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

Since prolactin has several modes of action on prostatic growth and physiology, the effect of the antiprolactin bromocriptine on plasma kinetics and intraprostatic metabolism of testosterone was studied in patients with untreated prostatic cancer; a therapy protocol was deduced which was controlled in 27 patients with advanced inoperable prostatic adenocarcinoma. Bromocriptine resulted in a significant suppression of prolactin and testosterone as well and favored testosterone elimination from the plasma pool. Prostatic androgen uptake was enhanced and the intraprostatic metabolism altered in relation to tumor grade. Adjunctive administration of bromocriptine to 27 patients, mostly in the state of hormone resistance, resulted in an overall objective regression of 22.2% and in stable disease in 55.6% of the patients. In half of the individuals a prompt relief of bone pain from osseous metastases was observed as well as improvement of micturition and decline of phosphatase activity. This preliminary data justify further investigations under controlled and randomized conditions.
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PMID:[Bromocriptine for palliation of advanced prostatic carcinoma. Experimental and clinical profile of a drug (author's' transl)]. 8 47

In previous studies the immunoperoxidase method was used to detect intracellular prolactin binding sites in epithelial cells of normal and neoplastic rat prostate. As an extension of this work, the same approach was used to test for and to localize prolactin binding sites in autopsy and biopsy specimens of formalin fixed, paraffin embedded human prostate. Rehydrated tissue sections were exposed to varying concentrations of human placental lactogen or human prolactin and then to human placental lactogen or human prolactin antisera. The loci of hormone binding were visualized by an immunoperoxidase staining sequence. Hormone pretreatment produced immunospecific, dose related staining inside epithelial cells of normal, hyperplastic, and neoplastic human prostate indicative of intracellular prolactin binding. The patterns of intracellular hormone binding in human prostate were similar to those seen previously in rat prostate tissue. The possible involvement of prolactin in prostatic cancer and the potential diagnostic value of the immunoperoxidase approach to hormone binding are discussed.
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PMID:The application of immunoperoxidase methodology for the visualization of prolactin binding sites in human prostate tissue. 9 68

This study reports the effect of a vegetarian diet and dexamethasone administration on the hormone status of healthy Caucasian men and premenopausal women. A lower nocturnal release of prolactin and testosterone occurred in men fed a vegetarian diet, while in women, dexamethasone administration decreased the nocturnal release of prolactin and caused a greater decrease of plasma dehydroepiandrosterone (DHEA). These results show that diet modification can induce hormonal changes, If similar changes occur in patients with breast and/or prostatic cancer, diet modification may be of benefit in these patients with tumors known to be hormonally dependent.
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PMID:Effect of a vegetarian diet and dexamethasone on plasma prolactin, testosterone and dehydroepiandrosterone in men and women. 15 72

Since Prolactin has intra- and extrapostatic effects on growth and function of the prostate, the influence of the anti-prolactin bromocriptine (PRAVIDEL) was investigated in 15 patients with untreated prostatic carcinoma of various grades of differentiation in vivo. A five-days treatment with 15 mg Pravidel daily significantly suppressed prostatic androgen uptake, unrelated to tumor grading. 5 alpha-Reductase was favored in poorly differentiated lesions with a decreased testosterone/dihydrotestosterone ratio. The pretherapeutic accumulation of 5 alpha-androstanediol was diminished after Pravidel and the tissue/plasma ratio decreased. The 17 beta-hydroxy-pathway of testosterone is predominant as compared to the 17-keto pathway; both pathways are favored after Pravidel in poorly differentiated tumors. Intraprostatic metabolic effects of Pravidel are not related to peripheral androgen levels nor are they dependent on altered prostatic hormone uptake. In the poorly differentiated prostatic tumors Pravidel initiates a metabolic situation as observed in prostate cancer responding to androgen depletion or estrogen therapy.
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PMID:[Bromocriptine and prostatic carcinoma: testosterone metabolism in relation to tumor grading (author's transl)]. 43 16

Eighty-eight patients with hormone-resistant Stage IV prostate cancer were treated with a five-drug chemotherapy program. Patient demographic data, prior therapy, symptoms, extent of disease, and laboratory studies were analyzed statistically to evaluate the association of these parameters with survival from the onset of chemotherapy. Factors associated with short survival included age greater than 65, severe bone pain, poor performance status, presence of soft tissue metastases, anemia, elevation of serum LDH, SGOT, alkaline and acid phosphatases, and prolactin, and hypoalbuminemia. Race, stage at initial diagnosis, prior radiation therapy, prior orchiectomy, and elevation of CEA had no prognostic association. We suggest that clinical trials of new therapies of hormone-resistant prostate cancer take into account the presence of these prognostic factors in the analysis of the results of therapeutic programs.
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PMID:Prognostic factors in metastatic and hormonally unresponsive carcinoma of the prostate. 47 83

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

In the light of the high incidence of cardiovascular side effects with oestrogen therapy in patients with prostatic cancer, other medications altering androgen metabolism are under investigation. The influence of the anti-prolactin bromocriptin (CB157) on plasma kinetics of testosterone and on endogenous hormones was studied and compared with the effect of ethinyl oestradiol in 25 patients with prostatic carcinoma. Bromocriptine significantly suppressed both prolactin and testosterone, inhibited the transfer of androgen from the inner pool into the deep compartment and favoured its degradation. Ethinyl oestradiol decreased testosterone, LH and FSH, and prolonged the biological half-life of testosterone. The effects of bromocriptine on androgen metabolism might be of therapeutic value in patients with prostatic carcinoma.
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PMID:Testosterone metabolism in patients with advanced carcinoma of the prostate: a comparative in vivo study of the effects of oestrogen and antiprolactin. 75 43

Plasma testosterone, androstenedione, oestradiol-17beta, follicle stimulating hormone (FSH) and luteinizing hormone (LH) were not significantly different in patients with prostatic cancer, with benign prostatic hyperplasia or in patients without prostatic disease. Plasma prolactin concentrations were significantly lower in the patients with benign disease than those with prostatic carcinoma. Endocrine therapy in the form of stilboestrol administration significantly decreased plasma levels of testosterone, oestradiol-17beta, FSH and LH within 7 days of the treatment. After 7 days therapy prolactin levels increased significantly in all patients studied. Changes in growth hormone concentrations were more varied in response to stilboestrol, being elevated in several patients and remaining unchanged in others. Treatment of a few prostatic carcinoma patients who were receiving stilboestrol therapy with CB154, an inhibitor of prolactin secretion, brought an immediate decrease in prolactin levels which was was sustained. Plasma testosterone, androstenedione and growth hormone were unchanged in these patients but a significant decrease in plasma oestradiol-17beta was noted in two patients during CB154 administration.
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PMID:Plasma steroid and protein hormone concentrations in patients with prostatic carcinoma, before and during oestrogen therapy. 94 55

The indications for and the results of hypophysectomy for advanced cancer of the breast or prostate gland are reviewed. The technic of open microsurgical transsphenoidal hypophysectomy is described. Since the metabolism of some breast cancers is influenced by estrogenic hormones, the major effect of hypophysectomy seems to be the complete suppression of estrogen production by the gonads and adrenal glands by removal of gonadotropin and ACTH, respectively. Other specific substances, such as growth hormone or prolactin, may also be factors. In cases of prostate cancer which relapse after castration, the adrenals seem to elaborate a significant amount of extradgonadal androgen. Hypophysectomy removes the source of ATCH and thus stops androgen production by the adrenal glands. Other hormones may also be important. In premenopausal patients with advancing cancer of the breast, oophorectomy should be the initial procedure. Most patients after a previous favorable response to oophorectomy get a subsequent objective improvement from hypophysectomy. In postmenopausal patients the effects of hormone therapy should 1st be tried. Many patients responding favorably to hormone therapy will also be benefited later by hypophysectomy. Remission rates are higher in older women. However, hypophysectomy should be carried out relatively early to obtain a useful remission. About 25% of those not responding to other methods will obtain a remission following hypophysectomy. Along interval after the mastectomy before metastases occurs is a favorable prognostic sign. While bony metastases respond best, other sites of metastases do not contraindicate the operation. Most patients with prostatic metastases obtain relief after hypophysectomy, even some of those who have not been benefited by other methods. Advanced age alone is not a contraindication. A preoperative evaluation should be done including a series of endocrine studies. Open microsurgical transsphenoidal hypophysectomy is considered the operation of choice. Complete removal of the gland is accomplished with less disturbance to the patient than an intracranial operation. General anesthesia is used. After the operation tests for pituitary reserve are repeated and a maintenance regimen of hydrocortisone prescribed. Thyroid replacement therapy is often needed. Subjective remissions are more common than objective ones, particularly relief of pain. This operation was done on 20 men with metastatic cancer of the prostate and 23 women and 1 man with metastatic cancer of the breast. Of the prostate cases, 3 patients died during the early postoperative period. Of the other 17, there have been 7 deaths from the cancers after 1-7 months. Of the 23 breast cases, severe body pain was the indication for the operation. Relief occurred in 19 (83%). There have been 7 deaths from the cancers. Hypophysectomy does not predispose to or lead to alterations in emotional state or mental function. Others with larger series of cases have reported that those responding favorably have lived an average of 25.8 months while average survival of those not so responding has been only 5.6 months.
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PMID:Hypophysectomy in the treatment of disseminated carcinoma of the breast and prostate gland. 127 14

Natural killer (NK) cell activity was studied together with tumor marker serotests (PSA, PAP) and blood testosterone, estradiol, cortisol, and prolactin concentrations in treated prostate cancer patients. NK cell activity data were correlated with tumor stage (stage D0 + D1 versus stage D2) and showed statistically insignificant differences. Both tumor progression and stabilization of metastatic disease, triggered by the application of more appropriate therapy in progressive subjects, yielded low NK activity data. By contrast, normal NK activity was found during both partial remission of stage D2 tumor and stabilization of the same disease, after an initial period of tumor remission. Differences between NK activity data from the aforementioned two groups are statistically significant (P less than 0.01). In subjects examined, the application of NK activity assay to those with advanced disease reflected changes in the outcome of the treatment more closely than it did routine tumor marker assessment. The activity of NK cells seems unaffected by changes in basal blood estradiol, cortisol, testosterone, and prolactin concentrations that occur during therapy with pharmacological agents (estradiol, cyproterone acetate, diethylstilbestrol, and flutamide) and during surgical castration. The reported NK activity recordings in treated prostate cancer patients might be indicative of the presence of tumor cells in the circulation. If this holds true, the measurement of NK activity would appear to furnish urological oncology with a new tool for early, rapid recognition of progressive metastatic tumors.
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PMID:NK cell activity in treated prostate cancer patients as a probe for circulating tumor cells: hormone regulatory effects in vivo. 138 13


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