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1. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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2. Hirai T, Tsujihata M, Ueda T, Nonomura N, Okuyama A: A case of polymyositis associated with adrenal carcinoma. Int J Urol; 2007 Oct;14(10):952-3
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  • [Title] A case of polymyositis associated with adrenal carcinoma.
  • Most descriptions have been of dermatomyositis-associated cancer, however, a few have been of polymyositis-associated adrenal cancer.
  • Here, we report a 69-year-old man in whom polymyositis-associated adrenal cancer was diagnosed.
  • Imaging studies showed a solid tumor measuring 14 x 9 cm in the retroperitoneum.
  • After surgical excision of the tumor, including the left kidney, the serum levels of creatine kinase and lactic dehydrogenase normalized, and symptoms of myositis disappeared.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Carcinoma / diagnosis. Polymyositis / diagnosis

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  • (PMID = 17880299.001).
  • [ISSN] 0919-8172
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 2.7.3.2 / Creatine Kinase
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3. Behrend EN, Weigand CM, Whitley EM, Refsal KR, Young DW, Kemppainen RJ: Corticosterone- and aldosterone-secreting adrenocortical tumor in a dog. J Am Vet Med Assoc; 2005 May 15;226(10):1662-6, 1659
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  • [Title] Corticosterone- and aldosterone-secreting adrenocortical tumor in a dog.
  • An adrenal gland tumor was visualized via ultrasonography and computed tomography.
  • Histologic examination confirmed that the mass was an adrenocortical carcinoma.
  • Excess adrenal secretion of corticosterone was hypothesized to be the cause of the signs of glucocorticoid excess.
  • Treatment with mitotane was instituted and successful for a period of 4-months until the dog was euthanatized for neurologic problems that were most likely unrelated to endocrine disease.
  • [MeSH-major] Adrenal Cortex Neoplasms / veterinary. Aldosterone / secretion. Antineoplastic Agents, Hormonal / therapeutic use. Corticosterone / secretion. Dog Diseases / diagnosis. Mitotane / therapeutic use

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  • (PMID = 15906564.001).
  • [ISSN] 0003-1488
  • [Journal-full-title] Journal of the American Veterinary Medical Association
  • [ISO-abbreviation] J. Am. Vet. Med. Assoc.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 4964P6T9RB / Aldosterone; 78E4J5IB5J / Mitotane; W980KJ009P / Corticosterone
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4. Hantel C, Beuschlein F: Mouse models of adrenal tumorigenesis. Best Pract Res Clin Endocrinol Metab; 2010 Dec;24(6):865-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mouse models of adrenal tumorigenesis.
  • Adrenocortical carcinomas (ACCs) are heterogeneous tumors with a poor prognosis.
  • The rarity of this disorder causes a lack of treatment experience and material availability which is necessary to optimize existing treatments and to develop novel therapeutic strategies.
  • Although surgery is still the treatment of choice, adjuvant therapies are urgently needed as the rate of recurrence for these tumors is high.
  • In recent years molecular characterization of surgical tumor specimen has aided in the understanding of disease mechanisms and definition of therapeutic targets also in adrenocortical carcinoma.
  • Here we give an overview on rodent models that have been described to either have adrenocortical tumors as part of their phenotype or have been utilized for therapeutic screens as adrenocortical tumor models.
  • [MeSH-major] Adrenal Cortex Neoplasms / therapy. Adrenal Gland Neoplasms / physiopathology. Adrenal Gland Neoplasms / therapy. Disease Models, Animal
  • [MeSH-minor] Animals. Animals, Genetically Modified. Mice. Neoplasm Transplantation

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  • [Copyright] 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 21115155.001).
  • [ISSN] 1878-1594
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
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5. Liang F, Kapoun AM, Lam A, Damm DL, Quan D, O'Connell M, Protter AA: B-Type natriuretic peptide inhibited angiotensin II-stimulated cholesterol biosynthesis, cholesterol transfer, and steroidogenesis in primary human adrenocortical cells. Endocrinology; 2007 Aug;148(8):3722-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] B-Type natriuretic peptide inhibited angiotensin II-stimulated cholesterol biosynthesis, cholesterol transfer, and steroidogenesis in primary human adrenocortical cells.
  • In this study, we demonstrate that B-type natriuretic peptide (BNP) opposed angiotensin II (Ang II)-stimulated de novo cholesterol biosynthesis, cellular cholesterol uptake, cholesterol transfer to the inner mitochondrial membrane, and steroidogenesis, which are required for biosynthesis of steroid hormones such as aldosterone and cortisol in primary human adrenocortical cells.
  • BNP dose-dependently stimulated intracellular cGMP production with an EC(50) of 11 nm, implying that human adrenocortical cells express the guanylyl cyclase A receptor. cDNA microarray and real-time RT-PCR analyses revealed that BNP inhibited Ang II-stimulated genes related to cholesterol biosynthesis (acetoacetyl coenzyme A thiolase, HMG coenzyme A synthase 1, HMG coenzyme A reductase, isopentenyl-diphosphate Delta-isomerase, lanosterol synthase, sterol-4C-methyl oxidase, and emopamil binding protein/sterol isomerase), cholesterol uptake from circulating lipoproteins (scavenger receptor class B type I and low-density lipoprotein receptor), cholesterol transfer to the inner mitochondrial membrane (steroidogenic acute regulatory protein), and steroidogenesis (ferredoxin 1,3beta-hydroxysteroid dehydrogenase, glutathione transferase A3, CYP19A1, CYP11B1, and CYP11B2).
  • Consistent with the microarray and real-time PCR results, BNP also blocked Ang II-induced binding of (125)I-labeled low-density lipoprotein and (125)I-labeled high-density lipoprotein to human adrenocortical cells.
  • Furthermore, BNP markedly inhibited Ang II-stimulated release of estradiol, aldosterone, and cortisol from cultured primary human adrenocortical cells.
  • This study provides new insights into the cellular mechanisms by which BNP modulates Ang II-induced steroidogenesis in the adrenal gland.
  • [MeSH-major] Adrenal Cortex / metabolism. Angiotensin II / metabolism. Cholesterol / metabolism. Natriuretic Peptide, Brain / metabolism. Vasoconstrictor Agents / metabolism
  • [MeSH-minor] Adrenal Cortex Hormones / biosynthesis. Adrenal Cortex Neoplasms. Adrenocortical Carcinoma. Adult. Cell Line, Tumor. Cells, Cultured. Cyclic GMP / metabolism. Drug Interactions. Gene Expression Profiling. Gene Expression Regulation / drug effects. Gene Expression Regulation / physiology. Humans. Lipoproteins / metabolism. Male. Middle Aged. Oligonucleotide Array Sequence Analysis / standards. Reproducibility of Results. Reverse Transcriptase Polymerase Chain Reaction. Steroids / biosynthesis

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  • (PMID = 17478552.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Lipoproteins; 0 / Steroids; 0 / Vasoconstrictor Agents; 11128-99-7 / Angiotensin II; 114471-18-0 / Natriuretic Peptide, Brain; 97C5T2UQ7J / Cholesterol; H2D2X058MU / Cyclic GMP
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6. McNicol AM: Lesions of the adrenal cortex. Arch Pathol Lab Med; 2008 Aug;132(8):1263-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lesions of the adrenal cortex.
  • CONTEXT: In surgical pathology practice adrenal cortical tumors are rare.
  • However, in autopsy series adrenal cortical nodules are found frequently.
  • These are now being identified more commonly in life when the abdomen is scanned for other disease.
  • It is important to differentiate between benign and malignant lesions as adrenal cortical carcinoma is an aggressive tumor.
  • Molecular genetic investigations are providing new information on both pathogenesis of adrenal tumors and basic adrenal development and physiology.
  • OBJECTIVE: To provide an overview of current knowledge on adrenal cortical development and structure that informs our understanding of genetic diseases of the adrenal cortex and adrenal cortical tumors.
  • CONCLUSIONS: The understanding of basic developmental and physiologic processes permits a better understanding of diseases of the adrenal cortex.
  • The information coming from investigation of the molecular pathology of adrenal cortical tumors is beginning to provide additional tests for the assessment of malignant potential in diagnosis but the mainstay remains traditional histologic analysis.
  • [MeSH-major] Adrenal Cortex. Adrenal Gland Diseases
  • [MeSH-minor] Adrenal Cortex Neoplasms / metabolism. Adrenal Cortex Neoplasms / pathology. Growth. Humans. Immunohistochemistry. Prognosis

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  • (PMID = 18684025.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 126
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7. Chen S: Advanced diagnostic approaches and current medical management of insulinomas and adrenocortical disease in ferrets (Mustela putorius furo). Vet Clin North Am Exot Anim Pract; 2010 Sep;13(3):439-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Advanced diagnostic approaches and current medical management of insulinomas and adrenocortical disease in ferrets (Mustela putorius furo).
  • Endocrine neoplasia is the most common tumor type in domestic ferrets, especially in middle-aged to older ferrets.
  • Islet cell tumors and adrenocortical tumors constitute the major types of endocrine neoplasms.
  • Insulinoma is a tumor that produces and releases excessive amounts of insulin.
  • Adrenocortical neoplasia in ferrets usually overproduces one or more sex hormones.
  • Abdominal ultrasonography and sex hormone assays can be used to diagnose adrenocortical neoplasms.
  • Drugs such as leuprolide acetate, deslorelin acetate, and the hormone melatonin can be used to treat adrenocortical neoplasms in ferrets when surgery is not an option.
  • [MeSH-major] Adrenal Cortex Diseases / veterinary. Adrenal Cortex Neoplasms / veterinary. Ferrets. Insulinoma / veterinary

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20682429.001).
  • [ISSN] 1558-4232
  • [Journal-full-title] The veterinary clinics of North America. Exotic animal practice
  • [ISO-abbreviation] Vet Clin North Am Exot Anim Pract
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
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8. Fassnacht M, Wittekind C, Allolio B: [Current TNM classification systems for adrenocortical carcinoma]. Pathologe; 2010 Sep;31(5):374-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Current TNM classification systems for adrenocortical carcinoma].
  • Adrenocortical carcinoma (ACC) is a rare malignancy and often difficult to diagnose.
  • Therefore, the European Network for the Study of Adrenal Tumours (ENSAT) developed a revised staging system, the superiority of which was recently confirmed in an independent American cohort.
  • In the ENSAT classification, stage I (tumors ≤ 5 cm) and II (tumors < 5 cm) are non-infiltrating tumors without positive lymph nodes and distant metastases.
  • Stage III is defined by the presence of positive lymph nodes, infiltration of surrounding tissue, or venous tumor thrombus.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Neoplasm Staging / methods
  • [MeSH-minor] Adrenal Cortex / pathology. Cohort Studies. Disease Progression. Humans. Lymphatic Metastasis / pathology. Neoplasm Invasiveness / pathology. Neoplastic Cells, Circulating. Prognosis. Registries

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  • (PMID = 20703482.001).
  • [ISSN] 1432-1963
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
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9. Mitchell IC, Auchus RJ, Juneja K, Chang AY, Holt SA, Snyder WH 3rd, Nwariaku FE: "Subclinical Cushing's syndrome" is not subclinical: improvement after adrenalectomy in 9 patients. Surgery; 2007 Dec;142(6):900-5; discussion 905.e1
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: A subgroup of patients with adrenal cortisol hypersecretion fails to meet the biochemical criteria for Cushing's syndrome.
  • METHODS: Between 2003 and 2006, all patients who underwent adrenalectomy for cortisol hypersecretion caused by an adrenal mass were examined.
  • RESULTS: Overall, 24 patients underwent adrenalectomy for adrenal cortisol hypersecretion, of which 9 were found to have subclinical CS.
  • [MeSH-minor] Adenoma / metabolism. Adenoma / pathology. Adenoma / surgery. Adrenal Cortex / metabolism. Adrenal Cortex / pathology. Adrenal Cortex / surgery. Adrenal Cortex Neoplasms / metabolism. Adrenal Cortex Neoplasms / pathology. Adrenal Cortex Neoplasms / surgery. Adult. Aged. Aged, 80 and over. Female. Humans. Hydrocortisone / secretion. Hyperplasia. Male. Middle Aged. Retrospective Studies. Treatment Outcome

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  • [ErratumIn] Surgery. 2008 Feb;143(2):302
  • (PMID = 18063074.001).
  • [ISSN] 1532-7361
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] WI4X0X7BPJ / Hydrocortisone
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10. Wen PY, Schiff D, Kesari S, Drappatz J, Gigas DC, Doherty L: Medical management of patients with brain tumors. J Neurooncol; 2006 Dec;80(3):313-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Medical management of patients with brain tumors.
  • The most common medical problems in brain tumor patients include the management of seizures, peritumoral edema, medication side effects, venous thromboembolism (VTE), fatigue and cognitive dysfunction.
  • There is increasing evidence that brain tumor patients who have not had a seizure do not benefit from prophylactic antiepileptic medications.
  • There is also growing evidence suggesting that anticoagulation may be more effective than inferior vena cava IVC) filtration devices for treating VTE in brain tumor patients and the risk of hemorrhage with anticoagulation is relatively small.
  • [MeSH-major] Brain Edema / etiology. Brain Neoplasms / complications. Epilepsy / etiology. Venous Thrombosis / etiology
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Anticoagulants / therapeutic use. Anticonvulsants / therapeutic use. Cognition Disorders / etiology. Cognition Disorders / therapy. Depressive Disorder / etiology. Depressive Disorder / therapy. Fatigue / etiology. Fatigue / therapy. Humans. Patient Care Planning

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  • (PMID = 16807780.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Anticoagulants; 0 / Anticonvulsants
  • [Number-of-references] 211
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11. 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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  • [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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12. Willenberg HS, Haase M, Papewalis C, Schott M, Scherbaum WA, Bornstein SR: Corticotropin-releasing hormone receptor expression on normal and tumorous human adrenocortical cells. Neuroendocrinology; 2005;82(5-6):274-81
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  • [Title] Corticotropin-releasing hormone receptor expression on normal and tumorous human adrenocortical cells.
  • Corticotropin-releasing hormone (CRH) is not only the principal regulator of the central hypothalamic-pituitary-adrenal (HPA) axis but also exerts direct actions on peripheral tissues.
  • We analyzed the expression of CRH receptors in microdissected preparations of normal human adrenal glands and in adrenocortical and adrenomedullary tumors, employing immunohistochemistry, quantitative RT-PCR of microdissected adrenal tissues, and in situ hybridization.
  • The effect of CRH on adrenal steroidogenesis was tested in adrenal cells.
  • In addition, we found a higher expression of CRH type-1 and 2 receptors mRNAs in preparations of adrenal cortices as compared to pheochromocytomas, a 6-fold increase in preparations of clinically unapparent adrenocortical adenomas, and a 10- to 60-fold increase in cortisol-producing adrenal adenomas.
  • Stimulation of the adrenal tumor cell line NCI-H295R with CRH elicited a 1.4-fold increase in DHEA secretion.
  • This result could be reproduced in a culture of primary human adrenocortical cells.
  • We conclude that adrenocortical cells exhibit a higher expression of functional CRH receptors than chromaffin cells and that CRH acts on adrenal DHEA production.
  • The data support the assertion of a direct action of CRH on human adrenocortical cells in addition to an intra-adrenal CRH receptor/adrenocorticotropin system.
  • Enhanced CRH1R expression may be involved in adrenocortical tumorigenesis.
  • [MeSH-major] Adrenal Cortex / chemistry. Adrenal Cortex Neoplasms / chemistry. Adrenocortical Adenoma / chemistry. Adrenocortical Carcinoma / chemistry. Pheochromocytoma / chemistry. Receptors, Corticotropin-Releasing Hormone / genetics

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  • (PMID = 16721033.001).
  • [ISSN] 0028-3835
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / CRF receptor type 1; 0 / CRF receptor type 2; 0 / RNA, Messenger; 0 / Receptors, Corticotropin-Releasing Hormone; 9015-71-8 / Corticotropin-Releasing Hormone
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13. Padberg BC, Rordorf T, Suter SL, Pfeiffer D, Wild D, Schröder S: [123I-Metaiodobenzylguanidine- (MIBG-) scintigraphy: paradoxical positivity in an oncocytic adrenocortical carcinoma]. Pathologe; 2007 Jul;28(4):281-4
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  • [Title] [123I-Metaiodobenzylguanidine- (MIBG-) scintigraphy: paradoxical positivity in an oncocytic adrenocortical carcinoma].
  • In contrast, the false-positive uptake of MIBG by adrenal cortical carcinoma is rare.
  • Here, we report a metastatic oncocytic adrenal cortical carcinoma with MIBG uptake used for therapeutic purposes.
  • [MeSH-major] 3-Iodobenzylguanidine. Adrenal Cortex Neoplasms / diagnostic imaging. Iodine Radioisotopes
  • [MeSH-minor] Adrenal Gland Neoplasms / diagnostic imaging. Diagnosis, Differential. Humans. Neoplasm Metastasis. Pheochromocytoma / diagnostic imaging. Pheochromocytoma / pathology. Radioisotopes. Radionuclide Imaging

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  • (PMID = 16673076.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Iodine Radioisotopes; 0 / Radioisotopes; 35MRW7B4AD / 3-Iodobenzylguanidine
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14. Petraglia F, Musacchio C, Luisi S, De Leo V: Hormone-dependent gynaecological disorders: a pathophysiological perspective for appropriate treatment. Best Pract Res Clin Obstet Gynaecol; 2008 Apr;22(2):235-49
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  • However, the correct functioning of other endocrine glands (thyroid, adrenal cortex, pancreas) is also crucial for correct reproductive function.
  • [MeSH-minor] Endometriosis / drug therapy. Endometriosis / physiopathology. Female. Fibroma / drug therapy. Fibroma / physiopathology. Humans. Hypogonadism / drug therapy. Hypogonadism / physiopathology. Hypothalamic Diseases / drug therapy. Hypothalamic Diseases / physiopathology. Polycystic Ovary Syndrome / drug therapy. Polycystic Ovary Syndrome / physiopathology. Uterine Neoplasms / drug therapy. Uterine Neoplasms / physiopathology

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  • (PMID = 17804298.001).
  • [ISSN] 1521-6934
  • [Journal-full-title] Best practice & research. Clinical obstetrics & gynaecology
  • [ISO-abbreviation] Best Pract Res Clin Obstet Gynaecol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 68
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15. Danilovic DL, Freire DS, Paraíba DB, Brandão Neto RA, Lucon AM, Pereira MA: [Primary aldosteronism caused by aldosteronoma: problems in the etiologic diagnosis]. Arq Bras Endocrinol Metabol; 2007 Apr;51(3):478-87
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  • [Title] [Primary aldosteronism caused by aldosteronoma: problems in the etiologic diagnosis].
  • We present a case of PA caused by an aldosteronoma associated with a contralateral nonfunctioning adrenal adenoma, which resulted in difficulties in the final diagnosis.
  • We discuss the most appropriated tests to screen, confirm the diagnosis of PA and define the etiology of the disorder, especially the adrenal veins sampling to distinguish the aldosteronoma and idiopathic hyperaldosteronism and to guide successful treatment.
  • [MeSH-major] Adenoma / diagnosis. Adrenal Cortex Neoplasms / diagnosis. Adrenocortical Adenoma / diagnosis. Hyperaldosteronism / diagnosis
  • [MeSH-minor] Aldosterone / blood. Diagnosis, Differential. Female. Humans. Hypertension / complications. Middle Aged. Renin / blood. Tomography, X-Ray Computed

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  • (PMID = 17546249.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] por
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone; EC 3.4.23.15 / Renin
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16. Gil J, Kalembkiewicz M, Polak E, Kostecka-Matyja M: [Disseminated adrenocortical carcinoma: case report]. Pol Arch Med Wewn; 2007 Jul;117(7):317-21
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  • [Title] [Disseminated adrenocortical carcinoma: case report].
  • [Transliterated title] Rozsiany rak kory nadnercza.
  • Adrenocortical carcinoma is a rare neoplasm occurring with a frequency of 1-2 cases per million.
  • This type of a tumor is slightly more frequent in women (58.6%) than in men (41.4%).
  • Etiology of adrenocortical carcinoma is still unclear, but a role of genetic and environmental factors has been largely considered.
  • The tumor size is still the best single predictor of prognosis.
  • Histopathology specimen from biopsy or obtained during operation should be stained for Melan A, which can confirm the adrenal origin of the tumor.
  • We presented the case of functioning adrenocortical cancer in 37-year-old patient who at time of diagnosis had 12 cm in diameter tumor of the left adrenal gland and metastases to the liver and lung.
  • In the article the symptoms associated with hormones produced by the carcinoma, diagnostics and treatment with regard to the progression of the disease have also been discussed.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Liver Neoplasms / secondary. Lung Neoplasms / secondary

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  • (PMID = 17966598.001).
  • [Journal-full-title] Polskie Archiwum Medycyny Wewnetrznej
  • [ISO-abbreviation] Pol. Arch. Med. Wewn.
  • [Language] pol
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Poland
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17. Nishimoto K, Nakagawa K, Li D, Kosaka T, Oya M, Mikami S, Shibata H, Itoh H, Mitani F, Yamazaki T, Ogishima T, Suematsu M, Mukai K: Adrenocortical zonation in humans under normal and pathological conditions. J Clin Endocrinol Metab; 2010 May;95(5):2296-305
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  • [Title] Adrenocortical zonation in humans under normal and pathological conditions.
  • CONTEXT: Aldosterone synthase (CYP11B2) and steroid 11 beta-hydroxylase (CYP11B1) catalyze the terminal steps for aldosterone and cortisol syntheses, respectively, thereby determining the functional differentiation of human adrenocortical cells.
  • OBJECTIVE: The objective of the study was to determine the localization of CYP11B2 and -B1 in human adrenal specimens by using developed antibodies capable of distinguishing the two enzymes from each other.
  • Adrenocortical cells lacking both enzymes were observed in the outer cortical regions.
  • In addition to conventional zonation, we found a variegated zonation consisting of a subcapsular cell cluster expressing CYP11B2, which we termed aldosterone-producing cell cluster, and a CYP11B1-expressing area.
  • CONCLUSION: Immunohistochemistry of the human normal adrenal cortex for CYP11B2 and CYP11B1 revealed a variegated zonation with cell clusters constitutively expressing CYP11B2.
  • This technique may provide a pathological confirmatory diagnosis of adrenocortical adenomas.
  • [MeSH-major] Adrenal Cortex / pathology. Adrenal Cortex / physiology
  • [MeSH-minor] Aldosterone / metabolism. Amino Acid Sequence. Animals. Antibodies. Carcinoma, Renal Cell / enzymology. Corticosterone / metabolism. Cushing Syndrome / enzymology. Cytochrome P-450 CYP11B2 / deficiency. Cytochrome P-450 CYP11B2 / metabolism. Humans. Kidney Neoplasms / enzymology. Mammals. Peptide Fragments / chemistry. Rabbits. Reference Values. Rodentia. Steroid 11-beta-Hydroxylase / metabolism. Zona Fasciculata / enzymology. Zona Glomerulosa / enzymology

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  • (PMID = 20200334.001).
  • [ISSN] 1945-7197
  • [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] 0 / Antibodies; 0 / Peptide Fragments; 4964P6T9RB / Aldosterone; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase; W980KJ009P / Corticosterone
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18. Wittekind C: [TNM 2010. What's new?]. Pathologe; 2010 Oct;31 Suppl 2:153-60
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  • In the seventh edition of the TNM Classification of Malignant Tumours there are several entirely new classifications: upper aerodigestive mucosal melanoma, gastrointestinal stromal tumour, gastrointestinal carcinoid (neuroendocrine tumour), intrahepatic cholangiocarcinoma, Merkel cell carcinoma, uterine sarcomas, and adrenal cortical carcinoma.
  • Significant modifications concern carcinomas of the oesophagus, oesophagogastric junction, stomach, appendix, biliary tract, lung, skin, prostate and ophthalmic tumours, which will be not addressed in this article.
  • For several tumour entities only minor changes were introduced which might be of importance in daily practice.
  • [MeSH-major] Neoplasm Staging / methods. Neoplasm Staging / trends. Neoplasms / pathology
  • [MeSH-minor] Adrenal Cortex Neoplasms / classification. Adrenal Cortex Neoplasms / pathology. Bile Duct Neoplasms / classification. Bile Duct Neoplasms / pathology. Bile Ducts, Intrahepatic. Carcinoid Tumor / classification. Carcinoid Tumor / pathology. Carcinoma, Merkel Cell / classification. Carcinoma, Merkel Cell / pathology. Cholangiocarcinoma / classification. Cholangiocarcinoma / pathology. Digestive System Neoplasms / classification. Digestive System Neoplasms / pathology. Female. Gastrointestinal Stromal Tumors / classification. Gastrointestinal Stromal Tumors / pathology. Humans. Respiratory Tract Neoplasms / classification. Respiratory Tract Neoplasms / pathology. Sarcoma / classification. Sarcoma / pathology. Skin Neoplasms / classification. Skin Neoplasms / pathology. Uterine Neoplasms / classification. Uterine Neoplasms / pathology

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  • (PMID = 20737151.001).
  • [ISSN] 1432-1963
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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19. Barlaskar FM, Spalding AC, Heaton JH, Kuick R, Kim AC, Thomas DG, Giordano TJ, Ben-Josef E, Hammer GD: Preclinical targeting of the type I insulin-like growth factor receptor in adrenocortical carcinoma. J Clin Endocrinol Metab; 2009 Jan;94(1):204-12
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  • [Title] Preclinical targeting of the type I insulin-like growth factor receptor in adrenocortical carcinoma.
  • CONTEXT: Drug therapy for adrenocortical carcinoma (ACC), a rare and lethal malignancy, is largely empirical and ineffective.
  • OBJECTIVE: The objective of the study was to profile human adrenal tumors and ACC cell lines to assess activated IGF signaling and determine the efficacy of two IGF receptor (IGF-1R) antagonists alone and in combination with mitotane.
  • EXPERIMENTAL DESIGN: ACC cell lines that display or lack activated IGF signaling are used to assess the effects of two IGF-1R antagonists in cultured cells and ACC xenograft tumors.
  • RESULTS: Transcriptional profiling data derived from DNA microarray analysis of human adrenal tumors implicate IGF2 as the single highest up-regulated transcript in the vast majority of carcinomas.
  • IGF inhibition markedly reduced tumor growth greater than that observed with mitotane treatment, and combination therapy with mitotane significantly enhanced tumor growth suppression.
  • CONCLUSION: These findings establish a critical role of IGF signaling in ACC pathophysiology and provide rationale for use of targeted IGF-1R antagonists to treat adrenocortical carcinoma in future clinical trials.

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  • (PMID = 18854392.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK062027; United States / NICHD NIH HHS / HD / T32 HD007505; United States / NIDDK NIH HHS / DK / DK 062027; United States / NICHD NIH HHS / HD / T-32-HD007505
  • [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 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; 67763-97-7 / Insulin-Like Growth Factor II; 78E4J5IB5J / Mitotane; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ PMC2630877
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20. Fulmer BR: Diagnosis and management of adrenal cortical carcinoma. Curr Urol Rep; 2007 Jan;8(1):77-82
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  • [Title] Diagnosis and management of adrenal cortical carcinoma.
  • Adrenal cortical carcinoma is a relatively uncommon malignancy that represents a significant clinical challenge for the development of optimal treatment strategies.
  • Although the framework of a successful treatment paradigm still relies on these steps, advances in diagnostic imaging have led to increased accuracy in diagnosis, and advances in laparoscopic surgical technique have served to reduce morbidity for patients facing treatment.
  • This review focuses on a discussion of advances in modalities for the diagnosis and treatment of adrenal cortical carcinoma amenable to curative therapy.
  • Patients that present with metastatic or locally advanced disease generally are treated with mitotane-based chemotherapy with or without the addition of cytotoxic drugs.
  • Contemporary results of this treatment approach are presented in this review as well as a discussion of further directions for the treatment of patients with advanced disease.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / therapy. Adrenocortical Carcinoma / diagnosis. Adrenocortical Carcinoma / therapy
  • [MeSH-minor] Adrenalectomy / methods. Chemotherapy, Adjuvant. Combined Modality Therapy. Female. Humans. Laparoscopy / methods. Male. Neoplasm Staging. Prognosis. Radiotherapy, Adjuvant. Risk Assessment. Survival Analysis

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  • (PMID = 17239320.001).
  • [ISSN] 1534-6285
  • [Journal-full-title] Current urology reports
  • [ISO-abbreviation] Curr Urol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 50
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21. Carbone M, Arduino PG, Carrozzo M, Gandolfo S, Argiolas MR, Bertolusso G, Conrotto D, Pentenero M, Broccoletti R: Course of oral lichen planus: a retrospective study of 808 northern Italian patients. Oral Dis; 2009 Apr;15(3):235-43
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  • We confirm the chronic nature of this disorder, rarely remissive and the treatment intend for alleviating symptoms.
  • OLP is established to be a disease with small frequency of malignant transformation.
  • [MeSH-major] Carcinoma, Squamous Cell / pathology. Lichen Planus, Oral / pathology. Mouth Neoplasms / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Aged. Chronic Disease. Female. Humans. Longitudinal Studies. Male. Middle Aged. Mouth Diseases / classification. Mouth Diseases / complications. Mouth Diseases / pathology. Retrospective Studies. Risk Assessment

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  • (PMID = 19222766.001).
  • [ISSN] 1601-0825
  • [Journal-full-title] Oral diseases
  • [ISO-abbreviation] Oral Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
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22. Pacella CM, Stasi R, Bizzarri G, Pacella S, Graziano FM, Guglielmi R, Papini E: Percutaneous laser ablation of unresectable primary and metastatic adrenocortical carcinoma. Eur J Radiol; 2008 Apr;66(1):88-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Percutaneous laser ablation of unresectable primary and metastatic adrenocortical carcinoma.
  • PURPOSE: To evaluate the feasibility, safety, and clinical benefits of percutaneous laser ablation (PLA) in patients with unresectable primary and metastatic adrenocortical carcinoma (ACC).
  • In one case the procedure was performed also on the primary tumor.
  • RESULTS: After three sessions of PLA, the primary tumor of 15 cm was ablated by 75%.
  • After 1-4 (median 1) sessions of PLA, five liver metastases ranging from 2 to 5 cm were completely ablated, while the sixth tumor of 12 cm was ablated by 75%.
  • After a median follow-up after PLA of 27.0 months (range, 9-48 months), two patients have died of tumor progression, while two other patients remain alive and free of disease.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenocortical Carcinoma / surgery. Laser Therapy / methods. Liver Neoplasms / surgery
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Combined Modality Therapy. Disease Progression. Feasibility Studies. Female. Humans. Male. Middle Aged. Mitotane / therapeutic use. Palliative Care. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 17498906.001).
  • [ISSN] 0720-048X
  • [Journal-full-title] European journal of radiology
  • [ISO-abbreviation] Eur J Radiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 78E4J5IB5J / Mitotane
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23. Basic-Jukic N, Kes P, Bubic-Filipi L, Brunetta B: Treatment of thrombotic microangiopathies with plasma exchange. Hematology; 2007 Feb;12(1):63-7
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  • Of the 17 patients, 13 achieved complete remission after 5-32 sessions, two had partial response, and two had no response and died of progressive disease.
  • Four patients developed chronic relapsing TMA, and three of them progressed to end-stage renal disease.
  • Overall, with the median follow up of 5 years, 6 patients died from consequences of TMA (35.3%); three with chronic TMA, and 2 in the acute phase of progressive disease.
  • A 74-year old male who developed TMA after prostate cancer died from disseminated malignant disease.
  • Development of end-stage renal disease was associated with poor prognosis.
  • Further studies, long term follow-up and establishment of international registries are needed to clarify many dilemmas associated with the diagnosis, treatment and outcomes of patients with TMA.
  • [MeSH-minor] Adenocarcinoma / complications. Adolescent. Adrenal Cortex Hormones / therapeutic use. Adult. Aged. Anaphylaxis / etiology. Catheters, Indwelling / adverse effects. Combined Modality Therapy. Confusion / etiology. Disease Progression. Escherichia coli Infections / complications. Female. Follow-Up Studies. Hemorrhage / etiology. Humans. Kidney Diseases / etiology. Kidney Transplantation. Male. Middle Aged. Plasma. Postoperative Complications / therapy. Prostatic Neoplasms / complications. Retrospective Studies. Syndrome. Thrombosis / etiology

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  • (PMID = 17364995.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
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24. Sbragia L, Oliveira-Filho AG, Vassallo J, Pinto GA, Guerra-Junior G, Bustorff-Silva J: Adrenocortical tumors in Brazilian children: immunohistochemical markers and prognostic factors. Arch Pathol Lab Med; 2005 Sep;129(9):1127-31
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  • [Title] Adrenocortical tumors in Brazilian children: immunohistochemical markers and prognostic factors.
  • CONTEXT: The behavior of adrenocortical tumors (ACTs) is usually difficult to establish in childhood, and the role of immunomarkers in predicting outcome has not yet been elucidated.
  • PATIENTS AND METHODS: Clinical data were evaluated retrospectively in 33 children with ACTs, including age at diagnosis, sex, time between first symptoms and diagnosis, clinical signs and symptoms, tumor position, and follow-up.
  • Histologic sections were reviewed, each tumor was classified, and staging was performed according to previously published criteria.
  • RESULTS: Sixty-four percent (n = 21) of the patients were female, and the age at diagnosis in the cohort ranged from 2 to 96 months.
  • Virilization alone affected 70% (n = 23) of the patients, and 18 patients had stage 1 disease, 9 had stage 2 disease, and 3 each had stage 3 and stage 4 disease.
  • Female sex and stage 1 and stage 2 disease were associated with good outcome.
  • Only tumors with a volume exceeding 200 mL were associated with malignant behavior.
  • Because only a small number of tumors expressed the antigens, results of these immunohistochemical tests were considered inconclusive.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / pathology. Adrenocortical Carcinoma / secondary
  • [MeSH-minor] Biomarkers, Tumor / analysis. Brazil / epidemiology. Cell Proliferation. Child. Child, Preschool. Female. Humans. Immunoenzyme Techniques. Infant. Male. Prognosis. Retrospective Studies. Survival Rate

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  • (PMID = 16119984.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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25. Hisanaga K, Iwasaki Y, Itoyama Y, Neuro-Sweet Disease Study Group: Neuro-Sweet disease: clinical manifestations and criteria for diagnosis. Neurology; 2005 May 24;64(10):1756-61
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  • [Title] Neuro-Sweet disease: clinical manifestations and criteria for diagnosis.
  • BACKGROUND: Sweet disease, also known as acute febrile neutrophilic dermatosis, is a multisystem inflammatory disorder characterized by painful erythematous plaques and aseptic neutrophilic infiltration of various organs.
  • Sweet disease responds to systemic corticosteroids.
  • METHODS: The authors performed a survey on neuro-Sweet disease (NSD) in Japan and obtained detailed information about 16 cases.
  • They analyzed 42 cases, including 26 cases documented in the literature, and assessed clinical and laboratory criteria for the diagnosis.
  • RESULTS: Thirteen cases also fulfilled the criteria for the diagnosis of Behcet disease.
  • CONCLUSIONS: Neuro-Sweet disease is a distinct entity that may account for some cases of idiopathic encephalomeningitis.
  • [MeSH-major] Central Nervous System / physiopathology. Meningoencephalitis / diagnosis. Meningoencephalitis / epidemiology. Neoplasms / epidemiology. Sweet Syndrome / diagnosis. Sweet Syndrome / epidemiology
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Adult. Age of Onset. Behcet Syndrome / diagnosis. Behcet Syndrome / epidemiology. Biopsy. Comorbidity. Diagnosis, Differential. Encephalitis / diagnosis. Encephalitis / drug therapy. Encephalitis / epidemiology. Female. HLA Antigens / blood. Humans. Japan / epidemiology. Male. Meningitis / diagnosis. Meningitis / drug therapy. Meningitis / epidemiology. Middle Aged. Sex Distribution. Skin / pathology

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  • (PMID = 15911805.001).
  • [ISSN] 1526-632X
  • [Journal-full-title] Neurology
  • [ISO-abbreviation] Neurology
  • [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 / HLA Antigens
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26. Lucha PA Jr, Fticsar JE, Francis MJ: The strictured anastomosis: successful treatment by corticosteroid injections--report of three cases and review of the literature. Dis Colon Rectum; 2005 Apr;48(4):862-5
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  • The reported rate averages 8 percent and has been attributed to tissue ischemia, localized sepsis, anastomotic leak, proximal fecal diversion, radiation injury, inflammatory bowel disease, and recurrent rectal cancer.
  • [MeSH-major] Adrenal Cortex Hormones / therapeutic use. Anus Diseases / surgery. Colonic Diseases / surgery. Ileostomy / methods. Postoperative Complications
  • [MeSH-minor] Abscess / etiology. Adult. Anastomosis, Surgical / adverse effects. Colorectal Neoplasms / surgery. Constriction, Pathologic / etiology. Dilatation. Female. Fibrosis / etiology. Humans. Male. Middle Aged. Risk Factors. Treatment Outcome

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  • (PMID = 15747075.001).
  • [ISSN] 0012-3706
  • [Journal-full-title] Diseases of the colon and rectum
  • [ISO-abbreviation] Dis. Colon Rectum
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
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27. Ziaja J, Chudek J, Król R, Stańczyk A, Pawlicki J, Gasińska T, Kajor M, Wiecek A, Cierpka L: [Long-term consequences of surgical excision of cortisol producing adrenocortical adenoma]. Endokrynol Pol; 2007 May-Jun;58(3):207-12
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  • [Title] [Long-term consequences of surgical excision of cortisol producing adrenocortical adenoma].
  • [Transliterated title] Odległe nastepstwa chirurgicznego usuniecia gruczolaka kory nadnercza wytwarzajacego kortyzol.
  • INTRODUCTION: Surgical excision of adrenocortical tumour in patients with ACTH-independent Cushing syndrome gives a chance for their entire cure.
  • The aim of the study was to analyse long term consequences of surgical excision of cortisol producing adrenocortical adenoma with a special attention on the influence of adrenalectomy on arterial blood pressure.
  • 46.7% of patients required supplementation with adrenal steroids.
  • 40% of patients reported a subjective withdrawal of all symptoms of the disease after surgery and 46.7% only partial remission.
  • CONCLUSION: Surgical excision of cortisol producing adrenocortical adenoma results in improvement of blood pressure control and body weight reduction in a large percentage of patients with Cushing syndrome.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenalectomy. Adrenocortical Adenoma / surgery. Cushing Syndrome / surgery. Hypertension / surgery

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  • (PMID = 17940986.001).
  • [ISSN] 0423-104X
  • [Journal-full-title] Endokrynologia Polska
  • [ISO-abbreviation] Endokrynol Pol
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] WI4X0X7BPJ / Hydrocortisone
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28. Jang KY, Chung MJ, Moon WS, Kang MJ, Lee DG, Park HS, Kim YK, Jeong YB: Adrenocortical adenoma with unusual myxoid histological pattern: a case report. Pathology; 2009 Feb;41(2):188-91
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  • [Title] Adrenocortical adenoma with unusual myxoid histological pattern: a case report.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / pathology

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  • (PMID = 19152192.001).
  • [ISSN] 0031-3025
  • [Journal-full-title] Pathology
  • [ISO-abbreviation] Pathology
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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29. Calò LA, Pagnin E, Davis PA, Armanini D, Mormino P, Rossi GP, Pessina AC: Oxidative stress-related proteins in a Conn's adenoma tissue. Relevance for aldosterone's prooxidative and proinflammatory activity. J Endocrinol Invest; 2010 Jan;33(1):48-53
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  • The normal adrenal tissue adjacent to the adenoma was used as control.
  • RESULTS: p22phox gene and protein expression were higher (31% and 53%, respectively) in the adrenal adenoma.
  • TGFbeta, PAI-1, and HO-1 gene expression were also higher (25%, 129%, and 25%, respectively) in the adrenal adenoma while AT1R gene expression was similar (8%).
  • [MeSH-major] Adrenal Cortex Neoplasms / physiopathology. Adrenocortical Adenoma / physiopathology. Aldosterone / physiology. Oxidative Stress / drug effects
  • [MeSH-minor] Adrenal Glands / metabolism. Adult. Female. Gene Expression. Heme Oxygenase-1 / genetics. Humans. Hyperaldosteronism / surgery. NADPH Oxidase / genetics. Plasminogen Activator Inhibitor 1 / genetics. Receptor, Angiotensin, Type 1 / genetics. Receptors, Mineralocorticoid / genetics. Transforming Growth Factor beta / genetics

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  • (PMID = 19625761.001).
  • [ISSN] 1720-8386
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Plasminogen Activator Inhibitor 1; 0 / Receptor, Angiotensin, Type 1; 0 / Receptors, Mineralocorticoid; 0 / Transforming Growth Factor beta; 4964P6T9RB / Aldosterone; EC 1.14.14.18 / Heme Oxygenase-1; EC 1.6.3.1 / CYBA protein, human; EC 1.6.3.1 / NADPH Oxidase
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30. Rodriguez FJ, Scheithauer BW, Erickson LA, Jenkins RB, Giannini C: Ectopic low-grade adrenocortical carcinoma in the spinal region: immunohistochemical and molecular cytogenetic study of a pediatric case. Am J Surg Pathol; 2009 Jan;33(1):142-8
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  • [Title] Ectopic low-grade adrenocortical carcinoma in the spinal region: immunohistochemical and molecular cytogenetic study of a pediatric case.
  • Ectopic adrenocortical neoplasms arising in the nervous system are very rare.
  • We encountered an intradural, extramedullary case of an adrenocortical neoplasm of indeterminate malignant potential affecting a spinal nerve root in the distal lumbar region of a 5-month-old girl.
  • The tumor in both resections had increased mitotic activity (5/10 high power fields) and MIB-1 labeling indices of 23% and 33% at initial resection and recurrence, respectively.
  • Both tumors demonstrated gains of chromosomes 5 and 12 by interphase cytogenetics, whereas insulin growth factor 2 was identified in the recurrent tumor by immunohistochemistry.
  • This report demonstrates that ectopic adrenocortical tumors in the nervous system may exhibit clinicopathologic and cytogenetic features suggestive of adrenocortical carcinoma.

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  • (PMID = 18941403.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / T32 NS007494; United States / NINDS NIH HHS / NS / T32 NS07494-04
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS396174; NLM/ PMC3427599
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31. Yener S, Ertilav S, Secil M, Akinci B, Demir T, Comlekci A, Yesil S: Natural course of benign adrenal incidentalomas in subjects with extra-adrenal malignancy. Endocrine; 2009 Aug;36(1):135-40
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  • [Title] Natural course of benign adrenal incidentalomas in subjects with extra-adrenal malignancy.
  • Patients with extra-adrenal malignancies are diagnosed increasingly with benign adrenal tumors, as well as non-oncology subjects.
  • We aimed to demonstrate the natural course of adrenal adenomas in terms of mass size and hormonal status in oncology and non-oncology subjects.
  • We also compared the characteristics and behavior of adrenal adenomas with adrenal malignancies.
  • In our registry of adrenal tumors (n = 335), we prospectively evaluated 29 oncology subjects (EAM+) and age, gender, and follow-up duration matched 110 non-oncology subjects (EAM-) with adrenal adenomas.
  • We also included 16 subjects with adrenal malignancies (primary; 3 and metastasis; 13).
  • Tumor size was followed-up with CT or MRI at 6th and 12th months and annually in subsequent visits.
  • Initial tumor size, mean increase in tumor size, and number of subjects who showed mass enlargement or developed subclinical Cushing Syndrome were comparable (P > 0.05) between EAM+ and EAM- groups.
  • Subjects with malignant adrenal tumors were older (P = 0.06), had larger tumors at presentation (P < 0.001), and showed mass enlargement during a shorter follow-up duration (P < 0.001).
  • Oncology subjects with adrenal adenomas featured similar baseline and follow-up parameters in terms of mass enlargement and development of subclinical Cushing Syndrome when compared with non-oncology subjects.
  • Malignant adrenal tumors were characterized with large, rapidly growing tumors of older ages.
  • Conservative approach can be suggested to oncology subjects for adrenal adenomas unless clinical and radiological suspicion of adrenal malignancy is present.
  • [MeSH-major] Adenoma / epidemiology. Adrenal Cortex Neoplasms / epidemiology. Cushing Syndrome / epidemiology. Neoplasms / epidemiology. Pheochromocytoma / epidemiology
  • [MeSH-minor] Adult. Aged. Carcinoma, Non-Small-Cell Lung / epidemiology. Carcinoma, Renal Cell / epidemiology. Disease Progression. Female. Follow-Up Studies. Humans. Incidental Findings. Kidney Neoplasms / epidemiology. Lung Neoplasms / epidemiology. Lymphoma, Non-Hodgkin / epidemiology. Male. Middle Aged. Pancreatic Neoplasms / epidemiology. Prevalence. Registries

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  • (PMID = 19381885.001).
  • [ISSN] 1355-008X
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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32. Katsumata N: [Virilizing adrenocortical tumor]. Nihon Rinsho; 2006 May 28;Suppl 1:705-7
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  • [Title] [Virilizing adrenocortical tumor].
  • [MeSH-major] Adrenal Cortex Neoplasms. Virilism
  • [MeSH-minor] Adrenalectomy. Androgens / biosynthesis. Androgens / secretion. Combined Modality Therapy. Diagnosis, Differential. Female. Humans. Mitotane / therapeutic use. Prognosis

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  • (PMID = 16776254.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Androgens; 78E4J5IB5J / Mitotane
  • [Number-of-references] 5
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33. Schlosser KA: Infantile hemangioma: how to treat this benign neoplasm of childhood. JAAPA; 2009 May;22(5):46-9
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  • [Title] Infantile hemangioma: how to treat this benign neoplasm of childhood.
  • [MeSH-major] Hemangioma / therapy. Skin Neoplasms / therapy
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Aminoquinolines / therapeutic use. Antineoplastic Agents / therapeutic use. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Interferon-alpha / therapeutic use. Laser Therapy. Male

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  • (PMID = 19469391.001).
  • [ISSN] 1547-1896
  • [Journal-full-title] JAAPA : official journal of the American Academy of Physician Assistants
  • [ISO-abbreviation] JAAPA
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Aminoquinolines; 0 / Antineoplastic Agents; 0 / Interferon-alpha; 99011-02-6 / imiquimod
  • [Number-of-references] 11
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34. Sheikh A, Haque N, Zuberi L, Jamal A: Laparoscopic adrenalectomy for Conn's syndrome. J Coll Physicians Surg Pak; 2006 Jan;16(1):76-8
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  • Laparoscopic adrenalectomy is now used worldwide to resect adrenal adenomas and other adrenal tumors recently introduced in Pakistan.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenalectomy. Adrenocortical Adenoma / surgery. Hyperaldosteronism / surgery. Laparoscopy

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  • (PMID = 16441999.001).
  • [ISSN] 1022-386X
  • [Journal-full-title] Journal of the College of Physicians and Surgeons--Pakistan : JCPSP
  • [ISO-abbreviation] J Coll Physicians Surg Pak
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Pakistan
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35. Yaneva M, Vandeva S, Zacharieva S, Daly AF, Beckers A: Genetics of Cushing's syndrome. Neuroendocrinology; 2010;92 Suppl 1:6-10
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  • Endogenous hypercortisolism is usually due to ACTH-secreting pituitary corticotropic adenomas and less often due to ectopic ACTH-secreting neuroendocrine neoplasms or ACTH-independent adrenal cortisol hypersecretion.
  • CS is a serious chronic disease leading to a several-fold increase in cardiovascular morbidity and mortality.
  • Sporadic adrenal adenomas and carcinomas may demonstrate dysfunction in genes such as TP53 among others.
  • Cushing's disease can be an inherited condition also.
  • Multiple endocrine neoplasia type 1 (MEN1) and familial isolated pituitary adenomas (FIPA) together account for 5% of pituitary adenomas.
  • Cushing's disease occurs infrequently in an inherited setting in both of these conditions.
  • To date only 2 cases of Cushing's disease have been described in association with mutations in AIP.
  • One case of Cushing's disease has been reported as part of MEN4, a rare MEN1-like syndrome due to mutation in the CDKN1B gene.
  • Carney complex (CNC) due to PRKAR1A mutations in most cases is associated with CS, mainly as a cause of bilateral adrenal hyperplasia.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics. Cushing Syndrome / genetics. Pituitary ACTH Hypersecretion / genetics. Pituitary Neoplasms / genetics


36. Kutzleb C, Busmann A, Wendland M, Maronde E: Discovery of novel regulatory peptides by reverse pharmacology: spotlight on chemerin and the RF-amide peptides metastin and QRFP. Curr Protein Pept Sci; 2005 Jun;6(3):265-78
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  • One decade spent pursuing orphan GPCR screening by this technique assigned over 30 ligand/receptor pairs and revealed previously known or novel undescribed ligands, mostly of a peptidic nature.
  • The novel RF-amide QRFP is implicated in food intake and aldosterone release from the adrenal cortex in the rat.
  • [MeSH-minor] Amino Acid Sequence. Animals. Drug Evaluation, Preclinical. Female. Humans. In Vitro Techniques. Intercellular Signaling Peptides and Proteins. Kisspeptins. Ligands. Models, Biological. Molecular Sequence Data. Neoplasms / etiology. Oligopeptides / chemistry. Oligopeptides / genetics. Oligopeptides / metabolism. Pharmacology / methods. Pregnancy. Rats. Receptors, G-Protein-Coupled / metabolism. Signal Transduction. Trophoblasts / cytology. Trophoblasts / physiology. Tumor Suppressor Proteins

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  • (PMID = 15974952.001).
  • [ISSN] 1389-2037
  • [Journal-full-title] Current protein & peptide science
  • [ISO-abbreviation] Curr. Protein Pept. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Chemokines; 0 / Intercellular Signaling Peptides and Proteins; 0 / KISS1 protein, human; 0 / Kisspeptins; 0 / Ligands; 0 / Oligopeptides; 0 / Proteins; 0 / Receptors, G-Protein-Coupled; 0 / Tumor Suppressor Proteins; 0 / chemerin protein, human
  • [Number-of-references] 139
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37. Tissier F: [Sporadic adrenocortical tumors: genetics and perspectives for the pathologist]. Ann Pathol; 2008 Oct;28(5):409-16
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  • [Title] [Sporadic adrenocortical tumors: genetics and perspectives for the pathologist].
  • [Transliterated title] Tumeurs corticosurrénaliennes sporadiques de l'adulte : aspects génétiques et perspectives pour le pathologiste.
  • Most adrenocortical tumors are benign; adrenocortical carcinomas are rare but their prognosis is poor and few therapeutic options are available.
  • In most adrenocortical tumors, the morphological approach provides enough elements to establish the differential diagnosis between a benign and a malignant tumor but in few cases, it is insufficient.
  • Moreover, morphology is limited for predicting prognosis of adrenocortical carcinomas.
  • The comprehension of the genetic syndromes associated with adrenocortical tumors led to progress in the identification of genetic abnormalities involved in sporadic adrenocortical tumorigenesis.
  • Thus, in sporadic adrenocortical tumorigenesis, IGF-II overexpression and cyclin E overproduction have been associated with 11p15 alterations which are observed in Bethwith-Wiedemann syndrome and TP53 inactivating mutations and 17p13 locus abnormalities which are observed in Li-Fraumeni syndrome.
  • Activation of the Wnt/ss-catenin signaling pathway which is observed in familial adenomatous polyposis has been found in adrenocortical adenomas and carcinomas associated to mutations of CTNNB1, the gene coding ss-catenin, suggesting a central role for this pathway in adrenocortical tumorigenesis.
  • These genetics findings already have had repercussions for patients via the development of molecular markers for diagnosis and prognosis; in the future they should be helpful in the development of new therapeutics.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / pathology

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  • (PMID = 19068395.001).
  • [ISSN] 0242-6498
  • [Journal-full-title] Annales de pathologie
  • [ISO-abbreviation] Ann Pathol
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human; 67763-97-7 / Insulin-Like Growth Factor II; EC 3.1.4.- / Phosphoric Diester Hydrolases; EC 3.1.4.35 / PDE11A protein, human
  • [Number-of-references] 73
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38. Khan A, Agarwal R: Lung cancer chemoprevention with inhaled corticosteroids? Am J Respir Crit Care Med; 2007 Dec 1;176(11):1169; author reply 1169
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Adrenal Cortex Hormones / administration & dosage. Lung Neoplasms / prevention & control. Pulmonary Disease, Chronic Obstructive / drug therapy

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  • [CommentOn] Am J Respir Crit Care Med. 2007 Apr 1;175(7):712-9 [17185647.001]
  • (PMID = 18042661.001).
  • [ISSN] 1535-4970
  • [Journal-full-title] American journal of respiratory and critical care medicine
  • [ISO-abbreviation] Am. J. Respir. Crit. Care Med.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
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39. Wang WJ, Zhang F, Xu GX, Chen C: [Calcium-binding protein secretagogin is a novel neuroendocrine marker]. Zhonghua Bing Li Xue Za Zhi; 2010 Sep;39(9):627-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Adenoma / metabolism. Adrenal Cortex Neoplasms / metabolism. Calcium-Binding Proteins / metabolism. Lung Neoplasms / metabolism. Neuroendocrine Tumors / metabolism. Small Cell Lung Carcinoma / metabolism
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Carcinoma, Neuroendocrine / metabolism. Humans. Neuroendocrine Cells / metabolism. Secretagogins

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  • (PMID = 21092592.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Calcium-Binding Proteins; 0 / SCGN protein, human; 0 / Secretagogins
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40. Mazzuco TL, Chabre O, Sturm N, Feige JJ, Thomas M: Ectopic expression of the gastric inhibitory polypeptide receptor gene is a sufficient genetic event to induce benign adrenocortical tumor in a xenotransplantation model. Endocrinology; 2006 Feb;147(2):782-90
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  • [Title] Ectopic expression of the gastric inhibitory polypeptide receptor gene is a sufficient genetic event to induce benign adrenocortical tumor in a xenotransplantation model.
  • Aberrant expression of ectopic G protein-coupled receptors (GPCRs) in adrenal cortex tissue has been observed in several cases of ACTH-independent macronodular adrenal hyperplasias and adenomas associated with Cushing's syndrome.
  • Although there is clear clinical evidence for the implication of these ectopic receptors in abnormal regulation of cortisol production, whether this aberrant GPCR expression is the cause or the consequence of the development of an adrenal hyperplasia is still an open question.
  • To answer it, we genetically engineered primary bovine adrenocortical cells to have them express the gastric inhibitory polypeptide receptor.
  • We observed the formation of an enlarged and hyperproliferative adenomatous adrenocortical tissue that secreted cortisol in a gastric inhibitory polypeptide-dependent manner and induced a mild Cushing's syndrome with hyperglycemia.
  • Moreover, we show that tumor development was ACTH independent.
  • Thus, a single genetic event, inappropriate expression of a nonmutated GPCR gene, is sufficient to initiate the complete phenotypic alterations that ultimately lead to the formation of a benign adrenocortical tumor.
  • [MeSH-major] Adenoma / genetics. Adrenal Cortex / metabolism. Adrenal Gland Neoplasms / genetics. Cell Transformation, Neoplastic / metabolism. Gene Expression Regulation, Neoplastic. Receptors, Gastrointestinal Hormone / metabolism

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  • (PMID = 16254030.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Gastrointestinal Hormone; 0 / gastric inhibitory polypeptide receptor; 128559-51-3 / RAG-1 protein; WI4X0X7BPJ / Hydrocortisone
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41. Namour F, Ayav A, Lu X, Klein M, Muresan M, Bresler L, Tramoy D, Guéant JL, Brunaud L: Lack of association between microsatellite instability and benign adrenal tumors. World J Surg; 2006 Jul;30(7):1240-6
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  • [Title] Lack of association between microsatellite instability and benign adrenal tumors.
  • BACKGROUND: The adrenal gland may give rise to pheochromocytomas, which are catecholamine-producing tumors originating from the adrenal medulla, or to adrenocortical tumors, which derive from the adrenocortical cortex and may be secreting or not.
  • The genetic mechanisms underlying the formation of these tumors include somatic mutations in susceptibility genes, especially in the familial forms, and allelic loss, especially in chromosome 1.
  • Microsatellite loci were analyzed in 32 benign tumors, including 11 pheochromocytomas and 21 adrenocortical tumors, in patients with and without familial syndrome.
  • No microsatellite instability was detected in any tumor.
  • A second patient with a MEN-2A syndrome and a two-sided pheochromocytoma exhibited a loss of heterozygosity for D2S123 in the right tumor only and a retention of heterozygosity for all markers in the left tumor.
  • CONCLUSIONS: These results suggest that microsatellite instability, evaluated by the five reference markers of the National Cancer Institute, is not a feature of benign adrenal tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Microsatellite Repeats / genetics. Pheochromocytoma / genetics
  • [MeSH-minor] Adult. Aged. Alleles. DNA, Neoplasm / analysis. Female. Humans. Loss of Heterozygosity. Male. Middle Aged. Polymerase Chain Reaction. Proto-Oncogene Proteins / genetics

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  • (PMID = 16715450.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Proto-Oncogene Proteins
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42. Xiao ZJ, Li CL: [Combined therapy of advanced adrenal cortical adenocarcinoma]. Zhonghua Yi Xue Za Zhi; 2010 Aug 10;90(30):2123-5
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  • [Title] [Combined therapy of advanced adrenal cortical adenocarcinoma].
  • OBJECTIVE: To analyze the clinical efficacy of combined therapy in the treatment of advanced adrenal cortical adenocarcinoma.
  • METHODS: The clinical data of 12 cases with advanced adrenal cortical adenocarcinoma at our hospital from 1986 - 2006 were analyzed.
  • Pathological diagnosis was all of adrenal cortical adenocarcinoma.
  • According to evaluation criterion of chemotherapeutic effect by WHO in 1987, the results were: CR (complete remission) (n = 0), PR (partial remission) (n = 7), SD (stable disease) (n = 3) and PD (progressive disease) (n = 2).
  • CONCLUSION: Combined therapy of adrenal cortical adenocarcinoma is effective to prolong the patient lifespan.
  • Making an early diagnosis and offering a novel therapy yield a better outcome.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenal Cortex Neoplasms / therapy. Adrenocortical Carcinoma / pathology. Adrenocortical Carcinoma / therapy
  • [MeSH-minor] Adult. Combined Modality Therapy. Female. Humans. Male. Middle Aged. Neoplasm Staging. Retrospective Studies. Treatment Outcome

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  • (PMID = 21029628.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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43. 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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44. Raparia K, Ayala AG, Sienko A, Zhai QJ, Ro JY: Myxoid adrenal cortical neoplasms. Ann Diagn Pathol; 2008 Oct;12(5):344-8
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  • [Title] Myxoid adrenal cortical neoplasms.
  • Myxoid adrenal cortical neoplasms are rare, and to our knowledge, only about 23 cases have been reported in the literature, including 13 carcinomas and 10 adenomas.
  • We recently experienced 4 cases of myxoid adrenal cortical neoplasms (3 benign and 1 borderline malignancy) and studied the clinical, histopathological, and immunohistochemical features of these neoplasms.
  • The tumors weighed from 24.1 to 94 g (size, 4.1-9.8 cm).
  • Histologically, the tumor cells were arranged in delicate arborizing cords or trabecula with myxoid areas varying from 30% to 70%.
  • Three tumors were benign and 1 was of borderline morphology with mitoses of 3/10 high-power fields and mild to moderate nuclear pleomorphism.
  • The tumor cells were positive for vimentin, synaptophysin, and inhibin but negative for cytokeratin.
  • All patients are alive with no recurrence of their tumors or evidence of metastasis (follow-up of 14-20 months).
  • Myxoid changes in adrenal cortical neoplasms are rare but can be seen in both an adenoma and a tumor of uncertain malignant potential.
  • Because of prominent myxoid changes, other myxoid tumors occurring in the retroperitoneum should be excluded.
  • The usual clinical and histological features can be applied to classify the lesions as benign, borderline tumor, or malignant.
  • In our series, there was no case with frank malignant tumor.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / pathology. Adrenocortical Carcinoma / pathology. Mucins / metabolism
  • [MeSH-minor] Adult. Biomarkers, Tumor / metabolism. Female. Humans. Immunoenzyme Techniques. Inhibins / metabolism. Male. Middle Aged. Synaptophysin / metabolism. Vimentin / metabolism

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  • (PMID = 18774497.001).
  • [ISSN] 1532-8198
  • [Journal-full-title] Annals of diagnostic pathology
  • [ISO-abbreviation] Ann Diagn Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Mucins; 0 / Synaptophysin; 0 / Vimentin; 57285-09-3 / Inhibins
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45. Cavalier ME, Davis MM, Croop JM: Germline p53 mutation presenting as synchronous tumors. J Pediatr Hematol Oncol; 2005 Aug;27(8):441-3
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  • [Title] Germline p53 mutation presenting as synchronous tumors.
  • Li-Fraumeni syndrome and the LF-like syndrome, rare heritable conditions that predispose to the development of malignancy, are associated with germline mutations of the tumor suppressor gene p53.
  • The authors describe a 14-month-old boy who presented with synchronous rhabdomyosarcoma and adrenal cortical carcinoma and a novel mutation of the p53 gene.
  • Although codon 273 is a known hotspot region for p53 mutation, the patient's mutation, R273H, has not been associated with development of adrenal cortical carcinoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Carcinoma / genetics. Genes, p53. Germ-Line Mutation. Li-Fraumeni Syndrome / complications. Neoplasms, Multiple Primary / genetics. Rhabdomyosarcoma / genetics

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  • (PMID = 16096528.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon
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46. Tömböl Z, Szabó PM, Patócs A, Rácz K, Igaz P: Differences in MicroRNA expression profiles of adrenocortical tumors--letter. Clin Cancer Res; 2010 May 15;16(10):2915; author reply 2915-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differences in MicroRNA expression profiles of adrenocortical tumors--letter.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. MicroRNAs / genetics

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  • (PMID = 20460475.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs
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47. Bertherat J, Coste J, Bertagna X: Adjuvant mitotane in adrenocortical carcinoma. N Engl J Med; 2007 Sep 20;357(12):1256-7; author reply 1259
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  • [Title] Adjuvant mitotane in adrenocortical carcinoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Adrenocortical Carcinoma / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Mitotane / therapeutic use
  • [MeSH-minor] Chemotherapy, Adjuvant. Disease-Free Survival. Humans. Patient Selection

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  • [CommentOn] N Engl J Med. 2007 Jun 7;356(23):2372-80 [17554118.001]
  • (PMID = 17881760.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 78E4J5IB5J / Mitotane
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48. 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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  • [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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49. Satter EK, Barnette DJ: Adrenocortical carcinoma with delayed cutaneous metastasis. J Cutan Pathol; 2008 Jul;35(7):677-80
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  • [Title] Adrenocortical carcinoma with delayed cutaneous metastasis.
  • Adrenal cortical carcinoma (ACC) is an uncommon and aggressive malignancy.
  • Patients often have metastatic disease at initial presentation, with the most common sites being the liver, local lymph nodes, lungs, peritoneum and bone.
  • Herein, we report a case of an 82-year-old woman who presented with a cyst-like lesion on her back, which on biopsy proved to be ACC metastatic from a primary tumor diagnosed 30 years previously.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / secondary. Skin / pathology. Skin Neoplasms / secondary
  • [MeSH-minor] Aged, 80 and over. Biomarkers, Tumor / metabolism. Diagnosis, Differential. Female. Humans. Lung / pathology. Lung Neoplasms / diagnosis. Lung Neoplasms / secondary. Middle Aged. Prognosis. Recurrence

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  • (PMID = 18201231.001).
  • [ISSN] 1600-0560
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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50. Papotti M, Volante M, Duregon E, Delsedime L, Terzolo M, Berruti A, Rosai J: Adrenocortical tumors with myxoid features: a distinct morphologic and phenotypical variant exhibiting malignant behavior. Am J Surg Pathol; 2010 Jul;34(7):973-83
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  • [Title] Adrenocortical tumors with myxoid features: a distinct morphologic and phenotypical variant exhibiting malignant behavior.
  • Myxoid changes have been rarely reported both in adrenocortical adenomas and carcinomas.
  • The recent observation by our group of an adrenal myxoid tumor with morphologically borderline features, but aggressive clinical behavior prompted us to review a series of 196 adrenocortical lesions, comprising 122 carcinomas and 74 adenomas, to define the morphologic, phenotypical and clinical characteristics of adrenocortical tumors with myxoid features.
  • Fourteen cases, including 12 carcinomas and 2 borderline tumors, formed the basis of this report, and were characterized by a variably abundant myxoid component (from 5% to 90% of tumor) and 2 distinct cellular growth patterns: the first (10 cases), mostly associated with a predominant myxoid stromal component, was made of small cells with mild atypia arranged in cords and microcysts; the second (4 cases) was characterized by focal myxoid changes in tumors otherwise similar to conventional adrenocortical carcinoma, with large atypical cells having an eosinophilic cytoplasm and a diffuse or nodular architecture.
  • A peculiar reactivity to neurofilaments was seen, mostly associated to the presence of predominant rather that focal myxoid stromal changes, and in 40% of conventional adrenocortical carcinomas, thus representing an undescribed potential pitfall in the differential diagnosis of adrenal lesions.
  • Myxoid adrenocortical tumors probably represent a rare but histologically and phenotipically distinct entity and, although rare cases of benign lesions are on record, they seem to be generally associated to morphologic and clinical features of malignancy.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / pathology. Adrenocortical Carcinoma / secondary. Mucins / metabolism
  • [MeSH-minor] Adrenal Glands / embryology. Adrenal Glands / metabolism. Adult. Aged. Biomarkers, Tumor / metabolism. Fatal Outcome. Female. Fetal Development. Humans. Male. Middle Aged

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  • (PMID = 20534995.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Mucins
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51. Khan S, Imtiaz KE: Adrenocortical carcinoma: a diagnostic and treatment dilemma. Br J Hosp Med (Lond); 2009 Jan;70(1):46-7
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  • [Title] Adrenocortical carcinoma: a diagnostic and treatment dilemma.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenalectomy / methods. Adrenocortical Carcinoma / surgery
  • [MeSH-minor] Diagnosis, Differential. Fatal Outcome. Female. Humans. Middle Aged. Neoplasm Seeding

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  • (PMID = 19357579.001).
  • [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] Case Reports; Journal Article
  • [Publication-country] England
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52. Trébol I, González-Pérez R, García-Rio I, Arregui MA, Saracibar N, Carnero L, Soloeta R: Paraneoplastic neutrophilic figurate erythema. Br J Dermatol; 2007 Feb;156(2):396-8
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  • [MeSH-major] Erythema / etiology. Hidradenitis / etiology. Hodgkin Disease / complications. Leukemia, Neutrophilic, Chronic / complications. Paraneoplastic Syndromes / complications
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Aged. Female. Humans. Skin Neoplasms / drug therapy. Treatment Outcome

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  • (PMID = 17223897.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
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53. Streeton CL, Gospodarevskaya E, Harris A: Treatment of basal cell carcinomas by general practitioners in Australia. Int J Dermatol; 2006 Apr;45(4):345-51
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  • [MeSH-major] Carcinoma, Basal Cell / therapy. Physicians, Family. Practice Patterns, Physicians' / statistics & numerical data. Skin Neoplasms / therapy
  • [MeSH-minor] Administration, Topical. Adrenal Cortex Hormones / therapeutic use. Antineoplastic Agents / therapeutic use. Australia. Cautery / utilization. Cryosurgery / utilization. Curettage / utilization. Female. Humans. Interferons / therapeutic use. Male. Mohs Surgery / utilization. Referral and Consultation / statistics & numerical data. Retrospective Studies. Surveys and Questionnaires

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  • (PMID = 16650155.001).
  • [ISSN] 0011-9059
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Antineoplastic Agents; 9008-11-1 / Interferons
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54. Mannelli M, Cantini G, Poli G, Mangoni M, Nesi G, Canu L, Rapizzi E, Borgogni E, Ercolino T, Piccini V, Luconi M: Role of the PPAR-γ system in normal and tumoral pituitary corticotropic cells and adrenal cells. Neuroendocrinology; 2010;92 Suppl 1:23-7
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  • [Title] Role of the PPAR-γ system in normal and tumoral pituitary corticotropic cells and adrenal cells.
  • In this minireview, we summarize the current knowledge on PPAR-γ in normal and tumoral corticotropic pituitary and adrenal cells.
  • The receptor expression has been shown in ACTH-secreting cells in both normal and adenomal pituitary as well as in normal and tumor adrenal cortex.
  • Preclinical studies conducted both in vitro on tumor cells and in vivo on xenograft tumor models obtained by subcutaneous injection of cancer cells have evidenced the anticancer properties of TZD, in particular rosiglitazone (RGZ) and pioglitazone (PIO).
  • In both pituitary and adrenocortical cancer, RGZ treatment results in inhibition of cell proliferation, through G0/G1 cell-cycle arrest and induction of cell apoptosis, leading to significant inhibition of tumor growth in the xenograft tumor models.
  • In addition, since RGZ can reduce ACTH and corticosterone secretion in mouse corticotropic pituitary tumors, both RGZ and PIO have been used in the treatment of Cushing's disease with variable but generally unsatisfactory results.
  • [MeSH-major] Adrenal Cortex / metabolism. Corticotrophs / metabolism. PPAR gamma / metabolism. Pituitary ACTH Hypersecretion / metabolism. Pituitary Gland / metabolism
  • [MeSH-minor] Adrenal Cortex Neoplasms / drug therapy. Adrenal Cortex Neoplasms / metabolism. Humans. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / metabolism. Thiazolidinediones / therapeutic use

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  • [Copyright] Copyright © 2010 S. Karger AG, Basel.
  • (PMID = 20829614.001).
  • [ISSN] 1423-0194
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / PPAR gamma; 0 / Thiazolidinediones; X4OV71U42S / pioglitazone
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55. Tokar EJ, Diwan BA, Waalkes MP: Arsenic exposure in utero and nonepidermal proliferative response in adulthood in Tg.AC mice. Int J Toxicol; 2010 May-Jun;29(3):291-6
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  • After birth, groups (n = 25) of offspring received topical 12-O-tetradecanoyl phorbol-13-acetate (TPA) (2 microg twice a week) for 36 weeks and were killed; nonskin tumors were assessed.
  • Arsenic increased adrenal cortical adenomas (ACAs; 25%-29%) compared with control (0%) independent of TPA in all male groups.
  • All arsenic-treated females had uterine hyperplasia (26%-40%; control 4%) independent of TPA, and 3 had uterine tumors.
  • [MeSH-minor] Adenoma / chemically induced. Adrenal Cortex Neoplasms / chemically induced. Aging. Animals. Dose-Response Relationship, Drug. Female. Hyperplasia / chemically induced. Male. Maternal Exposure / adverse effects. Mice. Papilloma / chemically induced. Precancerous Conditions / chemically induced. Pregnancy. Random Allocation. Sex Characteristics. Tetradecanoylphorbol Acetate / toxicity. Urinary Bladder Neoplasms / chemically induced. Uterine Neoplasms / chemically induced

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  • (PMID = 20448261.001).
  • [ISSN] 1092-874X
  • [Journal-full-title] International journal of toxicology
  • [ISO-abbreviation] Int. J. Toxicol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arsenites; 0 / Carcinogens; 0 / Sodium Compounds; 48OVY2OC72 / sodium arsenite; N712M78A8G / Arsenic; NI40JAQ945 / Tetradecanoylphorbol Acetate
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56. Caetano MS, Vilar L, Kater CE: [Subclinical Cushing's syndrome in populations at risk]. Arq Bras Endocrinol Metabol; 2007 Nov;51(8):1185-90
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  • [Transliterated title] Síndrome de Cushing subclínica em populações de risco.
  • Based on autopsy studies, adrenal masses are among the most common tumors in humans.
  • Endogenous Cushing's syndrome (CS) is unusual and adrenal adenomas account for 10% of all cases of CS.
  • The prevalence of hypercortisolism in clinically inapparent adrenal masses has been reported as 9%.
  • Adrenal incidentalomas and subclinical CS are related to metabolic disorders, in special to type-2 diabetes.
  • [MeSH-minor] Adrenal Cortex Neoplasms / complications. Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / therapy. Adrenocortical Adenoma / complications. Adrenocortical Adenoma / diagnosis. Adrenocortical Adenoma / therapy. Humans. Hydrocortisone / blood. Hydrocortisone / urine. Hypertension / diagnosis. Hypertension / therapy. Incidental Findings. Obesity / diagnosis. Risk Factors

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  • (PMID = 18209855.001).
  • [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
  • [Chemical-registry-number] WI4X0X7BPJ / Hydrocortisone
  • [Number-of-references] 33
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57. Bourdeau I, Lampron A, Costa MH, Tadjine M, Lacroix A: Adrenocorticotropic hormone-independent Cushing's syndrome. Curr Opin Endocrinol Diabetes Obes; 2007 Jun;14(3):219-25
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  • Primary Cushing's syndrome is most often secondary to adrenocortical adenomas or carcinomas, and more rarely to bilateral adrenal hyperplasias.
  • Corticotropin-independent cortisol-producing hyperplasia is caused by micronodular diseases, including primary pigmented nodular adrenocortical disease and nonpigmented micronodular hyperplasia and adrenocorticotropic hormone-independent macronodular adrenal hyperplasia.
  • Primary pigmented nodular adrenocortical disease can be found either alone or in the context of Carney complex, a multiple endocrine neoplasia syndrome.
  • RECENT FINDINGS: In recent years, the pathophysiology of adrenocortical tumors and hyperplasias became better understood following the identification of genes responsible for syndromes associated with corticotropin-independent Cushing's syndrome and the demonstration of aberrant expression and function of various hormone receptors in adrenocortical adenomas and adrenocorticotropic hormone-independent macronodular adrenal hyperplasia.
  • This article reviews findings on the molecular and genetic aspects of corticotropin-independent Cushing's syndrome including recent gene expression profiling studies of adrenocortical tumors and hyperplasias and animal models that provided clues on the pathogenesis of primary Cushing's syndrome.
  • SUMMARY: A better understanding of molecular mechanisms involved in adrenocortical tumors and hyperplasias may lead to improved diagnostic and prognostic markers and treatment strategies to assist clinicians in the management of corticotropin-independent Cushing's syndrome.
  • [MeSH-major] Adrenal Cortex Diseases / complications. Adrenal Cortex Neoplasms / complications. Adrenocorticotropic Hormone / metabolism. Cushing Syndrome / etiology

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  • (PMID = 17940443.001).
  • [ISSN] 1752-2978
  • [Journal-full-title] Current opinion in endocrinology, diabetes, and obesity
  • [ISO-abbreviation] Curr Opin Endocrinol Diabetes Obes
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
  • [Number-of-references] 63
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58. Assié G: [Gene profiling and classification of adrenocortical tumors]. Ann Endocrinol (Paris); 2009 Jun;70(3):186-91
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  • [Title] [Gene profiling and classification of adrenocortical tumors].
  • [Transliterated title] Etudes génomiques à haut débit et classification des tumeurs de la corticosurrénale.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Gene Expression Profiling
  • [MeSH-minor] Adrenal Cortex / pathology. DNA, Neoplasm / genetics. Humans. Neoplasm Metastasis. Transcription, Genetic

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  • (PMID = 19296923.001).
  • [ISSN] 0003-4266
  • [Journal-full-title] Annales d'endocrinologie
  • [ISO-abbreviation] Ann. Endocrinol. (Paris)
  • [Language] fre
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / DNA, Neoplasm
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59. Tenenbaum F: [Adrenal incidentaloma and nuclear medicine examination]. J Radiol; 2009 Mar;90(3 Pt 2):444-8
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  • [Title] [Adrenal incidentaloma and nuclear medicine examination].
  • In the setting of adrenal incidentaloma, nuclear medicine evaluation is only indicated after biological and imaging work-up has been completed.
  • In lesions without MIBG uptake, 18F FDG or 18F DOPA PET can be considered to characterize chromaffin cell tumours.
  • To characterize lesions of the adrenal cortex, iodocholesterol scintigraphy is performed to confirm the origin of the adenoma and the benign or malignant nature of the lesion since benign adenomas show tracer uptake and malignant lesions show no tracer uptake.
  • [MeSH-major] Adenoma / radionuclide imaging. Adrenal Cortex Neoplasms / radionuclide imaging. Adrenal Gland Neoplasms / radionuclide imaging. Incidental Findings. Pheochromocytoma / radionuclide imaging. Positron-Emission Tomography / methods

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  • (PMID = 19421135.001).
  • [ISSN] 0221-0363
  • [Journal-full-title] Journal de radiologie
  • [ISO-abbreviation] J Radiol
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Fluorine Radioisotopes; 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18; 2C598205QX / fluorodopa F 18; 30461-91-7 / 19-Iodocholesterol; 35MRW7B4AD / 3-Iodobenzylguanidine; 63-84-3 / Dihydroxyphenylalanine
  • [Number-of-references] 16
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60. Stephens JW, Fielding A, Verdaguer R, Freites O: A steroid-cell tumor of the ovary resulting in massive androgen excess early in the gonadol steroidogenic pathway. Gynecol Endocrinol; 2008 Mar;24(3):151-3
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  • [Title] A steroid-cell tumor of the ovary resulting in massive androgen excess early in the gonadol steroidogenic pathway.
  • We describe the case of a 35-year-old woman with an ovarian steroid-cell tumor secreting markedly elevated levels of testosterone (28.3 nmol/l), dehydroepiandrosterone sulfate (19.7 mumol/l), androstenedione (>34.7 nmol/l) and 17-hydroxyprogesterone (100.5 nmol/l) into plasma.
  • We also discuss the differential diagnosis, investigation and interpretation of androgens of adrenal and ovarian origin.
  • [MeSH-major] Adrenal Cortex Hormones / secretion. Androgens / secretion. Ovarian Neoplasms / secretion
  • [MeSH-minor] 17-alpha-Hydroxyprogesterone / blood. Adrenal Glands / metabolism. Adrenal Glands / pathology. Adult. Androstenedione / blood. Dehydroepiandrosterone Sulfate / blood. Diagnosis, Differential. Fallopian Tubes / surgery. Female. Humans. Ovariectomy. Ovary / metabolism. Testosterone / blood. Tomography, X-Ray Computed. Ultrasonography

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  • [CommentIn] Gynecol Endocrinol. 2008 Sep;24(9):502-4 [18958769.001]
  • [ErratumIn] Gynecol Endocrinol. 2012 Apr;28(4):340
  • (PMID = 18335330.001).
  • [ISSN] 0951-3590
  • [Journal-full-title] Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology
  • [ISO-abbreviation] Gynecol. Endocrinol.
  • [Language] eng
  • [Publication-type] Case Reports; Duplicate Publication; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Androgens; 3XMK78S47O / Testosterone; 409J2J96VR / Androstenedione; 57B09Q7FJR / Dehydroepiandrosterone Sulfate; 68-96-2 / 17-alpha-Hydroxyprogesterone
  • [Number-of-references] 5
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61. Terzolo M, Bovio S, Reimondo G, Pia A, Osella G, Borretta G, Angeli A: Subclinical Cushing's syndrome in adrenal incidentalomas. Endocrinol Metab Clin North Am; 2005 Jun;34(2):423-39, x
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  • [Title] Subclinical Cushing's syndrome in adrenal incidentalomas.
  • This article reviews the available evidence on subclinical Cushing's syndrome in patients who have adrenal incidentalomas.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenal Cortex Neoplasms / diagnosis. Cushing Syndrome / diagnosis. Cushing Syndrome / etiology

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  • (PMID = 15850851.001).
  • [ISSN] 0889-8529
  • [Journal-full-title] Endocrinology and metabolism clinics of North America
  • [ISO-abbreviation] Endocrinol. Metab. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 87
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62. Müssig K, Wehrmann M, Horger M, Maser-Gluth C, Häring HU, Overkamp D: Adrenocortical carcinoma producing 11-deoxycorticosterone: a rare cause of mineralocorticoid hypertension. J Endocrinol Invest; 2005 Jan;28(1):61-5
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  • [Title] Adrenocortical carcinoma producing 11-deoxycorticosterone: a rare cause of mineralocorticoid hypertension.
  • Computed tomography (CT) scans showed a large right adrenal mass without signs of metastatic disease.
  • The tumor was removed by open laparotomy, and histology revealed an adrenocortical carcinoma.
  • Two yr after diagnosis, the patient is in good general condition and there is no sign of recurrence or metastatic disease, despite the large tumor size.
  • DOC producing adrenocortical carcinomas causing mineralocorticoid hypertension are very rare, so far only 10 cases have been described in the literature.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Desoxycorticosterone / biosynthesis. Hypertension / etiology. Hypertension / physiopathology. Mineralocorticoids / physiology. Pheochromocytoma / metabolism
  • [MeSH-minor] Adrenal Cortex Hormones / blood. Adrenal Cortex Hormones / urine. Adrenalectomy. Adult. Aldosterone / blood. Aldosterone / urine. Catecholamines / urine. Humans. Hypokalemia / etiology. Hypokalemia / physiopathology. Male. Renin / blood. Tomography, X-Ray Computed

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  • (PMID = 15816373.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Catecholamines; 0 / Mineralocorticoids; 40GP35YQ49 / Desoxycorticosterone; 4964P6T9RB / Aldosterone; EC 3.4.23.15 / Renin
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63. Johnsen IK, Kappler R, Auernhammer CJ, Beuschlein F: Bone morphogenetic proteins 2 and 5 are down-regulated in adrenocortical carcinoma and modulate adrenal cell proliferation and steroidogenesis. Cancer Res; 2009 Jul 15;69(14):5784-92
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  • [Title] Bone morphogenetic proteins 2 and 5 are down-regulated in adrenocortical carcinoma and modulate adrenal cell proliferation and steroidogenesis.
  • Bone morphogenetic proteins (BMP) have been shown to affect tumorigenesis in a variety of tumors.
  • Quantitative PCR analysis revealed down-regulation of BMP2 and BMP5 in tissue samples from adrenocortical carcinoma and adrenocortical tumor cell lines compared with normal adrenal glands.
  • Taken together, we show that loss of expression of members of the BMP family of ligands is a common finding in adrenocortical tumors and we provide evidence that BMP-dependent pathways are likely to be involved in the modulation of the malignant and functional phenotype of adrenocortical cancer cells.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Bone Morphogenetic Protein 2 / genetics. Bone Morphogenetic Protein 5 / genetics
  • [MeSH-minor] Aldosterone / metabolism. Blotting, Western. Bone Morphogenetic Protein Receptors / genetics. Bone Morphogenetic Protein Receptors / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Colforsin / pharmacology. Dose-Response Relationship, Drug. Down-Regulation / drug effects. GATA6 Transcription Factor / genetics. GATA6 Transcription Factor / metabolism. Humans. Hydrocortisone / metabolism. Insulin-Like Growth Factor I / genetics. Insulin-Like Growth Factor I / pharmacology. Phosphorylation / drug effects. Proto-Oncogene Proteins c-akt / metabolism. Recombinant Proteins / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Steroid 17-alpha-Hydroxylase / genetics. Steroid 17-alpha-Hydroxylase / metabolism. Time Factors. Tretinoin / pharmacology. Tumor Cells, Cultured

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  • (PMID = 19584291.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bone Morphogenetic Protein 2; 0 / Bone Morphogenetic Protein 5; 0 / GATA6 Transcription Factor; 0 / GATA6 protein, human; 0 / Recombinant Proteins; 1F7A44V6OU / Colforsin; 4964P6T9RB / Aldosterone; 5688UTC01R / Tretinoin; 67763-96-6 / Insulin-Like Growth Factor I; EC 1.14.99.9 / Steroid 17-alpha-Hydroxylase; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.30 / Bone Morphogenetic Protein Receptors; WI4X0X7BPJ / Hydrocortisone
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64. 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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65. Ribeiro RC, Pinto EM, Zambetti GP: Familial predisposition to adrenocortical tumors: clinical and biological features and management strategies. Best Pract Res Clin Endocrinol Metab; 2010 Jun;24(3):477-90
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  • [Title] Familial predisposition to adrenocortical tumors: clinical and biological features and management strategies.
  • The incidence of adrenocortical tumors (ACTs) is increased in several familial cancer syndromes resulting from abnormalities in genes that encode transcription factors implicated in cell proliferation, differentiation, senescence, apoptosis, and genomic instability.
  • Adenomas are the most common ACTs, but adrenocortical carcinomas occur rarely as well.
  • The clinical manifestations of ACTs, which result from increased secretion of adrenocortical hormones, are similar in the familial and sporadic forms of the disease.
  • The analysis of gene expression profiles of ACTs in these constitutional syndromes have contributed to our understanding of adrenal tumorigenesis and revealed new molecular diagnostic and prognostic markers and candidate genes for targeted therapies.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Li-Fraumeni Syndrome / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Genes, p53. Genetic Predisposition to Disease. Humans. Male

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  • [Copyright] Copyright 2010. Published by Elsevier Ltd.
  • (PMID = 20833338.001).
  • [ISSN] 1878-1594
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
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66. Karaosmanoglu AD, Gee MS: Sonographic findings of an adrenal leiomyosarcoma. J Ultrasound Med; 2010 Sep;29(9):1369-73
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  • [Title] Sonographic findings of an adrenal leiomyosarcoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / ultrasonography. Leiomyosarcoma / ultrasonography
  • [MeSH-minor] Biopsy. Diagnosis, Differential. Fatal Outcome. Humans. Male. Middle Aged. Splenomegaly / radiography. Splenomegaly / ultrasonography. Tomography, X-Ray Computed

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  • (PMID = 20733196.001).
  • [ISSN] 1550-9613
  • [Journal-full-title] Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine
  • [ISO-abbreviation] J Ultrasound Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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67. Springinsfeld G, Guillaume JC, Boeckler P, Tortel MC, Cribier B: [Two cases of subcutaneous panniculitis-like T-cell lymphoma (CD4- CD8+ CD56-)]. Ann Dermatol Venereol; 2009 Mar;136(3):264-8
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  • [Transliterated title] Lymphome T sous-cutané (CD4- CD8+ CD56-) à type de panniculite: deux cas.
  • BACKGROUND: Subcutaneous T-cell lymphoma is a rare disease and diagnosis is often difficult.
  • Lymphocyte immunophenotyping and genotyping led to a diagnosis of subcutaneous T-cell lymphoma of CD4- CD8+ CD56- phenotype.
  • Differential diagnosis with regard to lupus panniculitis can be difficult because of its slow progression.
  • [MeSH-major] Antigens, CD4 / analysis. Antigens, CD56 / genetics. Antigens, CD8 / analysis. Lymphoma, T-Cell / pathology. Panniculitis / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Aged. Antigens, CD / analysis. Antigens, CD / genetics. Diagnosis, Differential. Female. Humans. Middle Aged. Phenotype

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  • (PMID = 19328310.001).
  • [ISSN] 0151-9638
  • [Journal-full-title] Annales de dermatologie et de vénéréologie
  • [ISO-abbreviation] Ann Dermatol Venereol
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Antigens, CD; 0 / Antigens, CD4; 0 / Antigens, CD56; 0 / Antigens, CD8
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68. Gupta AA, Tyrrell P, Valani R, Benseler S, Abdelhaleem M, Weitzman S: Experience with hemophagocytic lymphohistiocytosis/macrophage activation syndrome at a single institution. J Pediatr Hematol Oncol; 2009 Feb;31(2):81-4
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  • BACKGROUND: Hemophagocytic lymphohistiocytosis/macrophage activation syndrome (HLH/MAS) is a serious and potentially life threatening histiocytic disorder in children and adults.
  • RESULTS: Thirty-eight patients had a median age of 9.1 years at diagnosis.
  • CONCLUSIONS: Patients with HLH are at high risk for death early in their disease course.
  • However, corticosteroids and/or IVIG may be sufficient as first-line therapy for patients with underlying rheumatologic disease who present with HLH/MAS.
  • Further prospective studies are required to more precisely define early risk factors for poor outcomes in this often fatal disease.
  • [MeSH-minor] Adolescent. Adrenal Cortex Hormones / therapeutic use. Cause of Death. Child. Child, Preschool. Cyclosporine / therapeutic use. Etoposide / therapeutic use. Female. Hematologic Neoplasms / complications. Humans. Immunoglobulins, Intravenous / therapeutic use. Infant. Male. Retrospective Studies. Rheumatic Diseases / complications. Steroids / therapeutic use. Virus Diseases / complications

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  • (PMID = 19194188.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Immunoglobulins, Intravenous; 0 / Steroids; 6PLQ3CP4P3 / Etoposide; 83HN0GTJ6D / Cyclosporine
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69. Vascik T: Case of the month. JAAPA; 2009 Dec;22(12):70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenocortical Adenoma / diagnosis
  • [MeSH-minor] Adrenalectomy. Adult. Diagnosis, Differential. Humans. Hypertension / etiology. Hypokalemia / etiology. Male

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  • (PMID = 24887476.001).
  • [ISSN] 1547-1896
  • [Journal-full-title] JAAPA : official journal of the American Academy of Physician Assistants
  • [ISO-abbreviation] JAAPA
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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70. Schön G: [Laparoscopic adrenalectomy]. Aktuelle Urol; 2010 Sep;41(5):329-38; quiz 339-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Adrenal Gland Neoplasms / surgery. Adrenalectomy / methods. Laparoscopy / methods. Neuroendocrine Tumors / surgery
  • [MeSH-minor] Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / surgery. Adrenocortical Adenoma / diagnosis. Adrenocortical Adenoma / surgery. Cushing Syndrome / diagnosis. Cushing Syndrome / surgery. Diagnosis, Differential. Diagnostic Imaging. Hormones / blood. Humans

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  • (PMID = 20824578.001).
  • [ISSN] 1438-8820
  • [Journal-full-title] Aktuelle Urologie
  • [ISO-abbreviation] Aktuelle Urol
  • [Language] ger
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Hormones
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71. Dluhy RG: Incidentaloma--role of the endocrinologist. Endocr Pract; 2008 Apr;14(3):267-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Adrenal Cortex Neoplasms / radiography. Adrenocortical Adenoma / radiography. Incidental Findings

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  • [CommentOn] Endocr Pract. 2008 Apr;14(3):279-84 [18463033.001]
  • [CommentOn] Endocr Pract. 2008 Apr;14(3):269-78 [18463032.001]
  • (PMID = 18463031.001).
  • [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] Comment; Editorial
  • [Publication-country] United States
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72. Vonend O, Rump LC: [Normokalemic primary hyperaldosteronism]. Dtsch Med Wochenschr; 2006 Nov;131(46 Spec No):H24-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-minor] Adenoma / complications. Adenoma / surgery. Adrenal Cortex Neoplasms / complications. Adrenal Cortex Neoplasms / surgery. Adrenalectomy. Diagnosis, Differential. Humans. Mass Screening. Prevalence

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  • (PMID = 17109245.001).
  • [ISSN] 1439-4413
  • [Journal-full-title] Deutsche medizinische Wochenschrift (1946)
  • [ISO-abbreviation] Dtsch. Med. Wochenschr.
  • [Language] ger
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Mineralocorticoid Receptor Antagonists; 4964P6T9RB / Aldosterone; EC 3.4.23.15 / Renin; RWP5GA015D / Potassium
  • [Number-of-references] 25
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73. Furtado SV, Venkatesh PK, Ghosal N, Hedge AS: Reduction in Size of a Large Rathke's Cleft Cyst on Treatment with Low Dose of Corticosteroid. Horm Metab Res; 2010 Apr;42(4):227-9
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  • [Title] Reduction in Size of a Large Rathke's Cleft Cyst on Treatment with Low Dose of Corticosteroid.
  • [MeSH-major] Adrenal Cortex Hormones / administration & dosage. Central Nervous System Cysts / drug therapy. Nervous System Neoplasms / drug therapy
  • [MeSH-minor] Adolescent. Humans. Male. Thyroid Hormones / metabolism. Tumor Burden / drug effects

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  • (PMID = 20013648.001).
  • [ISSN] 1439-4286
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Thyroid Hormones
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74. Katoulis AC, Liakou A, Bozi E, Theodorakis M, Alevizou A, Zafeiraki A, Mistidou M, Stavrianeas NG: Erythema multiforme following vaccination for human papillomavirus. Dermatology; 2010;220(1):60-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Clinico-histologically, a diagnosis of EM minor was made.
  • [MeSH-major] Erythema Multiforme / etiology. Papillomavirus Vaccines / adverse effects. Uterine Cervical Neoplasms / prevention & control. Vaccination / adverse effects
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Capsid / immunology. Female. Histamine Antagonists / therapeutic use. Human Papillomavirus Recombinant Vaccine Quadrivalent, Types 6, 11, 16, 18. Humans. Young Adult


75. Weng SW, Yang CH, Huang WT, Chen MC, Wang PW: Malignant hypertension secondary to cortisol-secreting adrenal tumour. N Z Med J; 2005 Jun 3;118(1216):U1498
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  • [Title] Malignant hypertension secondary to cortisol-secreting adrenal tumour.
  • Adrenal cortical tumour-induced malignant hypertension is rare, except for some documented aldosterone-producing adenomas.
  • This case in Taiwan is only the second reported case with malignant hypertension secondary to a cortisol-secreting adrenal tumour.
  • The immunohistochemical study of the excised tumour showed strong positive staining of interleukin (IL)-6.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenal Cortex Neoplasms / secretion. Adrenocortical Adenoma / complications. Adrenocortical Adenoma / secretion. Hydrocortisone / secretion. Hypertension, Malignant / etiology

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  • (PMID = 15937532.001).
  • [ISSN] 1175-8716
  • [Journal-full-title] The New Zealand medical journal
  • [ISO-abbreviation] N. Z. Med. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antihypertensive Agents; WI4X0X7BPJ / Hydrocortisone
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76. Trezzi R, Poli F, Fellegara G: "Dedifferentiated" adrenal cortical neoplasm. Int J Surg Pathol; 2009 Aug;17(4):343-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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77. Jaber JJ, Thomas FJ, Carfrae MJ, Galati LT: Radiotherapy-associated euthyroid Graves ophthalmopathy following floor-of-mouth surgery: a case report. Ear Nose Throat J; 2008 Sep;87(9):533-6
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  • The thyroid gland is commonly included in the radiation field during treatment of nonthyroidal neoplastic disease of the head and neck.
  • [MeSH-major] Carcinoma, Squamous Cell / radiotherapy. Graves Ophthalmopathy / etiology. Mouth Neoplasms / pathology. Mouth Neoplasms / radiotherapy. Radiation Injuries / diagnosis
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Follow-Up Studies. Humans. Male. Middle Aged. Mouth Floor / pathology. Mouth Floor / surgery. Oral Surgical Procedures / methods. Radiotherapy Dosage. Radiotherapy, Adjuvant. Risk Assessment. Thyroid Function Tests. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 18800329.001).
  • [ISSN] 1942-7522
  • [Journal-full-title] Ear, nose, & throat journal
  • [ISO-abbreviation] Ear Nose Throat J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
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78. Burke MJ, Cohn SL: Rituximab for treatment of opsoclonus-myoclonus syndrome in neuroblastoma. Pediatr Blood Cancer; 2008 Mar;50(3):679-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Adrenal Gland Neoplasms / complications. Antibodies, Monoclonal / therapeutic use. Ganglioneuroblastoma / complications. Immunotherapy. Opsoclonus-Myoclonus Syndrome / etiology
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Antibodies, Monoclonal, Murine-Derived. Child Behavior Disorders / etiology. Child, Preschool. Combined Modality Therapy. Diagnostic Errors. Humans. Immunoglobulins, Intravenous / therapeutic use. Immunosuppressive Agents / therapeutic use. Learning Disorders / etiology. Male. Psychomotor Disorders / etiology. Recurrence. Rituximab

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 16900484.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Immunoglobulins, Intravenous; 0 / Immunosuppressive Agents; 4F4X42SYQ6 / Rituximab
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79. Tadjine M, Lampron A, Ouadi L, Horvath A, Stratakis CA, Bourdeau I: Detection of somatic beta-catenin mutations in primary pigmented nodular adrenocortical disease (PPNAD). Clin Endocrinol (Oxf); 2008 Sep;69(3):367-73
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  • [Title] Detection of somatic beta-catenin mutations in primary pigmented nodular adrenocortical disease (PPNAD).
  • BACKGROUND: Primary pigmented nodular adrenocortical disease (PPNAD) leads to Cushing syndrome (CS) and is often associated with Carney complex (CNC).
  • Recent studies have demonstrated that beta-catenin mutations are frequent in adrenocortical adenomas and carcinomas and that the Wnt-signalling pathway is involved in PPNAD tumorigenesis.
  • We hypothesized that adrenocortical adenomas that form in the context of PPNAD may harbour beta-catenin mutations.
  • Tumor DNA was extracted from pigmented adrenocortical adenoma and nodular adrenal hyperplasia.
  • Sections from formalin-fixed, paraffin-embedded tumour samples were studied by immunohistochemistry with an antibody against beta-catenin.
  • Tumor DNA analysis revealed a heterozygous ACC-to-GCC missense mutation in codon 41 (T41A) and a TCT-to-CCT missense mutation in codon 45 (S45P) of exon 3 of the beta-catenin gene that was confirmed at the cDNA level.
  • CONCLUSIONS: We report, for the first time, beta-catenin mutations in adenomas associated with PPNAD, further implicating Wnt-beta-catenin signalling in tumorigenesis linked to bilateral adrenal hyperplasias.
  • [MeSH-major] Adrenal Cortex Diseases / genetics. beta Catenin / genetics
  • [MeSH-minor] Adenoma / complications. Adenoma / genetics. Adenoma / pathology. Adolescent. Adrenal Cortex Neoplasms / complications. Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / pathology. Adult. Child. Child, Preschool. Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / genetics. DNA Mutational Analysis. Female. Genetic Testing. Humans. Male. Middle Aged. Mutation. Phosphoric Diester Hydrolases / genetics. Pigmentation Disorders / complications. Pigmentation Disorders / genetics. Young Adult

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  • (PMID = 18419788.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / ZIA HD000642-13
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human; 0 / beta Catenin; EC 3.1.4.- / Phosphoric Diester Hydrolases; EC 3.1.4.35 / PDE11A protein, human
  • [Other-IDs] NLM/ NIHMS307371; NLM/ PMC3138207
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80. Kumara TL, Kollure SK: A case of peritoneal encapsulation syndrome. Ceylon Med J; 2009 Mar;54(1):17-8
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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 / complications. Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / surgery. Adult. Female. Humans. Incidental Findings. Intestinal Obstruction / diagnosis. Intestinal Obstruction / etiology. Syndrome

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  • (PMID = 19391451.001).
  • [ISSN] 0009-0875
  • [Journal-full-title] The Ceylon medical journal
  • [ISO-abbreviation] Ceylon Med J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Sri Lanka
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81. Maynard JW, Christopher-Stine L, Gelber AC: Testicular pain followed by microscopic hematuria, a renal mass, palpable purpura, polyarthritis, and hematochezia. J Clin Rheumatol; 2010 Dec;16(8):388-91
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  • We present the instructive case of a man who developed progressively severe testicular pain.
  • What began with focal testicular pain evolved over the ensuing weeks to a multisystem disorder affecting at least 3 additional organ systems beyond the genitourinary tract.
  • This case illustrates and reinforces both the importance of considering an occult malignancy in a patient who presents with symptoms suggestive of a systemic vasculitis as well as the importance of considering an occult vasculitis in the adult male patient presenting with testicular pain.
  • [MeSH-major] Arthritis / etiology. Gastrointestinal Hemorrhage / etiology. Hematuria / etiology. Kidney Neoplasms / complications. Pain / etiology. Purpura, Schoenlein-Henoch / complications. Testicular Diseases / etiology
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Adult. Carcinoma, Renal Cell / complications. Carcinoma, Renal Cell / diagnosis. Carcinoma, Renal Cell / surgery. Humans. Male. Prednisone / therapeutic use. Treatment Outcome


82. Melstrom LG, Melstrom KA Jr, Ding XZ, Adrian TE: Mechanisms of skeletal muscle degradation and its therapy in cancer cachexia. Histol Histopathol; 2007 07;22(7):805-14
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  • Severe or chronic disease can lead to cachexia which involves weight loss and muscle wasting.
  • Cancer cachexia contributes significantly to disease morbidity and mortality.
  • The Ub-proteasome pathway seems to account for the majority of skeletal muscle degradation in cancer cachexia and is stimulated by several cytokines including tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, interferon-gamma and proteolysis-inducing factor.
  • [MeSH-major] Adrenal Cortex Hormones / therapeutic use. Appetite Stimulants / therapeutic use. Cachexia / drug therapy. Cachexia / metabolism. Muscle Proteins / metabolism. Muscle, Skeletal / drug effects. Pancreatic Neoplasms / complications

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  • (PMID = 17455154.001).
  • [ISSN] 1699-5848
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Appetite Stimulants; 0 / Cytokines; 0 / Muscle Proteins; 0 / Ubiquitin; EC 3.4.- / Peptide Hydrolases; EC 3.4.25.1 / Proteasome Endopeptidase Complex; TJ2M0FR8ES / Megestrol Acetate
  • [Number-of-references] 96
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83. Gomez-Rivera F, Medina-Franco H, Arch-Ferrer JE, Heslin MJ: Adrenocortical carcinoma: a single institution experience. Am Surg; 2005 Jan;71(1):90-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenocortical carcinoma: a single institution experience.
  • Adrenocortical carcinoma (ADCC) ranks among the least common malignant endocrine tumors.
  • Surgical resection is considered the most important treatment for this neoplasm.
  • Medical records of patients with the diagnosis of ADCC between 1990 and 2000 were reviewed.
  • Twelve per cent presented as an asymptomatic mass, 41 per cent as a functional tumor, and 47 per cent as a nonfunctioning tumor.
  • Older age, distant metastasis, nonoperative management, positive margins, advanced tumor stage, and venous invasion were significantly associated with worse overall actuarial survival.
  • Factors associated with a worse prognosis were stage of disease, nonoperative management, positive surgical margins, vascular invasion, and older age.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenocortical Carcinoma / surgery
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Angiography. Female. Follow-Up Studies. Humans. Liver Neoplasms / radiography. Liver Neoplasms / secondary. Lung Neoplasms / radiography. Lung Neoplasms / secondary. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Recurrence, Local. Neoplasm Staging. Prognosis. Retrospective Studies. Survival Rate. Tomography, X-Ray Computed

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  • (PMID = 15757066.001).
  • [ISSN] 0003-1348
  • [Journal-full-title] The American surgeon
  • [ISO-abbreviation] Am Surg
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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84. Nishikawa T, Saito J, Omura M: Adrenal venous sampling is absolutely requisite for definitively diagnosing primary aldosteronism as well as for detecting laterality of the adrenal lesion. Hypertens Res; 2007 Nov;30(11):1009-10
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  • [Title] Adrenal venous sampling is absolutely requisite for definitively diagnosing primary aldosteronism as well as for detecting laterality of the adrenal lesion.
  • [MeSH-major] Adenoma / diagnosis. Adrenal Cortex Neoplasms / diagnosis. Aldosterone / blood. Blood Specimen Collection / methods. Hydrocortisone / blood. Hyperaldosteronism / diagnosis
  • [MeSH-minor] Adrenal Glands / blood supply. Adrenocorticotropic Hormone. Humans

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  • [CommentOn] Hypertens Res. 2007 Nov;30(11):1083-95 [18250558.001]
  • (PMID = 18250546.001).
  • [ISSN] 0916-9636
  • [Journal-full-title] Hypertension research : official journal of the Japanese Society of Hypertension
  • [ISO-abbreviation] Hypertens. Res.
  • [Language] eng
  • [Publication-type] Comment; Editorial
  • [Publication-country] Japan
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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85. Hwang WR, Ma WY, Tso AL, Pan CC, Chang YH, Lin HD: Pheochromocytoma and adrenocortical adenoma in the same gland. J Chin Med Assoc; 2007 Jul;70(7):289-93
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  • [Title] Pheochromocytoma and adrenocortical adenoma in the same gland.
  • A right adrenal tumor was found incidentally during abdominal computed tomography exam in a 51-year-old female patient, who had had diabetes and hypertension for more than 10 years.
  • Therefore, adrenal cortical adenoma with subclinical Cushing's syndrome was highly suspected; however, further imaging studies, including magnetic resonance image and 131I-6beta-iodomethylnorcholesterol adrenal scintigraphy failed to discriminate an additional tumor.
  • After right adrenalectomy, a small adrenal cortical adenoma and a large pheochromocytoma were noted.
  • This is an extremely rare case of an adrenal incidentaloma consisting of both medullary and cortical tumors in the same gland.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenal Gland Neoplasms / diagnosis. Adrenocortical Adenoma / diagnosis. Neoplasms, Multiple Primary / diagnosis. Pheochromocytoma / diagnosis

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  • (PMID = 17631466.001).
  • [ISSN] 1726-4901
  • [Journal-full-title] Journal of the Chinese Medical Association : JCMA
  • [ISO-abbreviation] J Chin Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China (Republic : 1949- )
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
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86. Volante M, Bollito E, Sperone P, Tavaglione V, Daffara F, Porpiglia F, Terzolo M, Berruti A, Papotti M: Clinicopathological study of a series of 92 adrenocortical carcinomas: from a proposal of simplified diagnostic algorithm to prognostic stratification. Histopathology; 2009 Nov;55(5):535-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinicopathological study of a series of 92 adrenocortical carcinomas: from a proposal of simplified diagnostic algorithm to prognostic stratification.
  • AIMS: Pathological diagnosis of adrenocortical carcinoma relies on several microscopic features commonly used in combination in different scoring systems that are sometimes subjective and/or time consuming.
  • The aim was to investigate the impact of individual pathological parameters in the diagnosis and prognosis of adrenocortical carcinoma.
  • The presence of disruption of the reticular network, as highlighted by histochemical staining, was present in all adrenocortical carcinomas and the inclusion of at least one of the three following additional parameters - mitotic index >5/50 high-power fields (HPF), presence of necrosis and presence of vascular invasion - gave an algorithm with 100% sensitivity and specificity to recognize malignant tumours according to the Weiss system, with easier and more practical applicability.
  • Moreover, on multivariate analysis, stage III/IV and mitotic count >9/50 HPF showed a strong adverse impact on disease-free and overall survival, leading to the identification of three risk groups affected by a significantly different prognosis.
  • CONCLUSIONS: We have defined an easy-to-perform and highly specific and sensitive algorithm for the diagnosis and prognostic categorization of adrenocortical tumours.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Algorithms
  • [MeSH-minor] Adenoma / pathology. Diagnosis, Differential. Disease-Free Survival. Humans. Prognosis. Proportional Hazards Models. Sensitivity and Specificity

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  • (PMID = 19912359.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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87. Arvieux C, Laval G, Mestrallet JP, Stefani L, Villard ML, Cardin N: [Treatment of malignant intestinal obstruction. A prospective study over 80 cases]. Ann Chir; 2005 Sep;130(8):470-6
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  • [Transliterated title] Traitement de l'occlusion intestinale sur carcinose péritonéale. Etude prospective à propos de 80 cas.
  • AIM: Of the work: evaluation of a multidisciplinary strategy and a prospective medicosurgical protocol for the treatment of occlusion due to unresectable peritoneal carcinomatosis.
  • [MeSH-major] Carcinoma / complications. Intestinal Obstruction / etiology. Intestinal Obstruction / surgery. Palliative Care. Peritoneal Neoplasms / complications
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Adult. Aged. Aged, 80 and over. Analgesics / therapeutic use. Antiemetics / therapeutic use. Female. Humans. Male. Middle Aged. Patient Care Team. Prospective Studies. Survival Analysis. Terminal Care. Treatment Outcome

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  • (PMID = 16084483.001).
  • [ISSN] 0003-3944
  • [Journal-full-title] Annales de chirurgie
  • [ISO-abbreviation] Ann Chir
  • [Language] fre
  • [Publication-type] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Analgesics; 0 / Antiemetics
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88. Lulsegged A: Lesson of the month. Clin Med (Lond); 2008 Feb;8(1):115
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenocortical Adenoma / diagnosis. Hyperaldosteronism / diagnosis

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  • [CommentOn] Clin Med (Lond). 2007 Oct;7(5):530-1 [17990731.001]
  • (PMID = 18335687.001).
  • [ISSN] 1470-2118
  • [Journal-full-title] Clinical medicine (London, England)
  • [ISO-abbreviation] Clin Med (Lond)
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.4.23.15 / Renin
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89. Lombardi CP, Raffaelli M, Pani G, Maffione A, Princi P, Traini E, Galeotti T, Rossi ED, Fadda G, Bellantone R: Gene expression profiling of adrenal cortical tumors by cDNA macroarray analysis. Results of a preliminary study. Biomed Pharmacother; 2006 May;60(4):186-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression profiling of adrenal cortical tumors by cDNA macroarray analysis. Results of a preliminary study.
  • Adrenocortical carcinoma (ACC) are highly malignant tumors with poor prognosis.
  • To verify if it is possible to assess their differential gene expression by a cDNA macroarray analysis using RNA extracted from paraffin sections, we analyzed two different cohorts of adrenal cortical adenoma (ACA) and ACC.
  • Heat shock protein 60 (HSP-60) (ratio>2), Ciclin D1 and topoisomerase I (ratio>1.5) were overexpressed in the ACC cohort, while jun proto-oncogene was down-regulated. cDNA macroarray analysis from paraffin sections of adrenal tumors is feasible, despite with a low success rate.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Gene Expression Profiling. Gene Expression Regulation, Neoplastic / genetics. Oligonucleotide Array Sequence Analysis
  • [MeSH-minor] Down-Regulation. Humans. Neoplasm Proteins / genetics. Up-Regulation


90. Nagata S, Ueda N, Yoshida Y, Matsuda H, Maehara Y: Severe interstitial pneumonitis associated with the administration of taxanes. J Infect Chemother; 2010 Oct;16(5):340-4
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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. Aged. Breast Neoplasms / drug therapy. Female. Humans. Male. Middle Aged. Stomach Neoplasms / drug therapy. Tomography, X-Ray Computed

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  • (PMID = 20354889.001).
  • [ISSN] 1437-7780
  • [Journal-full-title] Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy
  • [ISO-abbreviation] J. Infect. Chemother.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Taxoids; 15H5577CQD / docetaxel; P88XT4IS4D / Paclitaxel
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91. Puech-Bret N, Bret J, Bennet A, Huyghe E, Mazerolles C, Zabraniecki L, Fournie B: Maffucci syndrome and adrenal cortex tumor. Joint Bone Spine; 2009 Oct;76(5):556-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Maffucci syndrome and adrenal cortex tumor.
  • We report the second known case of Maffucci syndrome associated with an adrenal cortex tumor.
  • Endocrine tumors have been reported in patients with multiple enchondromas, although the underlying mechanism of this combination is unknown.
  • Therefore, routine evaluation for involvement of the adrenal cortex may be warranted to improve our knowledge of this syndrome and of its pathophysiology.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Enchondromatosis / complications
  • [MeSH-minor] Abdomen / pathology. Adrenocorticotropic Hormone / blood. Adult. Amputation. Bone Neoplasms / pathology. Bone Neoplasms / radiography. Female. Femoral Neoplasms / pathology. Femoral Neoplasms / radiography. Fingers / surgery. Hemangioma / complications. Hemangioma / pathology. Humans. Hydrocortisone / blood. Leg / pathology. Magnetic Resonance Imaging. Sarcoma / pathology. Sarcoma / surgery. Uterine Neoplasms / pathology

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  • (PMID = 19782627.001).
  • [ISSN] 1778-7254
  • [Journal-full-title] Joint, bone, spine : revue du rhumatisme
  • [ISO-abbreviation] Joint Bone Spine
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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92. Sun H, Nemecek AN: Optimal management of malignant epidural spinal cord compression. Emerg Med Clin North Am; 2009 May;27(2):195-208
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • MESCC is a medical emergency that needs rapid diagnosis and treatment to prevent paraplegia.
  • If indicated, patients should undergo maximal tumor resection and stabilization, followed by postoperative radiotherapy.
  • [MeSH-major] Emergency Service, Hospital. Spinal Cord Compression / therapy. Spinal Neoplasms / complications
  • [MeSH-minor] Adrenal Cortex Hormones / administration & dosage. Combined Modality Therapy. Continuity of Patient Care. Humans. Infusions, Intravenous. Radiosurgery. Referral and Consultation. Spinal Fusion

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  • [ReprintIn] Hematol Oncol Clin North Am. 2010 Jun;24(3):537-51 [20488352.001]
  • (PMID = 19447306.001).
  • [ISSN] 1558-0539
  • [Journal-full-title] Emergency medicine clinics of North America
  • [ISO-abbreviation] Emerg. Med. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
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93. Bilimoria KY, Shen WT, Elaraj D, Bentrem DJ, Winchester DJ, Kebebew E, Sturgeon C: Adrenocortical carcinoma in the United States: treatment utilization and prognostic factors. Cancer; 2008 Dec 1;113(11):3130-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenocortical carcinoma in the United States: treatment utilization and prognostic factors.
  • BACKGROUND: Adrenocortical carcinoma (ACC) is a rare tumor with a relatively poor prognosis.
  • Patient, tumor, treatment, and hospital factors associated with survival after resection were examined.
  • Median age at diagnosis was 55 years.
  • Median tumor size was 13 cm.
  • Multivariable analysis demonstrated a higher risk of death with increasing age, poorly differentiated tumors, involved margins, and nodal or distant metastases.
  • CONCLUSIONS: ACC carries a poor prognosis for patients commonly presenting with large, locally invasive tumors, involved margins, and metastatic disease.
  • Survival is not affected by size but is diminished with increasing age, poorly differentiated tumors, involved margins, and the presence of regional and distant disease.
  • [MeSH-major] Adrenal Cortex Neoplasms / therapy. Adrenocortical Carcinoma / therapy
  • [MeSH-minor] Adult. Aged. Disease-Free Survival. Female. Humans. Male. Middle Aged. Prognosis. Registries. Survival Analysis. Treatment Outcome. United States

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  • [Copyright] (c) 2008 American Cancer Society
  • (PMID = 18973179.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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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. Ragazzon B, Cazabat L, Rizk-Rabin M, Assie G, Groussin L, Fierrard H, Perlemoine K, Martinez A, Bertherat J: Inactivation of the Carney complex gene 1 (protein kinase A regulatory subunit 1A) inhibits SMAD3 expression and TGF beta-stimulated apoptosis in adrenocortical cells. Cancer Res; 2009 Sep 15;69(18):7278-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inactivation of the Carney complex gene 1 (protein kinase A regulatory subunit 1A) inhibits SMAD3 expression and TGF beta-stimulated apoptosis in adrenocortical cells.
  • The cyclic AMP signaling pathway can be altered at multiple levels in endocrine tumors.
  • Carney complex (CNC) is a hereditary multiple neoplasia syndrome resulting from inactivating mutations of the gene encoding the PKA type I alpha regulatory subunit (PRKAR1A).
  • Primary pigmented nodular adrenocortical disease is the most frequent endocrine tumor of CNC.
  • Transforming growth factor beta (TGFbeta) regulates adrenal cortex physiology and signals through SMAD2/3.
  • We used an interference approach to test the effects of PRKAR1A inactivation on PKA and TGFbeta pathways and on apoptosis in adrenocortical cells.
  • PRKAR1A silencing stimulates PKA activity and increases transcriptional activity of a PKA reporter construct and expression of the endogenous PKA target, NR4A2, under basal conditions or after forskolin stimulation.
  • SMAD3 expression was also inhibited by adrenocorticorticotropic hormone in the mouse adrenal gland and by forskolin in H295R cells.
  • Inactivating mutations of PRKAR1A observed in adrenocortical tumors alter SMAD3, leading to resistance to TGFbeta-induced apoptosis.
  • [MeSH-major] Adrenal Cortex Neoplasms / enzymology. Adrenocortical Carcinoma / enzymology. Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / genetics. Smad3 Protein / biosynthesis. Transforming Growth Factor beta / metabolism
  • [MeSH-minor] Animals. Apoptosis / genetics. Cell Line, Tumor. Colforsin / pharmacology. Cyclic AMP-Dependent Protein Kinases / genetics. Cyclic AMP-Dependent Protein Kinases / metabolism. Gene Silencing. Humans. Male. Mice. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. RNA, Small Interfering / genetics. Transcription, Genetic. Transfection

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  • (PMID = 19738044.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / SMAD3 protein, human; 0 / Smad3 Protein; 0 / Transforming Growth Factor beta; 1F7A44V6OU / Colforsin; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
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96. Miquel M, Soler A, Vaqué A, Ojanguren I, Costa J, Planas R: Suspected cross-hepatotoxicity of flutamide and cyproterone acetate. Liver Int; 2007 Oct;27(8):1144-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The occurrence of hepatotoxicity associated with flutamide and CPA on separated occasions suggests the possibility of a common mechanism of injury.
  • A closer monitoring of liver enzymes might be necessary in such cases, as an increased risk of a new severe hepatotoxicity event cannot be ruled out.
  • [MeSH-major] Adenocarcinoma / drug therapy. Androgen Antagonists / adverse effects. Antineoplastic Agents, Hormonal / adverse effects. Cyproterone Acetate / adverse effects. Drug-Induced Liver Injury / etiology. Flutamide / adverse effects. Liver / drug effects. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Acute Disease. Adrenal Cortex Hormones / pharmacology. Adrenal Cortex Hormones / therapeutic use. Aged. Drug Monitoring / methods. Humans. Liver Function Tests. Male. Severity of Illness Index. Treatment Outcome

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  • (PMID = 17845544.001).
  • [ISSN] 1478-3223
  • [Journal-full-title] Liver international : official journal of the International Association for the Study of the Liver
  • [ISO-abbreviation] Liver Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 4KM2BN5JHF / Cyproterone Acetate; 76W6J0943E / Flutamide
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97. Werner JA, Eivazi B, Folz BJ, Dünne AA: [State of the art of classification, diagnostics and therapy for cervicofacial hemangiomas and vascular malformations]. Laryngorhinootologie; 2006 Dec;85(12):883-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Arteriovenous Malformations. Face / blood supply. Facial Neoplasms. Head and Neck Neoplasms. Hemangioma. Neck / blood supply
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Adult. Age Factors. Child. Child, Preschool. Cryotherapy. Diagnosis, Differential. Female. Humans. Infant. Infant, Newborn. Laser Therapy. Lymphangioma / diagnosis. Lymphangioma / therapy. Male. Middle Aged


98. Vuorenoja S, Rivero-Müller A, Ziecik AJ, Huhtaniemi I, Toppari J, Rahman NA: Targeted therapy for adrenocortical tumors in transgenic mice through their LH receptor by Hecate-human chorionic gonadotropin beta conjugate. Endocr Relat Cancer; 2008 Jun;15(2):635-48
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeted therapy for adrenocortical tumors in transgenic mice through their LH receptor by Hecate-human chorionic gonadotropin beta conjugate.
  • Novel strategies are needed for the treatment of adrenocortical tumors that are usually resistant to chemotherapy.
  • To prove the principle that Hecate-CGbeta conjugate may eradicate tumors ectopically expressing plasma membrane receptors, transgenic (TG) inhibin alpha-subunit promoter (inhalpha)/Simian Virus 40 T-antigen mice, expressing LHR in their adrenal gland tumors, were used as the experimental model.
  • Wild-type control littermates and TG mice with adrenal tumors were treated with either Hecate or Hecate-CGbeta conjugate at the age of 6.5 months for 3 weeks and killed 7 days after the last treatment.
  • The Hecate-CGbeta conjugate reduced the adrenal tumor burden significantly in TG male but not in female mice, in comparison with Hecate-treated mice.
  • Hecate-CGbeta conjugate treatment did not affect normal adrenocortical function as the serum corticosterone level between Hecate and Hecate-CGbeta conjugate groups were similar.
  • The mRNA and protein expressions of GATA-4 and LHR colocalized only in tumor area, and a significant downregulation of gene expression was found after the Hecate-CGbeta conjugate in comparison with Hecate- and/or non-treated adrenal tumors by western blotting.
  • This finding provides evidence for a selective destruction of the tumor cells by the Hecate-CGbeta conjugate.
  • Hereby, our findings support the principle that Hecate-CGbeta conjugate is able to specifically destroy tumor cells that ectopically express LHR.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Adrenocortical Adenoma / drug therapy. Antineoplastic Agents / pharmacology. Melitten / analogs & derivatives. Receptors, LH / genetics
  • [MeSH-minor] Animals. Chorionic Gonadotropin, beta Subunit, Human / pharmacology. Disease Models, Animal. Female. GATA4 Transcription Factor / genetics. GATA4 Transcription Factor / metabolism. Gene Expression Regulation, Neoplastic. Luteinizing Hormone / blood. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. RNA, Messenger / metabolism

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  • (PMID = 18509010.001).
  • [ISSN] 1351-0088
  • [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 / Antineoplastic Agents; 0 / Chorionic Gonadotropin, beta Subunit, Human; 0 / GATA4 Transcription Factor; 0 / RNA, Messenger; 0 / Receptors, LH; 0 / hecate-chorionic gonadotropin beta-subunit conjugate; 20449-79-0 / Melitten; 9002-67-9 / Luteinizing Hormone
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99. Lee JE: Adjuvant mitotane in adrenocortical carcinoma. N Engl J Med; 2007 Sep 20;357(12):1258; author reply 1259
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adjuvant mitotane in adrenocortical carcinoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Adrenocortical Carcinoma / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Mitotane / therapeutic use
  • [MeSH-minor] Chemotherapy, Adjuvant. Follow-Up Studies. Humans. Neoplasm Staging

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  • [CommentOn] N Engl J Med. 2007 Jun 7;356(23):2372-80 [17554118.001]
  • (PMID = 17891836.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 78E4J5IB5J / Mitotane
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100. Wagnerova H, Lazúrová I, Habalová V, Dudásová D, Vrzgula A: The prevalence of 21-hydroxylase deficiency in adrenal incidentalomas - hormonal and mutation screening. Exp Clin Endocrinol Diabetes; 2008 May;116(5):272-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The prevalence of 21-hydroxylase deficiency in adrenal incidentalomas - hormonal and mutation screening.
  • The aim of the present study was to evaluate and compare the response of 17 OHP to ACTH stimulation in patients with various types of adrenal incidentalomas and to examine the occurence of germline CYP21 mutation in these patients.
  • 21 of them had unilateral adrenal adenoma, 13 patients had adrenal hyperplasia (six of them unilateral) and 6 patients had CT characteristics of other tumors (myelolipomas, cysts, adrenocortical carcinoma).
  • Stimulated plasma values of DHEA and 17OHP after ACTH administration were significantly higher in patients with adenomas (p < 0.05 and p < 0.01) and with hyperplasia (p < 0.05 and p < 0.05) compared with those with other tumors.
  • SUMMARY: Although 12 % of patients with adrenal incidentalomas had an exaggerated response of 17 OHP after ACTH administration indicating a possible 21-hydroxylase deficiency, these findings are not associated with CYP21 mutation estimated in peripheral blood samples.
  • There was found no germline CYP21 mutation in all patients with various adrenal incidentalomas.
  • [MeSH-major] Adenoma / epidemiology. Adrenal Gland Neoplasms / epidemiology. Adrenal Hyperplasia, Congenital / genetics. Hormones / secretion. Incidental Findings. Steroid 21-Hydroxylase / genetics
  • [MeSH-minor] 17-alpha-Hydroxyprogesterone / blood. Adrenal Cortex Function Tests. Adrenocorticotropic Hormone. Adult. Aged. DNA Mutational Analysis. Female. Germ-Line Mutation. Humans. Hyperplasia / blood. Hyperplasia / epidemiology. Hyperplasia / genetics. Male. Middle Aged. Prevalence

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  • (PMID = 18589890.001).
  • [ISSN] 0947-7349
  • [Journal-full-title] Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
  • [ISO-abbreviation] Exp. Clin. Endocrinol. Diabetes
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Hormones; 68-96-2 / 17-alpha-Hydroxyprogesterone; 9002-60-2 / Adrenocorticotropic Hormone; EC 1.14.99.10 / Steroid 21-Hydroxylase
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