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)

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

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

Several somatostatin analogs with recently synthesized acetylated N terminus were assayed in vivo for their effects on sodium pentobarbital-stimulated growth hormone (GH) levels in fed male rats and gastrin-releasing peptide (14-27)-stimulated gastrin levels in fasted male rats. The binding characteristics of these analogs to somatostatin receptors were also examined in various human tumors and normal tissues. The analog RC-101-I, injected at a dose of 0.1 micrograms/100 g body wt, significantly suppressed GH release (P less than 0.01) for at least 2 hr. Analog RC-160-II caused the longest inhibition of GH release, greater than that induced by nonacetylated parent analog RC-160, with GH levels showing significant suppression (P less than 0.01) for more than 3 hr. Analogs RC-160-II and RC-101-I and RC-160, injected at a dose of 1.0 micrograms/100 g body wt, significantly (P less than 0.01) suppressed gastrin-releasing peptide (14-27)-stimulated serum gastrin. Analog RC-101-I was active in this test at a dose of 0.1 micrograms/100 g body wt. RC-160-II showed significant binding to somatostatin-14 receptors in all investigated tissues (human colon, human colon cancer, breast cancer, human pancreas and pancreatic cancer, human prostate and prostate cancer, and rat cerebral cortex), but there were marked variations in binding affinities among various normal and cancerous tissues. The highest affinity was found in membranes of colon cancer (Ka = 18.4 nM-1) and breast cancer (Ka = 12.46 nM-1). The binding affinity of RC-160-II to somatostatin receptors in membranes of the breast cancer was similar to that of RC-160. RC-101-I showed higher binding affinity to somatostatin-14 receptors than RC-160 in human breast, pancreatic, and prostate cancer. With the exception of breast cancer tissue, the binding affinity of RC-101-I was significantly lower than that of RC-160-II in membranes of all investigated tissues. It can be concluded that acetylated somatostatin analogs RC-101-I and RC-160-II possess prolonged and enhanced biological activities in suppressing serum GH and gastrin in rats. Significant variations in binding affinities for these analogs in different tissues and various tumors suggest that differences may exist between somatostatin receptors in normal versus malignant tissues. This raises the possibility that some of these analogs could be used more selectively in the treatment of various neoplasms.
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PMID:Biological activity and receptor binding characteristics to various human tumors of acetylated somatostatin analogs. 134 89

The effects of treatment with a bombesin receptor antagonist [D-Tpi6, Leu13 psi (CH2NH) Leu14]BN(6-14)(RC-3095) and the combination of an agonist of luteinizing hormone-releasing hormone [D-Trp6]-LH-RH and somatostatin analog D-Phe-Cys-Tyr-D-Trp-Lys-Val- Cys-Trp-NH2 (RC-160) were studied in nude mice bearing xenografts of the hormone-dependent human prostate tumor PC-82. During the 5 weeks of treatment, tumor growth was decreased in all treated groups compared with controls. Bombesin antagonist RC-3095 and the combination of [D-Trp6]-LH-RH and RC-160 caused a greater inhibition of tumor growth than [D-Trp6]-LH-RH or RC-160 alone as based on measurement of tumor volume and percentage change in tumor volume. The largest decrease in tumor weight was also seen in the groups treated with the bombesin antagonist and with the combination of RC-160 and [D-Trp6]-LH-RH. Serum prostatic-specific antigen levels were greatly decreased, and insulin-like growth factor I (IGF-I) as well as growth hormone levels were reduced in all treated groups. Specific binding sites for [D-Trp6]-LH-RH, epidermal growth factor (EGF), IGF-I, and somatostatin (SS-14) were found in the tumor membranes. Receptors for EGF were significantly down-regulated by treatment with the bombesin antagonist or RC-160. Combination of LH-RH agonists with somatostatin analog RC-160 might be considered for improvement of hormonal therapy for prostate cancer. The finding that bombesin antagonist RC-3095 inhibits the growth of PC-82 prostate cancer suggests the merit of further studies to evaluate the possible usefulness of antagonists of bombesin in the management of prostatic carcinoma.
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PMID:Inhibition of growth of PC-82 human prostate cancer line xenografts in nude mice by bombesin antagonist RC-3095 or combination of agonist [D-Trp6]-luteinizing hormone-releasing hormone and somatostatin analog RC-160. 137 10

High-dose medroxyprogesterone acetate (MPA) was given orally to 7 patients with advanced prostatic cancer and severe pain due to bone metastases; 5 patients had stable and 2 had progressive disease. Pain relief was obtained in 6 patients. Two patients who reported complete relief of pain showed suppressed levels of gonadotrophins after MPA treatment. In the other patients, suppression of plasma gonadotrophin levels was observed before treatment. The plasma levels of prolactin, growth hormone and thyroid stimulating hormone were not affected by MPA. Only 1 patient showed suppression of plasma adrenocortical trophic hormone. The plasma levels of cortisol and dihydroepiandrosterone sulphate were suppressed in 6 patients, but there was no correlation between the suppression and the occurrence of pain relief. These findings suggest that the mechanism of pain relief by high-dose MPA may be very complicated.
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PMID:Effect of high-dose medroxyprogesterone acetate on plasma hormone levels and pain relief in patients with advanced prostatic cancer. 169 98

Circulating osteocalcin (OC) and cortisol levels were measured in blood samples from 93 patients with dissaminated prostate cancer. Among these subjects 79 had not responded to therapy, while 14 had responded to a variety of anticancer treatment strategies (orchiectomy, cyproterone acetate (CPA), flutamide, Buserelin, diethylstilbestrol (DES), Estracyt, and polyestradiol phosphate). The control group consisted of 19 patients with benign prostatic hypertrophy. In the majority of these patients blood adrenocorticotropic hormone (ACTH), estradiol human growth hormone (hGH), and thyroid stimulating hormone (TSH) levels were also assessed. In nonresponders to therapy with DES and Estracyt subnormal circulating OC levels were measured, while normal OC values were found in nonresponders to other treatment strategies. In patient given Estracyt highly elevated estradiol levels were recorded. Subnormal and/or low-normal estradiol concentrations were found in patients subjected to CPA and DES. Elevated blood cortisol levels were assessed in subjects treated with DES and Estracyt while at the same time either subnormal and low-normal plasma ACTH concentrations were measured in these same patients. Accordingly, the decline observed in OC concentration seems to be a consequence of the well-established inhibitory effect of glucorticoids on osteoblast activity. The decline in blood cortisol levels obtained after administration of dexamethasone in patients given DES and Estracyt may be attributed both to possible changes in catabolic pathways and to the contribution of the negative neuroendocrinological feedback.
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PMID:Plasma osteocalcin values and related hormonal parameters in patients subjected to a variety of prostate anticancer agents. 185 47

Newly developed somatostatin analogues may be useful agents in the treatment of breast and prostate cancer. Potential mechanisms of antitumor action include suppression of circulating levels of trophic hormones and growth factors as well as direct effects at the tumor level, potentially involving autocrine/paracrine mechanisms. Pilot clinical trials conducted in heavily pretreated women with advanced breast cancer indicate that SMS 201-995 (Sandostatin R) has minimal toxicity and moderately suppresses stimulated growth hormone secretion and basal somatomedin-C level. Somatostatin analogues have also been found to retard the growth of experimental prostate cancer, particularly when used in combination with LHRH analogues. The therapeutic efficacy of these compounds used alone or in combination with other agents in the treatment of breast and prostate cancer remains to be established in larger clinical trials involving less heavily pretreated patients.
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PMID:Somatostatin analogues in the treatment of breast and prostate cancer. 198 Oct 12

The serum levels of the pineal hormone melatonin were determined by radioimmunoassay (RIA) in 4-h intervals throughout a 24-h period in elderly men with different types of prostate tumors: benign prostatic hyperplasia (BPH, n = 13), incidental carcinoma (PCi, n = 5), and nonmetastasizing carcinoma (PC, n = 9), as well as in young men (YM, n = 10). Simultaneously, the pituitary hormones prolactin, growth hormone, luteinizing hormone and follicle-stimulating hormone were measured by RIA. All subjects were untreated and free of serious complaints, and they stayed in the same environment. The data were analyzed by the population mean-cosinor method, and linear correlation coefficients between the five hormones were calculated for each group. Melatonin showed significant circadian rhythms in young men and patients with BPH and PCi but not in patients with PC. Twenty-four-hour mean concentration (mesor) and amplitude were significantly increased in patients with PCi as compared to patients with PC. Prolactin showed significant circadian rhythms in young men and in patients with BPH, whereas patients with PCi and PC appeared to have ultradian variations. Growth hormone did not show significant rhythms in any of the groups; the mesors were elevated in all tumor groups as compared to young men. Gonadotropin mesors were elevated in all tumor patients as compared to young men; rhythms were not detected. Carcinoma patients showed different interhormonal correlations than all other groups. These results indicate that modulation of melatonin secretion, accompanied by changes in the pituitary hormone levels, may be related to development and growth of prostate cancer.
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PMID:Evidence for modulation of melatonin secretion in men with benign and malignant tumors of the prostate: relationship with the pituitary hormones. 242 Sep 60

The effects of parenteral and parenteral plus oral estrogen therapy on the serum levels of sex hormone binding globulin (SHBG), pregnancy-associated alpha 2-macroglobulin (alpha 2-PAG), growth hormone (GH), and somatomedin C (SmC) were studied in 26 patients with prostatic cancer. Intramuscular polyestradiol phosphate treatment, yielding a mean serum level of estradiol-17 beta of 1,446 pM and a mean testosterone level of 4.5 nM, had no significant effects on alpha 2-PAG, GH, and SmC and increased SHBG levels only marginally. Combined treatment with intramuscular polyestradiol phosphate and oral ethinyl estradiol greatly increased SHBG and alpha 2-PAG levels and caused elevated GH and decreased SmC levels. The route of estrogen administration is probably of major importance for the hormonal effects on hepatic activity as reflected by SHBG and alpha 2-PAG levels. Bypassing the portal circulation might be advantageous with respect to liver-related side effects of estrogen therapy. GH and SmC might act as mediators of estrogen effects on the human liver.
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PMID:Steroid-sensitive proteins, growth hormone and somatomedin C in prostatic cancer: effects of parenteral and oral estrogen therapy. 244 14


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