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)

Fifty-one female patients with prolactin producing tumors (PRL 1100 to 88,000 microU/ml) and 26 male patients with prolactin producing tumors (PRL 6500 to 400,000 microU/ml) were studied. Only 25% of the females had visual field defects which were present in 70% of the males. All females had amenorrhea but only 35 had galactorrhea. Hypopituitarism was rarely seen in the females but in most of the male patients. Twenty-four females and all male patients were operated (transphenoidal or transfrontal operation). PRL normalized in only eight females and in none of the males. Two patients became pregnant postoperatively, four after postoperative treatment with bromocriptine. Bromocriptine induced regular menses in 4 other patients operated by transsphenoidal route. Eight patients with microadenoma (PRL less than 4000 microU/ml) were treated with bromocriptine alone of whom two became pregnant. The males were also treated with bromocriptine leading to a significant fall of the PRL level accompanied by improvement of libido, sexual potency and headache. Two patients received radiation postoperatively, which led to a fall of PRL and improvement of visual fields. Since PRL levels remained low after withdrawal of bromocriptine for several months an antiproliferative effect of this drug is suggested. Thus differential therapy of PRL producing tumors is possible: In females selective neurosurgery can alone or combined with medical therapy normalize PRL secretion and ovarian function. In patients with microadenoma bromocriptine alone can be successful. In patients with inoperable large tumors radiation should be advocated. Additional bromocriptine therapy may be helpful to stop tumor growth and alleviate the effects of hyperprolactinemia.
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PMID:Treatment of patients with prolactinomas. 75 42

There has been increasing interest regarding the use of Corynebacterium parvum (CP) with other modalities in the management of primary cancer. Due to the paucity of specific information available relative to CP toxicity, a Phase I study was carried out in patients with advanced disease. The purpose of the investigation was not to evaluate the effect of CP on tumor growth. from 273 injections of CP in 40 patients it was observed that following intravenous (i.v.) infusion of CP: a) a febrile response and chills of considerable severity occured in almost all patients and did not appreciably diminish in intensity following repetitive administrations; b) nausea, vomiting, headache, and confusion were not infrequent; c) a "flu-like" syndrome lasting 24 to 48 hours occurred following almost all courses of CP; d) blood pressure elevations occurred on occasion and were related to the severity of other-side-effects; hyper- or hypo- tension was not a problem; e) ther were no anaphalactic reactions. Pretreatment with a single administration of 100 mg of hydrocortisone prior to CP infusion markedly and in some instances dramatically diminished the toxicity and made acceptable the use of i.v. CP on an outpatient basis. The use of i.v. CP in patients with cerebral metasteses may be hazardous. Subcutaneously administered CP resulted in a significant number of undesirable local reactions. Evaluation of delayed cutaneous hypersensitivity response, immunoglobulins, complement, and E- and EAC-rosette-forming cells during CP administration failed to demonstrate significant change from injection values. Results were similar whether hydrocortisone pretreatment was or was not employed. From the standpoint of toxicity it now seems appropriate to use i.v. CP, particularly following pretreatment with hydrocortisone, in a controlled clinical trial to evaluate its therapeutic effectiveness in the management of primary cancer.
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PMID:Observations following Corynebacterium parvum administration to patients with advanced malignancy. a phase I study. 94 9

Anti-CD3 monoclonal antibodies induce the proliferation of human T-cells in vitro and activate specific and nonspecific cytolysis by human T-cell clones and human peripheral blood lymphocytes. In vivo administration of anti-CD3 prevents tumor growth of a UV-induced mouse fibrosarcoma. We conducted a phase I trial to determine the toxicity and immunomodulatory properties of low doses of anti-CD3 in 36 patients with cancer. In 23 patients, anti-CD3 was given i.v. over 3 h at 1, 10, 30, and 100 mcg/patient. Five other patients received anti-CD3 at 30 mcg by i.v. bolus. Patients were treated every 3 days for a total of four doses. An additional eight patients received anti-CD3 daily for 14 days at 3 mcg by i.v. bolus, 3-h infusion, or 24-h infusion. Dose-limiting toxicity was headache. Headache was often accompanied by signs and symptoms of meningeal irritation leading to performance of a lumbar puncture in nine patients. The opening pressure was usually elevated, and six patients had a cerebrospinal fluid lymphocytosis with an elevated protein. Increased levels of interleukin 6 were identified in the cerebrospinal fluid. The maximum tolerated dose by 3-h infusion was 30 mcg. There were no objective tumor responses. There was a dose-related increase in the number of peripheral blood lymphocytes expressing the T-cell activation antigen CD69 (Leu 23), but no changes were seen in CD25 (interleukin 2 receptor) expression, and no changes were observed in the serum levels of the soluble interleukin 2 receptor. Even at these low doses of anti-CD3, 8 of 16 patients tested developed human anti-mouse antibodies.
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PMID:Anti-CD3 monoclonal antibody treatment of patients with CD3-negative tumors: a phase IA/B study. 153 72

Meningiomas are common brain tumors which are generally benign, well circumscribed, and slow growing. In a minority of patients, complete surgical removal is not possible and regrowth of tumor tissue is a major clinical problem. Most meningiomas contain progesterone receptors and the antiprogestational drug mifepristone (RU 486) binds to these receptors. 10 patients were treated with 12 recurrent or primary inoperable meningiomas, all of whom had shown recent neuroradiological and/or ophthalmological evidence of tumor growth. They received 200 mg mifepristone daily for 12 months. Most patients initially had complaints of nausea, vomiting, and/or tiredness. In 4 patients, prednisone (7.5 mg/day) was given, after which these side effects subsided. CT scan analysis of tumor size showed a progression of growth of 5 meningiomas in 4 patients, stable disease in 3 with 3 tumors, and regression of 3 tumors in 3 patients. A decrease in the complaints of headache and an improved general well being was observed in 5 patients. 2 patients died during the treatment period from unrelated causes. Mifepristone treatment resulted in control of tumor growth (stable disease) in 6 of 10 patients who had shown recent evidence of tumor growth. In 3 of these 6 patients, consistent tumor shrinkage was seen.
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PMID:Mifepristone (RU 486) treatment of meningiomas. 161 17

Retinoids have shown a tumor growth inhibition and a synergistic activity with hormonal manipulations in human breast cancer cell lines and rat mammary carcinoma. To investigate the potential usefulness of this synergistic activity in human breast cancer, 33 postmenopausal patients with advanced disease were treated with the combination of tamoxifen (10 mg p.o. three times a day) and retinyl acetate (300,000 IU p.o. daily). Out of 31 evaluable patients, 3 achieved complete response, 9 partial response (overall response rate: 38.5%, 95% confidence interval = 21%-56%) and 16 (52%) showed no change. The median duration of response was 11.5 months (range: 3-19+ months), while the 2-year overall survival rate for the entire group of patients was 63%. Toxicity was generally mild, hot flushes, nausea (and/or vomiting), headache and cutaneous itching being the most frequent side-effects. Only 1 patient discontinued treatment for severe toxicity. These preliminary results suggest that the combination of tamoxifen and high-dose retinyl acetate is a safe and effective regimen for breast cancer patients. However, the study design does not allow us to establish whether the very low rate of early disease progression we observed might be related to a possible synergistic effect between retinoids and antiestrogens or rather to the quite indolent disease of the patients who have been selected for entry into this trial.
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PMID:Phase II study of tamoxifen and high-dose retinyl acetate in patients with advanced breast cancer. 222 42

Twelve patients with malignant brain tumors who had failed to respond to conventional therapies were treated with thermotherapy. Hyperthermic temperatures (approximately 43 degrees C) were induced in the tumors using microwaves at a frequency of 2450 MHz that were guided into the tumors by one or more semirigid coaxial applicators. These applicators fit into 16 gauge tubes or needles and can be inserted into the brain with minimal damage to healthy tissues. During each treatment, the tumors were maintained at hyperthermic temperatures for 1 hour. Several treatments spaced a few days apart were usually administered. The procedure used for producing hyperthermia in brain tumors with microwaves proved to be safe and could be repeated several times without producing toxic effects. Objective tumor responses were obtained in 75% of the patients (decrease in tumor size, 3 patients; slowing of tumor growth, 2 patients; necrosis of tumor tissues verified by pathological examination, 4 patients). Favorable clinical responses were observed in 75% of the patients (rapid decrease in intractable headaches, 5 patients; improvements in clinical deficits, 4 patients). Also, in all patients, the microwave power required to heat for a given time or a given volume decreased during most of the thermotherapy sessions, possibly because of heat damage to the tumor vasculature. Our results, taken together with the results of other investigators, indicate that thermotherapy is a promising modality for treating malignant brain tumors, either as the sole therapy or in combination with radiotherapy and chemotherapy. The next logical steps would be Phase I/II type trials of subjects whose disease is less advanced than the disease of patients treated in the current series of investigations.
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PMID:Microwave hyperthermia for brain tumors. 299 66

Men with PRL-producing macroadenomas often present with hypogonadism and impotence. This report documents exacerbation of a PRL-secreting tumor after two separate 200-mg testosterone enanthate (T) injections despite continued bromocriptine (BRC) therapy. A 37-yr-old man with a 60-mm invasive tumor and a serum PRL level of 13,969 +/- 332 ng/ml (mean +/- SD) responded to BRC therapy with rapid disappearance of visual field defect, headache, and facial pain as well as decrease in serum PRL to 5,103 +/- 1,446 ng/ml. T injection was followed by severe headache, facial pain, and increase in PRL to 13,471 ng/ml. Visual field deterioration and increased tumor size (height, 40-43 mm) by computed tomography were documented. A relationship between T injection and exacerbation of the prolactinoma was not recognized until after a second T injection 3 months later. After that therapy, baseline PRL increased from 6,900 to 12,995 ng/ml. The hypothesis that T was aromatized to estradiol, directly stimulating lactotrophs, was supported by an increase in serum estradiol from 24 to 51 pg/ml after the second T injection. Although T treatment is accepted as appropriate therapy for hypogonadism in men with prolactinomas, it may not only interfere with the response of the tumor to BRC therapy, but even stimulate tumor growth and secretion.
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PMID:Testosterone-related exacerbation of a prolactin-producing macroadenoma: possible role for estrogen. 379 56

Subarachnoid hemorrhage attributable to brain tumor, particularly due to benign tumor, is not common. A case of subependymoma in the lateral ventricle, which manifested itself with an episode of subarachnoid hemorrhage was reported. A 33-year-old woman was admitted to our hospital because of severe headache and transient loss of consciousness, but neurological examination revealed no abnormality except for slight disturbance of consciousness and nuchal rigidity. Lumbar puncture showed an opening pressure over 350mmH2O and grossly bloody CSF. CT scan revealed an enhanced mass occupying the left ventricular trigone. Angiography, however, demonstrated no tumor stain or other vascular abnormality. Preoperative diagnosis was an intraventricular tumor of benign nature. A soft tumor arose from the lateral wall of the trigone was removed subtotally by paramedian parieto-occipital approach. Histology of the tumor was of typical subependymoma with scanty vascularity. Intraventricular or subarachnoid hemorrhage from cerebral neoplasm reported so far, is mostly due to a highly vascularized tumor. Subependymoma is of benign nature with poor vascularity, and therefore, intraventricular hemorrhage from the subependymoma was rarely reported in the literature. On the basis of the findings of angiography, serial CT scans and histological examination, it is reasonable to assume that intraventricular bleeding in our case is not attributed to the tumor per se, but to tearing of subependymal or ependymal veins extremely extended by the tumor growth.
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PMID:[A case of subependymoma in the lateral ventricle with intraventricular hemorrhage]. 646 67

A 29-year-old female who had undergone resection of an abdominal paraaortic pheochromocytoma weighing 33 g at the age of 20 had had severe headaches, hypertension and hyperhidrosis 3 years prior to the surgery. Postoperatively, her symptoms completely disappeared and urinary catecholamines were normalized. She was well and had married and had had 2 children. She was admitted to our hospital on August 22, 1982, for further evaluation of hypertension (154/100), which had been diagnosed 2 months previously. Endocrinological studies confirming the presence of a pheochromocytoma were as follows: 1) Plasma noradrenaline level was significantly elevated to 1750 pg/ml. 2) Urinary catecholamine and their metabolites (Metanephrines and VMA) were markedly elevated. Her blood pressure was borderline hypertension and its diurnal rhythm was lost. Her blood pressure decreased to normal values after the oral administration of labetalol (100 mg). Plasma noradrenaline level was still high at 180 minutes after the oral administration of clonidine (150 micrograms). Hypertensive response to insulin-induced hypoglycemia (regular insulin 0.1 u/kg i.v.) was observed, but blood pressure returned to normal after the infusion of glucose alone. Hypertensive response to both metoclopramide (5 mg i.v.) and sulpiride (50 mg per os) was observed accompanying the significant elevation of plasma noradrenaline. Computed tomography and ultrasonography revealed a tumor localized between the aorta and the vena cava inferior. Selective venous sampling also revealed an intrathoracic pheochromocytoma. On October 8, 1982, a 28 g mass was removed from the mediastinum just above the diaphragma. Histologically, it was typical of a pheochromocytoma. Electron microscopy showed large polygonal cells with numerous large secretory granules characteristic of noradrenaline-granules. Postoperative blood pressure was normal, but repeated measurements of plasma and urinary catecholamines were still slightly high. We, therefore, followed her case carefully at our out-patient clinic. In order to clarify the mechanism of catecholamine release by metoclopramide and sulpiride, tissue cultures of removed pheochromocytoma with and without these drugs were carried out. The in vitro studies revealed that metoclopramide released noradrenaline eight-fold and sulpiride 13-fold as compared with noradrenaline in a control medium. We concluded that both drugs stimulated catecholamine secretion directly from the tumor and thus, careless administration of these drugs should be avoided when pheochromocytoma was suspected, large or small. Finally, the rate of tumor growth seemed to be very slow because it took 9 years to ach
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PMID:[Case of intrathoracic pheochromocytoma occurring 9 years after resection of intraabdominal paraaortic pheochromocytoma: effect of metoclopramide and sulpiride on catecholamine secretion in vitro]. 666 41

A 59 yr old man presented with headaches and was shown to have a posterior fossa tumor arising from the inferior surface of the tentorium cerebelli. At operation the tumor was discrete from the cerebellum and was thought to be a meningioma. Pathological examination showed the tumor had features similar to those of a meningioma. It consisted of interlacing bundles of spindle cells with a considerable amount of connective tissue. Some mitoses were present. The tumor cells, however, showed abundant staining for glial fibrillary acidic protein indicating their astrocytic nature. The tumor was diagnosed as astrocytoma Grade 2. The tumor 'recurred' 4 mths later and a second surgical removal was attempted. Pathological examination showed features similar to those in the first operative specimen but this time invasion of the cerebellum was present. Deep x-ray treatment (D.X.R.T.) did not alter the tumor growth which proved fatal 7 mths after presentation. The differential diagnosis of an apparently meningeal-based tumor includes the rare entity of primary meningeal glioma. The case is presented as an example of this rare entity which both clinically and pathologically may be mistaken for a meningioma. The prognosis of intracranial solitary primary leptomeningeal gliomas is variable with recurrence and survival being months to years.
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PMID:Primary meningeal glioma. 816 33


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