Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 62-year-old woman developed neurologic deficits 7 months after pulmonary lobectomy for alveolar cell carcinoma of the lung. CT scan of the head demonstrated two metastases with marked peritumoral edema. Administration of Decadron, chemotherapy and 3,000 rad cranial radiation resulted in dramatic improvement of dysphasia and right hand paresis. Almost 2 months later, rhythmic, involuntary movements of the left hand developed. There was progression to multifocal seizures, grand mal seizures, postictal depression, status epilepticus, and coma, with death 9 days after onset of the movement disorder. Bronchoalveolar carcinoma was widely disseminated in lungs and bones, and as three metastases in brain. Bland "ischemic" necrosis in a pseudolaminar pattern was present in the neocortex. Innumerable Cowdry type A intranuclear inclusion bodies were seen in neurons, astrocytes, and oligodenodroglia. Immunofluorescence demonstrated Herpes simplex virus type 2 antigen and electron microscopy revealed virions with the morphology of the Herpes group. The case is significant for (1) the concurrence of intracranial metastases and Herpes simplex encephalitis, and (2) the causal agent, Herpes simplex virus type 2. The implication for the clinical neurocientist is the potential in a patient with systemic cancer, for the causation of neurologic complications by more than one factor or mechanism.
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PMID:Herpes simplex type 2 encephalitis concurrent with known cerebral metastases. 22 22

A 73-year-old female was admitted to our hospital because of weight loss and pretibial edema. Plasma levels of adenocorticotropic hormone (ACTH) and cortisol were elevated, and neither hormone showed circadian rhythm. Dexamethasone (2 mg for 2 days) failed to reduce the urinary excretion of 17-hydroxycorticosteroids and the plasma cortisol level. The stomach biopsy specimens showed a moderately-differentiated papillo-tubular adenocarcinoma. Computed tomography of the abdomen showed multiple metastases to the liver. Immunohistochemical staining of the autopsy specimens showed immunoreactive ACTH in the primary tumor cells of the stomach as well as the metastatic tumor cells of the liver. On the basis of the clinical, histological and immunohistochemical findings, we diagnosed this patient as having ectopic ACTH syndrome caused by adenocarcinoma of the stomach.
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PMID:Ectopic ACTH-producing adenocarcinoma of the stomach. 145 35

The effects of dexamethasone on protein synthesis were studied in human fibrosarcoma (HT-1080) cells. Dexamethasone induced a new protein of 46 kD which was rapidly secreted into the medium, while neither progesterone nor estradiol would induce the synthesis of this protein and only a small increase in its amount could be seen in the presence of testosterone. The 46 kD protein was partially purified by ammonium sulfate precipitation and gel filtration and mouse monoclonal antibodies to it were produced in mouse hybrid cells. Altogether 13 positive clones were found, of which six reacted only with native and seven reacted with the unreduced 46 kD protein in Western blotting. It was possible by using polyclonal antibodies to plasminogen activator inhibitor type I (PAI-1) and purified plasminogen activator inhibitor type I to confirm that the 46 kD protein purified and characterized here was PAI-1. In addition, the 46 kD protein clearly inhibited plasminogen activation, thus further confirming that protein isolated was an inhibitor of plasminogen activator. Since the induction of PAI-1 by dexamethasone was very extensive, it is possible that glucocorticoids regulate proteolysis and fibrinolysis in vivo by increasing the amount of the inhibitor of plasminogen activator and thus preventing the activation of plasminogen to plasmin. The reduction of activation of plasminogen to plasmin by glucocorticoid-induced inhibitor could be of great importance, e.g., in various blistering diseases, in metastases from malignant cells, and in the migration of inflammatory cells.
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PMID:Dexamethasone-induced plasminogen activator inhibitor: characterization, purification, and preparation of monoclonal antibodies. 214 2

Putrescine is a potential scanning agent for metastases of prostatic carcinoma. We examined the in vivo uptake of [14C]-putrescine by the Dunning R3327H Copenhagen rat prostatic tumor and by other tissues, and conclude that: The uptake of [14C]-putrescine by the tumor was higher than that of the normal dorsolateral prostate, but similar to that of the ventral prostate. Tumor accumulation of [14C]-putrescine was enhanced 38% in intact and 45% in castrated animals by pretreatment with alpha-difluoromethylornithine (DFMO), a polyamine synthesis inhibitor. Further enhancement of tumor uptake (94% in intact and 201% in castrated animals) was achieved by combining DFMO pretreatment with androgen stimulation. Oral administration of methyl-glyoxal bis (guanylhydrazone) (MGBG) increased intestinal uptake of [14C]-putrescine, while oral administration of unlabeled spermine and putrescine decreased it. Dexamethasone decreased the uptake of [14C]-putrescine by the spleen and intestine, but also reduced the prostatic uptake to a considerable extent. These observations are useful for the design of a putrescine-based scan for metastases of prostatic carcinoma.
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PMID:alpha-Difluoromethylornithine enhancement of 14C-putrescine uptake by an androgen-dependent prostatic tumor. 309 95

Primary lymphoma of the central nervous system (CNS) is difficult to diagnose because of the difficulty in differentiating it from multiple sclerosis, sarcoidosis, metastatic disease, chronic granulomatous disease, and cerebral cysticercosis. With the patient presented in this report, no abnormalities were found after performing laboratory tests, using radiographic modalities, and taking biopsies. Dexamethasone treatment was initiated, and patient's symptoms improved.Primary CNS lymphoma was not diagnosed until a year after presentation, due to lack of tissue diagnosis. CNS must be suspected when a diagnosed tumor treated with steroid is not found at surgery. It is suggested that a computerized tomographic scan be requested before the start of steroid therapy, as the lesion can disappear with steroid treatment.
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PMID:Primary lymphoma of the central nervous system: a diagnostic problem. 356 Feb 50

The expression of steroid receptors and the in vitro responsiveness to steroids were used to investigate the cell heterogeneity of a BALB/c mammary carcinoma cell line (TS/A) by means of its high- and low-metastatic clones previously selected in vitro. All the clones studied contained appreciable levels of receptors for oestrogens and for glucocorticoids. The in vitro responses of clones to 17 beta-oestradiol were very poor and comparable; conversely, a heterogeneous pattern of responsiveness to glucocorticoids was observed. In the presence of dexamethasone, the in vitro growth of high-metastatic clones was either unaffected or stimulated and dome formation was significantly increased. Dexamethasone treatment of low-metastatic clones caused inhibition of in vitro proliferation and a morphological shift from a fibroblast-like growth pattern towards the epithelial phenotype. One out of the three low-metastatic clones tested acquired the ability to form domes in the presence of dexamethasone, albeit sporadically. The in vitro treatment with dexamethasone significantly increased the lung colonization ability of the two low-metastatic clones studied, whereas no significant effect was observed with high-metastatic clones. Data presented here suggest that TS/A cell line consists of heterogeneous populations with peculiar proliferative and differentiative responses to glucocorticoids.
Clin Exp Metastasis
PMID:Dexamethasone modulation of in vitro growth pattern and of lung colonization ability in clones of a metastatic BALB/c mammary carcinoma cell line. 369 65

6 cases of breast cancer in women aged 19-45 years are reported. All underwent radical mastectomy (5 had presented with lymph node involvement) and were then treated with combined estrogen-gestagen preparations (Lyndiol, Lutestral, Dectancyl). After 1-4 years there is no evidence of local recurrence, regional lymph node involvement, or distant metastases. These encouraging results have led the authors to continue research into the possibility of slowing down the spread of metastases in young women by the use of estrogen-gestagen combinations administered in contraceptive-level dosage.
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PMID:[Remarks about some still young patients treated with the gestagen-estrogen association immediately after radical treatment of malignant tumors of the breast]. 409 66

Spinal cord compression from metastatic cancer is a medical emergency. Prompt intervention affords the best chance for successful recovery, while delay may result in devastating neurologic impairment. In the appropriate clinical setting, emergency myelography should be done to confirm the diagnosis of metastatic disease. Dexamethasone should then be started, followed by immediate radiation therapy or surgical decompression.
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PMID:Metastatic spinal cord compression. 682 90

Seventy-seven adult patients with suspected skeletal metastases were divided into two groups. In group A (n = 30), following intravenous administration of 20 mCi (740 MBq) of technetium-99m methylene diphosphonate (99mTc-MDP), 3- and 24-h scintigraphy of bone lesions was performed. The 24/3 h lesion to bone background radiouptake ratio (RUR) was calculated for each lesion. In group B (n = 47), the same procedure was followed with dexamethasone intervention (10 mg in 24 h) following the 3-h acquisition. In group A, after determination of the critical point, malignant and degenerative bone lesions could be separated with a sensitivity, specificity and accuracy of 0.76, 0.72 and 0.73, respectively. The mean RUR of the malignant lesions was 1.20 +/- 0.23, and that of the benign lesions, 0.95 +/- 0.15. In group B cases, significantly increased sensitivity, specificity and accuracy of 0.87, 0.94 and 0.92, respectively, were found (P < 0.001). The mean RUR of the malignant lesions was 1.48 +/- 0.34, and that of degenerative lesions, 0.88 +/- 0.19. Dexamethasone interventional bone scintigraphy seems to be a new cost-effective method for differentiating malignant from degenerative bone lesions using the RUR.
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PMID:Differentiation of malignant and degenerative bone lesions using dexamethasone interventional 3- and 24-hour bone scintigraphy. 795 46

We analysed the glucocorticoid receptor (GR) function and its ability to modulate cell-cell interactions between the PA-III rat prostate cancer and UMR 106 osteoblast-like rat osteosarcoma cells as an in vitro model for studying GR function in PA-III cell-induced tumor and blastic reaction in rat bone. Intact GR was detected by ligand binding assays, DNA band-shift, and GR trans-activation analysis of PA-III and UMR 106 cells transiently transfected with the mouse mammary tumor virus thymidine kinase-chloramphenicol acetyltransferase reporter gene. Dexamethasone and transforming growth factor beta 1 (TGFbeta1) inhibited the growth of PA-III and UMR 106 cells. Dexamethasone's inhibition of PA-III and UMR 106 cells was reversed by anti-TGFbeta1 antibody and exogenous insulin-like growth factor I (IGF-I). Exogenous IGF-I, urokinase-type plasminogen activator (uPA), UMR 106 conditioned media (CM) and PA-III CM stimulated the proliferation of PA-III and UMR 106 cells. The mitogenic activity exerted by uPA and PA-III CM in UMR 106 cells was completely neutralized by anti-IGF-I specific antibody. In addition, dexamethasone up-regulated TGFbeta1 mRNA and down-regulated uPA mRNA expression in PA-III cells without affecting TGFbeta1 and uPA mRNA expression in UMR 106 cells. These data suggested that TGFbeta1, uPA, and IGF-I mediate at least in part cell-cell interactions and GR function in PA-III prostate cancer and UMR 106 osteosarcoma cells.
Clin Exp Metastasis 1997 May
PMID:Glucocorticoid receptor function possibly modulates cell-cell interactions in osteoblastic metastases on rat skeleton. 917 22


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