Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Growth hormone (GH) serum levels in response to the administration of aminergic drugs and thyroliberine (TRH) were determined in a group of 34 acromegalics. Administration of bromocriptine (10 mg single oral dose) was followed by a decrease in GH below 60% control values in 35% of the cases. Administration of diazepam (10 mg single oral dose) to those cases not responding to bromocriptine induced a decrease in GH in 58% of the cases and an increase in GH in 42%. Administration of cyproheptadine (24 mg/day for one month) to those cases not responding to bromocriptine or with increased GH after the administration of diazepam, decreased GH in 75%, while increased GH in 25% of the cases. TRH 200 micrograms single I.V. dose induced increase of 128% GH basal level in 65% of cases (TRH positive) which correlated with more benign clinical course, decreased GH levels in response to bromocriptine, increased PRL levels, PRL-GH mixed secreting adenomas in immunohistochemistry studies, presence of granulated cells in electron microscopy studies and normalization of GH in the majority of surgically treated cases. By contrast, TRH negative cells correlated with aggressive tumor growth, lack of response to bromocriptine, normal PRL levels, pure GH secreting adenomas by immunohistochemistry, poorly granulated cells and lack of response to surgical treatment. Results suggest that there is more than one type of acromegaly that might be distinguished by the aminergic control on GH secretion.
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PMID:Differential response to aminergic stimuli and biological behavior of growth hormone secreting pituitary adenomas. 210 17

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

Growth hormone has been shown to stimulate muscle protein synthesis, improve nitrogen balance and promote wound healing in a variety of catabolic states. Its role in the tumor-bearing host is controversial because of its potential to stimulate tumor growth. Twenty-seven Lobund/Wistar rats bearing a subcutaneous prostate tumor implant (PA-III), were randomized to receive growth hormone (1,000 mU/kg/day) or placebo (saline) in the protein-fed and protein-depleted states. Body weight, primary tumor growth and tumor metastasis were assessed to determine the effect of growth hormone and dietary protein intake on these parameters. Growth hormone significantly increased carcass weight in protein-fed animals and reduced carcass weight loss in protein-depleted animals. No stimulation of primary tumor growth occurred and tumor:body weight ratio was similar in all treatment groups. Inhibition of spontaneous pulmonary metastasis occurred following growth hormone therapy in protein-fed and protein-depleted animals. Thus, in this tumor model, growth hormone was found to support host growth selectively and inhibit pulmonary metastasis and may be used as an adjunct to treat cancer cachexia effectively in the future.
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PMID:Growth hormone and prostate cancer growth and metastasis in tumor-bearing animals. 837 96

The role of human growth hormone (hGH) as a nutritional adjunct for cancer patients is controversial because of its potential mitogenic effects on tumor growth. No studies to date have examined the effect of hGH on human tumor response in vivo. In Vitro: Athymic mice were injected (s.c.) daily with hGH (GH, n=14) or saline (CTL, n=14). On Day 10, serum was collected and added to human pancreatic carcinoma cells in culture. In Vivo: Athymic mice were inoculated (s.c.) with human pancreatic carcinoma cells. On Day 14, mice were randomized to receive daily either hGH (GH, n=14) or saline (CTL, n=12). On Day 29, animals received [3H]phenylalanine for tissue protein fractional synthetic rate (FSR) measurement. Tumors were excised and cell cycle kinetics analyzed. Data are expressed as mean +/- SEM. Statistical analysis was performed by unpaired t test and/or ANOVA where appropriate. In Vitro: Serum from GH-treated animals had elevated IGF-1 levels (287 +/- 34 ng/ml vs 157 +/- 53 ng/ml, P<0.001) and significantly stimulated cell growth (No. cells x 10(3)/well) compared with CTL serum (925 +/- 31 vs 747 +/- 38, P<0.001). In Vivo: Serum for GH-treated animals had elevated IGF-1 levels (287 +/- 34 ng/ml vs 157 +/- 53 ng/ml, P<0.001) and significantly stimulated cell growth (No. cells x 10(3)/well) compared with CTL serum (925 +/- 31 vs 747 +/- 38, P<0.001). In Vivo: Growth hormone had no significant effect on tumor growth rate (mm3/day) (1.45 +/- 0.47 CTL vs 1.57 +/- 0.66 GH), final tumor weight (mg) (0.19 +/- 0.15 CTL vs 0.17+/- 0.06 GH), DNA Index (1.5 +/- 0.1 CTL vs 1.5 +/- 0.1 GH), percent S phase (20.3 +/- 3.3 CTL vs 22.1 +/- 3.0 GH), or tumor FSR (%/day) (51.1 +/- 17.8 CTL vs 70.2 +/- 61.1 GH). Growth hormone significantly elevated serum IGF-1 levels (ng/ml) (176 +/- 48 CTL vs 222 +/- 53 GH, P<0.005) and liver FSR (%/day) (62.8 +/- 17.8 CTL vs 79.7 +/- 12.7 GH, P<0.005). Serum of GH-treated mice increased human pancreatic cell growth in vitro. In vivo, GH administration raised serum IGF-1 levels and increased liver protein FSR, without tumor growth, cell cycle kinetics, or protein FSR.
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PMID:Effect of human growth hormone on human pancreatic carcinoma growth, protein, and cell cycle kinetics. 865 2

Forty-four adult acromegalic patients carrying growth hormone-producing pituitary macroadenomas were investigated with neuroradiological and endocrinological techniques. Plasma growth hormone and somatomedin-C levels were repeatedly measured before surgical removal of tumors and during the follow-up period. Twenty-five patients presented preoperatively with an invasive adenoma that involved the cavernous sinus (CS). Diagnosis of tumor invasivity was made according to distinct neuroradiological criteria and was confirmed or rejected during surgery Significantly higher basal growth hormone levels were found in patients with CS invasion than in cases without tumor growth in the CS. Evidence is presented that plasma growth hormone level in acromegalics is a more sensitive indicator for predicting tumor invasiveness than somatomedin-C. Growth hormone basal values before surgery and the extent of their decrease after removal of tumor correlate with adenoma growth in the parasellar compartments and should be used as a prognostic factor to aid in planing adjuvant tumor treatment.
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PMID:Factors predicting pituitary adenoma invasiveness in acromegalic patients. 929 20

Cancer registration statistics of economically advanced countries indicate that bladder carcinoma incidence ranks fourth in men and eighth in women, but a reliable tumor marker for predicting the disease course is still lacking. We designed an immunohistochemical study to comprehensively assess the trophoblastic hormone production profile of transitional cell carcinoma (TCC) of the bladder. Moreover, we correlated histological differentiation and tumor stages with marker expression and, finally, evaluated a potential tumor origin of hCGbeta core-fragment (hCGbetacf). To this end, formalin-fixed, paraffin-embedded tumor tissues from 104 patients with urothelial neoplasms of various histological grades (23 GI, 24 GII, and 38 GIII) and stage (19pTis, 21pTa, 29pT1, and 35pT2-T4) were analyzed by the immunoperoxidase technique using our own well-characterized monoclonal antibodies against the glycoprotein hormones human chorionic gonadotropin (hCG) and its derivatives hCGalpha, hCGbeta, hCGbetacf, luteinizing hormone (LH, LHbeta), follicle-stimulating hormone (FSH, FSHbeta), and the protein hormones placental lactogen (hPL) and growth hormone (hGH-V/N). Overall, trophoblastic hormone immunoreactivity was found in 36% of TCC. Detailed analysis showed 35% hCGbeta, 17% hCGbetacf, 9% hCGalpha, 4% hCG, and 2% hPL-positive cases. The tumors produced neither GH-N, placental GH-V, nor the pituitary gonadotropins FSH/FSHbeta and LH/LHbeta. Marker positivity significantly increased with high-grade lesions (26% GI- v 55% GIII-TCC) and advanced tumor stages (24% pTa v 63% > or = pT2). Hormone immunoreactivity was frequently observed in highly proliferating areas. Our findings, together with recent structural and clinical studies, strongly suggest that these hormones, or derivates thereof, might act as local tumor growth factors. Normal urothelium, urothelial papillomas, and carcinoma in situ showed no positive reactions. All tumors producing hCG-derived molecules were negative for the concommitantly analyzed neuroendocrine markers chromogranin A, synaptophysin, and neuron-specific enolase (NSE). In summary, one third of TCC ectopically produce trophoblastic hormones, which is specifically correlated with stage and grade. Apart from hCGbeta (97% of the marker-positive cases), the intracellular occurrence of hCGbetacf, apparently the second most frequently produced marker, was surprising, and there was also a lesser degree free hCGalpha and intact holo-hormone expression. The placental protein hormones PL and GH-V are not appropriate tumor marker candidates. Finally, our histogenetic findings support a metaplastic origin of the hCG producing choriocarcinomatous phenotype of some TCC.
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PMID:Production of trophoblastic hormones by transitional cell carcinoma of the bladder: association to tumor stage and grade. 956 88

Bone marrow transplantation is increasingly being used for treatment of patients with malignant and hematologic disorders. The process requires 4-6 wk of waiting for recovery from conditioning regimens and for engraftment. Patients undergo intensive monitoring and supportive care, yet their requirements for deep uninterrupted sleep often go unrecognized. We suggest that deep sleep may promote recovery and stem cell proliferation through production of growth hormone and melatonin, and through other mechanisms. Growth hormone production occurs primarily during deep, rapid-eye-movement (REM) sleep. Growth hormone promotes nutritional recovery, mucosal healing, cellular uptake of amino acids, and promotes proliferation of bone marrow cell lines in animal models. Melatonin is also secreted during nighttime and during sleep. Melatonin increases immune response, inhibits tumor growth, counteracts stress-induced immunosuppression, protects against viral infections, stimulates GM-CSF, salivary IgA, antioxidant properties and enhances sleep. In our preliminary studies, we have found that most patients undergoing bone marrow transplantation complain of sleep disturbances related to laminar air flow noise-beepers, and lights. We recommend several simple methods of enhancing sleep and for more research in the pathophysiology of sleep and bone marrow transplantation.
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PMID:Does sleep promote recovery after bone marrow transplantation?--A hypothesis. 1008 61

In a recent study we demonstrated that recombinant human growth hormone (r-hGH; Saizen) delayed tumor-induced cachexia in human tumor xenografts in vivo. Such a therapeutic effect could have a great impact in the supportive care of advanced cancer patients. Before large clinical studies are initiated possible growth stimulation should be excluded. This question was investigated in vitro in 20 human tumor models, which had been established in serial passage in nude mice. The effect of continuous exposure of r-hGH was investigated at dose levels ranging from 0.3 ng/ml up to 0.1 microg/ml in colorectal (n=2), gastric (n=1), non-small cell lung (n=4), small cell lung (n=1), mammary (n=3), ovarian (n=2), prostate (n=2) and renal cancers (n=2), and melanoma (n=3) using a modified Hamburger and Salmon clonogenic assay. The results show that there was neither tumor growth inhibition nor any evidence for tumor growth stimulation in any of the tumors studies. Therefore this preclinical study in 20 human tumor models indicated no direct risk for tumor growth enhancement.
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PMID:No evidence of tumor growth stimulation in human tumors in vitro following treatment with recombinant human growth hormone. 1108 60

Growth hormone releasing hormone (GHRH) is known to have multiple anabolic effects and immune-stimulatory effects. Previous studies suggest that treatment with anabolic hormones also has the potential to mitigate the deleterious effects of cancer cachexia in animals. We studied the effects of plasmid-mediated GHRH supplementation on tumor growth and the role of antitumor immune cells with two different human tumor cell lines, NCI-H358 human bronchioalveolar carcinoma and MDA-MB-468 human breast adenocarcinoma, subcutaneously implanted in nude mice. GHRH supplementation by delivery of human GHRH from a muscle-specific GHRH expression plasmid did not increase tumor progression in tumor-bearing nude mice. Male animals implanted with the NCI-H358 tumor cell line and treated with the GHRH-expressing plasmid exhibited a 40% decrease in the size of the tumors (P<.02), a 48% increase in white blood cells (P<.025) and a 300% increase in monocyte count (P<.0001), as well as an increase in the frequency of activated CD3+ and CD4+ cells in the tumors, compared to tumors of control animals. No adverse effects were observed in animals that received the GHRH-plasmid treatment. The present study shows that physiological stimulation of the GHRH-GH-IGF-I axis in mice with cancer does not promote tumor growth and may provide a viable treatment for cancer cachexia in humans.
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PMID:Growth hormone releasing hormone plasmid supplementation, a potential treatment for cancer cachexia, does not increase tumor growth in nude mice. 1537 78

Growth hormone (GH) hypersecretion leads to acromegaly which is associated with several co-morbidities and increased mortality. Despite of the typical clinical features and modern diagnostic tools, it often takes years from the onset of the disease until the diagnosis. The aims of the treatment are to reduce or control the tumor growth, inhibit the GH hypersecretion, normalize the insulin-like growth factor-I (IGF-I) levels, treat the co-morbidities and therefore reduce mortality. There are three approaches for therapy: surgery, medical management (dopamine agonist, somatostatin analogues and GH receptor antagonist), and radiotherapy. Efficient therapy of the disease is based on the appropriate multidisciplinary team management.
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PMID:[Treatment of acromegaly]. 2070 53


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