Prostate cancer is a very common
malignancy among Western males. Although most
tumors are indolent and grow slowly, some grow and metastasize aggressively. Because
prostate cancer growth is usually
androgen-dependent,
androgen ablation offers a therapeutic option to treat post-resection
tumor recurrence or primarily metastasized
prostate cancer. However, patients often relapse after the primary response to
androgen ablation
therapy, and there is no effective cure for cases of
castration-resistant
prostate cancer (CRPC). The mechanisms of
tumor growth in CRPC are poorly understood. Although the
androgen receptors (ARs) remain functional in CRPC, other mechanisms are clearly activated (e.g., disturbed
growth factor signaling). Results from our laboratory and others have shown that dysregulation of
fibroblast growth factor (FGF) signaling, including
FGF receptor 1 (FGFR1) activation and FGF8b overexpression, has an important role in
prostate cancer growth and progression. Several experimental models have been developed for prostate
tumorigenesis and various stages of
tumor progression. These models include genetically engineered mice and rats, as well as induced
tumors and xenografts in immunodeficient mice. The latter was created using parental and genetically modified cell lines. All of these models greatly helped to elucidate the roles of different genes in prostate
carcinogenesis and
tumor progression. Recently, patient-derived xenografts have been studied for possible use in testing individual, specific responses of
tumor tissue to different treatment options. Feasible and functional CRPC models for
drug responsiveness analysis and the development of effective
therapies targeting the FGF signaling pathway and other pathways in
prostate cancer are being actively investigated.