Celebrating the 80th anniversary of hormone ablation for prostate cancer (original) (raw)
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Androgen Ablation Therapy and Prostate Cancer: An Update
British Journal of Medicine and Medical Research, 2013
It is now generally accepted that prostate cancer is the leading form of cancer in men. Current evidence indicates that countries including America and West Africa have more cases of aggressive progressive prostate cancer. Many treatment strategies have been used in management of prostate cancer. Since the discovery of androgen deprivation protocol seventy years ago, more treatment strategies have been reported which added more values to treatment outcome. However, death from this disease is due to resistance to androgen ablation therapy (AAT). Until recently, treatment of patients with disseminated prostate cancer was based on modalities that reduce AR signalling, either by direct androgen depletion (castration, e.g., surgical orchiectomy, luteinizing hormonereleasing hormone agonists), by blockage of the androgen receptor (AR) (e.g., flutamide, bicalutamide), or by combinations. In literature there is wide range of reports on diverse treatment strategies for prostate cancer; this often lead to serious confusion among clinicians and scientists, especially those new to the field. This study reviewed all the current available treatment strategies for androgen ablation therapy in management of hormone sensitive progressive prostate cancer, and highlights the merits and challenges involved in each of the treatments options. Thus, providing a
Urologia Internationalis, 2010
Background: It is not known whether androgen ablation therapy (AAT) influences TRAIL death ligand and its receptors expression of prostate cancer (PCa) cells. Aim: To investigate whether hormonal therapy alters the expression of TRAIL death ligand and TRAIL receptors in patients with advanced PCa. Patients and Methods: 26 untreated and 20 AAT-treated advanced PCa patients were included in the study. The patients who received AAT were divided into two groups based on hormone sensitivity status. TRAIL ligand and receptor expression were determined by a conventional immunohistochemistry method. Results: TRAIL death ligand and TRAIL-R2 death receptor were upregulated in PCa patients who received AAT. Hormone-refractory PCa patients exhibited lower levels of TRAIL death receptor (TRAIL-R1 and TRAIL-R2) expression compared to hormone-sensitive PCa patients. Conclusions : AAT alters TRAIL death ligand and its receptors expression in patients with PCa.
Hormone therapy in the management of prostate cancer: evidence-based approaches
Therapeutic advances in urology, 2010
Hormonal therapy has been the standard for advanced prostate cancer for over 60 years. Recently, the utility of androgen ablation through various means has been demonstrated for earlier stages of disease. In particular, the strongest evidence to date involves the use of hormonal therapy in combination with radiation therapy. In this article we review the basic concepts in hormonal ablation for prostate cancer and review the evidence-based studies that support the use of hormonal therapy in early stage prostate cancer.
Journal of Clinical Oncology, 2011
Purpose Clinicians are increasingly willing to treat prostate cancer within the primary site in the presence of regional lymph node or even limited distant metastases. However, no formal study on the merits of this approach has been reported. We used a preoperative clinical discovery platform to prioritize pathways for assessment as therapeutic targets and to test the hypothesis that the primary site harbors potentially lethal tumors after aggressive treatment. Patients and Methods Patients with locally advanced or lymph node–metastatic prostate cancer underwent 1 year of androgen ablation and three cycles of docetaxel therapy, followed by prostatectomy. All specimens were characterized for stage by accepted criteria. Expression of select molecular markers implicated in disease progression and therapy resistance was determined immunohistochemically and compared with that in 30 archived specimens from untreated patients with high-grade prostate cancer. Marker expression was divided i...
Modern approaches for antiandrogen-resistant prostate cancer therapy
Journal of Mind and Medical Sciences, 2021
Prostate cancer represents the leading malignant tumor in men over 50 years of age with 400,000 new cases being diagnosed yearly in Europe. Even if the incidence rate is higher than the mortality rate, still there is an increasing trend when speaking of its mortality. The increasing incidence of the metabolic syndrome, the unhealthy lifestyle, the high lipid and Calcium intake, the high spread of infections with Human Papilloma Virus, Human Herpes Virus, the excess of androgen consumption and the longer life expectancy, are few of the main causes of prostate cancer increasing incidence. The new systemic therapies such as immunotherapy with Checkpoint Inhibitors or Poly, ADP-Ribose Polymerase inhibitors and local experimental procedures addressing tumor destruction, such as High- Intensity Focused Ultrasound, the Cryo and Focal Laser Ablation, provide good outcomes and become new promising tools for prostate cancer therapy. Physicians consider these methods worth using; the efficacy ...
Androgen receptor as a target in androgen-independent prostate cancer
Urology, 2002
Prostate cancer is dependent on androgen stimulation mediated by the androgen receptor (AR), a member of the steroid hormone receptor family of ligand-dependent nuclear receptors. Most patients respond to standard androgen ablation therapies, but virtually all patients eventually relapse with disease that has been termed hormone-refractory or androgen-independent disease. Efforts to use AR antagonists, such as flutamide or bicalutamide, to enhance responses to primary androgen ablation therapy or to treat androgenindependent prostate cancer have been disappointing, which has diminished enthusiasm for more aggressive or alternative methods to block AR function. However, many lines of evidence indicate that AR function contributes to tumor cell survival after androgen ablation and to growth of androgen-independent prostate cancer. This article outlines a number of mechanisms that may contribute to AR activity in androgenindependent prostate cancer, including AR amplification, AR mutation, altered expression of AR coactivator and corepressor proteins, and activation of other pathways that can enhance AR function. Understanding the mechanisms responsible for AR function in androgen-independent prostate cancer should allow the more rational development of antagonists that can enhance the efficacy of androgen ablation therapies. UROLOGY 60 (Suppl 3A): 132-139, 2002.