Abstract
Recent progress in the study of c-Myc has convincingly demonstrated that it possesses a dual role in regulating both proliferation and apoptosis; however, the manner in which c-Myc influences these cellular response pathways remains incompletely characterized. Deregulation of c-Myc expression, via many mechanisms, is a common feature of multiple cancers and is an especially prominent feature of many breast cancers. Of significant interest to those who study mammary gland development and neoplasia is the unresolved nature and contribution of apoptosis to breast tumorigenesis. Recently, the use of transgenic mice and gene-knockout mice has allowed investigators to evaluate the pathological mechanisms by which different genes influence tumor development and progression. In this review, we address two distinct c-myc-containing bitransgenic murine mammary tumor models and discuss the contribution and possible future directions for resolution of cancer-relevant molecular pathways influenced by c-Myc.
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