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)

Hypophysectomy was studied for its possible effects on cancer by alt eration of the endorcines at the New York Hospital-Cornell Medical Center beginning in 1953. The major effort has been the treatment of 850 cases of metastic breast cancer. In 80 patients with other types of metastatic cancer benefit was found only in 50 cases of prostatic cancer. Prolactin is mediated directly from the anterior pituitary to breast tissue where it aids and abets the growth of breast cancer; its secretion is largely dependent on the estrogen produced in ovaries and adrenals. In humans estrogen given after total hypophysectomy is found to be ineffective in altering metastases. Growth hormone is also produced in the anteriod lobe of the pituitary but its production is not dependent on an estrogen feed-back mechanism. If the primary cancer is dependent on the presence of prolactin, failures with hypophysectomy are explained the tumor having gained autonomy and being no longer so dependent. Contraindications to hypophysectomy include extensive pulmonary, liver, or brain metastases and any systemic disease that would preclude major surgery. Following a remission after oophorectomy, another remission with hypophysectomy may often be obtained. Neither the pathological type of a breast cancer nor the location of metastases alter the results. However the longer the interval between mastectomy and reactivation of the tumor, the more favorable the outlook. Maintenance substitution therapy following removal of the pituitary employs daily hydrocortisone, 17.5 mg orally, or equivalent steroid preparations. The mortality rate is 2% in the first 30 days after operation. In 88 patients evaluated 2 years after operation those who had received a remisssion lasting over 6 months survived nearly 5 times longer than those unbenefitted by the operation. The intracranial procedure is preferred. In cases of failure or when a remission terminates, male hormone therapy, chemotherapy, or radiation may have limited value.
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PMID:Hypophysectomy for metastatic cancer. 466 60

Testosterone (T), dihydrostestosterone (DHT) and prolactin (HPr) levels were determined in normal males and females, in patients with benign prostatic hypertrophy (BPH) and in clinically stable patients with prostatic carcinoma (CAP), intact and orchiectomized. CAP patients were either untreated or on different modalities of therapy. The HPr levels were higher in prostatic cancer patients, in BPH patients, and in subjects on estrogen therapy. No significant differences were found between controls or patients treated with 5-Fu plus cytoxan. The T and DHT levels were decreased in all noncontrol subjects. The levels of DHT in intact, untreated CAP patients or those receiving 5-FU plus cytoxan were significantly higher than in BPH patients. Based on these observations, it appears that HPr could be involved with T and DHT in a feedback control role, especially in BPH. The alterations in these hormone levels in CAP treated or untreated patients are in marked contrast and must be evaluated further.
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PMID:Measurements of prolactin and androgens in patients with prostatic diseases. 615 26

To investigate the possible role of circulatory levels of prolactin on the development of prostatic tumors, and to gain insight into the prolactin-androgen relationship, serum prolactin and testosterone were determined in 73 patients with newly diagnosed prostatic adenocarcinoma. Controls consisted of 32 patients with benign prostatic hyperplasia before treatment, 19 age-matched controls, and 21 young individuals. Hormones were measured under standardized conditions by highly specific and sensitive radioimmunoassays. There was no difference in prolactin in the elderly men regardless of prostate pathology, but a significant increment was found in young controls. Individual prolactin values did not correlate with serum testosterone, and there was no statistical regression in prolactin values of patients in the age range between 50 and 80 years. In a second study, serum testosterone and prolactin were measured in 7 patients with prostate cancer and in 6 individuals with benign prostatic hyperplasia before and 30 and 60 minutes after stimulation with an iv bolus of 200 microgram TRH. Both hormones were within the normal range at time T0, and a significant stimulation of prolactin was achieved (p less than 0.001). Prolactin values did not differ between patients with benign and malignant prostatic disease. Thus, when investigating the role of prolactin in neoplastic prostatic growth in the human, it seems necessary to investigate receptor-mediated prostatic tumor responsiveness, and interferences with androgen converting enzymes on a cellular level, rather than circulating prolactin concentrations.
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PMID:Serum prolactin and tumors of the prostate: unchanged basal levels and lack of correlation to serum testosterone. 615 29

Three experiments were performed to determine whether human prolactin (hPr) affects prostatic uptake and metabolism of testosterone (T). 1) Patients with prostatic cancer were infused twice with radio-labelled androgens, the first time with basal hPR, the second time with oral thyrotrophin-releasing hormone (TRH)-elevated hPr. In 5/7, significant increases in metabolic clearance of dihydrotestosterone (DHT) and in conversion of T to DHT accompanied increased hPR. 2) The incorporation of labelled T into minced benign prostatic hypertrophy (BPH) tissue from subjects with high (40 ng/ml) hPR was measured and was found to be more than twice the uptake into tissue from those with low hPR (6.5 +/- 1.9 ng/ml). 3) Uptake and metabolism in vivo of a bolus of 3H-T by BPH and carcinomatous prostates was measured and was far greater in subjects whose hPR was elevated by chlorpromazine than in untreated controls. It is concluded that prolactin increases prostatic uptake and metabolism of T. It is suggested that the best management of prostatic cancer should include depletion of prolactin as well as androgen.
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PMID:Interaction of prolactin and testosterone in the human prostate. 616 28

Bromocriptine mesylate lowers the serum concentration of prolactin and TSH in patients with prostatic hypertrophy as a function of drug administration time. The effect of a 2.5-mg dose in lowering these two hormones in presumably similar patients is statistically highly significant and relatively large at unusual test times (in the evening); at other, conventional test or administration times (early morning or midday), it is smaller, questionable, or not demonstrable with the dose and conditions used. Dosing without timing may lead to reduced effect or lack of effect, ambiguity and controversy, and lack of timing may account for the circumstance that an effect of bromocriptine upon TSH in human serum was not previously established. Rigorous assessment of the effect of bromocriptine mesylate upon circulating TSH and prolactin requires consideration of the entire spectrum of rhythms, ultradian and infradian as well as circannual. The circadian approach here analyzed represents a step toward that goal and indicates that the circadian frequency is a critical determinant of this response. Manipulation of TSH concentration in serum, in turn, is of interest in view of the demonstrated alteration of the circannual TSH rhythm in patients with prostatic cancer.
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PMID:Circadian aspects of serum prolactin and TSH lowering by bromocriptine in patients with prostatic hypertrophy. 617 Sep 68

The nature of hormonal changes with age and the possible role of these changes in the development of benign prostatic hyperplasia (BPH) and prostatic cancer (PC) were studied by assaying the plasma levels of total and free testosterone (T), estradiol (E2), prolactin, and sex hormone binding globulin binding capacity (SHBG) in 20 normal healthy men aged 40-59 years, in 30 patients with BPH aged 63-79 years, and in 30 patients with PC of similar height, weight, and age as the BPH patients. The mean E2 was highly significantly (P less than 0.0005) lower in the PC patients and in the young controls than in the BPH patients. The mean free T was significantly higher in the young controls than in the BPH patients (P less than 0.025) and PC patients (P less than 0.0005). The PC patients had a slightly lower (P less than 0.05) mean free T and mean E2/free T ratio than the BPH patients. The mean E2/free T ratio was significantly higher in the BPH patients (P less than 0.0005) and in the PC patients (P less than 0.0025) than in the young controls. It seems possible that the observed age-dependent significant increase in plasma estrogen concentration in the BPH patients may act as a protective factor against prostatic cancer.
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PMID:Plasma estradiol, free testosterone, sex hormone binding globulin binding capacity, and prolactin in benign prostatic hyperplasia and prostatic cancer. 618 6

The goals of hormonal therapy for prostatic cancer are to decrease circulating plasma testosterone to castration levels; prevent a rise in or reduce circulating prolactin; and block residual androgen at the cell level. Orchiectomy is very effective but does not prevent residual adrenal androgens from being converted to dihydrotestosterone (DHT); also, it has no effect on plasma prolactin. Estrogen has no known effect on androgen-receptor concentration or DHT binding to receptor and raises plasma prolactin. It also has significant side effects. Megestrol acetate, the only antiandrogen currently available for use in the United States, has been shown to block androgen from all sources. It produces a transient reduction in plasma testosterone to levels somewhat higher than those in castrated men, and it has no effect on plasma prolactin. When used in a dose of 120 mg/day in combination with 0.5 to 1.5 mg of estradiol per day, it acts synergistically to suppress pituitary gonadotropins and maintain plasma testosterone at castration levels for periods of up to 1 year. Newer therapies being studied include flutamide, a nonsteroidal antiandrogen, and luteinizing hormone-releasing hormone (LHRH). Data on these agents are limited and comparisons with standard therapies are needed.
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PMID:Comparison of various hormonal therapies for prostatic carcinoma. 619 46

The authors begin by stressing the importance of the role of prolactin in the metabolism of testosterone in the cells of the prostate. They studied three groups of patients: 9 patients with prostatic cancer, 15 patients with benign prostatic adenoma and 11 healthy young men. Inhibition of the dopaminergic receptors by metoclopramide only resulted in a significant increase in serum prolactin in the patients with prostatic cancer, while the serum prolactin level remained unchanged in the young men and in the patients with prostatic adenoma. The authors believe that this increased secretion of prolactin in patients with prostatic cancer is related to a decrease in the testosterone: oestradiol ratio. They suggest the use of bromocriptine in patients with prostatic cancer no longer responding to oestrogen therapy in the event of prolactin over-secretion. Some papers have reported the beneficial effect of bromocriptine on the general health of these patients.
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PMID:[Increased secretion of prolactin after inhibition of dopaminergic receptors by metoclopramide in patients with cancer of the prostate]. 620 86

We have investigated the effects of chronic administration of D-Trp6-LH-RH on the growth of various hormone dependent tumors in rats and mice. Treatment of male Copenhagen F-1 rats bearing the Dunning R-3327H prostate adenocarcinoma with 25 micrograms of D-Trp6-LH-RH bid for 21 days significantly reduced tumor weight and volume as compared to controls. Serum LH, prolactin and testosterone levels in Copenhagen F-1 rats bearing Dunning tumors were significantly decreased after treatment with D-Trp6-LH-RH. Administration of D-Trp6-LH-RH in doses of 25 micrograms/day for 21 days to mice bearing the MXT mammary carcinoma significantly decreased tumor weight and volume. In rats bearing the MT/W9A mammary adenocarcinoma, D-Trp6-LH-RH, at a dose of 25 micrograms bid for 28 days significantly decreased tumor weight and volume. Administration of D-Trp6-LH-RH in a dose of 25 micrograms/day, 3-18 days after inoculation with the tumor, inhibited the growth of the prolactin (PRL) and ACTH-secreting pituitary tumor 7315a in female Buffalo rats. In three experiments D-Trp6-LH-RH (30-60 micrograms/day) decreased tumor weight and/or volume of the Swarm chondrosarcoma. Regression of these hormone-dependent tumors in rats and mice in response to chronic administration of D-Trp6-LH-RH suggests that this compound can be used for treatment of prostate cancer and breast cancer, and also considered for the development of a new endocrine therapy for chondrosarcomas, osteosarcomas, pituitary tumors and other hormone-dependent neoplasias. The demonstration of the successful use of LH-RH agonists for the palliative management of stage C and D prostate cancer has already shown that this treatment could be employed instead of surgical orchiectomy or estrogen therapy. Preliminary clinical trials suggest that agonists of LH-RH might also be of help in the treatment of breast cancer in premenopausal women.
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PMID:Inhibition of the growth of some hormone dependent tumors by D-Trp6-LH-RH. 624 77

A x C rat prostate cancer cells were established in continuous culture. The polygonal epithelial cells had granular cytoplasm and well-defined cell margins, contained round to oval nuclei with prominent nucleoli, and were tumorigenic when inoculated into A x C male rats. The tumors produced by the injected prostate cancer cells grew as well-vascularized, solid, cribriform adenocarcinomas. The rat prostate cancer cells and derived tumors contained cytoplasmic and nuclear androgen receptors and prolactin receptors. Androgen regulation of prolactin receptor content and androgen receptor distribution in A x C rat prostate cancer cells were comparable to those of the normal ventral prostate gland. These studies suggest that the A x C rat prostate cancer cells and tumors may represent a unique model for studies of hormonal regulation of prostate cancer cell behavior.
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PMID:A x C rat prostate adenocarcinoma: initial characterization of testosterone regulation of hormone receptors of cultured cancer cells and derived tumors. 625 2


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