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Paul Mathew, M.D., Assistant Professor, Department of Genitourinary Medical Oncology |
The prostate-specific antigen (PSA) screening era has resulted in a stageshift in the pattern of newly diagnosed prostate cancer such that the most common form of advanced disease is the locally advanced form. As metastasis is the principal cause of mortality, treatment failure with surgery or radiation therapy implies in large part the existence of micrometastatic disease at the very outset of the disease. Neoadjuvant or adjuvant therapy in prostate cancer is directed toward eliminating such sources of treatment failure.
Hormonal therapy is highly effective in inducing regressions in advanced prostate cancer, but invariably clones with hormone-independent biology emerge and proliferate. Systemic chemotherapy is being further studied in both the adjuvant and neoadjuvant settings, particularly with the current appreciation of the survival benefits of docetaxel-containing regimens in advanced hormone-independent disease.
One of the hallmarks of effective neoadjuvant therapy in cancer is the achievement of complete pathologic remission at the time of surgery. This landmark has been associated with markedly improved prognosis in many tumor types, but for reasons that are incompletely understood, complete pathologic remissions are rarely achieved in prostate cancer with neoadjuvant therapy.
At M. D. Anderson, a neoadjuvant multidisciplinary group directs the clinical and scientific approach to high-risk prostate cancer. An important focus is on understanding the molecular mechanisms of prostate cancer, including those that mediate resistance to hormonal therapy and chemotherapy as well as those that contribute to the early events of metastatic disease. A range of therapeutics, including angiogenesis inhibitors and signal transduction inhibitors (alone and in combination), is being studied, with molecular and pathologic endpoints in mind.
For example, we are completing a trial of hormone ablation, docetaxel, and imatinib followed by radical prostatectomy in men with high-risk localized disease. Imatinib is a tyrosine kinase receptor inhibitor. The kinase is found not only in primary tumors but also in the bone microenvironment where metastatic prostate cancer cells gain a particular advantage. It has also been implicated in hormone-independent signaling pathways. By challenging cancer cells simultaneously with imatinib, hormone therapy, and chemotherapy, we hope to gain an important advantage that will translate into long-term benefit. Residual cancer cells at the time of surgery will be profiled using genomic and tissue-based platforms to provide insights into resistance pathways. Such insights will be influential in defining future directions in the treatment of prostate cancer.
For more information on this topic or for questions about M. D. Anderson’s treatments, programs, or services, call the M. D. Anderson Information Line at (800) 392-1611 (in the United States) or (713) 792-3245 (in Houston and outside the United States).
Other articles in OncoLog, December 2004 issue:
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