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1. Gómez J, Prado C, López P, Suárez A, Gutiérrez C: Conserved anti-proliferative effect and poor inhibition of TNFalpha secretion by regulatory CD4+CD25+ T cells in patients with systemic lupus erythematosus. Clin Immunol; 2009 Sep;132(3):385-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Interleukin-2 Receptor alpha Subunit / metabolism. Lupus Erythematosus, Systemic / immunology. T-Lymphocytes, Regulatory / immunology. Tumor Necrosis Factor-alpha / secretion
  • [MeSH-minor] Adrenal Cortex Hormones / pharmacology. Adult. Antimalarials / pharmacology. Cell Count. Cell Proliferation / drug effects. Dendritic Cells / immunology. Female. Humans. Lymphocyte Activation / drug effects. Lymphocyte Activation / immunology. Middle Aged. Young Adult

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  • (PMID = 19540813.001).
  • [ISSN] 1521-7035
  • [Journal-full-title] Clinical immunology (Orlando, Fla.)
  • [ISO-abbreviation] Clin. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Antimalarials; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Tumor Necrosis Factor-alpha
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2. Takahashi K, Shoji I, Shibasaki A, Kato I, Hiraishi K, Yamamoto H, Kaneko K, Murakami O, Morimoto R, Satoh F, Ito S, Totsune K: Presence of kisspeptin-like immunoreactivity in human adrenal glands and adrenal tumors. J Mol Neurosci; 2010 May;41(1):138-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Presence of kisspeptin-like immunoreactivity in human adrenal glands and adrenal tumors.
  • Kisspeptins have also been reported to stimulate the aldosterone secretion from the adrenal cortex.
  • However, the expression of kisspeptins in human adrenal glands and adrenal tumors has not been clarified yet.
  • We, therefore, studied the presence of kisspeptin-like immunoreactivity (LI) in human adrenal glands and adrenal tumors (adrenocortical adenomas, adrenocortical carcinomas, and pheochromocytomas) by radioimmunoassay and immunocytochemistry.
  • Kisspeptin-LI was detected in all the tissues examined; normal portions of adrenal glands (3.0 +/- 2.3 pmol/g wet weight, n = 21, mean +/- SD), aldosterone-producing adenomas (4.6 +/- 3.3 pmol/g wet weight, n = 10), cortisol-producing adenomas (2.7 +/- 1.4 pmol/g wet weight, n = 14), adrenocortical carcinomas (1.7 +/- 0.2 pmol/g wet weight, n = 4), and pheochromocytomas (1.8 +/- 0.8 pmol/g wet weight, n = 6).
  • Immunocytochemistry showed positive kisspeptin-immunostaining in normal adrenal glands, with stronger immunostaining found in the medulla.
  • Furthermore, positive kisspeptin-immunostaining was found in all types of adrenal tumors examined; adrenocortical adenomas, adrenocortical carcinomas, and pheochromocytomas.
  • The intensity of kisspeptin-immunostaining in these adrenal tumors was, however, not so strong as that in normal adrenal medulla.
  • The present study has shown for the first time the presence of kisspeptin-LI in adrenal glands and adrenal tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / metabolism. Adrenal Glands / metabolism. Tumor Suppressor Proteins / metabolism

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  • (PMID = 19898965.001).
  • [ISSN] 1559-1166
  • [Journal-full-title] Journal of molecular neuroscience : MN
  • [ISO-abbreviation] J. Mol. Neurosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KISS1 protein, human; 0 / Kisspeptins; 0 / Tumor Suppressor Proteins
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3. Asif AR, Steffgen J, Metten M, Grunewald RW, Müller GA, Bahn A, Burckhardt G, Hagos Y: Presence of organic anion transporters 3 (OAT3) and 4 (OAT4) in human adrenocortical cells. Pflugers Arch; 2005 May;450(2):88-95
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  • [Title] Presence of organic anion transporters 3 (OAT3) and 4 (OAT4) in human adrenocortical cells.
  • Since the organic anion transporter-1 (OAT1) has been implicated in cortisol release from bovine and rat adrenal zona fasciculata cells, we addressed the question of whether OATs are present in human adrenal cortical cells.
  • In the human adrenal cell line NCI-H295R, 24-h cortisol secretion increased up to 30-fold on exposure to forskolin.
  • RT-PCR did not reveal expression of human OAT1 and OAT2, but OAT3 and OAT4 mRNAs were detected in both NCI-H295R cells and human adrenal tissue.
  • [MeSH-major] Adrenal Cortex / metabolism. Organic Anion Transporters, Sodium-Independent / metabolism
  • [MeSH-minor] Adrenocorticotropic Hormone / pharmacology. Animals. Biological Transport / drug effects. Colforsin / pharmacology. Estrone / analogs & derivatives. Estrone / pharmacokinetics. Humans. Hydrocortisone / pharmacokinetics. Oocytes / metabolism. Tritium. Tumor Cells, Cultured. Xenopus laevis

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  • (PMID = 15864504.001).
  • [ISSN] 0031-6768
  • [Journal-full-title] Pflugers Archiv : European journal of physiology
  • [ISO-abbreviation] Pflugers Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Organic Anion Transporters, Sodium-Independent; 0 / SLC22A9 protein, human; 0 / organic anion transport protein 3; 10028-17-8 / Tritium; 1F7A44V6OU / Colforsin; 2DI9HA706A / Estrone; 9002-60-2 / Adrenocorticotropic Hormone; QTL48N278K / estrone sulfate; WI4X0X7BPJ / Hydrocortisone
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4. Brassard P, Kezouh A, Suissa S: Antirheumatic drugs and the risk of tuberculosis. Clin Infect Dis; 2006 Sep 15;43(6):717-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: We aimed to quantify the rate of Mycobacterium tuberculosis disease (TB) among a cohort of patients with rheumatoid arthritis (RA) and to assess whether the independent use of disease-modifying antirheumatic drugs (DMARDs) is associated with the risk of developing TB.
  • The cohort consisted of all subjects with > or =1 occurrence of a diagnosis of RA during an inpatient or outpatient visit during the period of September 1998 through December 2003.
  • RESULTS: The cohort consisted of 112,300 patients with RA.
  • RRs of developing TB disease with the use of biological or traditional DMARD were lower among current users of corticosteroids than among noncurrent users of corticosteroids.
  • CONCLUSION: We found that the use of biological and traditional DMARDs is associated with an increased risk of developing TB in patients with RA, mainly among noncurrent users of corticosteroids.
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Adult. Arthritis, Rheumatoid / drug therapy. Case-Control Studies. Cohort Studies. Etanercept. Female. Humans. Infliximab. Interleukin 1 Receptor Antagonist Protein. Male. Middle Aged. Receptors, Tumor Necrosis Factor / therapeutic use. Risk Factors

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  • [CommentIn] Clin Infect Dis. 2007 Feb 15;44(4):619-20; author reply 620-1 [17243073.001]
  • (PMID = 16912945.001).
  • [ISSN] 1537-6591
  • [Journal-full-title] Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
  • [ISO-abbreviation] Clin. Infect. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Antibodies, Monoclonal; 0 / Antirheumatic Agents; 0 / IL1RN protein, human; 0 / Immunoglobulin G; 0 / Interleukin 1 Receptor Antagonist Protein; 0 / Receptors, Tumor Necrosis Factor; 0 / Sialoglycoproteins; B72HH48FLU / Infliximab; OP401G7OJC / Etanercept
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5. Gleizniene R, Bucinskas U, Lukosevicius S, Vaitkus A, Letautiene S, Apanaviciūte D, Galvonaite M: Gliomatosis cerebri. Medicina (Kaunas); 2010;46(5):341-4
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  • Gliomatosis cerebri is a rare diffusely infiltrating glial tumor involving two or more lobes and is frequently is bilateral.
  • Infiltrative extent of tumor is out of proportion to histological and clinical features.
  • We present a case in which finally the diagnosis of gliomatosis cerebri was made.
  • Diagnosis of gliomatosis cerebri was suspected, stereotaxic biopsy was performed, and pathological examination revealed changes typical of diffuse glial tumor.
  • [MeSH-major] Brain Neoplasms. Neoplasms, Neuroepithelial
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Biopsy. Brain / pathology. Brain / radiography. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Tomography, X-Ray Computed

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  • (PMID = 20679750.001).
  • [ISSN] 1648-9144
  • [Journal-full-title] Medicina (Kaunas, Lithuania)
  • [ISO-abbreviation] Medicina (Kaunas)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Lithuania
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
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6. Szekeres M, Turu G, Orient A, Szalai B, Süpeki K, Cserzo M, Várnai P, Hunyady L: Mechanisms of angiotensin II-mediated regulation of aldosterone synthase expression in H295R human adrenocortical and rat adrenal glomerulosa cells. Mol Cell Endocrinol; 2009 Apr 29;302(2):244-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mechanisms of angiotensin II-mediated regulation of aldosterone synthase expression in H295R human adrenocortical and rat adrenal glomerulosa cells.
  • In adrenal zona glomerulosa cells angiotensin II (Ang II) is a key regulator of steroidogenesis.
  • Our purpose was to compare the mechanisms of Ang II-induced changes in the expression level of early transcription factors NR4A1 (NGFIB) and NR4A2 (Nurr1) genes, and the CYP11B2 gene encoding aldosterone synthase in H295R human adrenocortical tumor cells and in primary rat adrenal glomerulosa cells.
  • Real-time PCR studies have demonstrated that Ang II increased the expression levels of NR4A1 and NR4A2 in H295R cells within 1 h after stimulation, which persisted up to 6 h; whereas in rat adrenal glomerulosa cells the kinetics of the expression of these genes were more rapid and transient.
  • Studies using MEK inhibitor (PD98059, 20 microM), protein kinase C inhibitor (BIM1, 3 microM) and calmodulin kinase (CAMK) inhibitor (KN93, 10 microM) revealed that in rat adrenal glomerulosa cells CAMK-mediated mechanisms play a predominant role in the regulation of CYP11B2.
  • These data suggest that the previously reported CAMK-mediated stimulation of early transcription factors NGFIB and Nurr1 has a predominant role in Ang II-induced CYP11B2 activation in rat adrenal glomerulosa cells, whereas in H295R cells ERK activation and G protein-independent mechanisms also contribute to this process.
  • [MeSH-major] Adrenal Cortex / cytology. Angiotensin II / pharmacology. Cytochrome P-450 CYP11B2 / genetics. Gene Expression Regulation / drug effects. Zona Glomerulosa / cytology

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  • (PMID = 19418629.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Transcription Factors; 11128-99-7 / Angiotensin II; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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7. Solís-López DR, Rodríguez-Hernández Z, Solís-López DH: Incidental adreno-cortical adenoma, why surgery? a case report. P R Health Sci J; 2010 Jun;29(2):130-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Incidental adreno-cortical adenoma, why surgery? a case report.
  • INTRODUCTION: Incidental adrenal tumors are commonly benign, but reports demonstrate that if the characteristics of the tumor are not clear, on images surgery is the procedure of choice.
  • Our objective through this case is to show that laparoscopic adrenalectomy is a safe approach for adrenal incidental tumor regardless of radiological findings.
  • She went for check up and a left adrenal mass on MRI described as myelolipoma was found incidentally.
  • The pathological report was adrenal cortical adenoma with central hemorrhage and not a myelolipoma as described in images on magnetic resonance imaging (MRI).
  • CONCLUSION: The use of imaging for diagnosis, clinical management and decision making is very controversial.
  • Laparoscopic surgery for adrenal masses is a safe procedure for tumors of 6 cm regardless of the radiological description.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenocortical Adenoma / surgery

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  • (PMID = 20496530.001).
  • [ISSN] 0738-0658
  • [Journal-full-title] Puerto Rico health sciences journal
  • [ISO-abbreviation] P R Health Sci J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Puerto Rico
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8. Moreland LW, Weinblatt ME, Keystone EC, Kremer JM, Martin RW, Schiff MH, Whitmore JB, White BW: Etanercept treatment in adults with established rheumatoid arthritis: 7 years of clinical experience. J Rheumatol; 2006 May;33(5):854-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: To evaluate safety and efficacy of longterm etanercept treatment in patients with disease modifying antirheumatic drug (DMARD) refractory rheumatoid arthritis (RA).
  • CONCLUSION: The safety profile of etanercept was consistent over time, with rates of adverse events similar to those reported for patients with RA in general.
  • [MeSH-major] Antirheumatic Agents / therapeutic use. Arthritis, Rheumatoid / drug therapy. Immunoglobulin G / therapeutic use. Receptors, Tumor Necrosis Factor / therapeutic use
  • [MeSH-minor] Adolescent. Adrenal Cortex Hormones / therapeutic use. Adult. Aged. Aged, 80 and over. Etanercept. Female. Humans. Infection / chemically induced. Infection / epidemiology. Joints / physiopathology. Longitudinal Studies. Male. Methotrexate / therapeutic use. Middle Aged. Neoplasms / chemically induced. Neoplasms / epidemiology. Risk. Risk Assessment. Time Factors. Treatment Outcome


9. Ozimek A, Diebold J, Linke R, Heyn J, Hallfeldt K, Mussack T: Bilateral primary adrenal non-Hodgkin's lymphoma and primary adrenocortical carcinoma--review of the literature preoperative differentiation of adrenal tumors. Endocr J; 2008 Aug;55(4):625-38
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  • [Title] Bilateral primary adrenal non-Hodgkin's lymphoma and primary adrenocortical carcinoma--review of the literature preoperative differentiation of adrenal tumors.
  • Most of the adrenal tumors that are incidentally detected are benign adenomas.
  • The incidence of malignant adrenal tumors including adrenocortical carcinoma (ACC) and primary adrenal lymphoma (PAL) is rather low.
  • As many patients with ACC and PAL are diagnosed at an advanced stage of disease, the overall survival time of both entities remains poor.
  • Unfortunately hitherto preoperative diagnosis of potentially malignant adrenal masses is still a main problem in the treatment of adrenal tumors.
  • We present the case of a 57-year-old male patient with ACC and the case of an 87-year-old male patient with PAL and provide a systematic comparison of the clinical and pathological features of both entities.
  • In both cases clinical and radiological features resulted in an initially false diagnosis.
  • The patient with ACC showed tumor progression with local and systemic recurrence despite adjuvant therapy with mitotane and additional surgical therapy.
  • We propose some guidelines for diagnosis and surgical management of adrenal tumors.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenal Gland Neoplasms / diagnosis. Adrenocortical Carcinoma / diagnosis. Lymphoma, Non-Hodgkin / diagnosis

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  • (PMID = 18490838.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 78E4J5IB5J / Mitotane
  • [Number-of-references] 55
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10. Bozdogan G, Dogu F, Güloglu D, Yuksek M, Aytekin C, Ikinciogullari A: CD27 expression on lymphocyte and sCD27 levels in children with asthma. Allergol Immunopathol (Madr); 2010 Nov-Dec;38(6):327-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: CD27, a lymphocyte specific member of the Tumour Necrosis Factor- Receptor (TNF-R) family is expressed on the majority of peripheral blood T cells.
  • Activation of T cells via TCR/CD3 induces high CD27 surface expression and release of a soluble form (sCD27) of the molecule. sCD27 level increases in patients suffering from a variety of chronic inflammatory diseases.
  • [MeSH-minor] Adolescent. Adrenal Cortex Hormones / administration & dosage. Child. Child, Preschool. Female. Gene Expression Regulation / immunology. Humans. Immunophenotyping. Lymphocyte Activation. Male. Withholding Treatment

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  • [Copyright] Copyright © 2009 SEICAP. Published by Elsevier Espana. All rights reserved.
  • (PMID = 20800938.001).
  • [ISSN] 1578-1267
  • [Journal-full-title] Allergologia et immunopathologia
  • [ISO-abbreviation] Allergol Immunopathol (Madr)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Antigens, CD27
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11. Silvestri M, Serpero L, Petecchia L, Sabatini F, Cerasoli F Jr, Rossi GA: Cytokine-activated bronchial epithelial cell pro-inflammatory functions are effectively downregulated in vitro by ciclesonide. Pulm Pharmacol Ther; 2006;19(3):210-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Ciclesonide, a new inhaled corticosteroid, is administered as a parent compound and converted in the airway mucosa into the active metabolite, desisobutyryl-(des-)ciclesonide.
  • A study was designed to evaluate the ability of ciclesonide to modulate pro-inflammatory functions of human bronchial epithelial cell (HBEC) primary cultures being converted into des-ciclesonide.
  • HBECs were stimulated with interleukin (IL)-4 and tumour necrosis factor (TNF)-alpha (20 ng/mL) in the presence of ciclesonide and intercellular adhesion molecule (ICAM)-1 expression, granulocyte-macrophage colony stimulating factor (GM-CSF) and IL-8 release evaluated respectively by FACS and ELISA.
  • Des-ciclesonide was detected in 24 h culture HBEC supernatants using high-performance liquid chromatography, while no parental compound ciclesonide was present.
  • [MeSH-minor] Adrenal Cortex Hormones / metabolism. Adrenal Cortex Hormones / pharmacology. Bronchi / cytology. Bronchi / drug effects. Bronchi / immunology. Cell Survival / drug effects. Cells, Cultured. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Granulocyte-Macrophage Colony-Stimulating Factor / secretion. Humans. Inflammation / immunology. Inflammation / metabolism. Inflammation / prevention & control. Intercellular Adhesion Molecule-1 / biosynthesis. Interleukin-4 / pharmacology. Interleukin-8 / secretion. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 16084120.001).
  • [ISSN] 1094-5539
  • [Journal-full-title] Pulmonary pharmacology & therapeutics
  • [ISO-abbreviation] Pulm Pharmacol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Cytokines; 0 / Interleukin-8; 0 / Pregnenediones; 0 / Tumor Necrosis Factor-alpha; 126547-89-5 / Intercellular Adhesion Molecule-1; 207137-56-2 / Interleukin-4; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; S59502J185 / ciclesonide
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12. Turan A, Dalton JE, Turner PL, Sessler DI, Kurz A, Saager L: Preoperative prolonged steroid use is not associated with intraoperative blood transfusion in noncardiac surgical patients. Anesthesiology; 2010 Aug;113(2):285-91
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  • Patients with current pneumonia, ventilator dependence, coma, tumor involving the central nervous system, disseminated cancer, preoperative open wound/wound infection, and/or bleeding disorders were excluded.
  • [MeSH-major] Adrenal Cortex Hormones / administration & dosage. Blood Transfusion. Digestive System Surgical Procedures. Intraoperative Complications / therapy. Preoperative Care


13. Brenner T, O'Shaughnessy KM: Both TASK-3 and TREK-1 two-pore loop K channels are expressed in H295R cells and modulate their membrane potential and aldosterone secretion. Am J Physiol Endocrinol Metab; 2008 Dec;295(6):E1480-6
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  • The rate of aldosterone synthesis by adrenal glomerulosa cells relies on the selective permeability of the glomerulosa cell to K(+) ions.
  • In rodent and bovine adrenal glomerulosa cells, this background potassium current is provided by a two-pore loop potassium (K2P) channel: largely TASK-3 in the rat and TREK-1 in the cow.
  • The nature of the K2P channel in the human adrenal cortex is not known, and we have addressed this issue here using the H295R human adrenal cell line.
  • Finally, transfection of a constitutively active mutant of Galpha(q) into H295R cells (GTPase-deficient Galpha(q)-QL) depolarized them and increased basal aldosterone secretion.
  • This suggests that human adrenal glomerulosa cells may utilize both of these K2P channels for their background potassium current.
  • [MeSH-major] Aldosterone / secretion. Cell Line, Tumor. Membrane Potentials / genetics. Potassium Channels, Tandem Pore Domain / genetics. Potassium Channels, Tandem Pore Domain / physiology
  • [MeSH-minor] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / metabolism. Adrenal Cortex Neoplasms / physiopathology. Adrenocortical Carcinoma / genetics. Adrenocortical Carcinoma / metabolism. Adrenocortical Carcinoma / physiopathology. Fluorescence. Gene Expression Regulation, Neoplastic / physiology. Humans. Transfection

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  • (PMID = 18854423.001).
  • [ISSN] 0193-1849
  • [Journal-full-title] American journal of physiology. Endocrinology and metabolism
  • [ISO-abbreviation] Am. J. Physiol. Endocrinol. Metab.
  • [Language] eng
  • [Grant] United Kingdom / British Heart Foundation / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KCNK9 protein, human; 0 / Potassium Channels, Tandem Pore Domain; 0 / potassium channel protein TREK-1; 4964P6T9RB / Aldosterone
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14. van Deursen D, Botma GJ, Jansen H, Verhoeven AJ: Down-regulation of hepatic lipase expression by elevation of cAMP in human hepatoma but not adrenocortical cells. Mol Cell Endocrinol; 2008 Nov 6;294(1-2):37-44
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  • [Title] Down-regulation of hepatic lipase expression by elevation of cAMP in human hepatoma but not adrenocortical cells.
  • cAMP reduced expression of the 45kDa C/EBPbeta protein and binding of C/EBPbeta to the proximal promoter region of the human HL gene by 50%, as determined by immunoblotting and chromatin immunoprecipitation assay, respectively.
  • In human H295R adrenocortical cells, cAMP failed to suppress HL promoter activity, and only slightly reduced C/EBPbeta expression.
  • We conclude that the fall in HL expression during prolonged fasting may be mediated through elevation of cAMP and lowering of C/EBPbeta expression.
  • [MeSH-major] Adrenal Cortex / cytology. Adrenal Cortex / enzymology. Carcinoma, Hepatocellular / enzymology. Cyclic AMP / metabolism. Down-Regulation / genetics. Lipase / genetics
  • [MeSH-minor] 8-Bromo Cyclic Adenosine Monophosphate / pharmacology. Animals. CCAAT-Enhancer-Binding Protein-beta / metabolism. Cell Line, Tumor. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Protein Biosynthesis / drug effects. Rats. Response Elements. Transfection

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  • (PMID = 18675312.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-beta; 23583-48-4 / 8-Bromo Cyclic Adenosine Monophosphate; E0399OZS9N / Cyclic AMP; EC 3.1.1.3 / Lipase; EC 3.1.1.3 / hepatic lipase, human; EC 3.1.1.3 / hepatic lipase, rat
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15. Chave TA, Mortimer NJ, Sladden MJ, Hall AP, Hutchinson PE: Toxic epidermal necrolysis: current evidence, practical management and future directions. Br J Dermatol; 2005 Aug;153(2):241-53
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  • Toxic epidermal necrolysis (TEN) is a rare disorder characterized by extensive epidermal death.
  • FasL is likely to be particularly important but tumour necrosis factor (TNF) may well contribute, via the TNF receptor 1 (TNF-R1) death pathway.
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Apoptosis / drug effects. Apoptosis / physiology. CD8-Positive T-Lymphocytes / immunology. Cyclosporine / therapeutic use. Fas Ligand Protein. Humans. Immunoglobulins, Intravenous / therapeutic use. Immunosuppressive Agents / therapeutic use. Insulin / therapeutic use. Membrane Glycoproteins / physiology. Models, Biological. Nutritional Physiological Phenomena / physiology. Tumor Necrosis Factor-alpha / antagonists & inhibitors. Tumor Necrosis Factor-alpha / physiology. Zinc / therapeutic use

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  • [CommentIn] Br J Dermatol. 2006 Oct;155(4):842-3 [16965441.001]
  • (PMID = 16086734.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Immunoglobulins, Intravenous; 0 / Immunosuppressive Agents; 0 / Insulin; 0 / Membrane Glycoproteins; 0 / Tumor Necrosis Factor-alpha; 83HN0GTJ6D / Cyclosporine; J41CSQ7QDS / Zinc
  • [Number-of-references] 148
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16. Pianovski MA, Maluf EM, de Carvalho DS, Ribeiro RC, Rodriguez-Galindo C, Boffetta P, Zancanella P, Figueiredo BC: Mortality rate of adrenocortical tumors in children under 15 years of age in Curitiba, Brazil. Pediatr Blood Cancer; 2006 Jul;47(1):56-60
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  • [Title] Mortality rate of adrenocortical tumors in children under 15 years of age in Curitiba, Brazil.
  • BACKGROUND: Several reports refer to an increased frequency of adrenal cortex tumors (ACT) among children in Southern Brazil, yet all data have been derived from hospital-based registries.
  • PROCEDURE: We reviewed all death certificates that mentioned ACT or adrenal neuroblastoma (NB) and which were reported to the Paraná State Department of Health between 1998 and 2003, for individuals younger than 15 years who resided in the Curitiba metropolitan region.
  • The ratio of the adrenal NB and ACT age-adjusted mortality rates was 1.43.
  • CONCLUSIONS: Our investigation of population-based mortality confirms the evidence from hospital-based registries of a clustering of ACT in Southern Brazil.
  • [MeSH-major] Adrenal Cortex Neoplasms / mortality

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16200634.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Chen XN, Zhu H, Meng QY, Zhou JN: Estrogen receptor-alpha and -beta regulate the human corticotropin-releasing hormone gene through similar pathways. Brain Res; 2008 Aug 5;1223:1-10
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  • [MeSH-minor] Activating Transcription Factor 2 / genetics. Activating Transcription Factor 2 / metabolism. Adrenal Cortex Hormones / metabolism. Adrenal Cortex Hormones / secretion. Animals. CHO Cells. Cell Line, Tumor. Cricetinae. Cricetulus. Estradiol / metabolism. Estradiol / pharmacology. Humans. Mice. Promoter Regions, Genetic / drug effects. Promoter Regions, Genetic / genetics. RNA, Messenger / drug effects. RNA, Messenger / metabolism. Rats. Response Elements / drug effects. Response Elements / genetics. Stress, Physiological / genetics. Stress, Physiological / metabolism. Stress, Physiological / physiopathology. Transcriptional Activation / drug effects. Transcriptional Activation / genetics

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  • (PMID = 18597742.001).
  • [ISSN] 0006-8993
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Activating Transcription Factor 2; 0 / Adrenal Cortex Hormones; 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / RNA, Messenger; 4TI98Z838E / Estradiol; 9015-71-8 / Corticotropin-Releasing Hormone
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18. Doghman M, Karpova T, Rodrigues GA, Arhatte M, De Moura J, Cavalli LR, Virolle V, Barbry P, Zambetti GP, Figueiredo BC, Heckert LL, Lalli E: Increased steroidogenic factor-1 dosage triggers adrenocortical cell proliferation and cancer. Mol Endocrinol; 2007 Dec;21(12):2968-87
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  • [Title] Increased steroidogenic factor-1 dosage triggers adrenocortical cell proliferation and cancer.
  • Steroidogenic factor-1 (SF-1/Ad4BP; NR5A1), a nuclear receptor transcription factor, has a pivotal role in adrenal and gonadal development in humans and mice.
  • A frequent feature of childhood adrenocortical tumors is SF-1 amplification and overexpression.
  • Here we show that an increased SF-1 dosage can by itself augment human adrenocortical cell proliferation through concerted actions on the cell cycle and apoptosis.
  • Consistent with these results, increased SF-1 levels selectively modulate the steroid secretion profile of adrenocortical cells, reducing cortisol and aldosterone production and maintaining dehydroepiandrosterone sulfate secretion.
  • On the other hand, sphingosine, which can compete with phospholipids for binding to SF-1, had no effect on the SF-1 dosage-dependent increase of adrenocortical cell proliferation and expression of the FATE1 promoter.
  • In mice, increased Sf-1 dosage produces adrenocortical hyperplasia and formation of tumors expressing gonadal markers (Amh, Gata-4), which originate from the subcapsular region of the adrenal cortex.
  • Our studies reveal a critical role for SF-1 dosage in adrenocortical tumorigenesis and constitute a rationale for the development of drugs targeting SF-1 transcriptional activity for adrenocortical tumor therapy.

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  • (PMID = 17761949.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE5911/ GSE5912
  • [Grant] United States / NICHD NIH HHS / HD / R01 HD038498; United States / NCI NIH HHS / CA / CA63230; United States / NCI NIH HHS / CA / CA71907; United States / NICHD NIH HHS / HD / U54-HD28934
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / STAT3 Transcription Factor; 0 / Steroidogenic Factor 1; 0 / Steroids; 4QD397987E / Histidine
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19. Krummen MB, Varga G, Steinert M, Stuetz A, Luger TA, Grabbe S: Effect of pimecrolimus vs. corticosteroids on murine bone marrow-derived dendritic cell differentiation, maturation and function. Exp Dermatol; 2006 Jan;15(1):43-50
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  • [MeSH-major] Adrenal Cortex Hormones / pharmacology. Bone Marrow Cells / drug effects. Cell Differentiation / drug effects. Dendritic Cells / drug effects. Tacrolimus / analogs & derivatives
  • [MeSH-minor] Animals. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Antigens, Surface / biosynthesis. Clobetasol / pharmacology. Interferon-gamma / secretion. Interleukin-12 / secretion. Interleukin-6 / secretion. Mice. Mice, Inbred BALB C. Mometasone Furoate. Phenotype. Pregnadienediols / pharmacology. Spleen / cytology. T-Lymphocytes. Tumor Necrosis Factor-alpha / secretion

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  • (PMID = 16364030.001).
  • [ISSN] 0906-6705
  • [Journal-full-title] Experimental dermatology
  • [ISO-abbreviation] Exp. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antigens, Surface; 0 / Interleukin-6; 0 / Pregnadienediols; 0 / Tumor Necrosis Factor-alpha; 04201GDN4R / Mometasone Furoate; 187348-17-0 / Interleukin-12; 7KYV510875 / pimecrolimus; 82115-62-6 / Interferon-gamma; ADN79D536H / Clobetasol; WM0HAQ4WNM / Tacrolimus
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20. Lin MT, Shieh JJ, Chang JH, Chang SW, Chen TC, Hsu WH: Early detection of adrenocortical carcinoma in a child with Li-Fraumeni syndrome. Pediatr Blood Cancer; 2009 Apr;52(4):541-4
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  • [Title] Early detection of adrenocortical carcinoma in a child with Li-Fraumeni syndrome.
  • The proband was a 3-year-old male with a primitive mesenchymal tumor.
  • The younger sister at risk was followed, and an asymptomatic adrenal cortical carcinoma was detected 3 years later.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenocortical Carcinoma / diagnosis. Early Detection of Cancer. Genetic Predisposition to Disease. Li-Fraumeni Syndrome / genetics
  • [MeSH-minor] Child, Preschool. DNA Mutational Analysis. Female. Genetic Counseling. Germ-Line Mutation. Humans. Male. Pedigree. Point Mutation. Tumor Suppressor Protein p53 / genetics

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  • [Copyright] Copyright 2008 Wiley-Liss, Inc.
  • (PMID = 19101993.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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21. Mete O, Kapran Y, Güllüoğlu MG, Kiliçaslan I, Erbil Y, Senyürek YG, Dizdaroğlu F: Anti-CD10 (56C6) is expressed variably in adrenocortical tumors and cannot be used to discriminate clear cell renal cell carcinomas. Virchows Arch; 2010 May;456(5):515-21
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  • [Title] Anti-CD10 (56C6) is expressed variably in adrenocortical tumors and cannot be used to discriminate clear cell renal cell carcinomas.
  • In the evaluation of retroperitoneal masses, the practicing pathologist faces a dilemma when making a diagnosis based on histology given the often overlapping morphologic appearances of the adrenocortical carcinoma, renal cell carcinoma (RCC), and hepatocellular carcinoma (HCC).
  • However, its expression is not well-investigated in adrenal cortical tumors.
  • We examined CD10 expression in 47 surgically resected adrenocortical tumors (26 adenomas and 21 carcinomas) and compared with 20 clear cell RCCs and 25 HCCs.
  • Twenty HCCs (80%), 18 RCCs (90%), 11 adrenocortical carcinomas (52%), and 18 adrenocortical adenomas (69%) were positive for CD10.
  • Adrenocortical tumors displayed mainly cytoplasmic staining.
  • Four adrenocortical carcinomas and one adenoma also displayed the membranous staining pattern.
  • Despite the relatively small number of samples, our preliminary results revealed that adrenocortical tumors may express CD10 (Clone: 56C6).
  • The most important point from this paper is the fact that anti-CD10 expression has not been previously reported in adrenocortical carcinomas.
  • This suggests that CD10 does not seem to be a useful marker for discriminating clear cell RCCs from adrenocortical tumors since CD10 expression does not rule out the possibility of adrenocortical tumors.
  • This feature should be kept in mind when constructing an antibody panel for an epithelial tumor that involves the adrenal gland and kidney, especially in small biopsy specimens.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Carcinoma, Renal Cell / diagnosis. Kidney Neoplasms / diagnosis. Neprilysin / biosynthesis
  • [MeSH-minor] Adult. Antigens, Neoplasm / analysis. Carcinoma, Hepatocellular / diagnosis. Carcinoma, Hepatocellular / immunology. Female. Humans. Liver Neoplasms / diagnosis. Liver Neoplasms / immunology. Male. Middle Aged

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  • [ISSN] 1432-2307
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
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22. McNicol AM: Assessment of malignancy in adrenal cortical tumors. Endocr Pathol; 2006;17(2):131-6
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  • [Title] Assessment of malignancy in adrenal cortical tumors.
  • The roles of the pathologist in assessing adrenal cortical tumors are, first, to differentiate adenoma from carcinoma, and, second, to assess prognosis when the diagnosis of malignancy is made.
  • [MeSH-major] Adenoma / pathology. Adrenal Cortex Neoplasms / pathology. Carcinoma / pathology. Neoplasm Invasiveness / diagnosis
  • [MeSH-minor] Biomarkers, Tumor / analysis. Humans. Immunohistochemistry. Molecular Biology. Prognosis

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  • (PMID = 17159245.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 36
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23. Sasaki Y, Toyota E: [Prevention of tuberculosis in medically high-risked patients]. Kekkaku; 2010 Jan;85(1):47-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-minor] Adrenal Cortex Hormones / adverse effects. Antibodies, Monoclonal / adverse effects. Arthritis, Rheumatoid / complications. Arthritis, Rheumatoid / drug therapy. HIV Infections / complications. Humans. Immunocompromised Host. Infliximab. Latent Tuberculosis / drug therapy. Latent Tuberculosis / prevention & control. Renal Dialysis / adverse effects. Risk. Risk Factors. Tumor Necrosis Factor-alpha / antagonists & inhibitors

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  • (PMID = 20232544.001).
  • [ISSN] 0022-9776
  • [Journal-full-title] Kekkaku : [Tuberculosis]
  • [ISO-abbreviation] Kekkaku
  • [Language] jpn
  • [Publication-type] Congresses
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Antibodies, Monoclonal; 0 / Tumor Necrosis Factor-alpha; B72HH48FLU / Infliximab
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24. D'Haens G: Infliximab for ulcerative colitis: finally some answers. Gastroenterology; 2005 Jun;128(7):2161-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Clinical Trials as Topic. Endpoint Determination. Humans. Infliximab. Treatment Outcome. Tumor Necrosis Factor-alpha

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  • [CommentIn] Gastroenterology. 2005 Oct;129(4):1358-9; author reply 1359 [16230092.001]
  • [CommentOn] Gastroenterology. 2005 Jun;128(7):1805-11 [15940615.001]
  • (PMID = 15940648.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Comment; Editorial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Antibodies, Monoclonal; 0 / Tumor Necrosis Factor-alpha; B72HH48FLU / Infliximab
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25. Fassnacht M, Hahner S, Polat B, Koschker AC, Kenn W, Flentje M, Allolio B: Efficacy of adjuvant radiotherapy of the tumor bed on local recurrence of adrenocortical carcinoma. J Clin Endocrinol Metab; 2006 Nov;91(11):4501-4
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  • [Title] Efficacy of adjuvant radiotherapy of the tumor bed on local recurrence of adrenocortical carcinoma.
  • CONTEXT: Local tumor recurrence is common in adrenocortical carcinoma (ACC) and is the most frequent cause for reoperation.
  • OBJECTIVE: The objective of the study was investigation of adjuvant tumor bed irradiation in the treatment of ACC.
  • PATIENTS: The German ACC Registry (n = 285) was screened for patients who had received tumor bed radiotherapy in an adjuvant setting (no macroscopic evidence for residual disease after surgery).
  • Fourteen patients without distant metastases (World Health Organization stage I, one patient; stage II, seven; stage III, three; and stage IV, three) were matched with 14 patients for resection status, adjuvant mitotane treatment, stage, and tumor size.
  • MAIN OUTCOME MEASURE: Survival without local recurrence and disease-free survival was the main outcome measure.
  • However, disease-free and overall survival were not significantly different between the two groups.
  • CONCLUSION: These data from the largest series of ACC patients treated with adjuvant tumor bed irradiation suggest that radiotherapy is effective in reducing the high rate of local recurrence in ACC.
  • [MeSH-major] Adrenal Cortex Neoplasms / radiotherapy. Adrenal Cortex Neoplasms / surgery. Adrenocortical Carcinoma / radiotherapy. Adrenocortical Carcinoma / surgery. Neoplasm Recurrence, Local / radiotherapy
  • [MeSH-minor] Adult. Antineoplastic Agents, Hormonal / therapeutic use. Chemotherapy, Adjuvant. Combined Modality Therapy. Disease-Free Survival. Humans. Middle Aged. Mitotane / therapeutic use. Radiotherapy / adverse effects. Radiotherapy, Adjuvant / adverse effects. Radiotherapy, Adjuvant / methods. Retrospective Studies. Survival Analysis. Treatment Outcome

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  • [CommentIn] J Clin Endocrinol Metab. 2006 Nov;91(11):4250-2 [17088440.001]
  • (PMID = 16895957.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 78E4J5IB5J / Mitotane
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26. Cano F, Poderoso C, Cornejo Maciel F, Castilla R, Maloberti P, Castillo F, Neuman I, Paz C, Podestá EJ: Protein tyrosine phosphatases regulate arachidonic acid release, StAR induction and steroidogenesis acting on a hormone-dependent arachidonic acid-preferring acyl-CoA synthetase. J Steroid Biochem Mol Biol; 2006 Jun;99(4-5):197-202
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-minor] Adrenal Cortex Neoplasms. Adrenocorticotropic Hormone / pharmacology. Animals. Cell Line. Cell Line, Tumor. Leydig Cell Tumor. Luteinizing Hormone / pharmacology. Male. Mice

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  • (PMID = 16630718.001).
  • [ISSN] 0960-0760
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Membrane Transport Proteins; 27YG812J1I / Arachidonic Acid; 9002-60-2 / Adrenocorticotropic Hormone; 9002-67-9 / Luteinizing Hormone; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 6.2.1.- / Coenzyme A Ligases
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27. Genovese MC, Bathon JM, Fleischmann RM, Moreland LW, Martin RW, Whitmore JB, Tsuji WH, Leff JA: Longterm safety, efficacy, and radiographic outcome with etanercept treatment in patients with early rheumatoid arthritis. J Rheumatol; 2005 Jul;32(7):1232-42
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  • OBJECTIVE: To evaluate safety, efficacy, and radiographic progression in patients with early rheumatoid arthritis (RA) undergoing longterm treatment with etanercept.
  • METHODS: Patients with early RA (disease duration of 3 years or less) who had completed a 2-year efficacy study comparing etanercept and methotrexate (MTX) were followed in an extension where they received 25 mg etanercept twice weekly.
  • Efficacy and radiographic progression were assessed using American College of Rheumatology response criteria, disease activity scores, and Total Sharp Score (TSS).
  • CONCLUSION: Etanercept treatment in patients with early RA was generally well tolerated for up to 5 years.
  • The rate of radiographic progression was low compared with other studies, emphasizing the benefit gained in patients with early aggressive RA who undergo longterm treatment with etanercept.
  • [MeSH-major] Antirheumatic Agents / administration & dosage. Arthritis, Rheumatoid / drug therapy. Arthritis, Rheumatoid / radiography. Immunoglobulin G / administration & dosage. Receptors, Tumor Necrosis Factor / administration & dosage
  • [MeSH-minor] Adrenal Cortex Hormones / administration & dosage. Adrenal Cortex Hormones / adverse effects. Adult. Aged. Aged, 80 and over. Disease Progression. Drug Therapy, Combination. Etanercept. Female. Humans. Male. Methotrexate / administration & dosage. Methotrexate / adverse effects. Middle Aged. Severity of Illness Index. Treatment Outcome


28. Nomikos IN, Zizi-Serbetzoglou A, Matsakis G, Elemenoglou J, Vamvakopoulos NC: Association of an oversized adrenal cortical adenoma with expression of pheochromocytoma-like neurosecretory features. J BUON; 2008 Jul-Sep;13(3):425-8
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  • [Title] Association of an oversized adrenal cortical adenoma with expression of pheochromocytoma-like neurosecretory features.
  • Abnormal stimulation of adrenal function may be either direct, affecting similarly cortical and medullary secretion, or indirect affecting primarily the medulla.
  • Indirect activation of clinically detectable adrenomedullary function may develop as a physical consequence of a non-functional adrenal tumor exerting pressure on the medulla by its size, location and direction of growth.
  • Our case of an oversized and overweight adrenal tumor associated with expression of late-onset pheochromocytoma-like clinical symptoms may be explained by the physical indirect rather than the biological direct activation of adrenomedullary function like hyperplasia or cancer.
  • [MeSH-major] Adenoma / pathology. Adrenal Cortex Neoplasms / pathology. Adrenal Medulla / pathology. Pheochromocytoma / pathology

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  • (PMID = 18979561.001).
  • [ISSN] 1107-0625
  • [Journal-full-title] Journal of B.U.ON. : official journal of the Balkan Union of Oncology
  • [ISO-abbreviation] J BUON
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 57285-09-3 / Inhibins
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29. Soon PS, Libe R, Benn DE, Gill A, Shaw J, Sywak MS, Groussin L, Bertagna X, Gicquel C, Bertherat J, McDonald KL, Sidhu SB, Robinson BG: Loss of heterozygosity of 17p13, with possible involvement of ACADVL and ALOX15B, in the pathogenesis of adrenocortical tumors. Ann Surg; 2008 Jan;247(1):157-64
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  • [Title] Loss of heterozygosity of 17p13, with possible involvement of ACADVL and ALOX15B, in the pathogenesis of adrenocortical tumors.
  • OBJECTIVE: To determine the minimal common region of loss on 17p13 in a cohort of adrenocortical carcinomas (ACCs) (defined by a Weiss score > or =3) and adrenocortical adenomas (ACAs) (defined by a Weiss score <3) and subsequently to assess 3 genes in this region that could be involved in adrenocortical tumorigenesis.
  • METHODS: Using 12 microsatellite markers across 17p13, LOH analysis was performed on 37 paired blood and adrenocortical tumor samples (23 ACC and 14 ACA samples) to determine the minimal common region of loss for ACCs and ACAs.
  • [MeSH-major] Acyl-CoA Dehydrogenases / genetics. Adrenal Cortex Neoplasms / genetics. Arachidonate 12-Lipoxygenase / genetics. Chromosomes, Human, Pair 17. Genes, Tumor Suppressor. Loss of Heterozygosity

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  • (PMID = 18156936.001).
  • [ISSN] 0003-4932
  • [Journal-full-title] Annals of surgery
  • [ISO-abbreviation] Ann. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers; EC 1.13.11.31 / Arachidonate 12-Lipoxygenase; EC 1.3.- / Acyl-CoA Dehydrogenases
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30. Rednic S, Marinescu C, Chira R, Rogojan L, Rednic N: Treatment with infliximab in a patient with ankylosing spondylitis and Crohn's disease. J Gastrointestin Liver Dis; 2006 Dec;15(4):379-82
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  • [Title] Treatment with infliximab in a patient with ankylosing spondylitis and Crohn's disease.
  • The association of Crohn's disease and ankylosing spondylitis is described in up to 30% of cases.
  • We present the case of a 53 year old woman, diagnosed with colonic Crohn's disease and ankylosing spondilitis, treated initially with increasing doses of sulphasalazine and moderate dose of corticosteroids, with the persistence of severe gastrointestinal and articular symptoms.
  • She underwent therapy with tumor necrosis factor alpha (TNFalpha) inhibitor infliximab, with a spectacular improvement of symptoms, signs and quality of life.
  • [MeSH-major] Anti-Inflammatory Agents / therapeutic use. Antibodies, Monoclonal / therapeutic use. Colon / drug effects. Crohn Disease / drug therapy. Spondylitis, Ankylosing / drug therapy
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Biopsy. Colonoscopy. Female. Humans. Infliximab. Middle Aged. Sulfasalazine / therapeutic use. Treatment Outcome


31. Schmitt A, Saremaslani P, Schmid S, Rousson V, Montani M, Schmid DM, Heitz PU, Komminoth P, Perren A: IGFII and MIB1 immunohistochemistry is helpful for the differentiation of benign from malignant adrenocortical tumours. Histopathology; 2006 Sep;49(3):298-307
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  • [Title] IGFII and MIB1 immunohistochemistry is helpful for the differentiation of benign from malignant adrenocortical tumours.
  • AIMS: The differentiation of adrenocortical carcinomas from adenomas may be difficult based on morphology alone.
  • Differential expression of insulin-like growth factor (IGF) II and cyclin-dependent kinase (CDK) 4 has recently been described in these tumours.
  • METHODS AND RESULTS: We examined 22 benign and 17 malignant adrenocortical tumours and compared IGFII and CDK4 expression with known immunohistochemical as well as morphological criteria of malignancy.
  • The combination of IGFII immunohistochemistry with MIB1 index led to high sensitivity and specificity in detecting adrenocortical carcinomas.
  • CONCLUSIONS: IGFII and MIB1 are helpful immunohistochemical markers to predict malignancy in adrenocortical neoplasms.
  • These markers can be used in addition to clinical, gross and morphological features to establish a diagnosis in difficult cases.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenocortical Adenoma / diagnosis. Adrenocortical Carcinoma / diagnosis. Insulin-Like Growth Factor Binding Protein 2 / biosynthesis. Ki-67 Antigen / biosynthesis
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / analysis. Cyclin-Dependent Kinase 4 / biosynthesis. Diagnosis, Differential. Golgi Apparatus / metabolism. Humans. Immunohistochemistry. Middle Aged. Sensitivity and Specificity. Tumor Suppressor Protein p53 / biosynthesis

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  • (PMID = 16918977.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Insulin-Like Growth Factor Binding Protein 2; 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53; EC 2.7.11.22 / Cyclin-Dependent Kinase 4
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32. Arima K, Origuchi T, Tamai M, Iwanaga N, Izumi Y, Huang M, Tanaka F, Kamachi M, Aratake K, Nakamura H, Ida H, Uetani M, Kawakami A, Eguchi K: RS3PE syndrome presenting as vascular endothelial growth factor associated disorder. Ann Rheum Dis; 2005 Nov;64(11):1653-5
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  • [Title] RS3PE syndrome presenting as vascular endothelial growth factor associated disorder.
  • METHODS: Vascular endothelial growth factor(165) (VEGF(165)), tumour necrosis factor alpha (TNFalpha), and interleukin 1beta (IL1beta) were measured by enzyme linked immunosorbent assay (ELISA) in serum samples from three patients with RS3PE syndrome.
  • As controls, serum samples from 26 healthy volunteers, 12 patients with rheumatoid arthritis, 10 patients with systemic lupus erythematosus, 13 patients with polymyositis/dermatomyositis, 13 patients with vasculitis syndrome, and 6 patients with mixed connective tissue disease were also analysed.
  • CONCLUSIONS: VEGF promotes synovial inflammation and vascular permeability in patients with RS3PE syndrome, suggesting that RS3PE can be classified as a VEGF associated disorder.
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Humans. Interleukin-1 / blood. Magnetic Resonance Imaging / methods. Subcutaneous Tissue / pathology. Syndrome. Tumor Necrosis Factor-alpha / analysis

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  • (PMID = 16227418.001).
  • [ISSN] 0003-4967
  • [Journal-full-title] Annals of the rheumatic diseases
  • [ISO-abbreviation] Ann. Rheum. Dis.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Interleukin-1; 0 / Tumor Necrosis Factor-alpha; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
  • [Other-IDs] NLM/ PMC1755286
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33. Trezzi R, Poli F, Fellegara G: "Dedifferentiated" adrenal cortical neoplasm. Int J Surg Pathol; 2009 Aug;17(4):343-4
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  • [Title] "Dedifferentiated" adrenal cortical neoplasm.
  • [MeSH-major] Adenoma / pathology. Adrenal Cortex Neoplasms / pathology. Cell Dedifferentiation. Cell Transformation, Neoplastic
  • [MeSH-minor] Aged. Antigens, CD56 / analysis. Antigens, Neoplasm / analysis. Biomarkers, Tumor / analysis. Female. Humans. MART-1 Antigen. Neoplasm Proteins / analysis. Synaptophysin / analysis

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  • (PMID = 19443867.001).
  • [ISSN] 1066-8969
  • [Journal-full-title] International journal of surgical pathology
  • [ISO-abbreviation] Int. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / MART-1 Antigen; 0 / MLANA protein, human; 0 / Neoplasm Proteins; 0 / Synaptophysin
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34. Tseng KF, Hsu HC, Wang FC, Fong YC: Nerve sheath ganglion of the tibial nerve presenting as a Baker's cyst: a case report. Knee Surg Sports Traumatol Arthrosc; 2006 Sep;14(9):880-4
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  • The occurrence of a nerve sheath ganglion in a patient's tibial nerve has been identified.
  • The initial presentation of the tumor mass has been very similar to that of a Baker's cyst, namely a soft undulating popliteal mass.
  • [MeSH-major] Ganglion Cysts / diagnosis. Tibial Nerve / ultrastructure
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Adult. Diagnosis, Differential. Drainage. Humans. Injections. Male. Popliteal Cyst / diagnosis

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  • (PMID = 16570194.001).
  • [ISSN] 0942-2056
  • [Journal-full-title] Knee surgery, sports traumatology, arthroscopy : official journal of the ESSKA
  • [ISO-abbreviation] Knee Surg Sports Traumatol Arthrosc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
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35. Fenichel P, Bstandig B, Roger C, Chevallier D, Michels JF, Sadoul JL, Hieronimus S, Brucker-Davis F: Unilateral testicular tumour associated to congenital adrenal hyperplasia: Failure of specific tumoral molecular markers to discriminate between adrenal rest and leydigioma. Ann Endocrinol (Paris); 2008 Nov;69(5):453-8
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  • [Title] Unilateral testicular tumour associated to congenital adrenal hyperplasia: Failure of specific tumoral molecular markers to discriminate between adrenal rest and leydigioma.
  • Testicular adrenal rest tumours are frequently associated with congenital adrenal hyperplasia (CAH).
  • These ACTH-dependent tumours cannot be easily distinguished histologically from Leydig-cell tumours.
  • We report the case of a 30-year-old man who was explored for infertility, azoospermia and unilateral testicular tumour.
  • High levels of 17-OH progesterone and ACTH, low cortisol and undetectable gonadotropins levels, associated to bilateral adrenal hyperplasia, led to the diagnosis of CAH by 21-OH deficiency with a composite heterozygoty.
  • The testicular tumour was first considered as adrenal rest.
  • However, histological analysis of this unilateral painful tumour showed a steroid-hormone-secreting cell proliferation with atypical and frequent mitosis.
  • To discriminate between a benign adrenal rest tumour and a possible malignant leydigioma, tumoral expression of specific gene products was analyzed by RT-PCR.
  • No 11-beta-hydroxylase nor ACTH receptor mRNAs could be found in the tumour, which did not behave like usual adrenal rest cells.
  • For this unilateral testicular tumour, the lack of adrenal-specific markers associated with a high rate of mitosis and pleiomorphism supported a leydigian origin with malignant potential.
  • However, lack of tumoral LH-R mRNA expression and a tumour-free 3-year follow-up led us to retain the diagnosis of adrenal rest tumour with loss of adrenal gene expression and progressive autonomous behaviour.
  • [MeSH-major] Adrenal Hyperplasia, Congenital / complications. Adrenal Hyperplasia, Congenital / diagnosis. Adrenal Rest Tumor / diagnosis. Leydig Cell Tumor / diagnosis. Testicular Neoplasms / complications. Testicular Neoplasms / diagnosis
  • [MeSH-minor] Adrenal Cortex Hormones / blood. Adrenal Cortex Hormones / genetics. Adult. Anti-Inflammatory Agents / therapeutic use. Azoospermia / etiology. Biomarkers, Tumor. Dexamethasone / therapeutic use. Diagnosis, Differential. Gonadal Steroid Hormones / blood. Gonadal Steroid Hormones / genetics. Gonadotropins / blood. Humans. Infertility, Male / etiology. Male. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Testis / pathology


36. Kelly SN, McKenna TJ, Young LS: Coregulatory protein-orphan nuclear receptor interactions in the human adrenal cortex. J Endocrinol; 2005 Jul;186(1):33-42
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  • [Title] Coregulatory protein-orphan nuclear receptor interactions in the human adrenal cortex.
  • The capacity of the adrenal to produce steroids is controlled in part through the transcriptional regulation of steroid enzymes.
  • We hypothesised that, in the presence of secretagogues, SF-1 and nur77 may differentially interact with coregulatory proteins in the human adrenal cortex.
  • Both coregulatory proteins, steroid receptor coactivator (SRC-1) and silencing mediator for retinoid and thyroid hormones (SMRT), were found to be expressed in the zona fasciculata and reticularis in the human adrenal cortex, but were largely absent from the zona glomerulosa.
  • In the H295R adrenal tumour cell line, SF-1 and nur77 transcripts were increased in cells in the presence of forskolin, whereas nur77 mRNA was also induced with angiotensin II (AII).
  • Orphan nuclear receptor-coregulatory protein interactions may have consequences for the regulation of key steroidogenic enzymes in the human adrenal cortex.
  • [MeSH-major] Adrenal Cortex / chemistry. DNA-Binding Proteins / analysis. Receptors, Cytoplasmic and Nuclear / analysis. Receptors, Steroid / analysis. Repressor Proteins / analysis. Transcription Factors / analysis
  • [MeSH-minor] Angiotensin II / pharmacology. Cell Line, Tumor. Cells, Cultured. Colforsin / pharmacology. Gene Expression / drug effects. Histone Acetyltransferases. Homeodomain Proteins. Humans. Nuclear Receptor Co-Repressor 2. Nuclear Receptor Coactivator 1. Nuclear Receptor Subfamily 4, Group A, Member 1. Protein Interaction Mapping / methods. RNA, Messenger / analysis. Steroidogenic Factor 1. Stimulation, Chemical. Zona Fasciculata / chemistry. Zona Reticularis / chemistry

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  • (PMID = 16002533.001).
  • [ISSN] 0022-0795
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / NCOR2 protein, human; 0 / NR4A1 protein, human; 0 / NR5A1 protein, human; 0 / Nuclear Receptor Co-Repressor 2; 0 / Nuclear Receptor Subfamily 4, Group A, Member 1; 0 / RNA, Messenger; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Steroid; 0 / Repressor Proteins; 0 / Steroidogenic Factor 1; 0 / Transcription Factors; 11128-99-7 / Angiotensin II; 1F7A44V6OU / Colforsin; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / NCOA1 protein, human; EC 2.3.1.48 / Nuclear Receptor Coactivator 1
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37. Antoniu SA: Effects of inhaled therapy on biomarkers of systemic inflammation in stable chronic obstructive pulmonary disease. Biomarkers; 2010 Mar;15(2):97-103
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  • [Title] Effects of inhaled therapy on biomarkers of systemic inflammation in stable chronic obstructive pulmonary disease.
  • In chronic obstructive pulmonary disease (COPD) airways inflammation is associated in more advanced stages with systemic inflammation.
  • [MeSH-major] Biomarkers / analysis. C-Reactive Protein / metabolism. Pulmonary Disease, Chronic Obstructive / drug therapy. Pulmonary Disease, Chronic Obstructive / physiopathology. Pulmonary Surfactant-Associated Protein D / metabolism
  • [MeSH-minor] Administration, Inhalation. Adrenal Cortex Hormones / therapeutic use. Adrenergic beta-Agonists / therapeutic use. Cholinergic Antagonists / therapeutic use. Drug Therapy, Combination. Fibrinogen / metabolism. Humans. Inflammation / drug therapy. Interleukin-6 / metabolism. Receptors, Adrenergic, beta-2 / drug effects. Scopolamine Derivatives / therapeutic use. Tiotropium Bromide. Treatment Outcome. Tumor Necrosis Factor-alpha / metabolism. Uteroglobin / metabolism

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  • (PMID = 19929747.001).
  • [ISSN] 1366-5804
  • [Journal-full-title] Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals
  • [ISO-abbreviation] Biomarkers
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Adrenergic beta-Agonists; 0 / Biomarkers; 0 / Cholinergic Antagonists; 0 / Interleukin-6; 0 / Pulmonary Surfactant-Associated Protein D; 0 / Receptors, Adrenergic, beta-2; 0 / SCGB1A1 protein, human; 0 / Scopolamine Derivatives; 0 / Tumor Necrosis Factor-alpha; 9001-32-5 / Fibrinogen; 9007-41-4 / C-Reactive Protein; 9060-09-7 / Uteroglobin; XX112XZP0J / Tiotropium Bromide
  • [Number-of-references] 61
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38. Pulitanò C, Aldrighetti L, Arru M, Finazzi R, Catena M, Guzzetti E, Soldini L, Comotti L, Ferla G: Preoperative methylprednisolone administration maintains coagulation homeostasis in patients undergoing liver resection: importance of inflammatory cytokine modulation. Shock; 2007 Oct;28(4):401-5
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  • Alterations in hemostatic parameters are a common finding after major hepatic resection.
  • [MeSH-minor] Adrenal Cortex Hormones / administration & dosage. Adrenal Cortex Hormones / pharmacology. Adult. Aged. Aged, 80 and over. Anti-Inflammatory Agents / administration & dosage. Anti-Inflammatory Agents / pharmacology. Antithrombin III / metabolism. Fibrin Fibrinogen Degradation Products / metabolism. Fibrinogen / metabolism. Humans. Interleukin-6 / blood. Middle Aged. Preoperative Care / methods. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 17577134.001).
  • [ISSN] 1073-2322
  • [Journal-full-title] Shock (Augusta, Ga.)
  • [ISO-abbreviation] Shock
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Anti-Inflammatory Agents; 0 / Cytokines; 0 / Fibrin Fibrinogen Degradation Products; 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha; 9000-94-6 / Antithrombin III; 9001-32-5 / Fibrinogen; X4W7ZR7023 / Methylprednisolone
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39. Sakamoto N, Tojo K, Saito T, Fujimoto K, Isaka T, Tajima N, Ikeda K, Yamada H, Furuta N, Sasano H: Coexistence of aldosterone-producing adrenocortical adenoma and pheochromocytoma in an ipsilateral adrenal gland. Endocr J; 2009;56(2):213-9
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  • [Title] Coexistence of aldosterone-producing adrenocortical adenoma and pheochromocytoma in an ipsilateral adrenal gland.
  • A 40-year-old female, diagnosed as essential hypertension, demonstrated a 2 cm mass in left adrenal gland by computed tomography without abnormal endocrinological findings. (131)I-adosterol and (123)I-metaiodobenzylguanidine (MIBG) scintigraphy at 39 years of age showed no abnormal accumulation.
  • Follow up (131)I-adosterol scintigraphy performed one year later showed apparently abnormal uptake and slightly elevated uptake in left adrenal gland.
  • Serial T2-weighted magnetic resonance imaging clearly demonstrated two distinct tumors.
  • Furthermore, selective adrenal venous sampling with intravenous ACTH infusion indicated aldosterone-producing adrenocortical adenoma (APA) in left adrenal gland.
  • During operation of adrenal tumor, blood pressure elevated markedly and complication of pheochromocytoma (PC) was suspected.
  • Immunohistochemical findings after left adrenolectomy revealed that the adrenal mass was compatible with APA and PC.
  • Herein, we present an extremely rare case of the simultaneous occurrence of both APA and PC in an ipsilateral adrenal gland.
  • [MeSH-major] Adrenal Gland Neoplasms / pathology. Adrenocortical Adenoma / pathology. Pheochromocytoma / pathology
  • [MeSH-minor] Adrenal Cortex Neoplasms / pathology. Adrenal Glands / pathology. Adult. Aldosterone / blood. Female. Humans. Hypokalemia / complications. Incidental Findings. Neoplasms, Multiple Primary. Tomography, X-Ray Computed

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  • (PMID = 19023159.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone
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40. Hu ZJ, Tian HY, Wang LT, Tian HY: [Changes in adrenal cortex function and protective effect of dexamethasone in septic rats during early phases]. Zhongguo Wei Zhong Bing Ji Jiu Yi Xue; 2009 Jan;21(1):40-3
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  • [Title] [Changes in adrenal cortex function and protective effect of dexamethasone in septic rats during early phases].
  • OBJECTIVE: To affirm the presence of relative adrenal insufficiency (RAI) in the early phases of sepsis and its probable mechanisms, and to study the optimal time for glucocorticoid replacement therapy.
  • Adrenocorticotrophic hormone (ACTH) test was conducted at 8 hours and 12 hours, and before and after 30 minutes of ACTH administration, the cortisol content in serum was determined with radioimmunoassay (RIA) and the expressions of Toll-like receptor 4 (TLR4), tumor necrosis factor-alpha (TNF-alpha) mRNA in adrenal glands were detected with semiquantitative reverse transcription-polymerase chain reaction (RT-PCR).
  • Ultrastructure of adrenal cortex was observed with transmission electron microscope.
  • But there was no marked change in the levels of cortisol between pre-and post-ACTH in rats with sepsis in the early phases. (2)The expressions of TLR4, TNF-alpha mRNA in adrenal both were significantly increased in CLP group, and they were higher than those in sham operation group (P<0.05 or P<0.01).
  • The expressions of TLR4, TNF-alpha mRNA in dexamethasone prevention group and treatment group were significantly lower than those in CLP group, and those in the dexamethasone prevention group were lower than those in sham operation group. (3)In the groups of CLP, dexamethasone prevention and treatment, ultrastructure changes were observed in the adrenal, especially in CLP group. (4)The survival rate of the dexamethasone prevention and treatment groups at 12 hours were higher than that of CLP group (76.92%, 40.00% vs. 33.33%, P<0.01 and P<0.05).
  • CONCLUSION: (1)RAI occurs during the early stage of sepsis. (2)The expressions of TLR4, TNF-alpha mRNA in adrenal and changes in corticoadrenal ultrastructure participates in the pathogenesis of RAI in the early stage of sepsis in rat. (3) Dexamethasone therapy could effectively increase the survival rate and improve outcome through down-regulating the expression changes in TLR4, TNF-alpha mRNA and alleviating changes in ultrastructure of adrenal glands.
  • [MeSH-major] Adrenal Cortex / physiopathology. Dexamethasone / therapeutic use. Glucocorticoids / therapeutic use. Sepsis / physiopathology
  • [MeSH-minor] Animals. Disease Models, Animal. Male. RNA, Messenger / genetics. Random Allocation. Rats. Rats, Wistar. Toll-Like Receptor 4 / genetics. Toll-Like Receptor 4 / metabolism. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 19141191.001).
  • [ISSN] 1003-0603
  • [Journal-full-title] Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue
  • [ISO-abbreviation] Zhongguo Wei Zhong Bing Ji Jiu Yi Xue
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / RNA, Messenger; 0 / Tlr4 protein, rat; 0 / Toll-Like Receptor 4; 0 / Tumor Necrosis Factor-alpha; 7S5I7G3JQL / Dexamethasone
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41. Rosati R, Cerrato F, Doghman M, Pianovski MA, Parise GA, Custódio G, Zambetti GP, Ribeiro RC, Riccio A, Figueiredo BC, Lalli E: High frequency of loss of heterozygosity at 11p15 and IGF2 overexpression are not related to clinical outcome in childhood adrenocortical tumors positive for the R337H TP53 mutation. Cancer Genet Cytogenet; 2008 Oct;186(1):19-24
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  • [Title] High frequency of loss of heterozygosity at 11p15 and IGF2 overexpression are not related to clinical outcome in childhood adrenocortical tumors positive for the R337H TP53 mutation.
  • A germline TP53 R337H mutation is present in childhood adrenocortical tumors (ACT) from southern Brazil.
  • Other genetic alterations are also frequently found in these tumors.
  • This study was designed to assess whether alterations of the 11p15 region exist in childhood ACT, accounting for IGF2 overexpression in these tumors, and how they are related to clinical outcome.
  • Tumor DNA of 12 children with ACT (4 adenomas and 8 carcinomas) and from the blood of their parents was analyzed.
  • All patients showed 11p15 loss of heterozygosity (LOH) in the tumor.
  • In contrast to the single case of paternal LOH, IGF2 was overexpressed in tumors with maternal allele loss.
  • Our data show that 11p15 LOH is a widespread finding in childhood ACT not related with malignancy, contrary to adult ACT.

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  • [Copyright] (c)2008 Elsevier Inc. All rights reserved.
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  • (PMID = 18786438.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA063230-13; United States / NCI NIH HHS / CA / R01 CA063230; United States / NCI NIH HHS / CA / CA63230; United States / NCI NIH HHS / CA / R01 CA063230-13
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 67763-97-7 / Insulin-Like Growth Factor II
  • [Other-IDs] NLM/ NIHMS70916; NLM/ PMC2603647
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42. Rodríguez-Hermosa JI, Roig J, Ortuño P, Quiles AM, Recasens M, Codina-Cazador A: [A large adrenal tumor]. Rev Esp Enferm Dig; 2008 Jun;100(6):363-4
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  • [Title] [A large adrenal tumor].
  • [Transliterated title] Gran tumor suprarrenal.
  • [MeSH-major] Adrenal Cortex Neoplasms. Adrenocortical Adenoma

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  • (PMID = 18752367.001).
  • [ISSN] 1130-0108
  • [Journal-full-title] Revista española de enfermedades digestivas : organo oficial de la Sociedad Española de Patología Digestiva
  • [ISO-abbreviation] Rev Esp Enferm Dig
  • [Language] spa
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Spain
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43. Guillevin L, Pagnoux C: Therapeutic strategies for systemic necrotizing vasculitides. Allergol Int; 2007 Jun;56(2):105-11
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  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Antibodies, Monoclonal, Murine-Derived. Antigens, CD20 / immunology. Antiviral Agents / therapeutic use. Blood Vessels / pathology. Churg-Strauss Syndrome / immunology. Churg-Strauss Syndrome / therapy. Cyclophosphamide / therapeutic use. Etanercept. Granulomatosis with Polyangiitis / immunology. Granulomatosis with Polyangiitis / therapy. HIV Infections / complications. Hepatitis B / complications. Hepatitis C / complications. Humans. Immunoglobulin G / therapeutic use. Immunosuppressive Agents / therapeutic use. Infliximab. Necrosis. Polyarteritis Nodosa / immunology. Polyarteritis Nodosa / therapy. Receptors, Tumor Necrosis Factor / therapeutic use. Rituximab. Treatment Outcome. Tumor Necrosis Factor-alpha / immunology

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  • (PMID = 17460440.001).
  • [ISSN] 1323-8930
  • [Journal-full-title] Allergology international : official journal of the Japanese Society of Allergology
  • [ISO-abbreviation] Allergol Int
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Antiviral Agents; 0 / Immunoglobulin G; 0 / Immunoglobulins, Intravenous; 0 / Immunologic Factors; 0 / Immunosuppressive Agents; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha; 4F4X42SYQ6 / Rituximab; 8N3DW7272P / Cyclophosphamide; B72HH48FLU / Infliximab; OP401G7OJC / Etanercept
  • [Number-of-references] 48
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44. Wagner SA, Mehta AC, Laber DA: Rituximab-induced interstitial lung disease. Am J Hematol; 2007 Oct;82(10):916-9
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  • [Title] Rituximab-induced interstitial lung disease.
  • The aim of this study is to characterize rituximab-induced interstitial lung disease (R-ILD).
  • This analysis focused on patient characteristics, underlying disease, rituximab dosing schedule, and R-ILD characteristic-like symptoms, diagnosis, treatment, and outcomes.
  • Prompt diagnosis and treatment with corticosteroids is essential.
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Antibodies, Monoclonal, Murine-Derived. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cough / etiology. Cyclophosphamide / administration & dosage. Doxorubicin / administration & dosage. Doxorubicin / analogs & derivatives. Dyspnea / etiology. Fatal Outcome. Fever / etiology. Humans. Lymphoma, Large B-Cell, Diffuse / complications. Lymphoma, Large B-Cell, Diffuse / drug therapy. Male. Middle Aged. Prednisone / administration & dosage. Prognosis. Rituximab. Tumor Necrosis Factor-alpha / secretion. Vincristine / administration & dosage

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  • (PMID = 17597477.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Tumor Necrosis Factor-alpha; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol, modified
  • [Number-of-references] 17
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45. Kraugerud M, Zimmer KE, Dahl E, Berg V, Olsaker I, Farstad W, Ropstad E, Verhaegen S: Three structurally different polychlorinated biphenyl congeners (Pcb 118, 153, and 126) affect hormone production and gene expression in the human H295R in vitro model. J Toxicol Environ Health A; 2010;73(16):1122-32
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  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Environmental Pollutants / toxicity. Gene Expression Regulation / drug effects. Hormones / biosynthesis. Polychlorinated Biphenyls / toxicity. Steroids / biosynthesis
  • [MeSH-minor] Cell Survival / drug effects. Dose-Response Relationship, Drug. Estradiol / biosynthesis. Humans. RNA, Messenger / genetics. RNA, Messenger / metabolism. Tumor Cells, Cultured

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  • (PMID = 20574914.001).
  • [ISSN] 1528-7394
  • [Journal-full-title] Journal of toxicology and environmental health. Part A
  • [ISO-abbreviation] J. Toxicol. Environ. Health Part A
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Environmental Pollutants; 0 / Hormones; 0 / RNA, Messenger; 0 / Steroids; 4TI98Z838E / Estradiol; DFC2HB4I0K / Polychlorinated Biphenyls
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46. de Lange J, van den Akker HP, van den Berg H: Central giant cell granuloma of the jaw: a review of the literature with emphasis on therapy options. Oral Surg Oral Med Oral Pathol Oral Radiol Endod; 2007 Nov;104(5):603-15
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Age Distribution. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antineoplastic Agents / therapeutic use. Benzamides. Bone Density Conservation Agents / therapeutic use. Calcitonin / therapeutic use. Denosumab. Giant Cell Tumor of Bone / pathology. Humans. Imatinib Mesylate. Interferons / therapeutic use. Osteoprotegerin / therapeutic use. Piperazines / therapeutic use. Pyrimidines / therapeutic use. RANK Ligand. Subgingival Curettage

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  • (PMID = 17703964.001).
  • [ISSN] 1528-395X
  • [Journal-full-title] Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics
  • [ISO-abbreviation] Oral Surg Oral Med Oral Pathol Oral Radiol Endod
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Bone Density Conservation Agents; 0 / Osteoprotegerin; 0 / Piperazines; 0 / Pyrimidines; 0 / RANK Ligand; 4EQZ6YO2HI / Denosumab; 8A1O1M485B / Imatinib Mesylate; 9007-12-9 / Calcitonin; 9008-11-1 / Interferons
  • [Number-of-references] 113
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47. Matyakhina L, Freedman RJ, Bourdeau I, Wei MH, Stergiopoulos SG, Chidakel A, Walther M, Abu-Asab M, Tsokos M, Keil M, Toro J, Linehan WM, Stratakis CA: Hereditary leiomyomatosis associated with bilateral, massive, macronodular adrenocortical disease and atypical cushing syndrome: a clinical and molecular genetic investigation. J Clin Endocrinol Metab; 2005 Jun;90(6):3773-9
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  • [Title] Hereditary leiomyomatosis associated with bilateral, massive, macronodular adrenocortical disease and atypical cushing syndrome: a clinical and molecular genetic investigation.
  • Hereditary leiomyomatosis and renal cell cancer (HLRCC) is an autosomal dominant disorder caused by mutations in the fumarate hydratase (FH) gene on chromosome 1q42.3-43.
  • Massive macronodular adrenocortical disease (MMAD) is a heterogeneous condition associated with Cushing syndrome (CS) and bilateral hyperplasia of the adrenal glands.
  • In MMAD, cortisol secretion is often mediated by ectopic, adrenocortical expression of receptors for a variety of substances; however, to date, no consistent genetic defects have been identified.
  • In a patient with HLRCC caused by a germline-inactivating FH mutation, we diagnosed atypical (subclinical) CS due to bilateral, ACTH-independent adrenocortical hyperplasia.
  • The tumor tissue harbored the germline FH mutation and demonstrated allelic losses of the 1q42.3-43 FH locus.
  • We then searched the National Institutes of Health (NIH) databases of patients with MMAD or HLRCC and found at least three other cases with MMAD that had a history of tumors that could be part of HLRCC; among patients with HLRCC, there were several with some adrenal nodularity noted on computed tomography but none with imaging findings consistent with MMAD.
  • From two of the three MMAD patients, adrenocortical tumor DNA was available and sequenced for coding FH mutations; there were none.
  • We conclude that in a patient with HLRCC, adrenal hyperplasia and CS were due to MMAD.
  • The latter was likely due to the FH germline mutation because in tumor cells, only the mutant allele was retained.
  • However, other patients with MMAD and HLRCC, or HLRCC patients with adrenal imaging findings consistent with MMAD, or MMAD patients with somatic FH mutations were not found among the NIH series.
  • Although a fortuitous association cannot be excluded, HLRCC may be added to the short list of monogenic disorders that have been reported to be associated with the development of adrenal tumors; FH may be considered a candidate gene for MMAD.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Cushing Syndrome / genetics. Leiomyomatosis / genetics
  • [MeSH-minor] Adrenal Glands / pathology. Aged. Chromosome Mapping. Chromosomes, Human, Pair 1. DNA / blood. DNA / genetics. DNA / isolation & purification. Female. Functional Laterality. Humans. In Situ Hybridization, Fluorescence. Skin / pathology. Treatment Outcome

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  • (PMID = 15741255.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9007-49-2 / DNA
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48. Vyvey M: Steroids as pain relief adjuvants. Can Fam Physician; 2010 Dec;56(12):1295-7, e415
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  • Ten years ago he was diagnosed with a pancreatic carcinoid tumour and underwent a Whipple procedure.
  • Since then, his symptoms have been well controlled with intermittent chemotherapy despite his known liver and multiple spinal metastases.One year ago, Mr. C. developed bony pain from his cervical spine disease and was started on hydromorphone.
  • [MeSH-major] Adrenal Cortex Hormones / adverse effects. Adrenal Cortex Hormones / therapeutic use. Analgesics / adverse effects. Analgesics / therapeutic use. Pain / drug therapy. Palliative Care
  • [MeSH-minor] Aged, 80 and over. Carcinoid Tumor / drug therapy. Carcinoid Tumor / secondary. Carcinoid Tumor / surgery. Chemotherapy, Adjuvant. Humans. Male. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / surgery. Sleep Initiation and Maintenance Disorders / chemically induced. Spinal Neoplasms / drug therapy. Spinal Neoplasms / secondary. Substance Withdrawal Syndrome / etiology. Substance Withdrawal Syndrome / prevention & control

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  • (PMID = 21156893.001).
  • [ISSN] 1715-5258
  • [Journal-full-title] Canadian family physician Médecin de famille canadien
  • [ISO-abbreviation] Can Fam Physician
  • [Language] eng; fre
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Analgesics
  • [Other-IDs] NLM/ PMC3001922
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49. Slater EP, Diehl SM, Langer P, Samans B, Ramaswamy A, Zielke A, Bartsch DK: Analysis by cDNA microarrays of gene expression patterns of human adrenocortical tumors. Eur J Endocrinol; 2006 Apr;154(4):587-98
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  • [Title] Analysis by cDNA microarrays of gene expression patterns of human adrenocortical tumors.
  • OBJECTIVES: Adrenocortical carcinoma (ACC) is a rare malignant neoplasm with extremely poor prognosis.
  • The molecular mechanisms of adrenocortical tumorigenesis are still not well understood.
  • The comparative analysis by cDNA microarrays of gene-expression patterns of benign and malignant adrenocortical tumors allows us to identify new tumor-suppressor genes and proto-oncogenes underlying adrenocortical tumorigenesis.
  • DESIGN AND METHODS: Total RNA from fresh-frozen tissue of 10 ACC and 10 benign adrenocortical adenomas was isolated after histologic confirmation of neoplastic cellularity of at least 85%.
  • The reference consisted of pooled RNA of 10 normal adrenal cortex samples.
  • Amplified RNA of tumor and reference was used to synthesize Cy3- and Cy5-fluorescently labeled cDNA in a flip-color technique.
  • RESULTS: The comparative analysis of gene expression revealed many genes with more than fourfold expression difference between ACC and normal tissue (42 genes), cortical adenoma and normal tissue (11 genes), and ACC and cortical adenoma (21 genes) respectively.
  • As confirmed by real-time PCR, the IGF2 gene was significantly upregulated in ACCs versus cortical adenomas and normal cortical tissue.
  • Genes that were downregulated in adrenocortical tumors included chromogranin B and early growth response factor 1.
  • CONCLUSIONS: Comprehensive expression profiling of adrenocortical tumors by the cDNA microarray technique is a very powerful tool to elucidate the molecular steps associated with the tumorigenesis of these ill-defined neoplasms.

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  • (PMID = 16556722.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 4964P6T9RB / Aldosterone; WI4X0X7BPJ / Hydrocortisone
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50. Figueiredo BC, Sandrini R, Zambetti GP, Pereira RM, Cheng C, Liu W, Lacerda L, Pianovski MA, Michalkiewicz E, Jenkins J, Rodriguez-Galindo C, Mastellaro MJ, Vianna S, Watanabe F, Sandrini F, Arram SB, Boffetta P, Ribeiro RC: Penetrance of adrenocortical tumours associated with the germline TP53 R337H mutation. J Med Genet; 2006 Jan;43(1):91-6
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  • [Title] Penetrance of adrenocortical tumours associated with the germline TP53 R337H mutation.
  • BACKGROUND: An inherited germline P53 mutation has been identified in cases of childhood adrenocortical carcinoma (ACT), a neoplasm with a high incidence in southern Brazil.

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  • (PMID = 16033918.001).
  • [ISSN] 1468-6244
  • [Journal-full-title] Journal of medical genetics
  • [ISO-abbreviation] J. Med. Genet.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / CA-71907
  • [Publication-type] Letter; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ PMC2564508
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51. Lubina A, Olchovsky D, Berezin M, Ram Z, Hadani M, Shimon I: Management of pituitary apoplexy: clinical experience with 40 patients. Acta Neurochir (Wien); 2005 Feb;147(2):151-7; discussion 157
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  • Serial sellar MRI showed disappearance of pituitary tumor in 63% of operated subjects.
  • Six patients (3 with PRL-secreting and 3 nonfunctional adenomas) were treated medically (corticosteroids, dopamine agonists), two patients (out of three) with visual deficits improved, and tumor shrinkage was noted in four.
  • [MeSH-major] Adenoma / complications. Decompression, Surgical / methods. Neurosurgical Procedures / methods. Pituitary Apoplexy / complications. Pituitary Apoplexy / surgery. Pituitary Neoplasms / complications
  • [MeSH-minor] Adolescent. Adrenal Cortex Hormones / therapeutic use. Adult. Aged. Aged, 80 and over. Clinical Protocols. Dopamine Agonists / therapeutic use. Female. Humans. Hypopituitarism / etiology. Hypopituitarism / physiopathology. Hypopituitarism / surgery. Magnetic Resonance Imaging. Male. Middle Aged. Optic Chiasm / physiopathology. Optic Chiasm / surgery. Optic Nerve / physiopathology. Optic Nerve / surgery. Pituitary Gland / pathology. Pituitary Gland / physiopathology. Pituitary Gland / surgery. Retrospective Studies. Sphenoid Bone / pathology. Sphenoid Bone / surgery. Treatment Outcome. Vision, Low / etiology. Vision, Low / physiopathology. Vision, Low / surgery

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  • (PMID = 15570437.001).
  • [ISSN] 0001-6268
  • [Journal-full-title] Acta neurochirurgica
  • [ISO-abbreviation] Acta Neurochir (Wien)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Dopamine Agonists
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52. Ikenoue Y, Tagami T, Murata M: Development and validation of a novel IL-10 deficient cell transfer model for colitis. Int Immunopharmacol; 2005 Jun;5(6):993-1006
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  • [Title] Development and validation of a novel IL-10 deficient cell transfer model for colitis.
  • A number of rodent models for inflammatory bowel disease (IBD) have been developed, but most cannot be used to develop and validate new therapies for IBD.
  • From the models developed, the IL-10 deficient mouse model is the one that results in a disease similar to human IBD; however, in this model, colitis occurs with variable incidence taking 3-4 months to develop.
  • In addition, we assessed several agents for inflammatory bowel disease to validate the general utility of this cell transfer model.
  • It is worth noting that TNFR-Ig or prednisolone, which is effective for treatment of patients with severe-fulminant Crohn's disease, markedly attenuated pathological clinical indices in this colitis model, whereas the immunosuppressive agents, azathioprine, tacrolimus, and cyclosporine A produced no significant effect.
  • [MeSH-minor] Adrenal Cortex Hormones / pharmacology. Animals. Antibodies, Monoclonal / pharmacology. Disease Models, Animal. Flow Cytometry. Immunosuppressive Agents / pharmacology. Lymph Nodes / cytology. Lymph Nodes / transplantation. Mice. Mice, Inbred C57BL. Mice, Knockout. Mice, SCID. Nitrates / blood. Nitrites / blood. Prednisolone / pharmacology. Reproducibility of Results. Spleen / cytology. Spleen / transplantation. Tumor Necrosis Factor-alpha / antagonists & inhibitors

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  • (PMID = 15829415.001).
  • [ISSN] 1567-5769
  • [Journal-full-title] International immunopharmacology
  • [ISO-abbreviation] Int. Immunopharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Antibodies, Monoclonal; 0 / Immunosuppressive Agents; 0 / Nitrates; 0 / Nitrites; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 9PHQ9Y1OLM / Prednisolone
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53. Almeida MQ, Fragoso MC, Lotfi CF, Santos MG, Nishi MY, Costa MH, Lerario AM, Maciel CC, Mattos GE, Jorge AA, Mendonca BB, Latronico AC: Expression of insulin-like growth factor-II and its receptor in pediatric and adult adrenocortical tumors. J Clin Endocrinol Metab; 2008 Sep;93(9):3524-31
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  • [Title] Expression of insulin-like growth factor-II and its receptor in pediatric and adult adrenocortical tumors.
  • BACKGROUND: Adrenocortical tumors are heterogeneous neoplasms with incompletely understood pathogenesis.
  • IGF-II overexpression has been consistently demonstrated in adult adrenocortical carcinomas.
  • OBJECTIVES: The objective of the study was to analyze expression of IGF-II and its receptor (IGF-IR) in pediatric and adult adrenocortical tumors and the effects of a selective IGF-IR kinase inhibitor (NVP-AEW541) on adrenocortical tumor cells.
  • PATIENTS: Fifty-seven adrenocortical tumors (37 adenomas and 20 carcinomas) from 23 children and 34 adults were studied.
  • Cell proliferation and apoptosis were analyzed in NCI H295 cells and a new cell line established from a pediatric adrenocortical adenoma.
  • RESULTS: IGF-II transcripts were overexpressed in both pediatric adrenocortical carcinomas and adenomas.
  • Otherwise, IGF-II was mainly overexpressed in adult adrenocortical carcinomas (270.5 +/- 130.2 vs. 16.1 +/- 13.3; P = 0.0001).
  • IGF-IR expression was significantly higher in pediatric adrenocortical carcinomas than adenomas (9.1 +/- 3.1 vs. 2.6 +/- 0.3; P = 0.0001), whereas its expression was similar in adult adrenocortical carcinomas and adenomas.
  • IGF-IR expression was a predictor of metastases in pediatric adrenocortical tumors in univariate analysis (hazard ratio 1.84; 95% confidence interval 1.28-2.66; P = 0.01).
  • CONCLUSION: IGF-IR overexpression was a biomarker of pediatric adrenocortical carcinomas.
  • Additionally, a selective IGF-IR kinase inhibitor had antitumor effects in adult and pediatric adrenocortical tumor cell lines, suggesting that IGF-IR inhibitors represent a promising therapy for human adrenocortical carcinoma.
  • [MeSH-major] Adenoma / genetics. Adrenal Cortex Neoplasms / genetics. Carcinoma / genetics. Insulin-Like Growth Factor II / genetics. Receptor, IGF Type 2 / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Female. Gene Expression Regulation, Neoplastic. Humans. Infant. Male. Middle Aged. Neoplasm Metastasis. Tumor Cells, Cultured

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  • (PMID = 18611974.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptor, IGF Type 2; 67763-97-7 / Insulin-Like Growth Factor II
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54. Vivarelli M, Dazzi A, Zanello M, Cucchetti A, Cescon M, Ravaioli M, Del Gaudio M, Lauro A, Grazi GL, Pinna AD: Effect of different immunosuppressive schedules on recurrence-free survival after liver transplantation for hepatocellular carcinoma. Transplantation; 2010 Jan 27;89(2):227-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Tumor recurrence represents the main limitation of liver transplantation in patients with hepatocellular carcinoma (HCC) and can be favored by exposure to calcineurin inhibitors.
  • METHODS: We investigated the effect of an immunosuppressant schedule that minimizes the exposure to calcineurin inhibitors on patients transplanted for HCC to ascertain whether this can reduce the tumor recurrence rate.
  • [MeSH-major] Carcinoma, Hepatocellular / surgery. Immunosuppressive Agents / therapeutic use. Liver Neoplasms / surgery. Liver Transplantation / immunology. Neoplasm Recurrence, Local / epidemiology. Sirolimus / therapeutic use. Tacrolimus / therapeutic use
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Adult. Aged. Cohort Studies. Disease-Free Survival. Drug Administration Schedule. Female. Hepatitis B / complications. Hepatitis C / complications. Humans. Male. Middle Aged. Risk Factors. Survivors. Young Adult

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  • (PMID = 20098287.001).
  • [ISSN] 1534-6080
  • [Journal-full-title] Transplantation
  • [ISO-abbreviation] Transplantation
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Immunosuppressive Agents; W36ZG6FT64 / Sirolimus; WM0HAQ4WNM / Tacrolimus
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55. Antonelli A, Ferri C, Ferrari SM, Galetta F, Franzoni F, Santoro G, De Marco S, Ghiri E, Fallahi P: High circulating N-terminal pro-brain natriuretic peptide and tumor necrosis factor-alpha in mixed cryoglobulinemia. World J Gastroenterol; 2009 Oct 28;15(40):5074-9
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  • [Title] High circulating N-terminal pro-brain natriuretic peptide and tumor necrosis factor-alpha in mixed cryoglobulinemia.
  • AIM: To evaluate serum levels of N-terminal pro-brain natriuretic peptide (NTproBNP) and tumor necrosis factor alpha (TNF-alpha) in a large series of patients with hepatitis C associated with mixed cryoglobulinemia (MC+HCV).
  • The increase of NTproBNP may indicate the presence of a subclinical cardiac dysfunction.
  • [MeSH-major] Cryoglobulinemia / blood. Natriuretic Peptide, Brain / blood. Peptide Fragments / blood. Tumor Necrosis Factor-alpha / blood
  • [MeSH-minor] Adrenal Cortex Hormones / metabolism. Aged. Case-Control Studies. Female. Heart Failure. Humans. Liver / metabolism. Male. Middle Aged

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  • (PMID = 19860001.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Peptide Fragments; 0 / Tumor Necrosis Factor-alpha; 0 / pro-brain natriuretic peptide (1-76); 114471-18-0 / Natriuretic Peptide, Brain
  • [Other-IDs] NLM/ PMC2768887
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56. Kubota K, Iida H, Fujisawa T, Ogawa M, Inamori M, Saito S, Kakuta Y, Oshiro H, Nakajima A: Clinical significance of swollen duodenal papilla in autoimmune pancreatitis. Pancreas; 2007 Nov;35(4):e51-60
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  • OBJECTIVES: To evaluate the clinical significance of a swollen main duodenal papilla and the associated immunohistopathologic findings in patients with autoimmune pancreatitis (AIP).
  • These findings in the AIP patients were compared with those in 12 patients with chronic alcoholic tumor-forming pancreatitis (CAP).
  • We suggest that these findings may be valuable adjuncts to the diagnosis of AIP as well as for selecting suitable candidates for corticosteroid therapy.
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Aged. Anti-Inflammatory Agents / therapeutic use. Antigens, CD3 / analysis. Antigens, CD79 / analysis. Cholangiopancreatography, Endoscopic Retrograde. Female. Humans. Immunoglobulin G / analysis. Immunohistochemistry. Male. Middle Aged. Patient Selection. Plasma Cells / pathology. Predictive Value of Tests. Retrospective Studies. Stromal Cells / pathology. T-Lymphocytes / pathology. Treatment Outcome

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  • (PMID = 18090232.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Anti-Inflammatory Agents; 0 / Antigens, CD3; 0 / Antigens, CD79; 0 / CD79A protein, human; 0 / Immunoglobulin G
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57. West AN, Neale GA, Pounds S, Figueredo BC, Rodriguez Galindo C, Pianovski MA, Oliveira Filho AG, Malkin D, Lalli E, Ribeiro R, Zambetti GP: Gene expression profiling of childhood adrenocortical tumors. Cancer Res; 2007 Jan 15;67(2):600-8
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  • [Title] Gene expression profiling of childhood adrenocortical tumors.
  • Pediatric adrenocortical tumors (ACT) are rare and often fatal malignancies; little is known regarding their etiology and biology.
  • To provide additional insight into the nature of ACT, we determined the gene expression profiles of 24 pediatric tumors (five adenomas, 18 carcinomas, and one undetermined) and seven normal adrenal glands.
  • Distinct patterns of gene expression, validated by quantitative real-time PCR and Western blot analysis, were identified that distinguish normal adrenal cortex from tumor.
  • Differences in gene expression were also identified between adrenocortical adenomas and carcinomas.
  • In addition, pediatric adrenocortical carcinomas were found to share similar patterns of gene expression when compared with those published for adult ACT.
  • Our findings lay the groundwork for establishing gene expression profiles that may aid in the diagnosis and prognosis of pediatric ACT, and in the identification of signaling pathways that contribute to this disease.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics. Adrenocortical Carcinoma / genetics

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  • (PMID = 17234769.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / CA63230; United States / NCI NIH HHS / CA / CA71907
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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58. Szabó D, Zsippai A, Bendes M, Tömböl Z, Szabó PM, Rácz K, Igaz P: [Pathogenesis of adrenocortical cancer]. Orv Hetil; 2010 Jul 18;151(29):1163-70
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  • [Title] [Pathogenesis of adrenocortical cancer].
  • Adrenocortical cancer is a rare tumor with poor prognosis.
  • Whereas most cases occur in a sporadic setting, there are very rare hereditary forms that are important for the understanding of tumor pathogenesis.
  • The hereditary syndromes associated with adrenocortical cancer are: Li-Fraumeni's syndrome, Beckwith-Wiedemann's syndrome and familial adenomatous polyposis, whereas multiple endocrine neoplasia type 1, Carney's complex and McCune-Albright's syndrome mostly predispose to benign adrenocortical tumors.
  • Options for medical treatment of adrenocortical cancer are rather limited.
  • In this study, the pathogenesis of hereditary tumor syndromes, the alterations in sporadic tumors and the most recent molecular-bioinformatical observations are discussed.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / metabolism
  • [MeSH-minor] Adenomatous Polyposis Coli / genetics. Beckwith-Wiedemann Syndrome / genetics. Carney Complex / genetics. Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / metabolism. Fibrous Dysplasia, Polyostotic / genetics. Gene Expression Regulation, Neoplastic. Genes, p53. Genetic Predisposition to Disease. Humans. Insulin-Like Growth Factor II / metabolism. Li-Fraumeni Syndrome / genetics. Multiple Endocrine Neoplasia Type 1 / genetics. Mutation. Proto-Oncogene Proteins / genetics. Signal Transduction. Up-Regulation. Wnt Proteins / metabolism. beta Catenin / metabolism

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  • (PMID = 20591784.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Wnt Proteins; 0 / beta Catenin; 67763-97-7 / Insulin-Like Growth Factor II
  • [Number-of-references] 37
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59. Kimura N, Kumamoto T, Hanaoka T, Hasama Y, Nakamura K, Okazaki T: Monofocal large inflammatory demyelinating lesion, mimicking brain glioma. Clin Neurol Neurosurg; 2009 Apr;111(3):296-9
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  • Here we report two cases of pathologically confirmed tumor-like demyelinating lesions.
  • In comparison with common primary demyelinating diseases, our cases demonstrated atypical radiologic features, such as a large monofocal lesion with mild brain edema, and open ring-like or focal enhancement on magnetic resonance images, suggesting brain tumors.
  • Histological analysis of brain biopsy specimens showed the inflammatory demyelination and preserved axons without tumor cells.
  • The present cases suggest the importance of considering inflammatory demyelinating disease in the different diagnosis of monofocal tumor-like lesion.
  • [MeSH-major] Brain / pathology. Demyelinating Diseases / diagnosis. Demyelinating Diseases / pathology. Glioma / diagnosis
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Astrocytes / metabolism. Biopsy. Brain Edema / etiology. Brain Edema / pathology. Diagnosis, Differential. Female. Humans. Macrophages / immunology. Magnetic Resonance Imaging. Male. Middle Aged

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  • (PMID = 19058908.001).
  • [ISSN] 1872-6968
  • [Journal-full-title] Clinical neurology and neurosurgery
  • [ISO-abbreviation] Clin Neurol Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
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60. Mokos I, Bernat MM, Mareković Z, Pasini J: Virilizing adrenal cancer and bail-out nephrectomy. Coll Antropol; 2005 Dec;29(2):753-5
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  • [Title] Virilizing adrenal cancer and bail-out nephrectomy.
  • We report a rare case of virilizing adrenal cancer with tumorous invasion of the left renal vein in which a retroperitoneal adrenalectomy with bail-out nephrectomy was performed.
  • A tumor thrombus infiltrated the wall of the left adrenal vein and extended into the left renal vein.
  • To the authors' awareness, this is the first report of a virilizing adrenal cancer with a tumor thrombus infiltration of the renal vein and surgical tendency for kidney preservation.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenal Cortex Neoplasms / surgery. Adrenalectomy. Neoplastic Cells, Circulating / pathology. Nephrectomy. Renal Veins / pathology. Virilism / etiology

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  • (PMID = 16417195.001).
  • [ISSN] 0350-6134
  • [Journal-full-title] Collegium antropologicum
  • [ISO-abbreviation] Coll Antropol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Croatia
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61. Rodriguez-Galindo C, Figueiredo BC, Zambetti GP, Ribeiro RC: Biology, clinical characteristics, and management of adrenocortical tumors in children. Pediatr Blood Cancer; 2005 Sep;45(3):265-73
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  • [Title] Biology, clinical characteristics, and management of adrenocortical tumors in children.
  • Childhood adrenocortical tumors (ACT) are very aggressive endocrine neoplasms whose incidence is quite low.
  • In recent years, however, new information has been derived from the International Pediatric Adrenocortical Tumor Registry (IPACTR), and new clues to its pathogenesis have emerged.
  • Two-thirds of patients have resectable tumors.
  • Cisplatin-based chemotherapy with mitotane is indicated for unresectable or metastatic disease, although its impact on overall outcome is slight.
  • In childhood ACT, age, tumor size, and tumor resectability are the most important prognostic indicators.
  • Outcome is stage-dependent; patients with small, resectable tumors have survival rates in excess of 80%, whereas the outcome for patients with unresectable disease is dismal.
  • Patients with large, resectable tumors have an intermediate outcome.
  • [MeSH-major] Adrenal Cortex Neoplasms
  • [MeSH-minor] Adolescent. Antineoplastic Agents, Hormonal / therapeutic use. Child. Child, Preschool. Genes, p53 / genetics. Humans. Infant. Mitotane / therapeutic use. Mutation. Neoplasm Staging. Research. Survival Rate

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15747338.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 21765; United States / NCI NIH HHS / CA / CA 71907
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 78E4J5IB5J / Mitotane
  • [Number-of-references] 83
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62. Adam P, Hahner S, Hartmann M, Heinrich B, Quinkler M, Willenberg HS, Saeger W, Sbiera S, Schmull S, Voelker HU, Ströbel P, Allolio B, Fassnacht M: Epidermal growth factor receptor in adrenocortical tumors: analysis of gene sequence, protein expression and correlation with clinical outcome. Mod Pathol; 2010 Dec;23(12):1596-604
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  • [Title] Epidermal growth factor receptor in adrenocortical tumors: analysis of gene sequence, protein expression and correlation with clinical outcome.
  • Adrenocortical carcinoma is a rare but highly malignant neoplasm with still limited treatment options.
  • Epidermal growth factor receptor (EGFR) has been shown to be overexpressed in many solid tumors, but its expression in adrenocortical carcinoma has been studied only in a limited number of cases.
  • Therefore, we analyzed the expression of EGFR in 169 adrenocortical carcinoma samples and compared it with 31 adrenocortical adenomas.
  • Additionally, in 30 cases of adrenocortical carcinoma, exons 18-21 of the EGFR gene were cloned and sequenced.
  • EGFR expression was found in 128 of 169 adrenocortical carcinoma samples (76%), and in 60 of these samples (=36%) strong membrane staining was detected.
  • In contrast, only 1 out of 31 adrenocortical adenomas weakly expressed the EGFR (3%).
  • In summary, EGFR was overexpressed in more than three-quarters of adrenocortical carcinoma cases of this series.
  • As EGFR is hardly expressed in adrenocortical adenomas, our results suggest that its expression in adrenocortical tumors indicates a malignant phenotype, which may be used in the differential diagnosis between adrenocortical adenomas and carcinomas.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / metabolism. Adrenocortical Adenoma / pathology. Receptor, Epidermal Growth Factor / biosynthesis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Female. Gene Expression. Gene Expression Profiling. Humans. Immunohistochemistry. Male. Middle Aged. Polymerase Chain Reaction. Prognosis. Tissue Array Analysis

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  • (PMID = 20693985.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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63. Clerc RG, Stauffer A, Weibel F, Hainaut E, Perez A, Hoflack JC, Bénardeau A, Pflieger P, Garriz JM, Funder JW, Capponi AM, Niesor EJ: Mechanisms underlying off-target effects of the cholesteryl ester transfer protein inhibitor torcetrapib involve L-type calcium channels. J Hypertens; 2010 Aug;28(8):1676-86
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-minor] Adrenal Cortex / drug effects. Adrenal Cortex / metabolism. Adrenal Cortex / pathology. Adrenal Gland Neoplasms. Aldosterone / metabolism. Angiotensin II / pharmacology. Animals. Blood Pressure / drug effects. Blood Pressure / physiology. Calcium / metabolism. Cell Line, Tumor. Cytochrome P-450 CYP11B2 / biosynthesis. Cytochrome P-450 CYP11B2 / genetics. Cytosol / drug effects. Cytosol / metabolism. Enzyme Induction / drug effects. Extracellular Signal-Regulated MAP Kinases / metabolism. Gene Expression / drug effects. Gene Expression Profiling. Humans. NAV1.1 Voltage-Gated Sodium Channel. Nerve Tissue Proteins / metabolism. RNA, Small Interfering / genetics. RNA, Small Interfering / metabolism. Rats. Rats, Inbred SHR. Sodium Channels / metabolism. Structure-Activity Relationship. Sulfhydryl Compounds / pharmacology

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  • [CommentIn] Nat Rev Cardiol. 2010 Oct;7(10):541 [21080555.001]
  • [CommentIn] J Hypertens. 2010 Aug;28(8):1614-6 [20647856.001]
  • (PMID = 20498617.001).
  • [ISSN] 1473-5598
  • [Journal-full-title] Journal of hypertension
  • [ISO-abbreviation] J. Hypertens.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticholesteremic Agents; 0 / Calcium Channels, L-Type; 0 / Cholesterol Ester Transfer Proteins; 0 / NAV1.1 Voltage-Gated Sodium Channel; 0 / Nerve Tissue Proteins; 0 / Quinolines; 0 / RNA, Small Interfering; 0 / SCN1A protein, human; 0 / Scn1a protein, rat; 0 / Sodium Channels; 0 / Sulfhydryl Compounds; 11128-99-7 / Angiotensin II; 3D050LIQ3H / dalcetrapib; 4964P6T9RB / Aldosterone; 4N4457MV2U / torcetrapib; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; SY7Q814VUP / Calcium
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64. Ronchi CL, Sbiera S, Kraus L, Wortmann S, Johanssen S, Adam P, Willenberg HS, Hahner S, Allolio B, Fassnacht M: Expression of excision repair cross complementing group 1 and prognosis in adrenocortical carcinoma patients treated with platinum-based chemotherapy. Endocr Relat Cancer; 2009 Sep;16(3):907-18
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  • [Title] Expression of excision repair cross complementing group 1 and prognosis in adrenocortical carcinoma patients treated with platinum-based chemotherapy.
  • Therapeutic progress in adrenocortical carcinoma (ACC) is severely hampered by its low incidence.
  • In other tumor entities, expression of excision repair cross complementing group 1 (ERCC1) predicts resistance to platinum compounds.
  • We have retrolectively established adrenal tissue microarrays and analyzed prospectively samples from 163 ACCs, 15 benign adrenal adenomas, and 8 normal adrenal glands by immunohistochemistry for ERCC1 protein expression.
  • ERCC1 protein was highly expressed in all normal adrenal glands, 14 benign tumors (93%) and in 75 ACCs (47%).
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / drug therapy. Adrenal Cortex Neoplasms / metabolism. Adrenocortical Carcinoma / diagnosis. Adrenocortical Carcinoma / drug therapy. Adrenocortical Carcinoma / metabolism. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. DNA-Binding Proteins / metabolism. Endonucleases / metabolism
  • [MeSH-minor] Adult. Biomarkers, Tumor / metabolism. Cohort Studies. Female. Follow-Up Studies. Humans. Male. Middle Aged. Platinum Compounds / administration & dosage. Prognosis. Retrospective Studies

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  • (PMID = 19240185.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Platinum Compounds; EC 3.1.- / ERCC1 protein, human; EC 3.1.- / Endonucleases
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65. Mikhaylova IV, Kuulasmaa T, Jääskeläinen J, Voutilainen R: Tumor necrosis factor-alpha regulates steroidogenesis, apoptosis, and cell viability in the human adrenocortical cell line NCI-H295R. Endocrinology; 2007 Jan;148(1):386-92
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  • [Title] Tumor necrosis factor-alpha regulates steroidogenesis, apoptosis, and cell viability in the human adrenocortical cell line NCI-H295R.
  • TNF-alpha regulates the hypothalamo-pituitary-adrenal axis at several levels.
  • It has been shown to modify adrenal steroidogenesis in many species, and it is supposed to act as an auto/paracrine factor.
  • However, its significance in human adrenocortical function remains unclear.
  • Therefore, we investigated the effect of TNF-alpha on adrenal steroidogenesis, expression of the key steroidogenic genes, apoptosis, and cell viability in the human adrenocortical cell line NCI-H295R.
  • These findings indicate that TNF-alpha is a potent regulator of steroidogenesis and cell viability in adrenocortical cells.
  • TNF-alpha may have physiological and/or pathophysiological significance as an endocrine and/or paracrine/autocrine regulator of adrenocortical function.
  • [MeSH-major] Adrenal Cortex / cytology. Apoptosis / drug effects. Steroids / biosynthesis. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] 3-Hydroxysteroid Dehydrogenases / genetics. 3-Hydroxysteroid Dehydrogenases / metabolism. 8-Bromo Cyclic Adenosine Monophosphate / pharmacology. Aldosterone / biosynthesis. Androstenedione / biosynthesis. Cell Line, Tumor. Cell Survival / drug effects. Dehydroepiandrosterone / biosynthesis. Dehydroepiandrosterone Sulfate / metabolism. Gene Expression Regulation, Enzymologic / drug effects. Humans. Hydrocortisone / biosynthesis. Phosphoproteins / genetics. Phosphoproteins / metabolism. RNA, Messenger / metabolism. Steroid 17-alpha-Hydroxylase / genetics. Steroid 17-alpha-Hydroxylase / metabolism

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  • (PMID = 17038555.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Phosphoproteins; 0 / RNA, Messenger; 0 / Steroids; 0 / Tumor Necrosis Factor-alpha; 0 / steroidogenic acute regulatory protein; 23583-48-4 / 8-Bromo Cyclic Adenosine Monophosphate; 409J2J96VR / Androstenedione; 459AG36T1B / Dehydroepiandrosterone; 4964P6T9RB / Aldosterone; 57B09Q7FJR / Dehydroepiandrosterone Sulfate; EC 1.1.- / 3-Hydroxysteroid Dehydrogenases; EC 1.14.99.9 / Steroid 17-alpha-Hydroxylase; WI4X0X7BPJ / Hydrocortisone
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66. Vuorenoja S, Rivero-Muller A, Kiiveri S, Bielinska M, Heikinheimo M, Wilson DB, Huhtaniemi IT, Rahman NA: Adrenocortical tumorigenesis, luteinizing hormone receptor and transcription factors GATA-4 and GATA-6. Mol Cell Endocrinol; 2007 Apr 15;269(1-2):38-45
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  • [Title] Adrenocortical tumorigenesis, luteinizing hormone receptor and transcription factors GATA-4 and GATA-6.
  • Luteinizing hormone (LH/hCG) responsiveness of normal and pathological human adrenal glands as well as the possibility of constitutive expressions of luteinizing hormone receptor (LHR) in adrenal cortex has been reported.
  • Some recent studies showed a correlation between the LHR and abundant GATA-4 expression in both metastasizing and non-metastasizing human adrenocortical tumors, but not in normal adrenals, implicating the putative relevance of LHR and GATA-4 for adrenocortical pathophysiology.
  • However, the physio- and pathophysiological significance of LHR and GATA-4 in the mechanism of adrenocortical tumorigenesis remains unclear.
  • The paucity of suitable models for adrenal tumorigenesis makes the establishment of proper animal models highly important.
  • LHR expression in the murine adrenal gland is an exception and not found in wild-type (WT) animal.
  • We have previously shown that ectopic LHR expression in the murine adrenal gland can be induced by chronically elevated LH levels.
  • We have generated a gonadotropin-responsive adrenal tumor model in gonadectomized transgenic (TG) mice expressing the inhibin alpha promoter/Simian Virus 40 T antigen transgene (inhalpha/Tag).
  • Given the induction of expression and regulation of GATA-4 and GATA-6 zinc finger transcription factors in the gonads by gonadotropins, this review will explore their relationship to LHR expression and their role in adrenocortical tumorigenesis.
  • A functional link between LHR and GATA-4 actions in the adrenal pathophysiology is proposed.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Carcinoma / genetics. GATA4 Transcription Factor / physiology. GATA6 Transcription Factor / physiology. Receptors, LH / physiology
  • [MeSH-minor] Animals. Disease Models, Animal. Humans. Inhibins / genetics. Mice. Mice, Transgenic

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  • (PMID = 17337116.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / GATA4 Transcription Factor; 0 / GATA4 protein, human; 0 / GATA6 Transcription Factor; 0 / GATA6 protein, human; 0 / Receptors, LH; 0 / inhibin-alpha subunit; 57285-09-3 / Inhibins
  • [Number-of-references] 87
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67. Miyoshi Y, Oue T, Oowari M, Soh H, Tachibana M, Kimura S, Kiyohara Y, Yamada H, Bessyo K, Mushiake S, Homma K, Hasegawa T, Sasano H, Ozono K: A case of pediatric virilizing adrenocortical tumor resulting in hypothalamic-pituitary activation and central precocious puberty following surgical removal. Endocr J; 2009;56(8):975-82
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  • [Title] A case of pediatric virilizing adrenocortical tumor resulting in hypothalamic-pituitary activation and central precocious puberty following surgical removal.
  • We present a 6-year-old boy with a virilizing adrenocortical tumor who initially presented with peripheral precocious puberty.
  • Both serum and urinary levels of adrenal androgens were elevated.
  • The histological diagnosis was adrenocortical carcinoma according to the criteria of Weiss.
  • Following surgical removal of the androgen-producing tumor, the patient subsequently developed hypothalamic-pituitary activation and demonstrated central precocious puberty.
  • Clinical follow-up of potential secondary effects of excess hormone secretion after removal is important in some pediatric patients with virilizing adrenocortical tumor.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenal Cortex Neoplasms / surgery. Adrenocortical Carcinoma / complications. Adrenocortical Carcinoma / surgery. Hypothalamo-Hypophyseal System / physiopathology. Puberty, Precocious / etiology

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  • (PMID = 19671995.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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68. Kamba T, Tam BY, Hashizume H, Haskell A, Sennino B, Mancuso MR, Norberg SM, O'Brien SM, Davis RB, Gowen LC, Anderson KD, Thurston G, Joho S, Springer ML, Kuo CJ, McDonald DM: VEGF-dependent plasticity of fenestrated capillaries in the normal adult microvasculature. Am J Physiol Heart Circ Physiol; 2006 Feb;290(2):H560-76
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  • However, VEGF is a survival factor for many tumor vessels, and there are clues that some normal blood vessels may also depend on VEGF.
  • In a study of 17 normal organs after VEGF inhibition, we found significant capillary regression in pancreatic islets, thyroid, adrenal cortex, pituitary, choroid plexus, small-intestinal villi, and epididymal adipose tissue.
  • The amount of regression was dose dependent and varied from organ to organ, with a maximum of 68% in thyroid, but was less in normal organs than in tumors in RIP-Tag2-transgenic mice or in Lewis lung carcinoma.
  • [MeSH-minor] Animals. Blood Pressure. Carcinoma, Lewis Lung / blood supply. Glucose Tolerance Test. Heart / physiology. Imidazoles. Indazoles / pharmacology. Islets of Langerhans / blood supply. Kidney / physiology. Mice. Mice, Inbred C57BL. Mice, Transgenic. Neoplasm Transplantation. Pancreatic Neoplasms / blood supply. Phenotype. Reference Values. Regeneration. Signal Transduction / drug effects. Signal Transduction / physiology. Vascular Endothelial Growth Factor Receptor-1 / metabolism. Vascular Endothelial Growth Factor Receptor-2 / metabolism

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  • [CommentIn] Am J Physiol Heart Circ Physiol. 2006 Feb;290(2):H509-11 [16403945.001]
  • (PMID = 16172168.001).
  • [ISSN] 0363-6135
  • [Journal-full-title] American journal of physiology. Heart and circulatory physiology
  • [ISO-abbreviation] Am. J. Physiol. Heart Circ. Physiol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL-24136; United States / NHLBI NIH HHS / HL / HL-59157; United States / NCI NIH HHS / CA / P50 CA-90270
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Imidazoles; 0 / Indazoles; 0 / Vascular Endothelial Growth Factor A; C9LVQ0YUXG / axitinib; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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69. Zeugswetter F, Hoyer MT, Pagitz M, Benesch T, Hittmair KM, Thalhammer JG: The desmopressin stimulation test in dogs with Cushing's syndrome. Domest Anim Endocrinol; 2008 Apr;34(3):254-60
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  • The V3-receptor is overexpressed in pituitary corticotrope tumors and the injection of desmopressin induces a marked ACTH and cortisol release in human patients with pituitary- (PDH), but not adrenal tumor (AT) dependent hyperadrenocorticism.
  • According to standard tests the dogs were divided into 3 groups (group 1=other disease, n=27; group 2=PDH, n=46; group 3=AT, n=7).
  • The results of this study suggest that the desmopressin test could be a useful tool in differentiating pituitary from adrenal dependent Cushing's syndromes.
  • Additional dogs with adrenocortical tumor must be tested in order to recommend its use in clinical practice.
  • [MeSH-major] Cushing Syndrome / diagnosis. Deamino Arginine Vasopressin. Dog Diseases / diagnosis
  • [MeSH-minor] Adrenal Gland Neoplasms / veterinary. Animals. Diagnosis, Differential. Dogs. Hydrocortisone / blood. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / veterinary. Prospective Studies. ROC Curve

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  • (PMID = 17851017.001).
  • [ISSN] 0739-7240
  • [Journal-full-title] Domestic animal endocrinology
  • [ISO-abbreviation] Domest. Anim. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] ENR1LLB0FP / Deamino Arginine Vasopressin; WI4X0X7BPJ / Hydrocortisone
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70. Juillerat P, Pittet V, Felley C, Mottet C, Froehlich F, Vader JP, Gonvers JJ, Michetti P: Drug safety in Crohn's disease therapy. Digestion; 2007;76(2):161-8
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  • [Title] Drug safety in Crohn's disease therapy.
  • The management of Crohn's disease usually consists of a succession of short-term acute phase treatments followed by a long-term maintenance therapy.
  • The drugs described in this article include 5-ASA compounds, antibiotics (metronidazole, ciprofloxacin and rifaximin), corticosteroids (budesonide, prednisone and equivalents), thiopurines (azathioprine and 6-mercaptopurine), methotrexate, anti-tumor necrosis factor inhibitors (infliximab, adalimumab, certolizumab), natalizumab, anticalcineurin inhibitors (cyclosporine, tacrolimus) and mycophenolate mofetil.
  • [MeSH-major] Adrenal Cortex Hormones / therapeutic use. Anti-Bacterial Agents / therapeutic use. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Crohn Disease / drug therapy. Immunosuppressive Agents / therapeutic use

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  • [Copyright] Copyright 2008 S. Karger AG, Basel.
  • (PMID = 18239408.001).
  • [ISSN] 1421-9867
  • [Journal-full-title] Digestion
  • [ISO-abbreviation] Digestion
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Anti-Bacterial Agents; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Immunosuppressive Agents
  • [Number-of-references] 85
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71. Else T: Telomeres and telomerase in adrenocortical tissue maintenance, carcinogenesis, and aging. J Mol Endocrinol; 2009 Oct;43(4):131-41
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  • [Title] Telomeres and telomerase in adrenocortical tissue maintenance, carcinogenesis, and aging.
  • Telomere maintenance mechanisms, such as telomerase activity and alternative telomere lengthening, provide the basis of malignant cell expansion independent of telomere shortening-induced apoptosis or senescence, ensuring tumor survival.
  • Recent advances highlight the importance of these mechanisms in adrenocortical carcinogenesis.
  • In this review, we will summarize the main models of telomere physiology and their impact on adrenocortical tissue maintenance, aging, and carcinogenesis.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenal Glands / metabolism. Adrenal Glands / pathology. Cell Aging / physiology. Telomerase / physiology. Telomere / physiology

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  • (PMID = 19411304.001).
  • [ISSN] 1479-6813
  • [Journal-full-title] Journal of molecular endocrinology
  • [ISO-abbreviation] J. Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.7.49 / Telomerase
  • [Number-of-references] 115
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72. Mizota M, Tamada I, Hizukuri K, Otsubo K, Arima S, Kawano Y, Ono S, Hayashida Y, Kaji T, Takamatsu H, Sasano H: Bilateral asynchronous adrenocortical adenoma in a girl with beckwith-wiedemann syndrome. Clin Pediatr Endocrinol; 2005;14(1):23-6
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  • [Title] Bilateral asynchronous adrenocortical adenoma in a girl with beckwith-wiedemann syndrome.
  • We report a case of asynchronous occurrence of bilateral adrenocortical adenoma in a 13-yr-old girl with Beckwith-Wiedemann syndrome.
  • A right virilizing adrenal adenoma was surgically removed at age 6, following clinical manifestation of virilization such as acne, voice change, clitoris hypertrophy and overgrowth.
  • Histopathological examination of the resected specimen revealed an adrenocortical adenoma predominantly composed of eosinophilic tumor cells expressing all the steroidogenic enzymes.
  • Abdominal ultrasonography demonstrated the presence of a left adrenocortical adenoma.
  • Pathological examination of the resected specimen revealed a circumscribed and well encapsulated tumor with essentially the same histological features as the tumor previously removed, except that the tumor cells showed a more prominent morphological similarity to the fetal adrenal cortex and did not express 3β HSD.

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  • (PMID = 24790306.001).
  • [ISSN] 0918-5739
  • [Journal-full-title] Clinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology
  • [ISO-abbreviation] Clin Pediatr Endocrinol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Other-IDs] NLM/ PMC4004928
  • [Keywords] NOTNLM ; Beckwith-Wiedemann syndrome / adrenal tumor / virilizing
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73. Kimura M, Irie A, Minei S, Ishii J, Okawa A, Takashima R, Kadowaki K, Morinaga S, Baba S: [A case of adrenocortical adenoma coexisting with gastrointestinal stromal tumor]. Hinyokika Kiyo; 2007 Aug;53(8):551-5
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  • [Title] [A case of adrenocortical adenoma coexisting with gastrointestinal stromal tumor].
  • A 48-year-old man was referred to our institute for the evaluation of a concomitant gastric submucosal tumor and right adrenal tumor, incidentally found by ultrasound examination.
  • Computed tomography showed a mass with a diameter of 6 cm adjacent to the stomach and the right adrenal tumor with a diameter of 3 cm.
  • These tumors had similar characteristics in both plain and enhanced imagings.
  • By magnetic resonance imaging, the intensity of the right adrenal tumor was equivalent to the liver in both T1 and T2 weighted images.
  • On the other hand, the gastric submucosal tumor showed low intensity in T1 weighted images and high intensity in T2 weighted images.
  • An adosterol scintigram showed slight accumulation at the region of adrenal tumor.
  • Pathological diagnosis of the adrenal tumor was a cortical adenoma, and that of the gastric submucosal tumor was gastrointestinal stromal tumor (GIST).
  • The gastric tumor was immunohistochemically stained positive with the C-kit and CD34 and negative for s-100 protein and desmin.
  • Histopathological diagnosis was coincident with gastric GIST and right adrenocortical adenoma, and the GIST was diagnosed as a high risk tumor because its diameter was over 5 cm.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenocortical Adenoma / surgery. Gastrointestinal Stromal Tumors / surgery. Laparoscopy. Stomach Neoplasms / surgery

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  • (PMID = 17874546.001).
  • [ISSN] 0018-1994
  • [Journal-full-title] Hinyokika kiyo. Acta urologica Japonica
  • [ISO-abbreviation] Hinyokika Kiyo
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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74. Lee SA, Kim EH, Lee YM, Lee W, Min WK, Lee YJ, Huh JR, Lee WJ: A novel mutation of the succinate dehydrogenase B gene in a Korean family with pheochromocytoma. Fam Cancer; 2010 Dec;9(4):643-6
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  • Pheochromocytoma is a tumor that originates from the adrenal cortex and sympathetic chains.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Mutation / genetics. Pheochromocytoma / genetics. Succinate Dehydrogenase / genetics

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  • (PMID = 20563860.001).
  • [ISSN] 1573-7292
  • [Journal-full-title] Familial cancer
  • [ISO-abbreviation] Fam. Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 1.3.5.1 / SDHB protein, human; EC 1.3.99.1 / Succinate Dehydrogenase
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75. Woo HS, Lee KH, Park SY, Han HS, Yoon CJ, Kim YH: Adrenal cortical adenoma in adrenohepatic fusion tissue: a mimic of malignant hepatic tumor at CT. AJR Am J Roentgenol; 2007 Mar;188(3):W246-8
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  • [Title] Adrenal cortical adenoma in adrenohepatic fusion tissue: a mimic of malignant hepatic tumor at CT.
  • [MeSH-major] Adenoma / radiography. Adrenal Cortex Neoplasms / radiography. Adrenal Glands / abnormalities. Adrenal Glands / radiography. Liver / abnormalities. Liver / radiography. Liver Neoplasms / radiography
  • [MeSH-minor] Aged. Diagnosis, Differential. Female. Humans. Tomography, X-Ray Computed

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  • (PMID = 17312030.001).
  • [ISSN] 1546-3141
  • [Journal-full-title] AJR. American journal of roentgenology
  • [ISO-abbreviation] AJR Am J Roentgenol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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76. Day CP: Treatment of alcoholic liver disease. Liver Transpl; 2007 Nov;13(11 Suppl 2):S69-75
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  • [Title] Treatment of alcoholic liver disease.
  • Severe alcoholic steatohepatitis (ASH) is the major complication of advanced alcoholic liver disease (ALD) and has a high mortality even when treated with corticosteroids.
  • New treatment modalities in ASH might involve antagonism of proinflammatory cytokines such as tumor necrosis factor (TNF) by specific antibodies or other TNF-interfering treatment strategies.
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Antioxidants / therapeutic use. Colchicine / therapeutic use. Dietary Supplements. Humans. Pentoxifylline / therapeutic use. Prognosis. Propylthiouracil / therapeutic use. Temperance. Time Factors. Treatment Outcome. Tumor Necrosis Factor-alpha / therapeutic use

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  • (PMID = 17969070.001).
  • [ISSN] 1527-6465
  • [Journal-full-title] Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society
  • [ISO-abbreviation] Liver Transpl.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Antioxidants; 0 / Tumor Necrosis Factor-alpha; 721M9407IY / Propylthiouracil; SD6QCT3TSU / Pentoxifylline; SML2Y3J35T / Colchicine
  • [Number-of-references] 34
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77. Gutenberg A, Lange B, Gunawan B, Larsen J, Brück W, Rohde V, Verheggen R: Spontaneous adrenal hemorrhage: a little-known complication of intracranial tumor surgery. Case report. J Neurosurg; 2007 Jun;106(6):1086-8
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  • [Title] Spontaneous adrenal hemorrhage: a little-known complication of intracranial tumor surgery. Case report.
  • Nontraumatic adrenal hemorrhage in adults is uncommon and unexpected in the context of intracranial surgery.
  • In this brief report they seek to draw attention to this rare but life-threatening complication, because rapid diagnosis can be life-saving.
  • [MeSH-major] Adrenal Gland Diseases / etiology. Adrenalectomy. Hemorrhage / etiology. Intraoperative Complications / etiology. Meningioma / surgery. Neurosurgical Procedures / adverse effects
  • [MeSH-minor] Adrenal Cortex Function Tests. Adrenal Cortex Hormones / therapeutic use. Aged. Humans. Male. Seizures / drug therapy. Seizures / etiology

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  • (PMID = 17564184.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
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78. Pereira RM, Michalkiewicz E, Pianovski MA, França SN, Boguszewski MC, Cat I, Lacerda Filho Ld, Sandrini R: [Treatment of childhood adrenocortical tumor]. Arq Bras Endocrinol Metabol; 2005 Oct;49(5):747-52
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  • [Title] [Treatment of childhood adrenocortical tumor].
  • [Transliterated title] Tratamento do tumor do córtex adrenal na infância.
  • Adrenocortical tumors (ACT) in children are uncommon.
  • However, the incidence of these tumors in Paraná is 15 times higher than that worldwide.
  • In our experience, disease stage I, absence of spillage during surgery and absence of intravenous thrombus are associated with better survival rates.
  • Preliminary data with the combination of etoposide, doxorubicin, cisplatin, and mitotane have shown that in some patients a complete remission is observed both of the tumor and metastasis.
  • Side effects due to these drugs are common and adrenal insufficiency may occur.
  • [MeSH-major] Adrenal Cortex Neoplasms. Adrenocortical Carcinoma
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Combined Modality Therapy. Female. Humans. Infant. Male. Neoplasm Staging. Prognosis. Survival Analysis

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  • (PMID = 16444357.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] por
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Brazil
  • [Number-of-references] 36
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79. Marshall GA, Doyle JJ: Long-term treatment of Hashimoto's encephalopathy. J Neuropsychiatry Clin Neurosci; 2006;18(1):14-20
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  • HE patients have positive antithyroid antibodies, are usually in a subclinical hypothyroid state, have elevated cerebral spinal fluid (CSF) protein, and have nonspecific electroencephalogram (EEG) and imaging abnormalities in the absence of CNS infection, tumor, or stroke.
  • [MeSH-major] Adrenal Cortex Hormones / therapeutic use. Antithyroid Agents / therapeutic use. Brain Damage, Chronic / drug therapy. Hashimoto Disease / drug therapy. Hypothyroidism / drug therapy. Methylprednisolone / therapeutic use. Thyroiditis, Autoimmune / drug therapy
  • [MeSH-minor] Administration, Oral. Adolescent. Adult. Aged. Anticonvulsants / therapeutic use. Autoantibodies / blood. Child. Cyclophosphamide / adverse effects. Cyclophosphamide / therapeutic use. Diagnosis, Differential. Dose-Response Relationship, Drug. Drug Therapy, Combination. Female. Follow-Up Studies. Humans. Infusions, Intravenous. Iodide Peroxidase / immunology. Long-Term Care. Male. Methotrexate / adverse effects. Methotrexate / therapeutic use. Middle Aged. Neurologic Examination / drug effects. Prednisone / adverse effects. Prednisone / therapeutic use. Recurrence

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  • (PMID = 16525066.001).
  • [ISSN] 0895-0172
  • [Journal-full-title] The Journal of neuropsychiatry and clinical neurosciences
  • [ISO-abbreviation] J Neuropsychiatry Clin Neurosci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Anticonvulsants; 0 / Antithyroid Agents; 0 / Autoantibodies; 8N3DW7272P / Cyclophosphamide; EC 1.11.1.8 / Iodide Peroxidase; VB0R961HZT / Prednisone; X4W7ZR7023 / Methylprednisolone; YL5FZ2Y5U1 / Methotrexate
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80. Varallyay CG, Muldoon LL, Gahramanov S, Wu YJ, Goodman JA, Li X, Pike MM, Neuwelt EA: Dynamic MRI using iron oxide nanoparticles to assess early vascular effects of antiangiogenic versus corticosteroid treatment in a glioma model. J Cereb Blood Flow Metab; 2009 Apr;29(4):853-60
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  • The vascular effects of antiangiogenic treatment may pose problems for evaluating brain tumor response based on contrast-enhanced magnetic resonance imaging (MRI).
  • Bevacizumab significantly decreased the blood volume and decreased permeability in tumors as determined by increased time-to-peak enhancement.

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  • (PMID = 19142191.001).
  • [ISSN] 1559-7016
  • [Journal-full-title] Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
  • [ISO-abbreviation] J. Cereb. Blood Flow Metab.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS053468; United States / NINDS NIH HHS / NS / R01 NS053468-03; United States / NINDS NIH HHS / NS / NS044687-26; United States / NCI NIH HHS / CA / R01 CA137488-14A1; United States / NINDS NIH HHS / NS / NS33618; United States / NINDS NIH HHS / NS / R37 NS044687-26; United States / NINDS NIH HHS / NS / R01 NS033618; United States / NINDS NIH HHS / NS / R37 NS044687; United States / NINDS NIH HHS / NS / NS053468-03; United States / NINDS NIH HHS / NS / NS44687; United States / NCI NIH HHS / CA / CA137488-14A1; United States / NINDS NIH HHS / NS / NS53468; United States / NINDS NIH HHS / NS / R01 NS044687; United States / NCI NIH HHS / CA / R01 CA137488
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Ferric Compounds; 1K09F3G675 / ferric oxide; 2S9ZZM9Q9V / Bevacizumab; 7S5I7G3JQL / Dexamethasone; 84F6U3J2R6 / gadodiamide; K2I13DR72L / Gadolinium DTPA
  • [Other-IDs] NLM/ NIHMS124822; NLM/ PMC2747492
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81. Vredenburgh JJ, Cloughesy T, Samant M, Prados M, Wen PY, Mikkelsen T, Schiff D, Abrey LE, Yung WK, Paleologos N, Nicholas MK, Jensen R, Das A, Friedman HS: Corticosteroid use in patients with glioblastoma at first or second relapse treated with bevacizumab in the BRAIN study. Oncologist; 2010;15(12):1329-34
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  • [MeSH-major] Adrenal Cortex Hormones / therapeutic use. Angiogenesis Inhibitors / therapeutic use. Antibodies, Monoclonal / therapeutic use. Brain Neoplasms / drug therapy. Glioblastoma / drug therapy. Neoplasm Recurrence, Local / drug therapy. Salvage Therapy
  • [MeSH-minor] Adult. Antibodies, Monoclonal, Humanized. Bevacizumab. Female. Humans. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Staging. Survival Rate. Treatment Outcome. Vascular Endothelial Growth Factor A / antagonists & inhibitors. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 21147867.001).
  • [ISSN] 1549-490X
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Vascular Endothelial Growth Factor A; 2S9ZZM9Q9V / Bevacizumab
  • [Other-IDs] NLM/ PMC3227925
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82. Fareau GG, Vassilopoulou-Sellin R: Diagnostic challenges in adrenocortical carcinoma: recommendations for surveillance after surgical resection of selected adrenal nodules. Endocr Pract; 2007 Oct;13(6):636-41
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  • [Title] Diagnostic challenges in adrenocortical carcinoma: recommendations for surveillance after surgical resection of selected adrenal nodules.
  • OBJECTIVE: To discuss challenges in the diagnosis of adrenocortical carcinoma and to suggest surveillance measures after removal of selected adrenal nodules.
  • METHODS: We present the case of a 65-year-old man with worsening hypertension and new-onset hypokalemia attributed to primary hyperaldosteronism due to a 3-cm right adrenal nodule.
  • RESULTS: A laparoscopic right adrenalectomy was performed, and the histologic diagnosis was a benign adenoma.
  • Magnetic resonance imaging showed an 8-cm mass in the right adrenal bed and multiple hepatic metastatic lesions.
  • Fine-needle biopsy confirmed the presence of adrenocortical carcinoma.
  • CONCLUSION: Despite a comprehensive biochemical, radiologic, and histologic assessment, the diagnosis of adrenocortical carcinoma can be missed.
  • Particularly, we caution against undue reliance on the initial tumor size.
  • We recommend that abdominal imaging be performed every 3 months for the first year and every 6 months for the second year after surgical removal of selected adrenal nodules.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenal Glands / surgery. Adrenocortical Carcinoma / surgery
  • [MeSH-minor] Adrenalectomy. Adrenocortical Adenoma / complications. Adrenocortical Adenoma / diagnosis. Adrenocortical Adenoma / surgery. Aged. Humans. Hyperaldosteronism / complications. Hyperaldosteronism / pathology. Hypertension / etiology. Hypokalemia / etiology. Magnetic Resonance Imaging. Male. Treatment Outcome

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  • (PMID = 17954420.001).
  • [ISSN] 1934-2403
  • [Journal-full-title] Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
  • [ISO-abbreviation] Endocr Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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83. Wagner AS, Fleitz JM, Kleinschmidt-Demasters BK: Pediatric adrenal cortical carcinoma: brain metastases and relationship to NF-1, case reports and review of the literature. J Neurooncol; 2005 Nov;75(2):127-33
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  • [Title] Pediatric adrenal cortical carcinoma: brain metastases and relationship to NF-1, case reports and review of the literature.
  • Adrenal cortical carcinoma (ACC) is a rare childhood neoplasm that seldom manifests brain metastases; hence few papers in the literature focus on neurological manifestations associated with ACC.
  • Although ACC is known to be a signature tumor type in several inherited cancer predisposition syndromes, particularly Li Fraumeni, ACC has not been previously associated with neurofibromatosis, type 1 (NF-1), an inherited disorder with frequent CNS lesions that might prompt concern for metastatic disease by neuroimaging studies.
  • The first child developed metastasis to the brain 4 years after resection of his adrenal primary and 2 and 1 years, respectively, after metastases to the liver and lungs.
  • Disseminated disease prompted concern that her complex intracranial lesions identified by neuroimaging studies might represent brain metastases, but this proved to be NF1-related hamartomatous lesions.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / diagnosis. Adrenocortical Carcinoma / pathology. Brain Neoplasms / secondary. Neurofibromatosis 1
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Chromosome Aberrations. Chylothorax / complications. Chylothorax / surgery. Diagnosis, Differential. Fatal Outcome. Female. Follow-Up Studies. Hamartoma / diagnosis. Humans. Liver Neoplasms / secondary. Lung Neoplasms / secondary. Magnetic Resonance Imaging. Male. Neoplasm Metastasis. Receptor, Epidermal Growth Factor / metabolism. Time Factors. Treatment Outcome

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  • (PMID = 16132517.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Number-of-references] 28
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84. Kim DJ, Chung JJ, Ryu YH, Hong SW, Yu JS, Kim JH: Adrenocortical oncocytoma displaying intense activity on 18F-FDG-PET: a case report and a literature review. Ann Nucl Med; 2008 Nov;22(9):821-4
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  • [Title] Adrenocortical oncocytoma displaying intense activity on 18F-FDG-PET: a case report and a literature review.
  • We report on the 18F-fluorodeoxyglucose positron emission tomography (18F-FDG-PET) findings in a case of adrenocortical oncocytoma, a rare tumor of the adrenal gland with the literature review of other imaging findings including ultrasonography, computed tomography, and magnetic resonance imaging.
  • To our knowledge, there have been no reports published in the English literature about 18F-FDG-PET findings in adrenocortical oncocytoma.
  • [MeSH-major] Adenoma, Oxyphilic / radionuclide imaging. Adrenal Cortex Neoplasms / radionuclide imaging. Fluorodeoxyglucose F18. Positron-Emission Tomography / methods

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  • (PMID = 19039562.001).
  • [ISSN] 0914-7187
  • [Journal-full-title] Annals of nuclear medicine
  • [ISO-abbreviation] Ann Nucl Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
  • [Number-of-references] 19
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85. Misior AM, Yan H, Pascual RM, Deshpande DA, Panettieri RA, Penn RB: Mitogenic effects of cytokines on smooth muscle are critically dependent on protein kinase A and are unmasked by steroids and cyclooxygenase inhibitors. Mol Pharmacol; 2008 Feb;73(2):566-74
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  • The inflammatory cytokines interleukin (IL)-1beta and tumor necrosis factor-alpha (TNF-alpha) have been shown previously to inhibit mitogen-stimulated smooth muscle growth through a mechanism presumed to be dependent on the induction of cyclooxygenase-2, prostaglandins, and activation of the cAMP-dependent protein kinase (PKA).
  • [MeSH-major] Adrenal Cortex Hormones / pharmacology. Cyclic AMP-Dependent Protein Kinases / physiology. Cyclooxygenase Inhibitors / pharmacology. Cytokines / physiology. Mitogens / physiology. Muscle, Smooth / drug effects. Muscle, Smooth / metabolism

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  • (PMID = 17993511.001).
  • [ISSN] 1521-0111
  • [Journal-full-title] Molecular pharmacology
  • [ISO-abbreviation] Mol. Pharmacol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL58506
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Cyclooxygenase Inhibitors; 0 / Cytokines; 0 / Interleukin-1beta; 0 / Mitogens; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
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86. Watanabe M, Noda M, Nakajin S: Effect of epidermal growth factor and prostaglandin on the expression of aromatase (CYP19) in human adrenocortical carcinoma cell line NCI-H295R cells. J Endocrinol; 2006 Jan;188(1):59-68
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  • [Title] Effect of epidermal growth factor and prostaglandin on the expression of aromatase (CYP19) in human adrenocortical carcinoma cell line NCI-H295R cells.
  • We investigated the effects of epidermal growth factor (EGF) and prostaglandins (PG) on the expression of aromatase (CYP19) in human adrenocortical carcinoma cell line NCI-H295R cells.
  • [MeSH-major] Adrenal Cortex Neoplasms / enzymology. Aromatase / metabolism. Epidermal Growth Factor / pharmacology. Prostaglandins / pharmacology
  • [MeSH-minor] Alprostadil / analogs & derivatives. Alprostadil / pharmacology. Benzylamines / pharmacology. Cell Line, Tumor. Dinoprost / pharmacology. Dinoprostone / analogs & derivatives. Dinoprostone / pharmacology. Exons. Flavonoids / pharmacology. Humans. Isoquinolines / pharmacology. Promoter Regions, Genetic. Prostaglandins A / pharmacology. Prostaglandins E / analysis. Prostaglandins E / pharmacology. Protein Kinase Inhibitors / pharmacology. RNA, Messenger / analysis. Receptors, Prostaglandin E / agonists. Receptors, Prostaglandin E, EP1 Subtype. Receptors, Prostaglandin E, EP2 Subtype. Reverse Transcriptase Polymerase Chain Reaction. Stimulation, Chemical. Sulfonamides / pharmacology

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  • (PMID = 16394175.001).
  • [ISSN] 0022-0795
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / 9-deoxy-9-chloro-15-deoxy-16-hydroxy-17,17-trimethylene-19,20-didehydroprostaglandin E2; 0 / Benzylamines; 0 / Flavonoids; 0 / Isoquinolines; 0 / ONO-DI-004; 0 / PTGER1 protein, human; 0 / PTGER2 protein, human; 0 / Prostaglandins; 0 / Prostaglandins A; 0 / Prostaglandins E; 0 / Protein Kinase Inhibitors; 0 / RNA, Messenger; 0 / Receptors, Prostaglandin E; 0 / Receptors, Prostaglandin E, EP1 Subtype; 0 / Receptors, Prostaglandin E, EP2 Subtype; 0 / Sulfonamides; 127243-85-0 / N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide; 139298-40-1 / KN 93; 62229-50-9 / Epidermal Growth Factor; B7IN85G1HY / Dinoprost; EC 1.14.14.1 / Aromatase; F5TD010360 / Alprostadil; K7Q1JQR04M / Dinoprostone; VYR271N44P / prostaglandin A1
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87. Märker-Hermann E, Schmidt WA: [Polymyalgia rheumatica]. Dtsch Med Wochenschr; 2009 Jan;134(4):135-42; quiz 143-4
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  • [MeSH-major] Polymyalgia Rheumatica / diagnosis
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Aged. Diagnosis, Differential. Female. Giant Cell Arteritis / complications. Humans. Immunosuppressive Agents / therapeutic use. Methotrexate / therapeutic use. Tumor Necrosis Factor-alpha / antagonists & inhibitors

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  • (PMID = 19148856.001).
  • [ISSN] 1439-4413
  • [Journal-full-title] Deutsche medizinische Wochenschrift (1946)
  • [ISO-abbreviation] Dtsch. Med. Wochenschr.
  • [Language] ger
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Immunosuppressive Agents; 0 / Tumor Necrosis Factor-alpha; YL5FZ2Y5U1 / Methotrexate
  • [Number-of-references] 30
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88. Ferrer I, Aubourg P, Pujol A: General aspects and neuropathology of X-linked adrenoleukodystrophy. Brain Pathol; 2010 Jul;20(4):817-30
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  • X-adrenoleukodystrophy (X-ALD) is a metabolic, peroxisomal disease affecting the nervous system, adrenal cortex and testis resulting from inactivating mutations in ABCD1 gene which encodes a peroxisomal membrane half-adenosine triphosphate (ATP)-binding cassette transporter, ABCD1 (or ALDP), whose defect is associated with impaired peroxisomal beta-oxidation and accumulation of saturated very long-chain fatty acids (VLCFA) in tissues and body fluids.
  • Several phenotypes are recognized in male patients including cerebral ALD in childhood, adolescence or adulthood, adrenomyeloneuropathy (AMN), Addison's disease and, eventually, gonadal insufficiency.
  • There is a lack of phenotype-genotype correlations, as the same ABCD1 gene mutation may be associated with different phenotypes in the same family, suggesting that genetic, epigenetic, environmental and stochastic factors are probably contributory to the development and course of the disease.
  • A different and more aggressive phenotype is secondary to cerebral demyelination, very often accompanied by inflammatory changes in the white matter of the brain and associated with activation of T lymphocytes, CD1 presentation and increased levels of cytokines, gamma-interferon, interleukin (IL)-1alpha, IL-2 and IL-6, Granulocyte macrophage colony-stimulating factor (GM-CSF), tumor necrosis factor-alpha, chemokines and chemokine receptors.


89. Takeda Y, Usukura M, Yoneda T, Oda N, Ito Y, Mabuchi H: The expression of messenger RNA for ADP-ribosyl cyclase in aldosterone-producing adenomas. Clin Endocrinol (Oxf); 2005 Apr;62(4):504-8
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  • To determine whether the cADPR system plays a signalling role in angiotensin II (Ang II)-induced aldosterone synthesis in the human adrenal gland, we investigated the effects of Ang II on ADP-ribosyl cyclase activity in human adrenal cortical tissue.
  • In addition, the expression of ADP-ribosyl cyclase messenger RNA was evaluated in aldosterone-producing adenomas (APAs) and compared with normal adrenal tissue and nonfunctioning adenomas.
  • DESIGN: ADP-ribosyl cyclase activity was measured in crude membrane fractions of human adrenocortical tissues with Ang II or with Ang II plus the Ang II receptor (AT(1)R) antagonist losartan or plus the AT(2)R antagonist PD123319.
  • The effect of 8-bromo-cADPR on Ang II-induced aldosterone production from adrenal tissue was estimated.
  • The expression of ADP-ribosyl cyclase, CYP11B2 and AT(1)R mRNA was measured in APAs, nonfunctioning adenomas, adjacent adrenal tissue and normal adrenal tissue.
  • The expression of ADP-ribosyl cyclase, CYP11B2 and AT(1)R mRNA was increased in APAs compared with that of nonfunctioning adenomas, adjacent adrenal tissue or normal adrenal tissue.
  • CONCLUSIONS: These results demonstrated the existence of a signalling pathway from the Ang II receptor to ADP-ribosyl cyclase in the human adrenal gland and suggest that the cADP-ribose signalling system might play an important role in the pathogenesis of APAs.
  • [MeSH-major] ADP-ribosyl Cyclase / genetics. Adenoma / secretion. Adrenal Cortex Neoplasms / secretion. Aldosterone / secretion. Angiotensins / pharmacology. Cyclic ADP-Ribose / analogs & derivatives. RNA, Messenger / analysis
  • [MeSH-minor] Case-Control Studies. Cytochrome P-450 CYP11B2 / genetics. Cytochrome P-450 CYP11B2 / metabolism. Dose-Response Relationship, Drug. Gene Expression. Humans. Imidazoles / pharmacology. In Vitro Techniques. Losartan / pharmacology. Pyridines / pharmacology. Receptor, Angiotensin, Type 1 / drug effects. Receptor, Angiotensin, Type 1 / genetics. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction / physiology. Tumor Cells, Cultured

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  • (PMID = 15807884.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 8-bromo-cyclic-ADP-ribose; 0 / Angiotensins; 0 / Imidazoles; 0 / Pyridines; 0 / RNA, Messenger; 0 / Receptor, Angiotensin, Type 1; 119340-53-3 / Cyclic ADP-Ribose; 130663-39-7 / PD 123319; 4964P6T9RB / Aldosterone; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 3.2.2.5 / ADP-ribosyl Cyclase; JMS50MPO89 / Losartan
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90. Utriainen P, Voutilainen R, Jääskeläinen J: Continuum of phenotypes and sympathoadrenal function in premature adrenarche. Eur J Endocrinol; 2009 Apr;160(4):657-65
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  • OBJECTIVES: Premature adrenarche (PA), the early rise in adrenal androgen (AA) production, can manifest with different clinical signs of androgen effect.
  • Secondly, we tested whether adrenomedullary function is altered in children with SAA, as it is in congenital adrenal hyperplasia (CAH) also causing adrenal hyperandrogenism.
  • Circulating adrenal steroid and catecholamine concentrations were measured and correlated with clinical parameters.
  • RESULTS: None of the children with SAA had CAH or virilizing tumor.

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  • (PMID = 19151133.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Androgens; 0 / Catecholamines; 0 / Gonadotropins; 0 / Steroids
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91. Powell AC, Stratakis CA, Patronas NJ, Steinberg SM, Batista D, Alexander HR, Pingpank JF, Keil M, Bartlett DL, Libutti SK: Operative management of Cushing syndrome secondary to micronodular adrenal hyperplasia. Surgery; 2008 Jun;143(6):750-8
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  • [Title] Operative management of Cushing syndrome secondary to micronodular adrenal hyperplasia.
  • BACKGROUND: We reviewed our experience with micronodular adrenal hyperplasia (MAH), its pigmented variant primary pigmented nodular adrenocortical disease (PPNAD), and the association with Carney's complex (CNC) to better characterize these disorders.
  • CONCLUSION: Cushing syndrome due to MAH and PPNAD may be cured by bilateral adrenal resection.
  • All patients should be screened for manifestations of CNC at the time of adrenal diagnosis with particular attention to cardiac disease.

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  • (PMID = 18549891.001).
  • [ISSN] 1532-7361
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / / NIH0012762233; United States / NICHD NIH HHS / HD / Z01 HD000642; United States / NICHD NIH HHS / HD / Z01HD000642-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS56801; NLM/ PMC2601697
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92. Else T, Giordano TJ, Hammer GD: Evaluation of telomere length maintenance mechanisms in adrenocortical carcinoma. J Clin Endocrinol Metab; 2008 Apr;93(4):1442-9
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  • [Title] Evaluation of telomere length maintenance mechanisms in adrenocortical carcinoma.
  • CONTEXT: Adrenocortical cancer (ACC) is a rare disease with an often fatal outcome.
  • The clinical and pathological diagnosis of a malignant vs. benign adrenocortical tumor is sometimes challenging.
  • Telomere maintenance mechanisms (TMMs) are critical for the persistence of the malignant phenotype, but little is known about these mechanisms or their diagnostic value in adrenocortical lesions.
  • OBJECTIVE: Tissue samples of diagnostically known adrenocortical neoplasms were evaluated for parameters of known TMMs, telomerase activity (TA), and alternative telomere lengthening (ALT).
  • DESIGN: The study analyzed retrospectively collected frozen adrenocortical tissue samples from the University of Michigan Health System.
  • PATIENT SAMPLES: Samples included 24 ACCs, 11 adrenocortical adenomas (ACAs), and three normal adrenal tissues.
  • None of the normal adrenal tissues (none of three) or ACA (none of 11) samples had signs of an active TMM.
  • Determination of telomere maintenance mechanisms in diagnostically challenging adrenocortical tumors might be of additional diagnostic value in the pathological diagnosis of malignant vs. benign lesions.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Telomere

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  • (PMID = 18198226.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.7.49 / Telomerase
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93. Kanwar AS, Bhutani KK: Effects of Chlorophytum arundinaceum, Asparagus adscendens and Asparagus racemosus on pro-inflammatory cytokine and corticosterone levels produced by stress. Phytother Res; 2010 Oct;24(10):1562-6
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  • The extracts were shown to exert an inhibitory effect on pro-inflammatory cytokines, namely interleukin 1β and tumour necrosis factor α, and on the production of nitric oxide in mouse macrophage cells RAW 264.7 stimulated by lipopolysaccharide in vitro.
  • Corticosterone levels in serum and adrenal glands were measured.
  • [MeSH-major] Asparagus Plant / chemistry. Corticosterone / analysis. Interleukin-1beta / analysis. Plant Extracts / pharmacology. Stress, Physiological. Tumor Necrosis Factor-alpha / analysis
  • [MeSH-minor] Adrenal Cortex / metabolism. Animals. Cell Line. Interleukin-2 / analysis. Male. Mice. Nitric Oxide / analysis. Plant Roots / chemistry

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  • [Copyright] Copyright © 2010 John Wiley & Sons, Ltd.
  • (PMID = 20564504.001).
  • [ISSN] 1099-1573
  • [Journal-full-title] Phytotherapy research : PTR
  • [ISO-abbreviation] Phytother Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interleukin-1beta; 0 / Interleukin-2; 0 / Plant Extracts; 0 / Tumor Necrosis Factor-alpha; 31C4KY9ESH / Nitric Oxide; W980KJ009P / Corticosterone
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94. Inomoto C, Sato H, Kanai G, Hirukawa T, Shoji S, Terachi T, Kajiwara H, Osamura RY: Black adrenal adenoma causing preclinical Cushing's syndrome. Tokai J Exp Clin Med; 2010 Jul;35(2):57-61
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  • [Title] Black adrenal adenoma causing preclinical Cushing's syndrome.
  • Functioning black adrenal adenoma (BAA) rarely causes preclinical Cushing's syndrome (CS).
  • Abdominal computed tomography showed that she had a 15-mm in diameter, round, left adrenal adenoma.
  • The left adrenal adenoma was laparoscopically removed.
  • Examination of the surgical specimen revealed unilateral double adrenal adenomas of the left adrenal gland, one of which was a BAA.
  • There were also foci of myelolipomatous degenerative changes in the tumor.
  • The compact cell zones remained in the adrenal cortex adjacent to the BAA showed atrophic change.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications. Cushing Syndrome / etiology

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  • (PMID = 21319027.001).
  • [ISSN] 2185-2243
  • [Journal-full-title] The Tokai journal of experimental and clinical medicine
  • [ISO-abbreviation] Tokai J. Exp. Clin. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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95. Gerstner ER, Batchelor TT: Primary central nervous system lymphoma. Arch Neurol; 2010 Mar;67(3):291-7
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  • It accounts for approximately 3% of all the primary CNS tumors diagnosed each year in the United States.
  • Congenital or acquired immunodeficiency is the only established risk factor for PCNSL, and individuals with human immunodeficiency virus (HIV) infection are at greater risk for developing this tumor.
  • Owing to the rarity of PCNSL, the disease has been challenging to study and an effective standard of care has been difficult to establish.
  • Unfortunately, although durable remissions may be achieved for some patients with PCNSL, the tumor relapses in most cases.
  • [MeSH-major] Central Nervous System Neoplasms / etiology. Lymphoma, Non-Hodgkin / etiology
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Antineoplastic Combined Chemotherapy Protocols. Clinical Trials as Topic. Combined Modality Therapy. Cranial Irradiation. Humans. Prognosis


96. Kostyuchenko N, Pushkarev V, Kashevarov G, Tronko M, Komisarenko I, Mikosha O: Effects of N-acylethanolamines and various antimitotic agents on apoptotic DNA fragmentation in conventionally normal and tumor tissue of human adrenals. Exp Oncol; 2005 Sep;27(3):215-9
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  • [Title] Effects of N-acylethanolamines and various antimitotic agents on apoptotic DNA fragmentation in conventionally normal and tumor tissue of human adrenals.
  • AIM: To study effects of N-acylethanolamines (NAE) and various antimitotic agents: taxol, colchicine, and cytochalasin B on the DNA fragmentation extent in conventionally normal (CNT) and tumor tissue of human adrenal cortex.
  • METHODS: Six types of adrenal tumor tissue of 84 patients were analyzed.
  • RESULTS: It was established that NAEs enhanced apoptosis in conventionally normal and tumor tissue of adrenal glands.
  • In general, tumor tissue was more sensitive to NAEs and antimitotic compounds than conventionally normal tissue.
  • NAEs in combination with colchicine and cytochalasin B enhanced DNA fragmentation in some types of tumor tissue and did not influence, or even reduced it in CNT.
  • Taxol revealed selective action depending on tumor tissue type.
  • Considerable individual differences were reported in sensitiveness of different types of tumors to the NAEs and antimitotic agents.
  • CONCLUSIONS: Taxol and combination of NAEs with colchicine and cytochalasin B are inductors of apoptosis in the adrenal tumor cells and thus promising for further investigation.
  • [MeSH-major] Adrenal Gland Neoplasms / pathology. Antimitotic Agents / pharmacology. Antineoplastic Agents, Phytogenic / pharmacology. DNA Damage. Ethanolamines / pharmacology. Paclitaxel / pharmacology
  • [MeSH-minor] Adrenal Glands / cytology. Apoptosis / drug effects. Humans. Tumor Cells, Cultured

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  • (PMID = 16244584.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Antimitotic Agents; 0 / Antineoplastic Agents, Phytogenic; 0 / Ethanolamines; 0 / N-acylethanolamines; P88XT4IS4D / Paclitaxel
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97. Kaneko T, Moriyama T, Tsubakihara Y, Horio M, Imai E: Prevalence of human polyoma virus (BK virus and JC virus) infection in patients with chronic renal disease. Clin Exp Nephrol; 2005 Jun;9(2):132-7
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  • [Title] Prevalence of human polyoma virus (BK virus and JC virus) infection in patients with chronic renal disease.
  • The prevalence of polyoma viruses (BK virus and JC virus) was investigated in 45 patients with renal disease who were future candidates as renal graft recipients.
  • In the patients with renal disease, 33.3% were positive for BK virus and 33.3% were positive for JC virus; the prevalence of BK virus infection was significantly higher than that in the normal subjects.
  • Patients with renal disease with corticosteroid therapy revealed an especially high prevalence of BK virus infection (55.6%), indicating the possibility of viral reactivation by corticosteroid therapy.
  • [MeSH-major] BK Virus / isolation & purification. JC Virus / isolation & purification. Kidney Failure, Chronic / epidemiology. Polyomavirus Infections / epidemiology. Tumor Virus Infections / epidemiology
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Adult. Aged. DNA, Viral / analysis. DNA, Viral / urine. Female. Graft Survival. Humans. Kidney Transplantation. Male. Middle Aged. Prevalence

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  • (PMID = 15980947.001).
  • [ISSN] 1342-1751
  • [Journal-full-title] Clinical and experimental nephrology
  • [ISO-abbreviation] Clin. Exp. Nephrol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / DNA, Viral
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98. Pan CC, Lee WL: Vaginal obliteration in a woman with a history of cutaneous T-cell lymphoma: the results of combined chemotherapy-induced gonadal toxicity and lymphoma relapse. Taiwan J Obstet Gynecol; 2010 Mar;49(1):69-71
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  • In this case, vaginal obliteration was an early sign of tumor recurrence, although menopause may have contributed to the vaginal obliteration.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Lymphoma, T-Cell, Cutaneous / pathology. Neoplasm Recurrence, Local. Surgically-Created Structures. Vagina / surgery. Vaginal Neoplasms / pathology
  • [MeSH-minor] Adrenal Cortex Hormones / administration & dosage. Adrenal Cortex Hormones / adverse effects. Adult. Bleomycin / administration & dosage. Bleomycin / adverse effects. Cyclophosphamide / administration & dosage. Cyclophosphamide / adverse effects. Doxorubicin / administration & dosage. Doxorubicin / adverse effects. Female. Humans. Prednisolone / administration & dosage. Prednisolone / adverse effects. Vincristine / administration & dosage. Vincristine / adverse effects

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  • (PMID = 20466296.001).
  • [ISSN] 1875-6263
  • [Journal-full-title] Taiwanese journal of obstetrics & gynecology
  • [ISO-abbreviation] Taiwan J Obstet Gynecol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 11056-06-7 / Bleomycin; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone
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99. Pritchard CW, Hawthorne AB: Managing immunosuppression in medical patients. Br J Hosp Med (Lond); 2009 Jul;70(7):394-8
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  • [MeSH-minor] Abnormalities, Drug-Induced / prevention & control. Adrenal Cortex Hormones / therapeutic use. Counseling. Female. Fractures, Bone / chemically induced. Humans. Male. Neoplasms / chemically induced. Pregnancy. Risk Factors. Tumor Necrosis Factor-alpha / antagonists & inhibitors. Vaccines / contraindications

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  • (PMID = 19584781.001).
  • [ISSN] 1750-8460
  • [Journal-full-title] British journal of hospital medicine (London, England : 2005)
  • [ISO-abbreviation] Br J Hosp Med (Lond)
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Immunosuppressive Agents; 0 / Purines; 0 / Tumor Necrosis Factor-alpha; 0 / Vaccines
  • [Number-of-references] 14
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100. Arima K, Yamakado K, Suzuki R, Matsuura H, Nakatsuka A, Takeda K, Sugimura Y: Image-guided radiofrequency ablation for adrenocortical adenoma with Cushing syndrome: outcomes after mean follow-up of 33 months. Urology; 2007 Sep;70(3):407-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Image-guided radiofrequency ablation for adrenocortical adenoma with Cushing syndrome: outcomes after mean follow-up of 33 months.
  • OBJECTIVES: To evaluate the feasibility, safety, and therapeutic effects of image-guided radiofrequency (RF) ablation used for the treatment of adrenocortical adenoma with Cushing syndrome.
  • METHODS: From February 2003 to May 2005, 4 consecutive patients with adrenocortical adenoma and Cushing syndrome received percutaneous RF ablation.
  • All tumors were in the left adrenal gland, with a mean tumor size of 2.7 +/- 0.6 cm (range 2.0 to 3.5).
  • Technical success was defined as disappearance of tumor enhancement on contrast-enhanced computed tomography imaging acquired within 1 week after RF ablation.
  • RESULTS: Tumor enhancement disappeared after initial RF ablation in 3 of 4 patients (technical success rate 75%).
  • The fourth patient underwent a repeat RF ablation session 3 years later, resulting in eradication of tumor enhancement.
  • All tumors showed involution (2.2 +/- 0.3 cm) at the end of the study.
  • CONCLUSIONS: Using RF ablation for adrenocortical adenoma with Cushing syndrome is a feasible, safe, and promising treatment method in selected patients.
  • [MeSH-major] Adenoma / surgery. Adrenal Cortex Neoplasms / surgery. Catheter Ablation / methods. Cushing Syndrome / surgery. Fluoroscopy / methods. Radiography, Interventional / methods. Surgery, Computer-Assisted / methods

  • Genetic Alliance. consumer health - Cushing's Syndrome.
  • MedlinePlus Health Information. consumer health - Cushing's Syndrome.
  • Hazardous Substances Data Bank. HYDROCORTISONE .
  • Hazardous Substances Data Bank. Corticotropin .
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  • (PMID = 17905083.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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