Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The work deals with the study at cell level of the action of Crinofizin on some target organs. The effect of various doses of Crinofizin (0.2, 0.1, 0.01 and 0.001 ml/culture tube) was tested on multiplication and protein synthesis in human mammary tissue cells (cystic mastosis) and human prostate adenoma in cell culture. The morphologic aspect, enzymatic activity (LDH, G-6-PDH) and mucopolysaccharides synthesis were also studied. It was found that administration of Crinofizin results in preferential development of epithelial cells at the expense of the connective-fibroblastic ones. LDH and G-6-PDH, higher in the control cultures of the epithelial type than in the fibroblastic ones, becomes uniform by decreasing in intensity in the treated lots. Acute experimentation carried out on prostate organ cultures from rats of various ages (30, 60, 90 days and 2 years) treated with 0.2ml Crinofizin/ml culture medium indicates a decrease in connective tissue intrafollicular stroma, which is well developed in the case of adenoma. LDH and G-6-PDH activity, which is higher in the case of adenoma, decreases under Crinofizin administration to the levels in the adult control. The histologic aspect of the hypertrophied prostate organ cultures from aged rats, becomes after Crinofizin administration similar to that of the adult rat organ cultures.
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PMID:Histochemical and histoenzymatic action of crinofizin in cystic mastosis and prostate adenoma studied in cell and organotypic cultures. 732 46

Leukemia inhibitory factor (LIF) is a pleiotropic cytokine of the IL-6 family that activates the hypothalamic-pituitary-adrenal axis and promotes corticotrope cell differentiation during development. The aim of this study was to investigate the expression of LIF and its receptor (LIFR) in the canine pituitary gland and in corticotrope adenomas, and to perform a mutation analysis of LIFR. Using immunohistochemistry, immunofluorescence, and quantitative expression analysis, LIF and LIFR expression were studied in pituitary glands of control dogs and in specimens of corticotrope adenoma tissue collected through hypophysectomy in dogs with pituitary-dependent hypercortisolism (PDH, Cushing's disease). Using sequence analysis, cDNA was screened for mutations in the LIFR. In the control pituitary tissues and corticotrope adenomas, there was a low magnitude of LIF expression. The LIFR, however, was highly expressed and co-localized with ACTH(1-24) expression. Cytoplasmatic immunoreactivity of LIFR was preserved in corticotrope adenomas and adjacent nontumorous cells of pars intermedia. No mutation was found on mutation analysis of the complete LIFR cDNA. Surprisingly, nuclear to perinuclear immunoreactivity for LIFR was present in nontumorous pituitary cells of the pars distalis in 10 of 12 tissue specimens from PDH dogs. These data show that LIFR is highly co-expressed with adrenocorticotropic hormone (ACTH) and alpha-melanocyte-stimulating hormone (alpha-MSH) in the canine pituitary gland and in corticotrope adenomas. Nuclear immunoreactivity for LIFR in nontumorous cells of the pars distalis may indicate the presence of a corticotrope adenoma.
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PMID:Expression of leukemia inhibitory factor and leukemia inhibitory factor receptor in the canine pituitary gland and corticotrope adenomas. 2003 83

Targeting mitochondrial energy metabolism is a novel approach in cancer research and can be traced back to the description of the Warburg effect. Dichloroacetate, a controversially discussed subject of many studies in cancer research, is a pyruvate dehydrogenase kinase inhibitor. Dichloroacetate causes metabolic changes in cancerous glycolysis towards oxidative phosphorylation via indirect activation of pyruvate dehydrogenase in mitochondria. Canine mammary cancer is frequently diagnosed but after therapy prognosis still remains poor. In this study, canine mammary carcinoma, adenoma and non-neoplastic mammary gland cell lines were treated using 10 mM Dichloroacetate. The effect on cell number, lactate release and PDH expression and cell respiration was investigated. Further, the effect on apoptosis and several apoptotic proteins, proliferation, and microRNA expression was evaluated. Dichloroacetate was found to reduce cell proliferation without inducing apoptosis in all examined cell lines.
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PMID:Dichloroacetate affects proliferation but not apoptosis in canine mammary cell lines. 2859 Nov 65