less in the tumors of the TA2 mice than in the mammary glands ( t = 12.245 and 10.933; P = 0.000 and 0.001, respectively ). The results of immunohistochemical staining indicated PCNA expression in the tumors of the pregnant group compared with the control group. This implies that the tumors in the pregnant TA2 mice have higher proliferation activity. Moreover, more tumor vessels were observed in the pregnant group than in the virgin group. Conclusion: The spontaneous breast cancer of TA2 mice is similar to the human pregnancy-associated breast cancer. Pregnancy can accelerate the breast cancer growth in the mice; however, the promoting effect of estradiol and progestin on cell proliferation of the TA2 breast cancer might be indirect.