Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Growth hormone (GH) release and cAMP content were measured in monolayer cultures of anterior pituitary cells after beta-adrenergic and GH-releasing factor (GRF) receptor activation. Isoproterenol (Iso, ED50-20 nM) was less potent than GRF (ED50-20 pM) in stimulating GH release. Iso caused a rapid stimulation of GH release that was maximal after 15 min and declined thereafter, while GRF caused a more gradual increase in GH secretion that was maximal after 30 min and remained elevated after 3 h. Both Iso- and GRF-stimulated GH release were preceded by an increase in cAMP content in the pituitary cells. Further, the addition of 3-isobutyl-1-methylxanthine (IBMX) to the medium enhanced the GH-stimulatory and cAMP-accumulating effects of both secretagogues. Experiments performed with native catecholamines and synthetic catecholamine agonists and antagonists indicated that the GH-stimulatory effect of Iso was mediated by a mixed population of beta 1-adrenergic and beta 2-adrenergic receptors. Additionally, experiments performed with cultured GH3 tumor cells, found that incubation with GRF, Iso, vasoactive intestinal polypeptide, forskolin, or cholera toxin caused an increase in cAMP content in the cells. However, compared to the responses observed in primary pituitary cultures the GH secretory response to these agents was comparatively small. Together, these studies suggest that a mixed population of beta 1-adrenergic and beta 2-adrenergic receptors may act, at least in part, on somatotrophs in the anterior pituitary to stimulate GH release. Although both GRF and beta 2-adrenergic receptor agents affect GH release through a common second messenger system, their differing pharmacokinetic properties suggest distinct intracellular mechanisms.
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PMID:Iso stimulation of GH and cAMP: comparison of beta-adrenergic- to GRF-stimulated GH release and cAMP accumulation in monolayer cultures of anterior pituitary cells in vitro. 247 79

A 24 year old female with amenorrhea-galactorrhea due to a pituitary macroprolactinoma that eventually responded to bromocriptine with improvement of visual fields and intracranial hypertension syndrome is presented. After 2 years of treatment with bromocriptine her symptoms relapsed and she underwent transphenoidal hypophysectomy. The high serum prolactin levels detected initially decreased under bromocriptine to ward normal levels and was not modified after surgery, while gonadotropin production remain scarce. Growth hormone (GH) serum levels despite its normal concentration decreased significantly (p = less than 0.5) after pituitary ablation. We assume that the lack of response to bromocriptine in this case could have been due to a mixed hormonal nature of the tumor without overproduction or clinical expression of GH activity.
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PMID:[Macroprolactinoma resistant to bromocriptine]. 266 70

A 26-year-old man with acromegaly secondary to ectopic growth hormone-releasing hormone (GHRH) secretion by a metastatic carcinoid tumor is the subject of this study. He previously failed to respond to conventional therapeutic modalities (partial hypophysectomy, pituitary irradiation, high-dose bromocriptine and a combination of streptozotocin and 5-fluorouracil) and was treated with long-acting somatostatin analogue SMS 201-995 (Sandoz, East Hanover, NJ). Growth hormone and somatomedin C concentrations became normal, and GHRH-LI (GHRH-like immunoreactivity) was suppressed by more than 60%. The growth hormone response to exogenous GHRH 1-40 was stopped and growth hormone rise to thyrotropin-releasing hormone (TRH) was significantly attenuated. A significant shrinkage of the pituitary gland was observed. Similarly, the size of the metastatic carcinoid lesions decreased dramatically and was accompanied by a normalization of liver function. After almost 2 years of SMS 201-995 therapy, the patient was well and had no clinical signs of acromegaly. Thus, SMS 201-995 appears to be a remarkably effective agent for treatment of acromegaly secondary to ectopic GHRH secretion.
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PMID:Acromegaly from ectopic growth hormone-releasing hormone secretion by a malignant carcinoid tumor. Successful treatment with long-acting somatostatin analogue SMS 201-995. 289 32

Recent studies showed that both the pineal gland and the endogenous opioid system are involved in the modulation of the immune system and in the regulation of tumor growth. Moreover, a relationship between pineal and opioid system has been demonstrated. In order get an overall view of the psychoneuroendocrine interactions in cancer patients, the levels of melatonin, the most important pineal hormone, and of beta-endorphin have been measured on blood samples collected during the morning. The study was carried out on 54 patients, 42 healthy subjects, and in 34 patients having illnesses other than cancer. Breast cancer, lung carcinoma, and colorectum cancer were the three neoplasms detected in the patients investigated. Growth hormone (GH), somatomedin-C and prolactin (PRL) levels were also determined. beta-endorphin levels were found to be substantially within the normal range in patients with cancer, whereas those of melatonin were raised in several cases. The beta-endorphin/melatonin ratio was higher than 2 in normal subjects, in non-neoplastic patients and in most cancer patients without metastases, whereas this ratio was lower than 2 in almost all patients in a metastatic stage of the disease. Neither melatonin levels nor those of beta-endorphin appeared to be significantly correlated with GH, somatomedin-C, and PRL concentrations. The low beta-endorphin/melatonin ratio observed in metastatic patients suggests the presence of an unbalanced relation between the pineal and the opioid system in those subjects. Therefore, an anomalous relationship between pineal function and opioid activity might play a role in the clinical course of neoplastic disease.
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PMID:A study on the relationship between the pineal gland and the opioid system in patients with cancer. Preliminary considerations. 296 35

Folliculo-stellate cells (FS cells) in 40 pituitary adenomas and portions of anterior pituitary adjacent to the tumor in 26 cases were investigated immunohistochemically, using polyclonal antisera to S-100 protein (S-100) and glial fibrillary acidic protein (GFAP). The objective was to clarify the histological behavior of the FS cells. In most pituitary adenomas there were few or no S-100- or GFAP-positive cells, in comparison with numerous positive cells in the parts of the adenohypophyses compressed by adenomas. However, positive FS cells were observed in some types of pituitary adenomas. Growth hormone and prolactin producing adenomas frequently contained significant amounts of FS cells. In non-functioning adenomas, an unique case of FS cell adenoma was present. The adenoma was composed mainly of FS cells and immature glandular cells. The FS cells were sometimes located around follicles containing Periodic acid Schiff-positive material. Therefore, the FS cell adenoma is characterized by S-100- and GFAP-positive FS cells and PAS-positive follicles. In this type of adenoma, FS cells seemed to be the main proliferating component. In parts of the adenohypophyses adjacent to the adenomas, GFAP-positive FS cells were numerous. In the pathological conditions FS cells may possess the potential of reactive proliferation.
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PMID:Proliferating potential of folliculo-stellate cells in human pituitary adenomas. Immunohistochemical and electron microscopic analysis. 302 33

Growth hormone (GH)- and prolactin (Prl)-producing pituitary adenomas were studied with immunoelectron microscopy using protein A-gold complex, and were compared with the normal pituitary gland. GH-producing cells were readily identifiable by numerous, uniformly dense, round secretory granules in both adenomas and normal pituitary gland. In contrast, Prl secretory granules in normal pituitary gland were much larger in size than the scarce, smaller, secretory granules of Prl-producing adenomas. Thus immunoelectron microscopic identification of Prl is more valuable for prolactinoma. With more specific antigens available as tumor markers, immunoelectron microscopy appears to be a powerful tool for tumor diagnosis.
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PMID:Immunoelectron microscopy for growth hormone and prolactin in pituitary adenomas. 354 33

Growth hormone, GH1, or growth hormone and prolactin, GH3, secreting tumors were induced in 1 week old female Wistar-Furth rats and 17 week old female Wistar-Furth rats. At 11 or 30 weeks of age the parametrial fat pad (PFP) was weighed and a portion fixed with osmium tetroxide for cell quantitation by a Coulter counter technique. Tumor induction increased the body weight of both young and mature rats by 50 and 100% respectively when compared to age matched controls. Serum GH was elevated about 100 fold in both young and old treated rats when compared to controls. Tumor induction decreased the weight of the PFP in both young and old rats when compared to controls but the effect was only significant in the GH3 tumor bearing rats weights. The PFP made up a much smaller percentage of the body weight in all the treated groups when compared to respective age matched controls. Mean PFP adipocyte number was not affected by treatment or age. Tumor induction decreased the mean diameter and mean volume of adipocytes in both young and old rats of both treatment groups compared to age matched controls. The distribution of adipocytes by cell diameter was shifted toward smaller cells in the tumor-bearing rats. In conclusion, induction of GH1 or GH3 tumors elevated serum GH concentrations, increased body weight and decreased relative fat pad weight but did not affect adipocyte cell number. Hence, the proposed adipogenic function of GH does not appear to function in this model in vivo.
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PMID:Effect of growth hormone-secreting tumors on adipose tissue cellularity in young and mature rats. 373 64

Growth hormone (GH) was elevated in young growing, intact female Wistar-Furth rats bearing growth hormone (GH1) or growth hormone and prolactin (GH3) secreting tumors. Animals were injected with GH1 or GH3 cells at 1 wk of age. Total feed intake was measured for the 8-wk period from weaning until killed at 11 wk of age. Animals were fed a commercial chow diet throughout the trial. Body composition and composition of the liver and tibialis anterior muscle were determined. Tumor-bearing rats were about 65% heavier than control rats at 11 wk of age: most of the difference in body weight gain was obtained during the last 4 wk of the trial. Total feed intake during the 8 wk after weaning was increased in both GH1 and GH3 tumor-bearing rats when compared with controls. Overall feed efficiency (grams feed consumed/gram body weight gain) was improved in tumor-bearing animals when compared with controls. The GH1 tumor-bearing rats were slightly hyperphagic during wk 8, 9 and 10 (grams feed consumed/gram body weight) when compared with controls. The total amount of body dry matter, protein and ash was increased in tumor-bearing rats when compared with controls. There was no effect on total body fat. Tumor-bearing rats had increased liver weight and increased fat, protein, RNA, DNA and dry matter content when compared with controls. Tumor induction increased the weight, total RNA and total fat content of the tibialis anterior muscle when compared with controls. There was no effect on muscle protein content.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of growth hormone-secreting tumors on body composition and feed intake in young female Wistar-Furth rats. 377 95

Growth hormone releasing hormone (GHRH) has recently been isolated and sequenced from pancreatic tumors secreting GHRH. Patients with untreated acromegaly due to a pituitary tumor respond to exogenous administration of GHRH with a further rise of their elevated basal growth hormone (GH) levels. For the first time, we report the effects of exogenously administered synthetic GHRH in a patient with acromegaly due to a GHRH secreting pancreatic tumor. The diagnosis was established by high peripheral IR-GHRH levels (1100 pg/ml) and an arterio- venous tumor gradient of IR-GHRH. In this patient GH failed to respond to 1 microgram/kg of exogenous GHRH with the pancreatic tumor in situ; however, further increase of serum GH levels occurred after TRH administration, hypoglycemia and oral glucose administration. After removal of the tumor, serum GH levels decreased and a normal response to GHRH and TRH were demonstrated. The extract of the tumor contained 1.7 micrograms IR-GHRH per g wet tissue. Thus, lack of response to exogenous GHRH in untreated acromegaly may indicate the presence of an ectopic GHRH producing tumor.
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PMID:Failure to respond to growth hormone releasing hormone (GHRH) in acromegaly due to a GHRH secreting pancreatic tumor: dynamics of multiple endocrine testing. 392 12


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