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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An overview of the sex hormones is presented. Testosterone is a natural androgen produced in the testes, adrenal glands, and ovaries. It has anabolic as well as androgenic effects. Testosterone is used to treat inoperable breast cancer and osteoporosis, and to stimulate erythropoesis. Androgens are absolutely counterindicated in cases of prostate cancer. Estrone, estradiol, and estriol are natural estrogens produced in the ovaries, placenta, testes, and adrenal glands. These hormones also influence the production of gonadotropins by the pituitary gland. Estrogens are used to treat menopausal disorders, ovarial insufficiency, estrogen-independent breast cancer, prostate cancer, and in some cases pregnancy disorders. Estrogens and progestagens are 2 components used in oral contraceptives. Progesterone, a natural progestagen, is produced by the corpus luteum. It promotes the proliferation phase of the endometrium, fertilization, and nidation, and it works to maintain pregnancy. Progesterone is used to treat spontaneous abortion, corpus luteum insufficiency, and endometrial cancer.
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PMID:[Sex hormones]. 24 26

Plasma concentrations of testosterone, oestradiol-17 beta, luteinising hormone (LH), follicle stimulating hormone (FSH), prolactin and growth hormone (GH) were measured in patients with histologically proven prostatic cancer, before any form of therapy was given for this disease. Patients were categorised according to UICC classification. No systemic change in the group means of any of these hormones was associated with the progression of the disease from the T0 to the T4 stage. When multivariate analysis was applied to the combined intraprostatic (T0 + T1 + T2) and extraprostatic (T3 + T4) tumour category in patients without clinically evident metastases (M0) a discrimination was observed, GH substantially contributing to the separation of the 2 groups. When plasma hormone data from patients classified as M0 (without metastases) were compared with M1 patients (with metastases), mean GH values were significantly larger (P less than 0.02) in patients with metastases. GH was also a major contributory factor to the discrimination between the M0 and M1 groups, using multivariate analysis. Testosterone group means for M0 versus M1 were also significantly different (P less than 0.02).
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PMID:Evaluation of plasma hormone concentrations in relation to clinical staging in patients with prostatic cancer. British Prostate Study Group. 53 96

A clinical and pathologic comparison of carcinoma of the prostate in a high-risk US (Washington, DC) black population and in a low-risk Nigerian (Ibadan) black population is presented. Fifty-two percent of American patients were in clinical stages I and II, whereas only 10% of Nigerian patients were in the same stages. Testosterone and estradiol blood levels were significantly lower (P less than 0.05) in patients with carcinoma of the prostate from Ibadan compared with American black prostate cancer patients from Washington, DC. Age-standardized incidence rates (world standard) for 1000 autopsies for micro (incidental)-carcinoma were approximately equal in American and African black men. The incidence rate of invasive carcinoma was, however, even after adjustment for age, higher in American black men than in African men.
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PMID:Characterization of prostatic carcinoma among blacks: a continuation report. 87 28

Twenty-eight patients affected with disseminated prostate cancer, which proved hormone resistant (after castration and oestrogen administration), have undergone combined treatment with Testosterone (for 13 days) and 32P (for the last 7 days of the Testosterone treatment). During the initial fase of the treatment (Testosterone only), 14 patients experienced pain exacerbation and/or fever and one experienced immediate improvement. The exacerbation quickly disappeared following 32P administration, and 26 of the patients had distinct improvement at some time during or after treatment, with a mean remission duration of 3 months and mean survival rate of 7 months. No lytic or soft part deposit showed improvement; improvement was noticeable only in the mixed type or osteo-sclerotic metastases. This observation suggests that the androgen stimulates uptake of the isotope not inside the tumor cells but in the bone matrix around the tumoral deposit. The patient who showed very early improvement had a subsequent relapse on oestrogens, but later responded to the androgen alone.
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PMID:[Treatment with 32P of carcinoma of the prostate (author's transl)]. 100 7

Human prostate carcinogenesis has been viewed as a multi-step process involving progression from low histologic grade, small, latent carcinoma to large, higher grade, metastasizing carcinoma. However, recent data suggest that a variety of pathogenetic pathways may exist. The precise etiology and pathogenesis of human prostate cancer remain largely undefined. It is difficult to investigate stages in the development of human prostate cancer, but some animal models provide opportunities in this regard. Short-term treatment of rats with chemical carcinogens produces a low incidence (5-15%) of prostate cancer, provided that prostatic cell proliferation is enhanced during carcinogen exposure. Chronic treatment with testosterone also produces a low prostate carcinoma incidence. A high carcinoma incidence can only be produced by chronic treatment with testosterone following administration of carcinogens such as N-methyl-N-nitrosourea (MNU) and 3,2'-dimethyl-4-aminobiphenyl (DMAB). Testosterone markedly enhances prostate carcinogenesis even at doses that do not measurably increase circulating testosterone. Thus, testosterone is a strong tumor promoter for the rat prostate. All such MNU- or DMAB-initiated and/or testosterone-promoted tumors are adenocarcinomas; most originate from the dorsolateral and anterior, but not ventral, prostate lobes. These tumors share a number of important characteristics with human prostate cancer. A high frequency (70%) of activation of the K-ras gene by a G35 to A mutation occurs in these carcinomas. Another high incidence prostate carcinogenesis model, representing a different pathogenetic pathway, involves chronic administration of estradiol-17 beta to rats in combination with low-dose testosterone. The resulting carcinomas are low-grade and originate exclusively from periurethral ducts of the dorsolateral and anterior prostate. While it is unknown whether testosterone is a tumor promoter in this system, preliminary studies indicate the formation of a DNA adduct in the target tissue, which suggests that estradiol-17 beta acts as a tumor initiating agent in this system. The high incidence models mentioned earlier are adequate for the study of chemoprevention of prostatic carcinogenesis. Analysis of shifts in the relative incidence of metastasizing carcinoma, grossly apparent but not-metastasizing carcinoma, microscopic-size carcinoma, and carcinoma in situ or atypical hyperplasia may allow study of the modifying effects of potential chemopreventive agents on tumor progression in these animal models of prostatic carcinogenesis.
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PMID:Animal models for the study of prostate carcinogenesis. 128 79

LNCap, a human prostate cancer cell line, possess androgen dependent growth characteristics. We studied anchorage independent proliferation of LNCap cells using semi-solid agarose double layer culture. The cells formed colonies in the semi-solid medium supplemented with charcoal filtered steroid free fetal calf serum and maximal colony formation was obtained in the medium with 10% serum. The addition of several steroids (testosterone, dihydrotestosterone, ethinylestradiol) influenced the colony formation. Testosterone at the concentration of 10(-8) M to 10(-10) M stimulated colony formation with optiman of 10(-9) M. When LNCap cells were placed under the basal layer of the semi-solid culture as feeder cells, also stimulated was the colony formation of the LNCap cells cultured in upper layer of semi-solid medium. The addition of EGF, TGF alpha and TGF beta to the medium also stimulated the colony formation. The combined effect of EGF and TGF alpha was shown to be cooperative with testosterone. TGF beta, however, did not show such cooperative effect with testosterone on colony formation. The addition of the anti-body to EGF, TGF alpha or TGF beta to the medium decreased the colony formation of LNCap cells. These results suggest that LNCap cells excrete EGF, TGF alpha, TGF beta and/or similar substances and these factors autocrinely decorate the cell proliferation of LNCap human prostate cancer cells.
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PMID:[Analysis of anchorage independent growth of human prostate cancer cell line LNCap]. 143 84

Epidermal growth factor (EGF) and insulin-like growth factor I (IGF-I) have been shown to regulate Leydig cell steroidogenesis in several species. We have investigated the effects, if any, of EGF and IGF-I on in vitro testosterone production of human Leydig cells. Interstitial cells or Percoll purified Leydig cells were isolated from the testes obtained from patients (n = 9) undergoing orchidectomies for treatment of prostate cancer and were cultured for different time periods with hCG, dibutyryl cAMP, EGF and IGF-I. Testosterone in the culture media was measured by radioimmunoassay. While EGF had a stimulatory effect on basal testosterone production of isolated interstitial cells or purified Leydig cells, IGF-I was ineffective. When the interstitial cells were cultured in the presence of hCG or EGF for 3, 6 or 24 h, the stimulatory effects of EGF on testosterone production were only evident after 24 h. On the other hand, hCG stimulated testosterone production at all time points (i.e after 3, 6, 24 h of incubation). When added in the presence of maximal concentrations of hCG and dibutyryl cAMP, EGF did not further enhance steroidogenesis. On the other hand, IGF-I potentiated the effects of hCG on testosterone production. These studies suggest that EGF and IGF-I may play a regulatory role in steroidogenic function of the human testes.
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PMID:Epidermal growth factor stimulates testosterone production of human Leydig cells in vitro. 164 16

Genitourinary problems, including neurogenic dysfunction, impotence, prostatism, urinary tract infections, and prostate cancer, are common in the elderly, and most of the symptoms can be alleviated through pharmacological management. Patients with neurogenic dysfunction who present with symptoms such as incontinence and urinary retention can be appropriately managed with bladder and sphincter relaxants or stimulants. Anticholinergic agents in the form of oxybutynin, flavoxate, and propantheline are effective bladder relaxants, and phenoxybenzamine, prazosin, and terazosin are commonly used as sphincter relaxants. Bethanechol chloride is the agent most commonly used to stimulate bladder contraction, but physicians should be careful when prescribing it for elderly patients with cardiovascular problems. Organic and psychogenic causes of impotence usually overlap, and oral agents have limited use in the treatment process. The use of yohimbine has increased recently, but its value and rate of success remains questionable. Testosterone is being used widely to treat impotence, but it is only helpful to patients with hypogonadism and should be used with discretion in the elderly, who have a high incidence of prostate cancer. Vasoactive intracavernous pharmacotherapy, on the other hand, is a recently discovered alternative to testosterone with promising results. Although the treatment of choice for benign prostatic hypertrophy is surgery, there have been important pharmacological advances in treating this disorder. alpha-Adrenergic antagonists and anti-androgenic agents have been found to relieve the symptoms of prostatic enlargement. The use of chemotherapeutic and antibiotic agents to treat and suppress acute and chronic urinary tract infections is reviewed; these are second only to pulmonary infections as the most frequent cause of febrile episodes in patients over the age of 65. Lower urinary tract infections can be treated with almost any antibacterial agent. Upper urinary tract infections require full genitourinary evaluation and appropriate antibiotics should be used according to the urine culture sensitivity studies. With the advent of new hormonal agents, more choices are now available for the management of prostate cancer, which is the second most common malignancy in men. Diethylstilbestrol (stilboestrol), an oral estrogen, remains a commonly used agent to achieve castrate levels of androgens in advanced prostatic carcinoma. Agonist analogues, such as goserelin and leuprorelin, of gonadotrophin-releasing hormone (GnRH) [luteinising hormone-releasing hormone (LHRH); or gonadorelin] achieve the same results as diethylstilbestrol but without the cardiovascular side effects. Antiandrogens are also being used in combination with GnRH agonists to produce complete androgen blockage, with mixed results.
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PMID:Current concepts in the treatment of genitourinary tract disorders in the older individual. 172 98

Leuprorelin (leuprolide acetate) is a synthetic analogue of gonadotrophin-releasing hormone (GnRH) [luteinising hormone-releasing hormone (LHRH)] which initially stimulates luteinising hormone (LH) and hence testicular androgen release; continuous administration then results in profound suppression of these hormones. Testosterone levels associated with castration are attained within 3 to 4 weeks. A biodegradable subcutaneous or intramuscular depot formulation of leuprorelin 3.75 or 7.5 mg, which releases the drug at a constant rate over 28 days, is available and may be preferred over daily subcutaneous injections. The progression of previously untreated advanced prostatic cancer is delayed in 70 to 90% of men receiving leuprorelin, with median survival of approximately 2 years. The efficacy of leuprorelin is equivalent to that of estrogen therapy, but the tolerability of the GnRH analogue is far better. In contrast to most other studies of GnRH agonists, a slight survival advantage has been reported for combined treatment with leuprorelin and the antiandrogen flutamide. Small noncomparative trials reveal that leuprorelin also causes regression of benign hyperplastic prostate tissue with corresponding relief of obstructive, but not irritative, symptoms although continuous treatment is necessary to maintain remission. Impotence and flushing occur in most leuprorelin recipients but, unlike diethylstilbestrol (stilboestrol), cardiovascular toxicity and gynaecomastia are not significant problems. Symptom flare, usually manifested as bone pain in prostate cancer patients and exacerbation of obstructive symptoms in those with benign prostatic hypertrophy, can occur in 4 to 29% at the beginning of treatment. Leuprorelin treatment is therefore an established effective palliative measure in men with previously untreated advanced prostatic cancer, and may have a role in those with benign hypertrophy who are unfit for surgery.
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PMID:Leuprorelin. A review of its pharmacology and therapeutic use in prostatic disorders. 179 35

This study evaluates the sleep-related erections in 5 patients with locally advanced prostate cancer (T3NOMO) during 6 months treatment with Casodex by multinight continuous monitoring of penile tumescence and rigidity. Mean serum LH, Testosterone and Estradiol levels shown a no statistically significant increase at the six months control. We found no significant modifications in the number of NPT episodes, maximum penile circumference and rigidity time before and after therapy. Penile arterial flow and neurologic examination were also unmodified. All patients had a stable disease and unchanged performance status after 6 months. This pure antiandrogen in a men with prostate cancer does not seem to interfere with self reported libido and erectile capability.
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PMID:[Monitoring of erection function in patients with prostatic carcinoma treated with Casodex]. 183 Apr 8


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