Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Models for testing new drugs for the treatment of hormone-dependent prostate cancer are restricted to a few in vivo rat tumour lines; most of them originating from the Dunning R3327 adenocarcinoma. The original tumour and the R3327-H line grow rather slowly leading to a long duration of therapeutic experiments. The R3327-G subline can be transplanted as a cell suspension or tumour fragments, which give rise to fast and rather homogeneously growing androgen-dependent tumours. Their growth is strongly inhibited by castration or administration of diethylstilbestrol. Experiments were terminated 5 weeks after transplantation. Best results were obtained when treatment was started 1 day after transplantation. Histological sections showed therapy-dependent changes in the microarchitecture of these prostate tumours. The direct inhibitory effect of antiandrogens on prostate tumours was demonstrated when castrated, testosterone-propionate-supplemented animals were used. The short duration of experiments and reproducible responses to standard therapies are the advantages of this tumour model.
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PMID:Dunning R3327-G prostate carcinoma of the rat: an appropriate model for drug evaluation. 158 64

A prospective randomized study has been carried out in order to compare three different treatment modalities for symptomatic metastatic hormone-resistant prostatic cancer. A total of 79 patients were included. One group was treated with estramustine phosphate, another with Epirubicin plus Medroxyprogesterone acetate (MPA), while the third arm consisted of Epirubicin plus placebo. Best palliation was obtained by the combination of Epirubicin and MPA. This combination also seemed to be associated with the longest response duration.
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PMID:A randomized study on hormone-resistant prostatic cancer: estramustine phosphate versus low dose epirubicin with or without medroxyprogesterone acetate. A Norwegian multicenter study. 214 30

Considering the worldwide threat to health and reproduction related to endocrine disruptors (by-products of the chemical industry); considering the untrammelled development of the industrialization and engineering of the living, ethics and gynaecology/obstetrics itself is at a crossroads. Endocrine disruptors (derived from organochlorines and persistent organic pollutants such as PCBs, dioxins and furans, and pesticides such as aldrin, chlordane and DDT), are prime suspects in the deterioration of fertility and intellectual faculties and possibly a key factor in endometriosis, breast cancer and prostate cancer. The long-term and pernicious impacts of endocrine disruptors show our poor understanding of the complexities of life's mechanisms. Paradoxically, with our short-term perspectives and predilection for a technological fix, the problem posed by endocrine disruptors may accelerate the use of reproductive technologies such as ICSI and even cloning, as well as the dissemination of genetically modified organisms. The cure could be worse than the disease. Given the gravity of the challenge to humanity related to the chemical erosion of human health, the mutation of human conception introduced by reproductive technologies and by the drive to genetically modify nature and even human nature, we must urgently re-evaluate the direction in which our societies are headed and the reliance on profit-oriented technology to save us from ourselves. In these circumstances, the collective exercise of wisdom, prudence and responsibility towards the essence and integrity of humanity has become, more than ever, an ethical, and perhaps even a survival, imperative.
Baillieres Best Pract Res Clin Obstet Gynaecol 1999 Dec
PMID:Will we be taught ethics by our clones? The mutations of the living, from endocrine disruptors to genetics. 1071 12

Brachytherapy of prostate cancer has become attractive in recent years in Germany. There are several radioactive sources available, which are physically different. Some of them are used as permanent or temporary implants. The permanent sources most frequently used are iodine 125, palladium 103, and gold 198. Iridium is a temporary implant. The techniques used in Germany are low-dose rate (LDR) and high-dose rate brachytherapy, which differ in dose distribution and patient population. The success of prostate cancer brachytherapy depends on patient selection and choosing the right source for the technique used. Best suited for LDR monotherapy is the low-risk patient with a prostate-specific antigen (PSA) level below 10 ng/ml, maximal tumor stage T2b, and a Gleason score of less than 7.
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PMID:[Brachytherapy of local prostatic carcinoma]. 1140 25

(CPG) series provides an overview of one CPG each month. The overview includes a brief summary of the guideline's content, as well as the identification of some factors by which the author has critiqued it. The first article in the series reviewed the steps of CPG critique. Subsequent columns have described CPGs related to viral upper respiratory illnesses, tobacco dependence, menopause and perimenopause, and musculoskeletal evaluation. This month, the column describes a CPG titled: Prostate-Specific Antigen (PSA) Best Practice Policy, from the American Urological Association (AUA). As prostate cancer is the leading cause of cancer deaths among U.S. men, this set of recommendations should have wide application.
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PMID:Use of PSA measurement in practice. 1193 Aug 66

Prostate cancer patients are at significant risk for SREs, with up to 50% of androgen-insensitive patients experiencing an SRE at 24 months. The risk increases with the duration and type of cancer treatment. SREs decrease HRQOL, increase the cost of care, and are associated negatively with overall survival. Screening men at greatest risk (slender white men and men with hormone refractory disease or metastatic disease) with BMD measurements, and initiating empiric therapy (vitamin D3, calcium, parenteral estrogens, bisphosphates) may be warranted.
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PMID:The impact of osteoporosis in men treated for prostate cancer. 1512 10

Prostate cancer patients are at risk for developing bone loss and bone metastases. Clinicians prescribing ADT should appreciate the potential effects of ADT on BMD as well as the morbidity and mortality that can result from osteoporotic fractures. Measures to address the evaluation of patients and when to treat patients with significant bone loss have been discussed. Bisphosphonates effectively prevent loss of BMD in prostate cancer patients. Treatment of prostate cancer patients with established bone metastases with zoledronic acid should be considered strongly based on the results of the Saad study and other studies of patients with bone metastases with other malignancies. Zoledronic acid is approved by the US FDA for use in men with metastatic hormone-refractory prostate cancer and in the European Union for any patient with bone metastases, including prostate cancer patients,because of the beneficial impact of zoledronic acid on skeletal-related events. There is no validated method to determine which patients might benefit most from bisphosphonate therapy in this setting. Many questions about the use of bisphosphonate therapy in men with prostate cancer must be addressed, both in terms of the use in bone loss and bone metastases. These questions include: What is the optimal timing of therapy? Which bisphosphonate is best? What is the best dose and dose schedule? Do bisphosphonates effectively decrease skeletal fracture rates in patients with osteoporosis? How long should patients receive therapy? Are bisphosphonate "holidays" warranted? What are the long-term skeletal and renal toxicities? Is there a role for sequencing bisphosphonate therapy either before or after chemotherapy? Is bisphosphonate therapy synergistic with certain chemotherapy or other bone-targeted therapies? Which patients are the most likely to benefit from bisphosphonate therapy? What are clinically significant endpoints of bisphosphonate trials in patients with metastatic disease? Does inhibiting bone turnover also inhibit formation of bone metastases? Preliminary work in these areas has been completed, but more questions than answers are available. Given the rising costs of health care, it is imperative that these questions be addressed to best use the health care dollar while offering high-risk patients the best available therapy. At present, no data suggest that bisphosphonates should be used routinely to prevent BMD loss in men with normal BMD or to prevent the development of bone metastases in men with biochemical relapse. Continuing trials may give us guidance in the future.
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PMID:Understanding treatments for bone loss and bone metastases in patients with prostate cancer: a practical review and guide for the clinician. 1512 12

Primary and secondary osteoporosis are prevalent in more than 2 million American men. One of the main causes of this is hypogonadism, in turn brought upon by early androgen deprivation therapy used in prostate cancer treatment. Androgen deprivation therapy produces a host of adverse effects on the skeleton, including an increase in bone turnover, a decrease in bone mineral density, and an increase in fracture risk. In addition, based on observations in preclinical models, these adverse effects on the skeletal integrity may promote the development of or progression of metastasis to bone. Loss of bone due to androgen deprivation therapy is an important clinical issue for many men with prostate cancer, but osteoporosis is not an inevitable consequence of androgen deprivation therapy. Because of interpatient variations in peak bone mass as well as differences in rates of treatment-related bone loss, not all men with prostate cancer require treatment for osteoporosis. All men on androgen deprivation therapy should receive calcium and multivitamin supplements and should be considered for bisphosphonate therapy; this is particularly so for men with either a low baseline BMD or observed high rates of bone loss during androgen deprivation therapy.
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PMID:The role of bisphosphonates in men with prostate cancer receiving androgen deprivation therapy. 1520 84

Cancer treatment-induced bone loss is an emerging problem for patients with breast and prostate cancer, who are often treated with cancer therapies earlier in the disease process. Bone loss associated with cancer therapy can also progress rapidly and may cause significant morbidity in these patients. Many patients with metastatic prostate or breast cancer develop bone metastases and subsequent skeletal-related events. Studies suggest that bisphosphonates can maintain bone health when introduced early in the continuum of cancer care. They have shown efficacy in the prevention of bone loss and the more potent i.v. bisphosphonate, zoledronic acid, has prevented bone loss in addition to increasing BMD in prostate cancer patients with cancer treatment-induced bone loss. Intravenous zoledronic acid or pamidronate can be considered the standard of care for the treatment of osteolytic bone metastases in breast cancer. Clinical trials addressing the treatment of bone metastases related to prostate cancer have shown zoledronic acid to be the only bisphosphonate to have a significant positive effect on skeletal-related events.
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PMID:New generation of bisphosphonates: broad clinical utility in breast and prostate cancer. 1520 85

Serum testosterone levels peak in early adulthood in men and fall progressively with age. Since sex hormone binding globulin increases with age, the unbound forms of testosterone (free and bioavailable testosterone) fall more steeply than total testosterone levels. Serum testosterone levels below the normal range for young healthy adult males provide chemical evidence of androgen deficiency independent of the age of the patient. When accompanied by signs or symptoms that are compatible with androgen deficiency, treatment with testosterone should be considered in older men without evidence of prostate or breast cancer. While such therapy for younger hypogonadal men has shown benefit on libido, mood, muscle mass, muscle strength, bone mineral density and haematocrit, similar benefits in older men have not been as adequately assessed. While there is no convincing evidence that testosterone treatment in older men will increase the risk of cardiovascular or prostate cancer, long-term, well-controlled studies are lacking and needed. Treatment options for older men include injectable, transdermal and transbuccal testosterone preparations.
Best Pract Res Clin Endocrinol Metab 2004 Sep
PMID:Androgens and the ageing male. 1526 42


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