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Charles Sawyers, MD, head of the new Human Oncology and Pathogenesis Program at Memorial Sloan-Kettering Cancer Center, is perhaps best known for his kinase inhibitor research leading to the development of imatinib (Gleevec) and dasatinib (Sprycel), drugs of unprecedented benefit for patients with chronic myelogenous leukemia.

past decade has witnessed a host of technologic improvements in prostate cancer therapy. The three major modalities offered in most managed care plans include radical prostatectomy, external-beam radiation therapy (EBRT), and interstitial brachytherapy (seed implant). Continued technologic advancement has led to incremental improvements in the safety and effectiveness of each modality. However, these improvements have led to a significant increase in the cost of treatment.

The randomized, double-blind satraplatin phase III registration trial (SPARC) has failed to meet its primary endpoint of overall survival in patients with hormone-refractory prostate cancer, Pharmion Corporation and GPC Biotech AG said in a news release.

Rising prostate-specific antigen (PSA) in nonmetastatic prostate cancer occurs in two main clinical settings: (1) rising PSA to signal failed initial local therapy and (2) rising PSA in the setting of early hormone-refractory prostate cancer prior to documented clinical metastases. Most urologists and radiation oncologists are very familiar with the initial very common clinical scenario, commonly called "biochemical recurrence." In fact, up to 70,000 men each year will have a PSA-only recurrence after failed definitive therapy. The ideal salvage therapy for these men is not clear and includes salvage local therapies and systemic approaches, of which the mainstay is hormonal therapy. Treatment needs to be individualized based upon the patient's risk of progression and the likelihood of success and the risks involved with the therapy. It is unknown how many men per year progress with rising PSA while on hormonal therapy without documented metastases. This rising PSA disease state is sometimes called, "PSA-only hormone-refractory prostate cancer." As in the setting of initial biochemical recurrence, evidence-based treatment options are limited, and taking a risk-stratified approach is justified. In this article, we will explore these prostate cancer disease states with an emphasis on practical, clinically applicable approaches.

Rising prostate-specific antigen (PSA) in nonmetastatic prostate cancer occurs in two main clinical settings: (1) rising PSA to signal failed initial local therapy and (2) rising PSA in the setting of early hormone-refractory prostate cancer prior to documented clinical metastases. Most urologists and radiation oncologists are very familiar with the initial very common clinical scenario, commonly called "biochemical recurrence." In fact, up to 70,000 men each year will have a PSA-only recurrence after failed definitive therapy. The ideal salvage therapy for these men is not clear and includes salvage local therapies and systemic approaches, of which the mainstay is hormonal therapy. Treatment needs to be individualized based upon the patient's risk of progression and the likelihood of success and the risks involved with the therapy. It is unknown how many men per year progress with rising PSA while on hormonal therapy without documented metastases. This rising PSA disease state is sometimes called, "PSA-only hormone-refractory prostate cancer." As in the setting of initial biochemical recurrence, evidence-based treatment options are limited, and taking a risk-stratified approach is justified. In this article, we will explore these prostate cancer disease states with an emphasis on practical, clinically applicable approaches.

Rising prostate-specific antigen (PSA) in nonmetastatic prostate cancer occurs in two main clinical settings: (1) rising PSA to signal failed initial local therapy and (2) rising PSA in the setting of early hormone-refractory prostate cancer prior to documented clinical metastases. Most urologists and radiation oncologists are very familiar with the initial very common clinical scenario, commonly called "biochemical recurrence." In fact, up to 70,000 men each year will have a PSA-only recurrence after failed definitive therapy. The ideal salvage therapy for these men is not clear and includes salvage local therapies and systemic approaches, of which the mainstay is hormonal therapy. Treatment needs to be individualized based upon the patient's risk of progression and the likelihood of success and the risks involved with the therapy. It is unknown how many men per year progress with rising PSA while on hormonal therapy without documented metastases. This rising PSA disease state is sometimes called, "PSA-only hormone-refractory prostate cancer." As in the setting of initial biochemical recurrence, evidence-based treatment options are limited, and taking a risk-stratified approach is justified. In this article, we will explore these prostate cancer disease states with an emphasis on practical, clinically applicable approaches.

A 58-year-old prostate cancer patient who developed stress urinary incontinence after successful prostatectomy was the first man at the University of Texas Southwestern Medical Center to receive a new type of sling to prevent leakage, the AdVance Male Sling System, from American Medical Systems, Minnetonka, Minnesota

If PSA rises in a prostate cancer patient after prostatectomy, should the man receive immediate androgen deprivation therapy? Two experts at the Third Annual Oncology Congress approached the question from different angles but reached essentially the same conclusion.

GPC Biotech announced that the Oncologic Drugs Advisory Committee (ODAC) for the US Food and Drug Administration (FDA) recommended (12–0) that the FDA should wait for the final survival analysis of the SPARC trial before deciding whether satraplatin is approvable for the treatment of hormone-refractory prostate cancer patients whose prior chemotherapy has failed.

GPC Biotech had sought accelerated approval for its drug for the treatment of hormone-refractory (androgen-independent) prostate cancer (HRPC) that had failed prior chemotherapy on the basis of findings from a protocol-specified preliminary analysis that showed a 33% reduction in the risk of disease progression

Prostate cancer patients who showed central abdominal uptake (CAU) on imaging with capromab pendetide (ProstaScint) had prostate-cancer-specific death rates 10 times higher than those without CAU

Prostatic acid phosphatase (PAP) emerged as the world's first clinically useful tumor marker in the 1940s and 1950s. With the introduction of the prostate-specific antigen (PSA) test in the 1980s, which performed significantly better than PAP in terms of screening and monitoring response to treatment, PAP fell into disfavor. An increasing number of recent studies have identified PAP as a significant prognostic factor for patients with intermediate- and high-risk prostate cancer. PAP appears to be particularly valuable in predicting distant failure in higher-risk patients for whom high levels of local control are achieved with aggressive initial local treatment. As prostate cancer care becomes increasingly focused on identifying the minority of patients who would benefit from aggressive systemic therapy, a reevaluation of the potential contribution of the prostatic acid phosphatase test seems timely.

LOS ANGELES—Cougar Biotechnology, Inc.'s CB7630 (abiraterone acetate) was well tolerated at doses as high as 2,000 mg/d with minimal toxicity in a phase I/II trial of chemotherapy-naive patients with castration-refractory prostate cancer, who had progressive disease despite treatment with LHRH analogs and multiple other hormonal therapies. Of 30 evaluable patients, 18 (60%) had a confirmed decline in PSA of greater than 50%, while 10 (33%) had declines greater than 90%. Of 20 evaluable patients with measurable lesions, 11 (55%) had a partial radiological response, while 7 had ongoing stable disease and 3 had regressing bone disease. The data were presented at the American Urological Association (AUA) annual meeting.