View clinical trials related to Prostatic Neoplasms.
Filter by:RATIONALE: Diindolylmethane may slow the growth of prostate cancer cells. PURPOSE: This phase I trial is studying the side effects and best dose of diindolylmethane in treating patients with nonmetastatic prostate cancer that has not responded to previous hormone therapy.
RATIONALE: Colony-stimulating factors, such as GM-CSF, may help the body build an effective immune response to kill tumor cells. Giving GM-CSF before surgery may be an effective treatment for localized prostate cancer. PURPOSE: This clinical trial is studying how well giving GM-CSF before surgery works in treating patients with localized prostate cancer.
This trial is designed to determine whether an 8-week course of escalated dose conformal radiation can be compressed safely, and with similar efficacy into a 4-week course.
RATIONALE: Questionnaires that assess symptoms caused by cancer and cancer therapy may help improve the ability to plan treatment for patients with invasive cancer to help them live longer and more comfortably. PURPOSE: This clinical trial is studying symptoms caused by cancer and cancer therapy in patients with invasive breast, lung, prostate, or colorectal cancer.
RATIONALE: Exercise and dietary counseling may improve physical activity, nutrition, and quality of life in older long-term cancer survivors who are overweight. PURPOSE: This randomized clinical trial is studying two different schedules of exercise and dietary counseling to compare how well they work in improving physical activity, nutrition, and quality of life in older long-term cancer survivors who are overweight.
This two part study will evaluate the safety and tolerability of MK0429 in addition to assessing it's pharmacokinetic profile and pharmacodynamic response.
- There are nearly 30,000 deaths per year in the United States from prostate cancer, making this a large and important target patient population for new cancer treatments. - SU011248 is an exciting, new, experimental drug that inhibits a number of proteins, or more specifically receptor tyrosine kinases, in tumor cells. These proteins are active in cellular pathways that are important for development and growth of a variety of different cancers. The targets of SU011248 include the receptors for vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), and others. By blocking the VEGF and PDGF pathways, SU011248 can induce death of the blood vessels that nourish the cancer cells and death of the cancer cells themselves. - SU011248 has demonstrated significant anti-tumor activity in renal cell carcinoma, gastrointestinal stromal tumors, and other cancers. Its effect against prostate cancer has not been studied to date. - This study is directed at two populations of men with advanced prostate cancer: 1. Men with advanced prostate cancer who have a rising PSA despite hormone therapy, but have not yet received any chemotherapy. 2. Men with metastatic prostate cancer who have received prior chemotherapy (with a docetaxel-based regimen) and have increasing disease following chemotherapy. - Men in this study will receive SU011248 on a six-week repeating schedule, with four weeks of daily treatment followed by a two-week rest. The goals of the study are: 1. to determine whether SU011248 is an important therapeutic agent in men with advanced prostate cancer, and 2. to identify predictive markers of anti-cancer activity within individual subjects that would allow selective treatment of appropriate subjects in the future.
Prostate cancer (CaP) is the most commonly diagnosed cancer among males in the U.S. and the second leading cause of cancer-related mortality. More than 230,000 men will be diagnosed with prostate cancer in the USA this year and more than 30,000 will die of this disease. Androgen deprivation, the elimination of testosterone and its active metabolites, remains the single most effective intervention available for the treatment of advanced prostate carcinoma. This is usually achieved by surgical removal of the testes (orchiectomy), by suppressing production of testosterone (LHRH agonists) and/or by blocking the androgens at receptor sites (antiandrogens). Unfortunately, androgen suppression does not cure the disease. Most patients progress within 0-5 years, and all patients ultimately progress if the cancer is not eliminated during initial therapy (usually prostatectomy or radiation). Hormone suppression treatment eliminates the detectable levels of testosterone in the blood. However, the testosterone levels in tissue remain high enough to stimulate androgen receptors. Overexpression of androgen receptors is present in all cell lines which demonstrate "androgen independence," i.e., are resistant to androgen-suppressive therapy. Approximately 95% of testosterone is supplied by the testes, with the remaining 5% supplied by the adrenal glands. The presumption that standard androgen deprivation achieves the optimal level of androgen suppression for patients is based on the levels of androgen which result from orchiectomy. However, because adrenal androgen levels are unaffected by standard modes of androgen deprivation, 5% of the body's testosterone remains despite hormone therapy. The hypothesis of this study is that more effective suppression of the androgen axis through elimination of adrenal androgens and more effective suppression of testosterone metabolites will lower intraprostatic androgen levels, minimizing activation of the androgen receptor and augmenting natural cell death (apoptosis). The investigators propose to test this hypothesis by administering neoadjuvant (pre-surgery) androgen deprivation therapy of different types before prostatectomy for patients with clinically localized prostate cancer. The investigators will assay serum and intraprostatic androgen levels, while assessing relative levels of apoptosis of normal and malignant tissue.
The study was a three-arm, active-control, multi-centre, parallel group study.
To evaluate anti-androgen (bicalutamide) induced biological and molecular changes in prostate comparison to chemical castration induced (goserelin) ones