Skip to main content Accessibility help
×
Hostname: page-component-848d4c4894-8bljj Total loading time: 0 Render date: 2024-06-28T12:43:25.451Z Has data issue: false hasContentIssue false

6 - Systemic therapy

Published online by Cambridge University Press:  23 December 2009

Hedvig Hricak
Affiliation:
Memorial Sloan-Kettering Cancer Center
Peter Scardino
Affiliation:
Memorial Sloan-Kettering Cancer Center
Get access

Summary

Introduction

In 2005, approximately 128 000 American men were newly diagnosed with recurrent or advanced prostate cancer. For the vast majority of these men, hormonal therapy is the most common first line of treatment [1, 2]. This first-line hormonal treatment is typically surgical or medical castration, which is known as androgen-deprivation therapy. Most patients show a response to androgen-deprivation therapy as manifested by a drop in prostate-specific antigen and/or symptomatic improvement. Ultimately, all patients on androgen-lowering therapy eventually fail this treatment, with the re-emergence of castration-resistant tumors. These tumors may still be susceptible to secondary hormonal therapies that block androgen receptors, decrease the adrenal production of androgens, or increase circulating estrogens. Like androgen-deprivation therapy, secondary hormonal therapies improve symptoms and induce variable decreases in prostate-specific antigen, but they also have not been shown to provide a survival advantage. These patients will ultimately progress despite an initial success with such hormonal maneuvers.

Clinical states model of prostate cancer

The clinical states model of prostate cancer developed at Memorial Sloan-Kettering Cancer Center defines milestones for assessing prognosis and defining therapeutic objectives and outcomes in patients with advanced prostate cancer (Figure 6.1) [3].

Type
Chapter
Information
Prostate Cancer , pp. 93 - 101
Publisher: Cambridge University Press
Print publication year: 2008

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

,American Cancer Society. Cancer Facts and Figures 2005. Atlanta, GA: American Cancer Society; 2005.
Ward, J. F., Moul, J. W., Treating the biochemical recurrence of prostate cancer after definitive primary therapy. Clin Prostate Cancer, 4 (2005), 38–44.CrossRefGoogle ScholarPubMed
Scher, H. I., Heller, G., Clinical states in prostate cancer: towards a dynamic model of disease progression. Urology, 55 (2000), 323–7.CrossRefGoogle Scholar
Pound, C. R., Partin, A. W., Eisenberger, M. A., et al., Natural history of progression to metastases and death from prostate cancer in men with PSA recurrence following radical prostatectomy. JAMA, 281 (1999), 1591–7.CrossRefGoogle ScholarPubMed
Byar, D. P., Proceedings: The Veterans Administration Cooperative Urological Research Group's studies of cancer of the prostate. Cancer, 32:5 (1973), 1126–30.3.0.CO;2-C>CrossRefGoogle ScholarPubMed
,The Medical Research Council Prostate Cancer Working Party Investigators Group, Immediate versus deferred treatment for advanced prostatic cancer: initial results of the Medical Research Council trial. Br J Urol, 79 (1997), 235–46.CrossRefGoogle Scholar
Holzbeierlein, J. M., Castle, E. P., Thrasher, J. B., Complications of androgen-deprivation therapy for prostate cancer. Clin Prostate Cancer, 2 (2003), 147–52.CrossRefGoogle ScholarPubMed
Slovin, S. F., Wilton, A. S., Heller, G., et al., Time to detectable metastatic disease in patients with rising prostate-specific antigen values following surgery or radiation therapy. Clin Cancer Res, 11 (2005), 8669–73.CrossRefGoogle ScholarPubMed
Zelefsky, M. J., Ben-Porat, L., Scher, H. I., et al., Outcome predictors for the increasing PSA state after definitive external-beam radiotherapy for prostate cancer. J Clin Oncol, 23 (2005), 826–31.CrossRefGoogle ScholarPubMed
Stewart, A. J., Scher, H. I., Chen, M. H., et al., Prostate-specific antigen nadir and cancer specific mortality following antigen failure. J Clin Oncol, 23 (2005), 6556–60.CrossRefGoogle ScholarPubMed
Waxman, J., Man, A., Hendry, W. F., et al., Importance of early tumour exacerbation in patients treated with long acting analogues of gonadotrophin releasing hormone for advanced prostatic cancer. Br Med J, 291 (1985), 1387–8.CrossRefGoogle ScholarPubMed
Caubet, J. F., Tosteson, T. D., Dong, E. W., et al., Maximum androgen blockade in advanced prostate cancer: a meta-analysis of published randomized controlled trials using nonsteroidal antiandrogens. Urology, 49 (1997), 71–8.CrossRefGoogle ScholarPubMed
Samson, D. J., Seidenfeld, J., Schmitt, B., et al., Systematic review and meta-analysis of monotherapy compared with combined androgen blockade for patients with advanced prostate carcinoma. Cancer, 95 (2002), 361–76.CrossRefGoogle ScholarPubMed
Tyrrell, C. J., Kaisary, A. V., Iversen, P., et al., A randomised comparison of ‘Casodex’ (bicalutamide) 150 mg monotherapy versus castration in the treatment of metastatic and locally advanced prostate cancer. Eur Urol, 33 (1998), 447–56.CrossRefGoogle ScholarPubMed
Sharifi, N., Gulley, J. L., Dahut, W. L., Androgen deprivation therapy for prostate cancer. JAMA, 294 (2005), 238–44.CrossRefGoogle ScholarPubMed
Akakura, K, Bruchovsky, N., Goldenberg, S. L., et al., Effects of intermittent androgen suppression on androgen-dependent tumors. Apoptosis and serum prostate-specific antigen. Cancer, 71 (1993), 2782–90.3.0.CO;2-Z>CrossRefGoogle ScholarPubMed
Pantuck, A. J., Zisman, A., Belldegrun, A. S., Gene therapy for prostate cancer at the University of California, Los Angeles: preliminary results and future direction. World J Urol, 18 (2000), 143–7.CrossRefGoogle Scholar
Grossfeld, G. D., Carroll, P. R., Prostate cancer early detection: a clinical perspective. Epidemiol Rev, 23 (2001), 173–80.CrossRefGoogle ScholarPubMed
Rashid, M. H., Chaudhary, U. B., Intermittent androgen deprivation therapy for prostate cancer. Oncologists, 9 (2004), 295–301.CrossRefGoogle ScholarPubMed
Wright, J. L., Higano, C. S., Lin, D. W., Intermittent androgen deprivation: clinical experience and practical applications. Urol Clin North Am, 33 (2006), 167–79.CrossRefGoogle ScholarPubMed
Kelly, W. K., Scher, H. I., Prostate specific antigen decline after antiandrogen withdrawal: the flutamide withdrawal syndrome. J Urol, 149 (1993), 607–9.CrossRefGoogle ScholarPubMed
Scher, H. I., Kolvenbag, G. J., The antiandrogen withdrawal syndrome in relapsed prostate cancer. Eur Urol, 31:Suppl 2 (1997), 3–7; discussion 24–7.CrossRefGoogle ScholarPubMed
Scher, H. I., Kelly, W. K., Flutamide withdrawal syndrome: its impact on clinical trials in hormone-refractory prostatic cancer. J Clin Oncol, 11 (1993), 1566–72.CrossRefGoogle Scholar
Miyamoto, H., Rahman, M. M., Chang, C., Molecular basis for the antiandrogen withdrawal syndrome. J Cell Biochem, 91 (2004), 3–12.CrossRefGoogle ScholarPubMed
Scholz, M., Jennrich, M., Strum, R., et al., Long-term outcome for men with androgen independent prostate cancer treated with ketoconazole and hydrocortisone. J Urol, 173 (2005), 1947–52.CrossRefGoogle ScholarPubMed
Pound, C. R., Partin, A. W., Epstein, J. I., et al., Prostate-specific antigen after anatomic radical retropubic prostatectomy. Patterns of recurrence and cancer control. Urol Clin North Am, 24 (1997), 395–406.CrossRefGoogle ScholarPubMed
Katz, M. S., Zelefsky, M. J., Venkatraman, E. S., et al., Predictors of biochemical outcome with salvage conformal radiotherapy after radical prostatectomy for prostate cancer. J Clin Oncol, 21 (2003), 483–9.CrossRefGoogle ScholarPubMed
Moore, M. J., Osoba, D., Murphy, K., et al., Use of palliative end points to evaluate the effects of mitoxantrone and low-dose prednisone in patients with hormonally resistant prostate cancer. J Clin Oncol, 12 (1994), 689–94.CrossRefGoogle ScholarPubMed
Tannock, I. F., Osoba, D., Stockler, M. R., et al., Chemotherapy with mitoxantrone plus prednisone or prednisone alone for symptomatic hormone-resistant prostate cancer: a Canadian randomized trial with palliative end points. J Clin Oncol, 14 (1996), 1756–64.CrossRefGoogle ScholarPubMed
Kantoff, P. W., Halabi, S., Conaway, M., et al., Hydrocortisone with or without mitoxantrone in men with hormone-refractory prostate cancer: results of the cancer and leukemia group B 9182 study. J Clin Oncol, 18 (1999), 2506–13.CrossRefGoogle Scholar
Tannock, I. F., deWit, R., Berry, W. R., et al., Docetaxel plus prednisone or mitoxantrone plus prednisone for advanced prostate cancer. New Engl J Med, 351 (2004), 1502–12.CrossRefGoogle ScholarPubMed
Petrylak, D. P., Tangen, C. M., Hussain, M. H., et al., Docetaxel and estramustine compared with mitoxantrone and prednisone for advanced refractory prostate cancer. New Engl J Med, 351 (2004), 1513–20.CrossRefGoogle ScholarPubMed
Scher, H. I., Sawyers, C. L., Biology of progressive, castration-resistant prostate cancer: directed therapies targeting the androgen-receptor signaling axis. J Clin Oncol, 23 (2005), 8253–61.CrossRefGoogle ScholarPubMed
Grossmann, M. E., Huang, H., Tindall, D. J., Androgen receptor signaling in androgen-refractory prostate cancer. J Natl Cancer Inst, 93 (2001), 1687–97.CrossRefGoogle ScholarPubMed
Berger, R., Febbo, P. G., Majumder, P. K., et al., Androgen-induced differentiation and tumorigenicity of human prostate epithelial cells. Cancer Res, 64 (2004), 8867–75.CrossRefGoogle ScholarPubMed
Cheng, L., Pan, C. X., Yang, X. J., et al., Small cell carcinoma of the urinary bladder: a clinicopathologic analysis of 64 patients. Cancer, 101 (2004), 957–62.CrossRefGoogle ScholarPubMed
Han, G., Buchanan, G., Ittmann, M., et al., Mutation of the androgen receptor causes oncogenic transformation of the prostate. Proc Natl Acad Sci USA, 102 (2005), 1151–60.CrossRefGoogle ScholarPubMed
Serafini, A. N., Therapy of metastatic bone pain. J Nucl Med, 42 (2001), 895–906.Google ScholarPubMed
Serafini, A. N., Houston, S. J., Resche, J., et al., Palliation of pain associated with metastatic bone cancer using samarium-153 lexidronam: a double-blind placebo-controlled clinical trial. J Clin Oncol, 16 (1998), 1574–81.CrossRefGoogle ScholarPubMed
Robinson, R. G., Preton, D. F., Schiefelbein, M., et al., Stronium 89 therapy for the palliation of pain due to osseous metastases. JAMA; 274 (1995), 420–4.CrossRefGoogle Scholar
Saad, F., Gleason, D. M., Murray, R., et al., A randomized, placebo-controlled trial of zoledronic acid in patients with hormone-refractory metastatic prostate carcinoma. J Natl Cancer Inst, 94 (2002), 1458–68.CrossRefGoogle ScholarPubMed

Save book to Kindle

To save this book to your Kindle, first ensure coreplatform@cambridge.org is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle.

Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

Find out more about the Kindle Personal Document Service.

Available formats
×

Save book to Dropbox

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Dropbox.

Available formats
×

Save book to Google Drive

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.

Available formats
×