Increased susceptibility to carcinogen-induced mammary tumors in MMTV-Cdc25B transgenic mice

Cdc25 phosphatases activate cyclin-dependent kinases (Cdks) by dephosphoryl ating critical phospho-tyrosine and phospho-threonine residues on these pro teins. Several types of studies indicate that Cdc25s can enhance cell proli feration and oncogenesis, Furthermore, overexpression of Cdc25A and/or B ha ve been detected in several types of primary human cancers, including breas t cancers. To further assess the oncogenic capacity of Cdc25B in vivo, we h ave generated transgenic mice that overexpress Cdc25B in the mammary epithe lium, driven by the MMTV-LTR promoter. Although these mice are grossly norm al for up to 18 months, the ectopic expression of Cdc25B in their mammary g lands increases the susceptibility of these mice to induction of mammary tu mors by the carcinogen 9,10-dimethyl-1,2-benzanthracene (DMBA).