The current model for murine mammary tumorigenesis indicates that discrete, morphologically identifiable preneoplastic lesions precede and give rise to mammary tumors. The hyperplastic alveolar nodule is the primary lesion that precedes and gives rise to mammary tumors in mice infected with the mammary tumor virus (Bittner) or its variants. In mice fed 7,12-dimethylbenzanthracene or urethan, hyperplastic alveolar nodules are present but infrequent, and the major mammary dysplasias present are ductal hyperplasias. The ductal hyperplasias can be divided into four general morphological types: (a) simple terminal duct hyperplasia; (b) lobular hyperplasia; (c) papillary hyperplasia; (d) end-bud hyperplasia. All types of ductal hyperplasias are characterized by intraductal epithelial hyperplasia and have been shown to give rise to mammal adenocarcinomas in situ or by transplantation into the mammary gland-free fat pads of syngeneic mice. Our current hypothesis is that murine mammary cancer can evolve through one of several intermediate stages. The intermediate stages can be either alveolar or ductal hyperplasias. The latter resemble, in many instances, ductal lesions seen in human breast cancer.