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Clinical Chemistry 44: 705-723, 1998;
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(Clinical Chemistry. 1998;44:705-723.)
© 1998 American Association for Clinical Chemistry, Inc.

Review

Growth factor involvement in progression of prostate cancer

Pamela J. Russell1,a, Suzanne Bennett1, and Phillip Stricker2

1 Oncology Research Centre, Prince of Wales Hospital, High Street, Randwick, New South Wales, Australia, 2031 and Division of Medicine, University of New South Wales, Kensington, New South Wales 2052, Australia.

2 Department of Urology, St. Vincent's Hospital, 438 Victoria St., Darlinghurst, New South Wales 2010, Australia.
a Address correspondence to this author at: Oncology Research Centre, Villa 1, Prince of Wales Hospital, High Street, Randwick, New South Wales 2031, Australia. Fax 61 2 9382 2629; e-mail P.Russell{at}usnw.edu.au.

Understanding how the regulation of growth factor pathways alters during prostate cancer (PC) progression may enable researchers to develop targeted therapeutic strategies for advanced disease. PC progression involves the shifting of cells from androgen-dependent growth to an androgen-independent state, sometimes with the loss or mutation of the androgen receptors in PC cells. Both autocrine and paracrine pathways are up-regulated in androgen-independent tumors and may replace androgens as primary growth stimulatory factors in cancer progression. Our discussion focuses on growth factor families that maintain homeostasis between epithelial and stromal cells in the normal prostate and that undergo changes as PC progresses, often making stromal cells redundant. These growth factors include fibroblast growth factor, insulin-like growth factors, epidermal growth factor, transforming growth factor {alpha}, retinoic acid, vitamin D3, and the transforming growth factor ß families. We review their role in normal prostate development and in cancer progression, using evidence from clinical specimens and models of PC cell growth.




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