PubMed · 14759625
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Mark J Tullman, Fred D Lublin. 2004-03-15. Evaluating multiple sclerosis.. https://doi.org/10.1016/j.jns.2003.11.001
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Prostate cancer is the most common cancer diagnosed and the second leading cause of cancer-related deaths in men in the United States. The etiological factors that give rise to prostate cancer are not known. Therefore, it is not possible to develop primary intervention strategies to remove the causative agents from the environment. However, secondary intervention strategies with selenium (Se) compounds and other agents represent a viable option to reduce the morbidity and mortality of prostate cancer. In this review, we discuss ongoing clinical trials. In addition, we discuss preclinical mechanistic studies that provide insights into the biochemical and molecular basis for the anti-carcinogenic activity of both inorganic and organic forms of Se.
OBJECTIVE: To review the pathogenesis of in-stent restenosis and the evolution of drug-eluting stents (DES). DATA SOURCES: Using the search terms sirolimus, paclitaxel, and drug-eluting stents, a literature review was conducted to identify peer-reviewed articles and abstracts in MEDLINE (1966-June 2003). Recent meeting abstracts were accessed through the American Heart Association and the American College of Cardiology Web sites. Citations from available articles were also reviewed for additional references. STUDY SELECTION AND DATA EXTRACTION: Published reviews and studies showing the effects of in-stent restenosis and drug-coated and -eluting stents were evaluated and reviewed. DATA SYNTHESIS: Coronary stent implantation is a common form of percutaneous coronary interventions. Approximately 20-30% of patients undergoing stent placement develop restenosis 6 months after the procedure. The primary cause of in-stent restenosis is neointimal proliferation and subsequent accumulation of extracellular matrix, collagen, and macrophages. Eluting stents with an antimitotic agent may reduce the extent of restenosis. Research is ongoing in terms of finding the ideal combination of antimitotic agent, stent, and eluting medium to create the perfect stent. CONCLUSIONS: Research over the last decade has led to a better understanding of the pathogenesis of in-stent restenosis and ways to prevent restenosis. DES are being developed as one of the strategies to prevent restenosis.
PURPOSE: To define methodology to show clinical benefit for patients in the state of a rising prostate-specific antigen (PSA). RESULTS HYPOTHESIS: A clinical states framework was used to address the hypothesis that definitive phase III trials could not be conducted in this patient population. PATIENT POPULATION: The Group focused on men with systemic (nonlocalized) recurrence and a defined risk of developing clinically detectable metastases. Models to define systemic versus local recurrence, and risk of metastatic progression were discussed. INTERVENTION: Therapies that have shown favorable effects in more advanced clinical states; meaningful biologic surrogates of activity linked with efficacy in other tumor types; and/or effects on a target or pathway known to contribute to prostate cancer progression in this state can be considered for evaluation. OUTCOMES: An intervention-specific posttherapy PSA-based outcome definition that would justify further testing should be described at the outset. Reporting: Trial reports should include a table showing the number of patients who achieve a specific PSA-based outcome, the number who remain enrolled onto the trial, and the number who came off study at different time points. The term PSA response should be abandoned. TRIAL DESIGN: The phases of drug development for this state are optimizing dose and schedule, demonstration of a treatment effect, and clinical benefit. To move a drug forward should require a high bar that includes no rise in PSA in a defined proportion of patients for a specified period of time at a minimum. Agents that do not produce this effect can only be tested in combination. The preferred end point of clinical benefit is prostate cancer-specific survival; the time to development of metastatic disease is an alternative. CONCLUSION: Methodology to show that an intervention alters the natural history of prostate cancer is described. At each stage of development, only agents with sufficient activity should be moved forward.