Abstract
Since the classical observation of Huggins and Hodges in 1941 [1], the efficacy of androgen-ablative therapy has been well established in the management of patients with advanced prostate cancer. However, this type of therapy remains palliative in nature. Although, initially patients with stage D disease are expected to experience beneficial responses to androgen ablation, the vast majority of them eventually will face progression of the disease despite the continuous androgen-depleted state [2]. This phenomenon is attributed to the presence in the primary and metastatic sites of an androgen-insensitive prostate cancer cell subset which is able to proliferate in the absence of any androgenic support [3]. Patients with androgenrefractory disease (stage D3) have a dismal prognosis with a mean survival period of less than one year [4], for existing therapeutic regimens are not effective for this group of patients [5]. Therefore, it is important to study the mechanisms through which these androgen-insensitive cells are able to escape androgendependency and become autonomous in cell proliferation.
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Lee, C., Hofer, D.R., Sherwood, E.R., Kozlowski, J.M. (1991). Transforming Growth Factor α: A Potential Autocrine Growth Regulator in Prostatic Carcinoma. In: Karr, J.P., Coffey, D.S., Smith, R.G., Tindall, D.J. (eds) Molecular and Cellular Biology of Prostate Cancer. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3704-5_12
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DOI: https://doi.org/10.1007/978-1-4615-3704-5_12
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