c-MYC induces mammary tumorigenesis by means of a preferred pathway involving spontaneous Kras2 mutations

摘要: Although the process of mammary tumorigenesis requires multiple genetic events, it is unclear to what extent carcinogenesis proceeds through preferred secondary pathways following a specific initiating oncogenic event. Similarly, which established tumors remain dependent on individual mutations for maintenance transformed state unknown. Here we use tetracycline regulatory system conditionally express human c-MYC oncogene in epithelium transgenic mice. MYC encodes transcription factor implicated cancers. In particular, amplification and overexpression breast cancers associated with poor prognosis, although mechanisms by promotes tumor progression are poorly understood. We show that deregulated expression this inducible results formation invasive adenocarcinomas, many fully regress deinduction. Approximately half these harbor spontaneous activating point ras family proto-oncogenes strong preference Kras2 compared Hras1. Nearly all lacking regressed deinduction, whereas bearing did not, suggesting contribute progression. These findings demonstrate c-MYC-induced pathway involving Kras2.