ERBB2 and breast neoplasm: Genetically engineered mouse models, such as over-expression of oncogenes (i.e. c-myc (McCormack et al., 1998; D’Cruz et al., 2001), ErbB2 (Guy et al., 1992; Moody et al., 2002, PyMT (Maglione et al., 2001), Wnt1 (Tsukamoto et al., 1988), and RAS (Nielsen et al., 1991)) or disruption of tumor suppressor genes (p53 (Lin et al., 2004), Brca1 (Venkitaraman 2002), or Pten (Di Cristofano and Pandolfi 2000) for example), are particularly useful in investigating the progression of in situ breast tumor development and spontaneous metastasis.