EGFR and prostate neoplasm: The results from studies with normal prostate tissues (Traish and Wotiz, 1987; St-Arnaud et al, 1988; Nishi et al, 1996; Itoh et al, 1998; Hammarsten et al, 2007) and those described above in cell culture studies and human prostate tumour tissue biopsies support the concept that EGFR-stimulated growth of PCa escaped androgen control because of a molecular switch in the cross-talk pathway between androgens and EGFR.