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Non-acute transforming retroviruses like mouse mammary tumor virus (MMTV) cause cancer, at least in part, through integration near cellular genes involved in growth control, thereby de-regulating their expression. It is well-established that MMTV commonly integrates near and activates expression of members of the  Wnt  and  Fgf  pathways in mammary tumors. However, there are a significant number of tumors for which the proviral integration sites have not been identified. Here, we used high through-put screening to identify common integration sites (CISs) in MMTV-induced tumors from C3H/HeN and BALB/c mice. As expected, members of both the  Wnt  and  Fgf  families were identified in this screen. In addition, a number of novel CISs were found, including  Tcf7l2 ,  Antxr1 / Tem8 , and  Arhgap18 . We show here that expression of these three putative oncogenes in normal murine mammary gland cells altered their growth kinetics and caused their morphological transformation when grown in three dimensional cultures. Additionally, expression of  Tcf7l2  and  Antxr1 / Tem8  sensitized cells to exogenous WNT ligand. As  Tcf7l2 ,  Antxr1 / Tem8 , and  Arhgap18  have been associated with human breast and other cancers, these data demonstrate that MMTV-induced insertional mutation remains an important means for identifying genes involved in breast cancer.

Novel Common Integration Sites Targeted by Mouse Mammary Tumor Virus Insertion in Mammary Tumors Have Oncogenic Activity