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1. Mazzuco TL, Chabre O, Feige JJ, Thomas M: Aberrant GPCR expression is a sufficient genetic event to trigger adrenocortical tumorigenesis. Mol Cell Endocrinol; 2007 Feb;265-266:23-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant GPCR expression is a sufficient genetic event to trigger adrenocortical tumorigenesis.
  • Aberrant expression of G protein-coupled receptors (GPCR) in the adrenal cortex is observed in some cases of ACTH-independent macronodular adrenal hyperplasias and adenomas associated with Cushing syndrome (CS).
  • Although there is clinical evidence for the implication of these receptors in abnormal regulation of cortisol secretion, whether this aberrant expression also directly causes the development of a benign adrenocortical tumor is an open question.
  • Cell transplantation provides a way to study genes that may be important in human tumor development.
  • The system we developed uses genetically modified adrenocortical cells transplanted into adrenalectomized immunodeficient mice, which form a functional tissue structure.
  • We observed that enforcing expression of the gastric inhibitory polypeptide (GIP) receptor or the luteinizing hormone (LH) receptor genes (taken as canonical examples of aberrantly expressed GPCRs) in adrenocortical cells resulted in the formation of hyperplastic tissues and the development of Cushing syndrome features in transplanted mice.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Receptors, G-Protein-Coupled / genetics
  • [MeSH-minor] Adrenal Cortex / cytology. Adrenal Cortex / metabolism. Animals. Cell Transplantation. Cushing Syndrome / genetics. Humans

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  • (PMID = 17250952.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Receptors, G-Protein-Coupled
  • [Number-of-references] 35
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2. Dichtchekenian V, de Bragança Pereira CA, Kuperman H, Della Manna T, Damiani D, Ferreira Alves VA, Filho AL, Setian N: Adrenocortical carcinoma: prognostic indices based on clinical and immunohistochemical markers. J Pediatr Endocrinol Metab; 2005 Apr;18(4):347-53
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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: prognostic indices based on clinical and immunohistochemical markers.
  • Adrenocortical carcinoma is a rare condition with an unpredictable prognosis as a rule.
  • Y = 1 when chronological age (CA) >33 mo, Y = 0 when CA < or =33 mo; L = 1 for right sided tumor and L = 0 for left sided tumor; H = 1 in presence of hypertension and H = 0 for normal blood pressure; T = length of disease in months; W = weight of tumor (g); O = 1 in the absence of p53 protein and O = 0 in the presence of p53.
  • The chance of bad prognosis was observed when age is >33 mo, tumor is on the right side, systemic hypertension is present, tumor weight >250 g, in the absence of p53, J1, J2, J3 >0.4 (p <0.001) and J4 >0.5 (p <0.01).
  • [MeSH-major] Adrenal Cortex Neoplasms / physiopathology. Adrenocortical Carcinoma / physiopathology. Biomarkers, Tumor / metabolism. Models, Biological

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  • (PMID = 15844468.001).
  • [ISSN] 0334-018X
  • [Journal-full-title] Journal of pediatric endocrinology & metabolism : JPEM
  • [ISO-abbreviation] J. Pediatr. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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3. Evang JA, Carlsen SM, Svartberg J, Aanderud S, Johannesen Ø, Schreiner T, Ramm-Pettersen J, Bakke SJ, Lund-Johansen M, Bollerslev J: [Endogenous Cushing's syndrome]. Tidsskr Nor Laegeforen; 2006 Feb 23;126(5):599-602
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The reason can be overproduction of ACTH or an adrenocortical pathology.
  • Diagnosis of Cushing's syndrome is often challenging.
  • The final diagnosis is often made after a combined evaluation of dynamic tests.
  • [MeSH-major] Cushing Syndrome / diagnosis
  • [MeSH-minor] Adrenocorticotropic Hormone / blood. Biomarkers, Tumor / blood. Chromogranin A. Chromogranins / blood. Circadian Rhythm. Diagnosis, Differential. Humans. Hydrocortisone / analysis. Pituitary Gland / pathology. Saliva / chemistry

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  • (PMID = 16505869.001).
  • [ISSN] 0807-7096
  • [Journal-full-title] Tidsskrift for den Norske lægeforening : tidsskrift for praktisk medicin, ny række
  • [ISO-abbreviation] Tidsskr. Nor. Laegeforen.
  • [Language] nor
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Chromogranin A; 0 / Chromogranins; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
  • [Number-of-references] 42
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4. Fallo F, Pezzi V, Sonino N, Altavilla G, Barzon L: Adrenal incidentaloma in pregnancy: clinical, molecular and immunohistochemical findings. J Endocrinol Invest; 2005 May;28(5):459-63
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  • [Title] Adrenal incidentaloma in pregnancy: clinical, molecular and immunohistochemical findings.
  • Adrenal incidentalomas detected during pregnancy are very rare, and the natural history of these tumors during gestation is unknown.
  • We report a case of a pregnant woman with an adrenal mass discovered serendipitously, who was followed-up during gestation and underwent adrenalectomy shortly after delivery.
  • Estrogens may indeed influence the function and proliferation of human adrenal cells, and a state of circulating estrogen excess can represent an in vivo model to test their effect on the adrenals.
  • No evidence of adrenal change in morphology and function was found in our patient throughout pregnancy, as shown by adrenal ultrasound imaging and adrenal hormone measurements.
  • Four months after delivery, the patient underwent laparoscopic right adrenalectomy, and pathologic analysis revealed a 2.7 cm benign adrenocortical adenoma.
  • The diameter of the adrenal mass at ultrasonography correlated highly with post-partum mass diameter measured by abdominal computed tomography (CT).
  • Quantitative expression of both ERalpha and ERbeta by real-time RT-PCR analysis and Western blotting findings did not differ among adenoma, normal adjacent adrenal and normal adrenal control tissues.
  • This case of an adrenal incidentaloma discovered during pregnancy shows that a close observation with endocrine investigations and ultrasonography could be an appropriate approach, delaying the decision of surgical intervention after delivery.
  • Estrogen receptor mRNA levels in the adrenal mass similar to those observed in normal adrenals suggest that estrogen oversecretion during pregnancy was not a risk factor for tumor progression.
  • [MeSH-major] Adrenal Gland Neoplasms / immunology. Adrenal Gland Neoplasms / pathology. Pregnancy Complications, Neoplastic / immunology. Pregnancy Complications, Neoplastic / pathology

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  • (PMID = 16075931.001).
  • [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 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta
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5. Singh R, Basturk O, Klimstra DS, Zamboni G, Chetty R, Hussain S, La Rosa S, Yilmaz A, Capelli P, Capella C, Cheng JD, Adsay NV: Lipid-rich variant of pancreatic endocrine neoplasms. Am J Surg Pathol; 2006 Feb;30(2):194-200
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  • [Title] Lipid-rich variant of pancreatic endocrine neoplasms.
  • Most pancreatic endocrine neoplasms (PENs) show characteristic and well-recognized endocrine morphology; however, a lipid-rich pattern, which can present a diagnostic problem in biopsies, has been reported, mostly as individual cases.
  • Pathology reports indicated substantial diagnostic challenge in these cases; on biopsies, 1 case was originally diagnosed as adrenal cortical carcinoma, another as renal cell carcinoma, a third as solid-pseudopapillary tumor, and a fourth had a fine needle aspiration cytologic diagnosis of adenocarcinoma.
  • Immunohistochemically, markers implicated in VHL-associated neoplasia, including HIF-1alpha, inhibin, and Melan-A (in clear-cell PENs) and MUC6 (in serous cystadenomas) were mostly negative in lipid-rich PENs (1 of 10, 1 of 10, 0 of 10 and 0 of 10, respectively).
  • In conclusion, the lipid-rich pattern, reminiscent of adrenal cortical cells, represents a distinct subset of PENs.
  • The findings suggest that the pathogenesis of lipid-rich tumors may be different from the VHL-associated clear-cell variants of PENs.
  • [MeSH-major] Endocrine Gland Neoplasms / pathology. Lipids. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Adrenocortical Carcinoma / pathology. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Carcinoma, Renal Cell / pathology. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Male. Microscopy, Electron, Transmission. Middle Aged. Multiple Endocrine Neoplasia Type 1 / pathology. von Hippel-Lindau Disease / complications

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  • (PMID = 16434893.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Lipids
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6. Zhang X, Yu RM, Jones PD, Lam GK, Newsted JL, Gracia T, Hecker M, Hilscherova K, Sanderson T, Wu RS, Giesy JP: Quantitative RT-PCR methods for evaluating toxicant-induced effects on steroidogenesis using the H295R cell line. Environ Sci Technol; 2005 Apr 15;39(8):2777-85
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  • One approach to monitoring these pathways has been to use a human adrenocortical carcinoma cell line (H295R) that expresses all the key enzymes necessary for steroidogenesis.
  • [MeSH-minor] Cell Line, Tumor. Gene Expression Regulation. Humans. Phosphoproteins / metabolism. RNA / analysis. RNA / metabolism. Tomography, X-Ray Computed / methods

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  • (PMID = 15884376.001).
  • [ISSN] 0013-936X
  • [Journal-full-title] Environmental science & technology
  • [ISO-abbreviation] Environ. Sci. Technol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Phosphoproteins; 0 / Steroids; 0 / steroidogenic acute regulatory protein; 63231-63-0 / RNA
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7. Yavascaoglu I, Yilmaz M, Kordan Y: Cardiac and caval invasion of left adrenocortical carcinoma. Urol Int; 2008;81(2):244-6
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  • [Title] Cardiac and caval invasion of left adrenocortical carcinoma.
  • Adrenocortical carcinoma (ACC) is a rare and highly malignant neoplasm.
  • We present the case of a 51-year-old male patient with a left-sided ACC admitted to hospital with ipsilateral flank pain, weight loss, difficulty in breathing, abdominal discomfort and swelling and bilateral leg edema.
  • Thoracoabdominal computed tomography revealed a huge adrenal mass with obvious tumor thrombus involvement of the inferior vena cava and right atrium.
  • This is the first report describing caval and opposite side renal vein invasion of a left-sided ACC treated with grafting of the vessels.
  • Histopathological examination of the tumors confirmed the diagnosis of ACC.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Heart Atria / pathology. Vena Cava, Inferior / pathology
  • [MeSH-minor] Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Invasiveness

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  • [Copyright] (c) 2008 S. Karger AG, Basel.
  • (PMID = 18758230.001).
  • [ISSN] 1423-0399
  • [Journal-full-title] Urologia internationalis
  • [ISO-abbreviation] Urol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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8. Doghman M, Cazareth J, Lalli E: The T cell factor/beta-catenin antagonist PKF115-584 inhibits proliferation of adrenocortical carcinoma cells. J Clin Endocrinol Metab; 2008 Aug;93(8):3222-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The T cell factor/beta-catenin antagonist PKF115-584 inhibits proliferation of adrenocortical carcinoma cells.
  • CONTEXT: Mutations of the beta-catenin (CTNNB1) gene are frequently found in adrenocortical tumors.
  • OBJECTIVE: The objective of the study was to investigate the effect of the small-molecule inhibitor of the T cell factor (Tcf)/beta-catenin complex PKF115-584 on beta-catenin-dependent transcription and proliferation of H295R adrenocortical tumor cells, which harbor mutations in CTNNB1 as well as the TP53 tumor suppressor gene.
  • CONCLUSIONS: Inhibitors of the Tcf/beta-catenin complex may prove useful in the treatment of adrenocortical tumors in which multiple genetic alterations have accumulated.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. TCF Transcription Factors / antagonists & inhibitors. beta Catenin / antagonists & inhibitors
  • [MeSH-minor] Cell Proliferation / drug effects. Genes, p53. Humans. Mutation. Tumor Cells, Cultured

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  • (PMID = 18544621.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / TCF Transcription Factors; 0 / beta Catenin
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9. Allolio B, Fassnacht M: Clinical review: Adrenocortical carcinoma: clinical update. J Clin Endocrinol Metab; 2006 Jun;91(6):2027-37
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical review: Adrenocortical carcinoma: clinical update.
  • CONTEXT: Adrenocortical carcinoma (ACC) is a rare and heterogeneous malignancy with incompletely understood pathogenesis and poor prognosis.
  • Patients present with hormone excess (e.g. virilization, Cushing's syndrome) or a local mass effect (median tumor size at diagnosis > 10 cm).
  • The following search terms were used in varying combinations: adrenal, adrenocortical, cancer, carcinoma, tumor, diagnosis, imaging, treatment, radiotherapy, mitotane, cytotoxic, surgery.
  • EVIDENCE SYNTHESIS: Tumors typically appear inhomogeneous in both computerized tomography and magnetic resonance imaging with necroses and irregular borders and differ from benign adenomas by their low fat content.
  • Hormonal analysis reveals evidence of steroid hormone secretion by the tumor in the majority of cases, even in seemingly hormonally inactive lesions.
  • Histopathology is crucial for the diagnosis of malignancy and may also provide important prognostic information.
  • Local recurrence is frequent, particularly after violation of the tumor capsule.
  • Surgery also plays a role in local tumor recurrence and metastatic disease.
  • In advanced disease, the most promising therapeutic options (etoposide, doxorubicin, cisplatin plus mitotane, and streptozotocin plus mitotane) are currently being compared in an international phase III trial (www.firm-act.org).
  • Adjuvant treatment options after complete tumor removal (e.g. mitotane, radiotherapy) are urgently needed because postoperative disease-free survival at 5 yr is only around 30%, but options have still not been convincingly established.
  • [MeSH-major] Adrenal Cortex Neoplasms / therapy
  • [MeSH-minor] Follow-Up Studies. Humans. Neoplasm Staging. Prognosis

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  • (PMID = 16551738.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 156
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10. Ozimek A, Diebold J, Linke R, Heyn J, Hallfeldt K, Mussack T: Bilateral primary adrenal non-Hodgkin's lymphoma and primary adrenocortical carcinoma--review of the literature preoperative differentiation of adrenal tumors. Endocr J; 2008 Aug;55(4):625-38
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  • [Title] Bilateral primary adrenal non-Hodgkin's lymphoma and primary adrenocortical carcinoma--review of the literature preoperative differentiation of adrenal tumors.
  • Most of the adrenal tumors that are incidentally detected are benign adenomas.
  • The incidence of malignant adrenal tumors including adrenocortical carcinoma (ACC) and primary adrenal lymphoma (PAL) is rather low.
  • As many patients with ACC and PAL are diagnosed at an advanced stage of disease, the overall survival time of both entities remains poor.
  • Unfortunately hitherto preoperative diagnosis of potentially malignant adrenal masses is still a main problem in the treatment of adrenal tumors.
  • We present the case of a 57-year-old male patient with ACC and the case of an 87-year-old male patient with PAL and provide a systematic comparison of the clinical and pathological features of both entities.
  • In both cases clinical and radiological features resulted in an initially false diagnosis.
  • The patient with ACC showed tumor progression with local and systemic recurrence despite adjuvant therapy with mitotane and additional surgical therapy.
  • We propose some guidelines for diagnosis and surgical management of adrenal tumors.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenal Gland Neoplasms / diagnosis. Adrenocortical Carcinoma / diagnosis. Lymphoma, Non-Hodgkin / diagnosis

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  • (PMID = 18490838.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 78E4J5IB5J / Mitotane
  • [Number-of-references] 55
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11. Bauditz J, Quinkler M, Wermke W: Radiofrequency thermal ablation of hepatic metastases of adrenocortical cancer--a case report and review of the literature. Exp Clin Endocrinol Diabetes; 2009 Jul;117(7):316-9
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  • [Title] Radiofrequency thermal ablation of hepatic metastases of adrenocortical cancer--a case report and review of the literature.
  • AIM: Radiofrequency thermal ablation (RFA) has shown promise as a technique for treating solid tumors.
  • This method has been suggested as an alternative to surgery in patients with adrenocortical carcinoma (ACC).
  • MATERIALS AND METHODS: We reviewed the literature, and report the case of a patient with stage 4 ACC who received intraoperative and percutaneous RFA of two liver metastasis according to a standard ablation protocol.
  • RESULTS: Post-interventional imaging in our patient demonstrated that after both interventions, a stellar-like structure of vital tumor tissue had remained within the coagulation necrosis.
  • This was the starting point of a fast and progressive tumor recurrence.
  • We suspect heat-sink effects of blood vessels in the highly vascularized metastasis to cause the tumor recurrence.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Carcinoma / pathology. Catheter Ablation. Liver Neoplasms / secondary. Liver Neoplasms / surgery
  • [MeSH-minor] Adult. Disease Progression. Female. Humans. Monitoring, Intraoperative / methods. Treatment Outcome

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  • (PMID = 19053031.001).
  • [ISSN] 1439-3646
  • [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] Case Reports; Evaluation Studies; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 23
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12. Dunn AJ: Effects of cytokines and infections on brain neurochemistry. Clin Neurosci Res; 2006 Aug;6(1-2):52-68
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  • The most well studied effect is the activation of the hypothalamo-pituitary-adrenocortical (HPA) axis, especially that by interleukin-1 (IL-1).
  • Like IL-6, tumor necrosis factor-α (TNFα) activates the HPA axis, but affects NE and tryptophan only at high doses.

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  • (PMID = 18079991.001).
  • [ISSN] 1566-2772
  • [Journal-full-title] Clinical neuroscience research
  • [ISO-abbreviation] Clin Neurosci Res
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS035370-12; United States / NIMH NIH HHS / MH / R01 MH050947; United States / NINDS NIH HHS / NS / R01 NS035370
  • [Publication-type] JOURNAL ARTICLE
  • [Publication-country] Netherlands
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13. Chesnokova V, Melmed S: Pituitary tumour-transforming gene (PTTG) and pituitary senescence. Horm Res; 2009 Apr;71 Suppl 2:82-7
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  • [Title] Pituitary tumour-transforming gene (PTTG) and pituitary senescence.
  • Pituitary tumours account for 15% of intracranial neoplasms and are benign monoclonal neoplasms that may be clinically silent or secrete hormones, including prolactin, growth hormone, adrenocorticotrophic hormone or, rarely, thyroid-stimulating hormone or gonadotrophins.
  • Our results provide further insights into the role of cell-cycle control and growth constraints on experimental and human pituitary tumours, which underlie their failure to progress to malignancy.
  • These results improve our understanding of pituitary syndromes associated with infertility, growth disorders, hypercortisolism or adrenal, thyroid and gonadal failure due to abrogated pituitary function.
  • [MeSH-major] Brain Neoplasms / metabolism. Cell Aging. Cell Cycle. Mutation. Neoplasm Proteins / metabolism. Pituitary Neoplasms / metabolism
  • [MeSH-minor] Adrenocortical Hyperfunction / etiology. Adrenocortical Hyperfunction / genetics. Adrenocortical Hyperfunction / metabolism. Adrenocortical Hyperfunction / therapy. Aneuploidy. Animals. Growth Disorders / etiology. Growth Disorders / genetics. Growth Disorders / metabolism. Growth Disorders / therapy. Humans. Infertility / etiology. Infertility / genetics. Infertility / metabolism. Infertility / therapy. Mice. Mice, Transgenic. Pituitary Hormones / metabolism. Retinoblastoma Protein / genetics. Retinoblastoma Protein / metabolism. Securin

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19407503.001).
  • [ISSN] 1423-0046
  • [Journal-full-title] Hormone research
  • [ISO-abbreviation] Horm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Pituitary Hormones; 0 / Retinoblastoma Protein; 0 / Securin; 0 / pituitary tumor-transforming protein 1, human
  • [Number-of-references] 38
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14. Hammer GD, Parker KL, Schimmer BP: Minireview: transcriptional regulation of adrenocortical development. Endocrinology; 2005 Mar;146(3):1018-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Minireview: transcriptional regulation of adrenocortical development.
  • The adrenal glands are comprised of two distinct endocrine organs: the outer cortex, which is derived from mesoderm and synthesizes steroid hormones, and the inner medulla, which contains neuroectodermal cells derived from the neural crest and produces the catecholamine hormones norepinephrine and epinephrine.
  • The developmental program that gives rise to the adrenal gland begins early during embryogenesis and continues throughout gestation and well after birth.
  • In this article, we review the molecular mechanisms of adrenal differentiation and development, focusing on the contributions of genes responsible for the development of the adrenal cortex as identified from studies of experimental animal models and human subjects with clinical diseases.
  • These studies identify a hierarchical network of transcription factors, including Wilms' tumor-1, steroidogenic factor-1, dosage-sensitive sex reversal, adrenal hypoplasia congenita, X-linked-1, PBX1, and CITED2, that both give rise to the adrenal cortex and subsequently determine its subsequent function in steroidogenesis.
  • [MeSH-major] Adrenal Cortex / embryology. Adrenal Cortex / physiology. Adrenal Glands / embryology. Gene Expression Regulation, Developmental. Transcription, Genetic

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  • (PMID = 15604207.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CITED2 protein, human; 0 / DAX-1 Orphan Nuclear Receptor; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / NR0B1 protein, human; 0 / NR5A1 protein, human; 0 / Nr0b1 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Retinoic Acid; 0 / Repressor Proteins; 0 / Steroidogenic Factor 1; 0 / Steroids; 0 / Trans-Activators; 0 / Transcription Factors; 0 / WT1 Proteins; 0 / pbx1 protein, human; 0 / steroidogenic factor 1, mouse; X4W3ENH1CV / Norepinephrine; YKH834O4BH / Epinephrine
  • [Number-of-references] 71
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15. Hah JO: Intensive chemotherapy with autologous PBSCT for advanced adrenocortical carcinoma in a child. J Pediatr Hematol Oncol; 2008 Apr;30(4):332-4
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  • [Title] Intensive chemotherapy with autologous PBSCT for advanced adrenocortical carcinoma in a child.
  • Adrenocortical carcinoma (ACC) is a rare tumor in children.
  • We report successful treatment of a 3-year-old girl with ACC and lung metastases.
  • She has been well for 2 years since the time of diagnosis.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Peripheral Blood Stem Cell Transplantation / methods

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  • (PMID = 18391707.001).
  • [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
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16. Erdogan S, Ergin M, Cevlik F, Yuksel B, Tuncer R, Tunali N, Polat S: Testicular adrenal rest hyperplasia due to 21-hydroxylase deficiency: a case report. Endocr Pathol; 2006;17(1):83-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Testicular adrenal rest hyperplasia due to 21-hydroxylase deficiency: a case report.
  • Bilateral testicular tumors are a rare complication of congenital adrenal hyperplasia.
  • It can be extremely difficult to distinguish histologically between Leydig cell tumors and adrenocortical rest hyperplasia, which may lead in some cases to unnecessary orchidectomy.
  • Hormonal studies established the diagnosis of congenital adrenal hyperplasia due to 21-hydroxylase deficiency.
  • Here we report a case of testicular adrenal rest hyperplasia in congenital adrenal hyperplasia and discuss the pathological and clinical features and origin of this rare lesion by using immunohistochemical evaluation.
  • [MeSH-major] Adrenal Hyperplasia, Congenital / enzymology. Adrenal Rest Tumor / enzymology. Puberty, Precocious / etiology. Steroid 21-Hydroxylase / metabolism. Testicular Neoplasms / enzymology. Testis / pathology

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  • [Cites] AJR Am J Roentgenol. 1999 May;172(5):1235-8 [10227495.001]
  • [Cites] J Clin Endocrinol Metab. 1990 May;70(5):1408-13 [2335578.001]
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  • (PMID = 16760584.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.14.14.16 / Steroid 21-Hydroxylase
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17. Zhang H, Bu H, Chen H, Wei B, Liu W, Guo J, Li F, Liao D, Tang Y, Zhang Z: Comparison of immunohistochemical markers in the differential diagnosis of adrenocortical tumors: immunohistochemical analysis of adrenocortical tumors. Appl Immunohistochem Mol Morphol; 2008 Jan;16(1):32-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparison of immunohistochemical markers in the differential diagnosis of adrenocortical tumors: immunohistochemical analysis of adrenocortical tumors.
  • Most adrenocortical tumors (ACTs) can be diagnosed directly by a combination of morphologic features and clinical findings.
  • However, sometimes it may be difficult to distinguish ACTs from other neoplasms such as pheochromocytomas and some metastatic tumors, particularly for small biopsy specimens because they may be morphologically similar.
  • Expression of calretinin has recently been suggested as a valuable immunomarker for the differential diagnosis between ACTs and other tumors; however, its diagnostic value is still under debate.
  • To determine the diagnostic value of calretinin in Chinese patients with adrenocortical and non-ACTs, we employed both polyclonal and monoclonal anticalretinin to characterize the expression of calretinin in adrenal tissues and compared its expression with that of inhibin alpha, Melan-A, cytokeratin, or CD99 by immunohistochemistry in tissue microarrays and standard tissue sections of 414 specimens.
  • Our results revealed that calretinin was expressed by adrenocortical cells, but not by the other cells tested and the percentage of calretinin-positive ACTs reached 99% when stained with polyclonal antibodies, which was higher than that with monoclonal anticalretinin (91.3%), anti-Melan-A (90.3%), antiinhibin alpha (81.6%).
  • Furthermore, unlike anti-Melan-A that stained all metastatic malignant melanoma, anticalretinin did not recognize other tested tumors.
  • Therefore, immunohistologic staining with polyclonal anticalretinin is more sensitive than other antibodies tested for the diagnosis of ACTs.
  • Importantly, our data suggested that the fried-egg-like staining pattern, but not the mere cytoplasmic staining, was characteristic of anticalretinin staining in adrenocortical tissues.
  • Thus, the combinational characterization of calretinin (either by polyclonal or monoclonal antibody), inhibin alpha, and Melan-A expression is of great significance in the differential diagnosis of ACTs.

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  • (PMID = 18091323.001).
  • [ISSN] 1541-2016
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / CALB2 protein, human; 0 / Calbindin 2; 0 / MART-1 Antigen; 0 / MLANA protein, human; 0 / Neoplasm Proteins; 0 / S100 Calcium Binding Protein G; 57285-09-3 / Inhibins
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18. Kwon HS, Kim SI, Yoo SJ, Yoon KH, Lee KW, Kang MW, Son HY, Kang SK, Cha BY: Adrenal tuberculosis in Cushing's disease with bilateral macronodular adrenocortical hyperplasia. Endocr J; 2006 Apr;53(2):219-23
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  • [Title] Adrenal tuberculosis in Cushing's disease with bilateral macronodular adrenocortical hyperplasia.
  • Cushing's disease is a disorder of hypercortisolism caused by a pituitary micro- or macro-adenoma.
  • Most patients with Cushing's disease have a bilateral adrenal enlargement, which depends on the duration of the disease, as a result of the long standing ACTH stimulation of both adrenal glands.
  • However, in macronodular adrenocortical hyperplasia (MNH) that is caused by Cushing's disease, if the MNH gains autonomy, a bilateral adrenalectomy, as well as the removal of pituitary adenoma, is often essential.
  • We encountered a patient diagnosed with Cushing's disease with bilateral adrenal tuberculosis simulating MNH.
  • Sellar MRI revealed a pituitary macroadenoma, but adrenal CT showed enlargement in both adrenal glands that appeared to be MNH.
  • A hormonal study and bilateral inferior petrosal sinus sampling revealed Cushing's disease.
  • However, the adrenal mass rapidly enlarged after removing the pituitary tumor without showing evidence of a recurrence or adrenal autonomy of hypercortisolism.
  • The resected left adrenal gland was pathologically determined to have a lesion of tuberculosis with some part of the intact cortex.
  • So we assumed that the cause of rapid adrenal enlargement might be due to adrenal tuberculosis.
  • In summary, to the best of our knowledge, this is the first case of Cushing's disease coexisting with both adrenal tuberculosis simulating a bilateral MNH.
  • [MeSH-major] Adrenal Gland Diseases / microbiology. Adrenal Glands / pathology. Pituitary ACTH Hypersecretion / complications. Tuberculosis, Endocrine / complications. Tuberculosis, Endocrine / diagnosis

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  • (PMID = 16618981.001).
  • [ISSN] 0918-8959
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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19. 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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20. Haase M, Ansurudeen I, Schinner S, Paramonova I, Schott M, Papewalis C, Bornstein SR, Scherbaum WA, Willenberg HS: Evidence for the involvement of endothelial cell products in adrenal CITED2 expression. Cell Tissue Res; 2009 May;336(2):337-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evidence for the involvement of endothelial cell products in adrenal CITED2 expression.
  • The adrenal gland contains a well-organized network of blood vessels, and adrenocortical cells are situated in close proximity to endothelial cells.
  • Recently, several new mechanisms have been characterized that control the release of aldosterone by adrenocortical cells, including the involvement of endothelial-cell-derived factors.
  • Interestingly, a CBP/p300-interacting transactivator with ED-rich tail 2 (CITED2), which is necessary for adrenal development, has been linked to aldosterone synthesis.
  • We have therefore examined the effects of endothelial-cell-conditioned medium (ECCM), as produced during the incubation of human umbilical vein endothelial cells for 24 h, on the promoter activity and mRNA and protein expression of CITED2 in adrenocortical cells as represented by the NCI-H295R cell line.
  • We conclude that products secreted by endothelial cells control not only steroidogenesis, but also factors that are important for adrenocortical development, thereby highlighting the role of cellular interactions within adrenocortical development and physiology.
  • [MeSH-major] Adrenal Glands / metabolism. Endothelial Cells / metabolism. Repressor Proteins / metabolism. Trans-Activators / metabolism
  • [MeSH-minor] Cell Line, Tumor. Humans. Immunohistochemistry. Promoter Regions, Genetic / genetics

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  • (PMID = 19319572.001).
  • [ISSN] 1432-0878
  • [Journal-full-title] Cell and tissue research
  • [ISO-abbreviation] Cell Tissue Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / CITED2 protein, human; 0 / Repressor Proteins; 0 / Trans-Activators
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21. De Padua M, Rajagopal V: Myxoid adrenal adenoma with focal pseudoglandular pattern. Indian J Med Sci; 2008 May;62(5):199-203
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  • [Title] Myxoid adrenal adenoma with focal pseudoglandular pattern.
  • Adrenal cortical tumors with myxoid change are rare tumors.
  • A pseudoglandular pattern has been described in 9 of these tumors.
  • We report a case of a myxoid adenoma of the left adrenal gland in a 67-year-old woman, with a focal pseudoglandular pattern involving about 20% of the studied tumor.
  • Rest of the tumor was composed of anastomosing cords of tumor cells.
  • Immunophenotype was consistent with an adrenal tumor, i.e., positive for vimentin, inhibin, and melan A.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / pathology

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  • (PMID = 18579979.001).
  • [ISSN] 0019-5359
  • [Journal-full-title] Indian journal of medical sciences
  • [ISO-abbreviation] Indian J Med Sci
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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22. Lachenmayer A, Lichtenauer UD, Cox T, Schott M, Malendowicz LK, Goretzki PE, Cupisti K, Scherbaum WA, Bornstein SR, Willenberg HS: Nestin as a marker in the classification of adrenocortical tumors. Horm Metab Res; 2009 May;41(5):397-401
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nestin as a marker in the classification of adrenocortical tumors.
  • However, nestin expression has recently been detected in several tumors.
  • Since adrenocortical carcinoma, a tumor entity still very difficult to classify, may gain the ability to aberrantly express neuroectodermal proteins including chromogranin A and synaptophysin, we asked the question whether nestin might also be detected in adrenocortical carcinomas, and if so, whether it might serve as a tool for clinical pathology.
  • Therefore, we studied the expression of nestin in normal adrenal glands, adrenocortical adenomas, and adrenocortical cancers using specific immunohistochemistry and semi-quantitative reverse transcriptase-polymerase chain reaction.
  • Immunostaining was nestin-positive in 1 out of 9 normal adrenal glands (11%), 2 out of 20 adrenocortical adenomas (10%), and 13 out of 16 adrenocortical carcinomas (81%).
  • We conclude that our findings provide further evidence that nestin, as a marker, is not restricted to neuronal stem cells and nestin expression is worth to be studied in adrenocortical tumors.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / classification. Adrenocortical Carcinoma / pathology. Biomarkers, Tumor / metabolism. Intermediate Filament Proteins / metabolism. Nerve Tissue Proteins / metabolism
  • [MeSH-minor] Adrenal Glands / metabolism. Adult. Aged. Aged, 80 and over. Female. Gene Expression. Humans. Male. Middle Aged. Nestin

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  • (PMID = 19294612.001).
  • [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] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin
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23. Achatz MI, Olivier M, Le Calvez F, Martel-Planche G, Lopes A, Rossi BM, Ashton-Prolla P, Giugliani R, Palmero EI, Vargas FR, Da Rocha JC, Vettore AL, Hainaut P: The TP53 mutation, R337H, is associated with Li-Fraumeni and Li-Fraumeni-like syndromes in Brazilian families. Cancer Lett; 2007 Jan 8;245(1-2):96-102
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A TP53 germline mutation, R337H, has been previously described in children from southern Brazil with adrenocortical tumours but no documented familial history of other cancers.
  • Families with the R337H mutation presented a wide spectrum of tumours, including breast cancers (30.4%), brain cancers (10.7%), soft tissue sarcomas (10.7%) and adrenocortical carcinomas (8.9%).
  • These results show that the TP53 R337H germline mutation predisposes to a larger spectrum of tumours, similar to the one reported for other TP53 mutations.
  • [MeSH-major] Germ-Line Mutation. Li-Fraumeni Syndrome / genetics. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Base Sequence. Brazil. DNA Mutational Analysis. Female. Genetic Predisposition to Disease / genetics. Humans. Male. Mutation, Missense. Neoplastic Syndromes, Hereditary / genetics. Neoplastic Syndromes, Hereditary / pathology

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  • [CommentIn] Cancer Lett. 2007 Mar 18;247(2):353-5; author reply 356-8 [16750598.001]
  • (PMID = 16494995.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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24. van Staveren WC, Solís DW, Delys L, Venet D, Cappello M, Andry G, Dumont JE, Libert F, Detours V, Maenhaut C: Gene expression in human thyrocytes and autonomous adenomas reveals suppression of negative feedbacks in tumorigenesis. Proc Natl Acad Sci U S A; 2006 Jan 10;103(2):413-8
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  • The cAMP signaling pathway regulates growth of many cell types, including somatotrophs, thyrocytes, melanocytes, ovarian follicular granulosa cells, adrenocortical cells, and keratinocytes.
  • Mutations of partners from the cAMP signaling cascade are involved in tumor formation.
  • Thyroid-stimulating hormone (TSH) receptor and Gsalpha activating mutations have been detected in thyroid autonomous adenomas, Gsalpha mutations in growth hormone-secreting pituitary adenomas, and PKAR1A mutations in Carney complex, a multiple neoplasia syndrome.
  • To gain more insight into the role of cAMP signaling in tumor formation, human primary cultures of thyrocytes were treated for different times (1.5, 3, 16, 24, and 48 h) with TSH to characterize modulations in gene expression using cDNA microarrays.
  • Some were down- or nonregulated in adenomas, suggesting a loss of negative feedback control in the tumors.
  • These results suggest that in tumorigenesis, activation of proliferation pathways may be complemented by suppression of multiple corresponding negative feedbacks, i.e., specific tumor suppressors.
  • [MeSH-major] Adenoma / genetics. Adenoma / pathology. Cell Transformation, Neoplastic / genetics. Gene Expression Regulation, Neoplastic. Thyroid Gland / cytology. Thyroid Neoplasms / genetics. Thyroid Neoplasms / pathology
  • [MeSH-minor] Down-Regulation / genetics. Feedback, Physiological. Gene Expression Profiling. Humans. Kinetics. Oligonucleotide Array Sequence Analysis. RNA, Messenger / genetics. Thyrotropin / pharmacology. Time Factors. Tumor Cells, Cultured

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  • (PMID = 16381821.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 9002-71-5 / Thyrotropin
  • [Other-IDs] NLM/ PMC1326163
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25. 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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  • [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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26. Arima K, Yamakado K, Suzuki R, Matsuura H, Nakatsuka A, Takeda K, Sugimura Y: Image-guided radiofrequency ablation for adrenocortical adenoma with Cushing syndrome: outcomes after mean follow-up of 33 months. Urology; 2007 Sep;70(3):407-11
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  • [Title] Image-guided radiofrequency ablation for adrenocortical adenoma with Cushing syndrome: outcomes after mean follow-up of 33 months.
  • OBJECTIVES: To evaluate the feasibility, safety, and therapeutic effects of image-guided radiofrequency (RF) ablation used for the treatment of adrenocortical adenoma with Cushing syndrome.
  • METHODS: From February 2003 to May 2005, 4 consecutive patients with adrenocortical adenoma and Cushing syndrome received percutaneous RF ablation.
  • All tumors were in the left adrenal gland, with a mean tumor size of 2.7 +/- 0.6 cm (range 2.0 to 3.5).
  • Technical success was defined as disappearance of tumor enhancement on contrast-enhanced computed tomography imaging acquired within 1 week after RF ablation.
  • RESULTS: Tumor enhancement disappeared after initial RF ablation in 3 of 4 patients (technical success rate 75%).
  • The fourth patient underwent a repeat RF ablation session 3 years later, resulting in eradication of tumor enhancement.
  • All tumors showed involution (2.2 +/- 0.3 cm) at the end of the study.
  • CONCLUSIONS: Using RF ablation for adrenocortical adenoma with Cushing syndrome is a feasible, safe, and promising treatment method in selected patients.
  • [MeSH-major] Adenoma / surgery. Adrenal Cortex Neoplasms / surgery. Catheter Ablation / methods. Cushing Syndrome / surgery. Fluoroscopy / methods. Radiography, Interventional / methods. Surgery, Computer-Assisted / methods

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  • (PMID = 17905083.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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27. Onoda N, Ishikawa T, Nishio K, Tahara H, Inaba M, Wakasa K, Sumi T, Yamazaki T, Shigematsu K, Hirakawa K: Cushing's syndrome by left adrenocortical adenoma synchronously associated with primary aldosteronism by right adrenocortical adenoma: report of a case. Endocr J; 2009;56(3):495-502
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  • [Title] Cushing's syndrome by left adrenocortical adenoma synchronously associated with primary aldosteronism by right adrenocortical adenoma: report of a case.
  • Synchronous associations of Cushing's syndrome (CS) and primary aldosteronism (PA) with multiple adrenocortical adenomas secreting each hormone independently have rarely been reported.
  • Bilateral adrenal masses with clinical symptoms of CS and PA were found in a 43-year-old woman.
  • Venous sampling demonstrated excess secretion of cortisol, and aldosterone from right, and left tumor, respectively.
  • The right adrenal tumor (3 cm) was yellow in color with abundant lipofuscin granules, and was composed of both eosinophilic compact cells and clear cells.
  • In situ hybridization showed that both mRNAs for HSD3B2 and CYP17A1 were strongly expressed in the tumor, suggesting cortisol synthesis.
  • Left adrenal tumor (2.4 cm) was golden-yellow in color, and composed of clear cells only.
  • Expression of HSD3B2 and CYP11B mRNAs were observed in the tumor compatible with the aldosterone synthesis.
  • Furthermore, minute nodules were found at the surface of normal-appearing cortex on both sides of the adrenal glands, and the expression of HSD3B2 and CYP11B mRNAs was clearly demonstrated within the nodules, indicating aldosterone synthesis.
  • We diagnosed that the present case had 1) cortisol-producing right adrenocortical adenoma, 2) aldosterone producing left adrenocortical adenoma, and 3) cortical minute nodules with aldosterone production in both adrenal glands compatible with idiopathic adrenal hyperplasia.
  • We reviewed the cases reported, and discussed the significance of the minute nodules in the adrenal cortex, often found in association with the adrenocortical adenoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications. Cushing Syndrome / etiology. Hyperaldosteronism / etiology

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  • (PMID = 19270420.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] EC 1.1.1.145 / 3 beta-hydroxysteroid dehydrogenase type II; EC 1.1.1.145 / Progesterone Reductase; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase
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28. Bednarek-Tupikowska G, Florczak A, Witkiewicz W, Tupikowski W, Cisarz E: [A long term survival of the patient treated due to advanced adrenocortical carcinoma]. Pol Arch Med Wewn; 2005 May;113(5):462-5
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  • [Title] [A long term survival of the patient treated due to advanced adrenocortical carcinoma].
  • [Transliterated title] Długoletnie przezycie chorej leczonej z powodu zaawansowanego raka kory nadnercza.
  • The authors presented a case of 52-years old woman with advanced adrenocortical carcinoma completely recovered after surgical resection followed by chemotherapy and mitotane treatment.
  • Two years later metastatic tumor of hepar was excised.
  • From the first diagnosis - patient lives 12 years, without any symptoms of recurrence until now.
  • The authors accentuate a big value of postoperative control, especially imaging studies for early diagnosis of recurrent of cancer and beginning therapy.
  • [MeSH-major] Adrenal Cortex Neoplasms / therapy. Liver Neoplasms / therapy
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Disease-Free Survival. Female. Humans. Middle Aged. Mitotane / therapeutic use

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  • (PMID = 16479829.001).
  • [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
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 78E4J5IB5J / Mitotane
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29. Palazzo FF, Sebag F, Sierra M, Ippolito G, Souteyrand P, Henry JF: Long-term outcome following laparoscopic adrenalectomy for large solid adrenal cortex tumors. World J Surg; 2006 May;30(5):893-8
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  • [Title] Long-term outcome following laparoscopic adrenalectomy for large solid adrenal cortex tumors.
  • INTRODUCTION: Laparoscopic adrenalectomy (LA) is the procedure of choice for small benign adrenal tumors.
  • In the absence of local invasion or metastases, the preoperative diagnosis of an adrenocortical carcinoma (ACC) is difficult, often leaving size as the principal predictor of malignancy.
  • Large tumors are resectable laparoscopically, but the long-term outcome and therefore appropriateness of LA for cortical tumors > 6 cm is not known.
  • METHODS: We reviewed the LA experience in our institution since its introduction in June 1994.
  • Patients who underwent LA for solid cortical tumors > or = 60 mm in diameter without preoperative or intraoperative evidence of malignancy were reviewed.
  • Follow-up data, including clinical examination, biochemical analysis, and repeat scans, were reviewed for evidence of local or systemic recurrent disease.
  • Among them, 19 were solid cortical tumors > or = 60 mm in diameter with no overt malignant preoperative or intraoperative characteristics: 9 nonsecreting tumors, 8 Cushing's syndrome tumors (including 2 virilizing variants), 1 virilizing tumor, and 1 aldosteronoma.
  • The mean age of the patients was 49.9 years (range 22-77 years), and the mean tumor size was 69.0 mm (range 60-80 mm).
  • Histology confirmed a cortical adenoma in eight patients, malignant tumors in three, and indeterminate tumors in eight.
  • Two patients died of systemic recurrent disease (liver metastases) at 10 and 19 months, respectively, following surgery; two other patients died 12 and 21 months, respectively following surgery owing to unrelated cardiovascular and cerebrovascular pathology.
  • One patient underwent surgery for local recurrence 54 months after primary surgery; the remaining 14 patients are well with no clinical or radiologic evidence of recurrent disease.
  • CONCLUSIONS: Laparoscopic adrenalectomy for large solid cortical tumors without pre- or intraoperative evidence of malignancy is not contraindicated, and it is unlikely to have a deleterious effect on long-term outcome.
  • We provide an algorithm for the approach to adrenocortical tumors > or = 6 cm.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenalectomy. Adrenocortical Adenoma / surgery. Adrenocortical Carcinoma / surgery
  • [MeSH-minor] Adult. Aged. Algorithms. Humans. Laparoscopy. Middle Aged. Neoplasm Staging. Retrospective Studies. Time Factors. Treatment Outcome

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  • (PMID = 16680605.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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30. Emerson RE, Ulbright TM: The use of immunohistochemistry in the differential diagnosis of tumors of the testis and paratestis. Semin Diagn Pathol; 2005 Feb;22(1):33-50
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  • [Title] The use of immunohistochemistry in the differential diagnosis of tumors of the testis and paratestis.
  • Although most testicular and paratesticular tumors can be recognized by their light microscopic features, some raise significant differential diagnostic questions.
  • OCT4 is virtually 100% sensitive and specific for seminoma, embryonal carcinoma, and intratubular germ cell neoplasia, unclassified type.
  • Inhibin-alpha, among testicular tumors, is limited to those in the sex cord-stromal category or those having adrenocortical-type differentiation (testicular tumor of the adrenogenital syndrome) or of trophoblastic lineage.
  • Calretinin is another positive marker for the sex cord-stromal tumors but has less specificity.
  • [MeSH-major] Immunohistochemistry. Testicular Neoplasms / diagnosis
  • [MeSH-minor] Adult. Biomarkers, Tumor / analysis. Child. Diagnosis, Differential. Humans. Male. Neoplasm Metastasis. Sensitivity and Specificity

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  • (PMID = 16512598.001).
  • [ISSN] 0740-2570
  • [Journal-full-title] Seminars in diagnostic pathology
  • [ISO-abbreviation] Semin Diagn Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 137
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31. Enberg U, Hennings J, Volpe C, Hellman P, Höög A, Hamberger B, Thorén M: Increased ratio of mRNA expression of the genes CYP17 and CYP11B1 indicates autonomous cortisol production in adrenocortical tumors. J Endocrinol Invest; 2009 Nov;32(10):810-5
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  • [Title] Increased ratio of mRNA expression of the genes CYP17 and CYP11B1 indicates autonomous cortisol production in adrenocortical tumors.
  • OBJECTIVE: Due to increased use of imaging techniques, adrenal incidentalomas are frequently detected.
  • The majority are non-hyperfunctioning adrenocortical tumors.
  • We have previously shown that expression of the gene CYP17, coding for the enzyme in the cortisol pathway, correlates with cortisol release from adrenocortical tumors in vitro.
  • The aim of this study was to compare clinical data with mRNA expression of CYP17 and CYP11B1 in adrenocortical tumors from patients with and without Cushing's syndrome and to identify adrenal tumors that may cause subclinical Cushing's syndrome.
  • DESIGN: A retrospective study of 34 patients undergoing adrenalectomy due to an adrenal tumor.
  • In the adrenal gland the mRNA expression of the genes CYP17 and CYP11B1 was studied with in situ hybridisation technique.
  • RESULTS: The median ratio of CYP17/CYP11B1 expression in tumors from patients with Cushing's syndrome was significantly higher than the median ratio in the non-hyperfunctioning tumors.
  • Tumors from 2 patients with subclinical Cushing's syndrome had ratios within the upper range for non-hyperfunctioning tumors.
  • CONCLUSIONS: The ratio between the expression of the genes CYP17 and CYP11B1 in tumors from patients with Cushing's syndrome is significantly higher than in the non-hyperfunctioning tumors.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenocortical Adenoma / metabolism. Hydrocortisone / biosynthesis. Steroid 11-beta-Hydroxylase / genetics. Steroid 17-alpha-Hydroxylase / genetics
  • [MeSH-minor] Adrenalectomy. Adrenocorticotropic Hormone / blood. Adult. Aged. Aldosterone / blood. Aldosterone / urine. Cushing Syndrome / diagnosis. Cushing Syndrome / genetics. Cushing Syndrome / metabolism. Female. Humans. In Situ Hybridization. Incidental Findings. Magnetic Resonance Imaging. Male. Middle Aged. RNA, Messenger / genetics. Retrospective Studies. Statistics, Nonparametric

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  • (PMID = 19564722.001).
  • [ISSN] 1720-8386
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / RNA, Messenger; 4964P6T9RB / Aldosterone; 9002-60-2 / Adrenocorticotropic Hormone; EC 1.14.14.19 / Steroid 17-alpha-Hydroxylase; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase; WI4X0X7BPJ / Hydrocortisone
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32. Song R, He Y, Murphy MB, Yeung LW, Yu RM, Lam MH, Lam PK, Hecker M, Giesy JP, Wu RS, Zhang W, Sheng G, Fu J: Effects of fifteen PBDE metabolites, DE71, DE79 and TBBPA on steroidogenesis in the H295R cell line. Chemosphere; 2008 May;71(10):1888-94
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  • In the present study, 15 PBDE metabolites, two BDE mixtures (DE71 and DE79), and TBBPA were studied individually to determine their effects on ten steroidogenic genes, aromatase activity, and concentrations of two steroid hormones (testosterone and 17beta-estradiol) in the H295R human adrenocortical carcinoma cell line.
  • [MeSH-minor] Aromatase / metabolism. Cell Line, Tumor. Cell Survival / drug effects. Cytochrome P-450 Enzyme System / genetics. Estradiol / metabolism. Humans. Hydroxysteroid Dehydrogenases / genetics. Phosphoproteins / genetics. Testosterone / metabolism

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  • (PMID = 18313098.001).
  • [ISSN] 0045-6535
  • [Journal-full-title] Chemosphere
  • [ISO-abbreviation] Chemosphere
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Phenyl Ethers; 0 / Phosphoproteins; 0 / Polybrominated Biphenyls; 0 / steroidogenic acute regulatory protein; 3XMK78S47O / Testosterone; 4TI98Z838E / Estradiol; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.1.- / Hydroxysteroid Dehydrogenases; EC 1.14.14.1 / Aromatase
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33. Lawnicka H, Kowalewicz-Kulbat M, Sicinska P, Kazimierczuk Z, Grieb P, Stepien H: Anti-neoplastic effect of protein kinase CK2 inhibitor, 2-dimethylamino-4,5,6,7-tetrabromobenzimidazole (DMAT), on growth and hormonal activity of human adrenocortical carcinoma cell line (H295R) in vitro. Cell Tissue Res; 2010 May;340(2):371-9
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  • [Title] Anti-neoplastic effect of protein kinase CK2 inhibitor, 2-dimethylamino-4,5,6,7-tetrabromobenzimidazole (DMAT), on growth and hormonal activity of human adrenocortical carcinoma cell line (H295R) in vitro.
  • CK2 kinase (casein kinase-2) has been suggested to be a constituent of a neoplastic milleu, and its inhibition might represent a new approach to cancer therapy.
  • Adrenocortical carcinomas (ACCs) are highly malignant neoplasms with poor overall prognosis.
  • We have examined the effects of 2-dimethylamino-4,5,6,7-tetrabromobenzimidazole (DMAT), a potent CK2 inhibitor, on the H295R human adrenocortical cancer cell line.
  • [MeSH-major] Adrenal Cortex Hormones / secretion. Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Benzimidazoles / pharmacology. Casein Kinase II / antagonists & inhibitors. Cell Proliferation / drug effects. Protein Kinase Inhibitors / pharmacology
  • [MeSH-minor] 17-alpha-Hydroxyprogesterone / metabolism. Aldosterone / secretion. Antineoplastic Agents / pharmacology. Cell Cycle / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Dehydroepiandrosterone Sulfate / metabolism. Drug Screening Assays, Antitumor. Humans. Hydrocortisone / secretion

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  • (PMID = 20383646.001).
  • [ISSN] 1432-0878
  • [Journal-full-title] Cell and tissue research
  • [ISO-abbreviation] Cell Tissue Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / 4,5,6,7-tetrabromobenzimidazole; 0 / Adrenal Cortex Hormones; 0 / Antineoplastic Agents; 0 / Benzimidazoles; 0 / Protein Kinase Inhibitors; 4964P6T9RB / Aldosterone; 57B09Q7FJR / Dehydroepiandrosterone Sulfate; 68-96-2 / 17-alpha-Hydroxyprogesterone; EC 2.7.11.1 / Casein Kinase II; WI4X0X7BPJ / Hydrocortisone
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34. Gasińska T, Pietrasik L, Kulawik G: [Adrenal cortical carcinoma. Progress in diagnosis, clinical and genetic features]. Pol Arch Med Wewn; 2005 Sep;114(3):901-5
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  • [Title] [Adrenal cortical carcinoma. Progress in diagnosis, clinical and genetic features].
  • [Transliterated title] Pierwotny rak kory nadnerczy. Postepy w diagnostyce, aspekty kliniczne i genetyczne.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis. Adrenal Gland Neoplasms / genetics. Adrenocortical Carcinoma / diagnosis. Adrenocortical Carcinoma / genetics
  • [MeSH-minor] Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Diagnosis, Differential. Humans. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 16708566.001).
  • [Journal-full-title] Polskie Archiwum Medycyny Wewnetrznej
  • [ISO-abbreviation] Pol. Arch. Med. Wewn.
  • [Language] pol
  • [Publication-type] Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Tumor Suppressor Protein p53
  • [Number-of-references] 40
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35. Gross MD, Djekidel M, Hay RV, Rubello D: Scintigraphic localization of adrenal tumors. Minerva Endocrinol; 2009 Jun;34(2):171-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Scintigraphic localization of adrenal tumors.
  • Scintigraphy has historically added much to the evaluation of adrenal dysfunction and tumor localization.
  • The early development of radiopharmaceuticals for adrenocortical imaging provided vital clinical information well before the widespread availability of computed tomography (CT), but beginning in the early 1980's nuclear imaging became supplanted in large part by high resolution CT and more recently by magnetic resonance imaging.
  • The parallel emergence of radiopharmaceuticals for adrenomedullary imaging also provided important functional insight in evaluating these neoplasms, but despite the clinical value of such nuclear probes they too, were relegated to a less prominent role in tumor characterization because of advances in anatomic imaging.
  • However, with the recent introduction of dual-modality imaging platforms that directly combine CT with scintigraphy, either as single photon emission tomography (SPECT)/CT or positron emission tomography (PET)/CT, nuclear medicine studies once again play an integral role in adrenal tumor evaluation.
  • [MeSH-major] Adrenal Gland Neoplasms / radionuclide imaging. Positron-Emission Tomography. Radiopharmaceuticals. Tomography, Emission-Computed, Single-Photon
  • [MeSH-minor] Adrenal Cortex Neoplasms / radionuclide imaging. Adrenal Gland Diseases / radionuclide imaging. Adrenocortical Carcinoma / radionuclide imaging. Cushing Syndrome / radionuclide imaging. Diagnosis, Differential. Humans. Incidental Findings. Pheochromocytoma / radionuclide imaging. Reproducibility of Results. Sensitivity and Specificity. Tomography, X-Ray Computed

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  • (PMID = 19333218.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Radiopharmaceuticals
  • [Number-of-references] 93
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36. Giacchetti G, Ronconi V, Rilli S, Guerrieri M, Turchi F, Boscaro M: Small tumor size as favorable prognostic factor after adrenalectomy in Conn's adenoma. Eur J Endocrinol; 2009 Apr;160(4):639-46
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  • [Title] Small tumor size as favorable prognostic factor after adrenalectomy in Conn's adenoma.

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  • (PMID = 19131503.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone
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37. Wen MJ, Lin YF, Chen JS: Newly developed hypertension as an early marker of recurrence of adrenocortical carcinoma with high renin expression. Int J Urol; 2008 Jun;15(6):540-2
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  • [Title] Newly developed hypertension as an early marker of recurrence of adrenocortical carcinoma with high renin expression.
  • Adrenocortical carcinoma can recur frequently after successful surgery but no adequate markers can detect this recurrence.
  • Here, we present a recurrence of adrenocortical carcinoma with a high renin expression, after successful surgery, where hypertension has developed again.
  • Tumor recurrence was observed via (18)F-fluorodeoxyglucose positron emission tomography and coregistered computed tomography.
  • Based on our findings, follow-up blood pressure assessment may effectively predict the recurrence of adrenocortical carcinoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenal Cortex Neoplasms / metabolism. Adrenocortical Carcinoma / complications. Adrenocortical Carcinoma / metabolism. Hypertension / etiology. Neoplasm Recurrence, Local / complications. Neoplasm Recurrence, Local / metabolism. Renin / biosynthesis

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  • (PMID = 18489644.001).
  • [ISSN] 1442-2042
  • [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 3.4.23.15 / Renin
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38. Goto J, Otsuka F, Kodera R, Miyoshi T, Kinomura M, Otani H, Mimura Y, Ogura T, Yanai H, Nasu Y, Makino H: A rare tumor in the adrenal region: neuron-specific enolase (NSE)-producing leiomyosarcoma in an elderly hypertensive patient. Endocr J; 2008 Mar;55(1):175-81
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  • [Title] A rare tumor in the adrenal region: neuron-specific enolase (NSE)-producing leiomyosarcoma in an elderly hypertensive patient.
  • Abdominal CT incidentally detected a right adrenal mass 8 cm in size.
  • The tumor exhibited isodensity by CT and contained high-intense lesion by T2-weighted MRI.
  • Positron emission tomography scan with (18) F-2-fluoro-D-deoxyglucose demonstrated an exclusive uptake in the right adrenal mass.
  • Adrenocortical hormone levels and catecholamine secretion were within normal range; however, the level of serum neuron-specific enolase (NSE) was found to be markedly high.
  • After controlling systemic blood pressure with an alpha1-blocker, the right adrenal tumor was surgically removed, along with the right kidney and inferior vena cava which adhered to it.
  • The tumor was pathologically proven to be leiomyosarcoma, which was immunohistochemically positive with alpha-smooth muscle actin and negative with CD57, S-100 and c-kit proteins.
  • Notably, NSE protein was massively expressed in the resected tumor.
  • The possibility of leiomyosarcoma should be kept in mind in adrenal incidentalomas with rapid growth and atypical radiological images.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis. Adrenal Gland Neoplasms / metabolism. Hypertension / complications. Leiomyosarcoma / diagnosis. Leiomyosarcoma / metabolism. Phosphopyruvate Hydratase / metabolism

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  • (PMID = 18250540.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / ACTA2 protein, human; 0 / Actins; 0 / Antigens, CD57; 0 / S100 Proteins; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 4.2.1.11 / Phosphopyruvate Hydratase
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39. Tömböl Z, Szabó PM, Molnár V, Wiener Z, Tölgyesi G, Horányi J, Riesz P, Reismann P, Patócs A, Likó I, Gaillard RC, Falus A, Rácz K, Igaz P: Integrative molecular bioinformatics study of human adrenocortical tumors: microRNA, tissue-specific target prediction, and pathway analysis. Endocr Relat Cancer; 2009 Sep;16(3):895-906
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  • [Title] Integrative molecular bioinformatics study of human adrenocortical tumors: microRNA, tissue-specific target prediction, and pathway analysis.
  • MicroRNAs (miRs) are involved in the pathogenesis of several neoplasms; however, there are no data on their expression patterns and possible roles in adrenocortical tumors.
  • Our objective was to study adrenocortical tumors by an integrative bioinformatics analysis involving miR and transcriptomics profiling, pathway analysis, and a novel, tissue-specific miR target prediction approach.
  • Thirty-six tissue samples including normal adrenocortical tissues, benign adenomas, and adrenocortical carcinomas (ACC) were studied by simultaneous miR and mRNA profiling.
  • To our knowledge, this is the first report describing miR expression patterns and pathway analysis in sporadic adrenocortical tumors. miR biomarkers may be helpful for the diagnosis of adrenocortical malignancy.
  • This tissue-specific target prediction approach may be used in other tumors too.
  • [MeSH-major] Adenoma / genetics. Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Computational Biology / methods. Gene Expression Profiling / methods. MicroRNAs / genetics. Signal Transduction / genetics
  • [MeSH-minor] Adult. Algorithms. Biomarkers, Tumor / analysis. Biomarkers, Tumor / genetics. Drug Delivery Systems / methods. Female. Forecasting / methods. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Models, Biological. Organ Specificity / genetics

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  • (PMID = 19546168.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MicroRNAs
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40. Lawnicka H, Kowalewicz-Kulbat M, Sicinska P, Altmann KH, Hofmann T, Stepien H: Resorcylic acid lactone L-783,277 inhibits the growth of the human adrenal cancer cell line H295R in vitro. Int J Immunopathol Pharmacol; 2009 Oct-Dec;22(4):889-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Resorcylic acid lactone L-783,277 inhibits the growth of the human adrenal cancer cell line H295R in vitro.
  • However, the role of this compound in the regulation of endocrine-related cancer cell growth and tumor progression remains unknown.
  • In the present study we have evaluated the effect of L-783,277 on the viability, proliferation and cell cycle of the human adrenocortical carcinoma cell line H295R.
  • At concentrations of 10(-6)-10(-8)M this effect was associated with the accumulation of H295R cells in S-phase, whereas at concentrations of 10(-9)-10(-10)M a prolonged G1-phase and reduced transition into S-phase were observed.
  • Our findings demonstrate for the first time the anti-proliferative action of L-783,277 on the human adrenocortical H295R cell line.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Antineoplastic Agents / pharmacology. Cell Proliferation / drug effects. Lactones / pharmacology. Mitogen-Activated Protein Kinase Kinases / antagonists & inhibitors. Protein Kinase Inhibitors / pharmacology. Resorcinols / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Cell Cycle / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Dose-Response Relationship, Drug. Humans. Inhibitory Concentration 50

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  • (PMID = 20074452.001).
  • [ISSN] 0394-6320
  • [Journal-full-title] International journal of immunopathology and pharmacology
  • [ISO-abbreviation] Int J Immunopathol Pharmacol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / L 783277; 0 / Lactones; 0 / Protein Kinase Inhibitors; 0 / Resorcinols; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases
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41. Atzeni F, Sarzi-Puttini P, DePortu S, Cutolo M, Carrabba M, Straub RH: In etanercept-treated psoriatic arthritis patients clinical improvement correlated with an increase of serum cortisol relative to other adrenal hormones. Clin Exp Rheumatol; 2008 Jan-Feb;26(1):103-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In etanercept-treated psoriatic arthritis patients clinical improvement correlated with an increase of serum cortisol relative to other adrenal hormones.
  • OBJECTIVE: In patients with rheumatoid arthritis (RA), long-term therapy with anti-tumor necrosis factor (TNF) antibodies sensitizes the pituitary gland and improves adrenal androgen secretion in prednisolone-naïve patients.
  • Clinical improvement was assessed using the Disease Activity Score-28 (DAS-28).
  • This indicates that improvement was linked to higher serum cortisol levels relative to others adrenal hormones.
  • An increase of serum cortisol relative to others adrenocortical hormones (i.e., androstenedione and ACTH) was accompanied by clinical improvement.
  • [MeSH-major] Antirheumatic Agents / therapeutic use. Arthritis, Psoriatic / blood. Arthritis, Psoriatic / drug therapy. Hydrocortisone / blood. Immunoglobulin G / therapeutic use. Receptors, Tumor Necrosis Factor / therapeutic use
  • [MeSH-minor] 17-alpha-Hydroxyprogesterone / blood. Adrenocorticotropic Hormone / blood. Adult. Androstenedione / blood. Etanercept. Female. Humans. Hypothalamo-Hypophyseal System / drug effects. Male. Middle Aged. Pituitary-Adrenal System / drug effects


42. Michalakis K, Ilias I: Medical management of adrenal disease: a narrative review. Endocr Regul; 2009 Jul;43(3):127-35
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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 adrenal disease: a narrative review.
  • Adrenal diseases comprise for a variety of medical endocrine issues, ranging from partial or complete gland insufficiency, to several kinds of adrenal hyperfunction, either of congenital or neoplastic etiology.
  • Patients with congenital adrenal hyperplasia caused by 21-hydroxylase deficiency are treated with glucocorticoids to control androgen excess.
  • Most benign neoplastic adrenal diseases that cause hyperfunction of the gland are surgically treated, however this may not be always feasible or effective.
  • For neoplastic adrenomedullary disease surgery is the treatment of choice; medical treatment is used preoperatively (mainly alpha blockers) and in case of disease persistence and /or recurrence (mainly metyrosine).
  • For malignant adrenocortical disease, surgical removal remains the indicated treatment, but if the potential for surgical intervention is limited due to tumor extension, medical treatment can alleviate symptoms of hormone hypersecretion; mitotane in selected patients has good results.
  • [MeSH-major] Adrenal Gland Diseases / drug therapy
  • [MeSH-minor] Adrenal Gland Neoplasms / drug therapy. Adrenal Gland Neoplasms / surgery. Adrenal Glands / surgery. Adrenal Hyperplasia, Congenital / drug therapy. Adrenal Insufficiency / drug therapy. Adrenocortical Carcinoma / drug therapy. Clinical Trials as Topic. Cushing Syndrome / drug therapy. Humans. Hyperaldosteronism / drug therapy. Pheochromocytoma / drug therapy. Pheochromocytoma / surgery

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  • (PMID = 19817507.001).
  • [ISSN] 1210-0668
  • [Journal-full-title] Endocrine regulations
  • [ISO-abbreviation] Endocr Regul
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Slovakia
  • [Number-of-references] 51
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43. 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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44. Li LA, Lin TC: Interacting influence of potassium and polychlorinated biphenyl on cortisol and aldosterone biosynthesis. Toxicol Appl Pharmacol; 2007 May 1;220(3):252-61
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  • Giving human adrenocortical H295R cells 14 mM KCl for 24 h significantly induced not only aldosterone biosynthesis but also cortisol biosynthesis.
  • [MeSH-minor] 17-alpha-Hydroxyprogesterone / metabolism. Cell Line, Tumor. Cytochrome P-450 CYP11B2 / genetics. Cytochrome P-450 CYP11B2 / metabolism. Dose-Response Relationship, Drug. Drug Synergism. Gene Expression / drug effects. Humans. Luciferases / genetics. Luciferases / metabolism. Progesterone / metabolism. Promoter Regions, Genetic / genetics. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Steroid 11-beta-Hydroxylase / genetics. Steroid 11-beta-Hydroxylase / metabolism. Time Factors. Transfection

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  • (PMID = 17350062.001).
  • [ISSN] 0041-008X
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 4964P6T9RB / Aldosterone; 4G7DS2Q64Y / Progesterone; 660YQ98I10 / Potassium Chloride; 68-96-2 / 17-alpha-Hydroxyprogesterone; DFC2HB4I0K / Polychlorinated Biphenyls; EC 1.13.12.- / Luciferases; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase; TSH69IA9XF / 3,4,5,3',4'-pentachlorobiphenyl; WI4X0X7BPJ / Hydrocortisone
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45. Imrich R, Lukac J, Rovensky J, Radikova Z, Penesova A, Kvetnansky R, Huckova M, Vigas M, Macho L, Koska J: Lower adrenocortical and adrenomedullary responses to hypoglycemia in premenopausal women with systemic sclerosis. J Rheumatol; 2006 Nov;33(11):2235-41
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  • [Title] Lower adrenocortical and adrenomedullary responses to hypoglycemia in premenopausal women with systemic sclerosis.
  • OBJECTIVES: To evaluate function of the hypothalamic-pituitary-adrenal (HPA) axis, adrenomedullary hormonal system (AMHS), and sympathetic noradrenergic system (SNS) in premenopausal women with systemic sclerosis (SSc).
  • METHODS: Insulin-induced hypoglycemia (0.1 IU/kg) was performed in 17 longterm, glucocorticoid-naive SSc patients with low disease activity and in 18 healthy women matched for age and body mass index (BMI).
  • Concentrations of glucose, adrenocorticotrophic hormone (ACTH), cortisol, androstenedione (ASD), dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEAS), 17a-hydroxyprogesterone (17OHP), epinephrine (EPI), norepinephrine (NE), interleukin 1ss (IL-1ss), IL-6, and tumor necrosis factor-a (TNF-a) were analyzed in plasma.
  • CONCLUSION: Our data indicate decreased adrenocortical and adrenomedullary functions in premenopausal women with SSc.
  • Whether the observed changes in the neuroendocrine system are secondary to chronic disease deserves further investigation.
  • [MeSH-major] Adrenal Cortex / physiology. Adrenal Medulla / physiology. Androgens / metabolism. Hypoglycemia / metabolism. Premenopause / metabolism. Progesterone / blood. Scleroderma, Systemic / metabolism


46. Sawazaki H, Segawa T, Yoshida K, Kawahara T, Inoue T, Soda T, Kamba T, Yoshimura K, Takahashi T, Nakamura E, Nishiyama H, Ito N, Kamoto T, Ogawa O: [Hemorrhagic adrenocortical adenoma with myelolipoma: a case report]. Hinyokika Kiyo; 2006 Oct;52(10):785-8
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  • [Title] [Hemorrhagic adrenocortical adenoma with myelolipoma: a case report].
  • We present a case of hemorrhagic adrenocortical adenoma with myelolipoma.
  • Based on abdominal computed tomography, magnetic resonance imaging and blood tests, preoperative diagnosis was a sarcoma of renal capsule origin.
  • En bloc resection of adrenal gland, tumor, and the kidney with lymph node dissection was performed.
  • Histologically, the mass was diagnosed as hemorrhagic adrenocortical adenoma with myelolipomatous foci.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenal Gland Neoplasms / etiology. Adrenocortical Adenoma / complications. Myelolipoma / etiology. Neoplasms, Multiple Primary

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  • (PMID = 17131868.001).
  • [ISSN] 0018-1994
  • [Journal-full-title] Hinyokika kiyo. Acta urologica Japonica
  • [ISO-abbreviation] Hinyokika Kiyo
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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47. Sasano H, Suzuki T, Moriya T: Recent advances in histopathology and immunohistochemistry of adrenocortical carcinoma. Endocr Pathol; 2006;17(4):345-54
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  • [Title] Recent advances in histopathology and immunohistochemistry of adrenocortical carcinoma.
  • Discerning malignancy in resected adrenocortical neoplasms can pose diagnostic difficulty.
  • Macroscopic examination is the first important step toward diagnosis and should include accurate measurement of weight and dimension of the specimens and description of the cut surface of the tumors.
  • It is also important to sample the specimens for histological diagnosis near foci of hemorrhage and/or necrosis.
  • Histological scoring systems evaluating multiple parameters, especially the criteria of Weiss, have been shown to be reliable in differential diagnosis between adrenocortical adenoma and carcinoma.
  • A tumor is defined as adrenocortical carcinoma when three or more of the following criteria are met;.
  • (1) high nuclear grade, (2) mitotic rate six or more per 50 high power fields, (3) atypical mitosis, (4) clear cells less than 25%, (5) a diffuse architecture pattern in more than one-third of the tumor, (6) confluent necrosis, (7) venous invasion, (8) sinusoidal invasion, and (9) capsular invasion.
  • The criteria are relatively straightforward and considered the most effective standard for diagnosis of adrenocortical malignancy.
  • However, great care should be taken in applying the criteria to histological evaluation of two relatively rare and peculiar adrenocortical tumors, adrenocortical oncocytoma and pediatric adrenocortical neoplasms.
  • At this juncture, ancillary biological or molecular markers are of little practical value in terms of differential diagnosis between adrenocortical adenoma and carcinoma but tumors with MIB1 or Ki-67 labeling index more than 2.5 may be considered malignant.
  • Prognostic markers of adrenocortical carcinoma have not been established other than complete respectability of the tumor.
  • It sometimes is important for surgical pathologists to differentiate adrenocortical carcinoma from metastatic malignancies of other sites.
  • An immunohistochemical evaluation of adrenal 4 binding protein (Ad4BP) or SF-1, a transcription factor of all steroidogenesis, can aid in this differential diagnosis because nuclear immunoreactivity for this transcription factor is relatively specific to steroid producing cells.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology
  • [MeSH-minor] Adrenocortical Adenoma / diagnosis. Biomarkers, Tumor / analysis. Cell Count. Cell Nucleus / pathology. Diagnosis, Differential. Humans. Immunohistochemistry / methods. Ki-67 Antigen / analysis. Mitotic Index. Ubiquitin-Protein Ligases / analysis

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  • (PMID = 17525483.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; EC 2.3.2.27 / MIB1 ligase, human; EC 2.3.2.27 / Ubiquitin-Protein Ligases
  • [Number-of-references] 33
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48. Sutter JA, Grimberg A: Adrenocortical tumors and hyperplasias in childhood--etiology, genetics, clinical presentation and therapy. Pediatr Endocrinol Rev; 2006 Sep;4(1):32-9
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  • [Title] Adrenocortical tumors and hyperplasias in childhood--etiology, genetics, clinical presentation and therapy.
  • Adrenocortical tumors are rare in children and are associated with a poor prognosis when malignant.
  • Evaluation of genetic disorders associated with the development of adrenocortical disorders has allowed researchers to identify a number of mutations that may be involved in tumorigenesis, including alterations in the GNAS1, PRKAR1A, TP53 and IGF2 genes.
  • Most children have localized disease at presentation which may be associated with a better prognosis when compared to adults.
  • Broader participation in multi-center research, such as the International Pediatric Adrenocortical Tumor Registry, is needed to collect sufficient data to better guide our clinical management.

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  • (PMID = 17021581.001).
  • [ISSN] 1565-4753
  • [Journal-full-title] Pediatric endocrinology reviews : PER
  • [ISO-abbreviation] Pediatr Endocrinol Rev
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / K08 DK064352; United States / NIDDK NIH HHS / DK / 5K08 DK64352
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Israel
  • [Number-of-references] 73
  • [Other-IDs] NLM/ NIHMS22957; NLM/ PMC1907361
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49. Machida T, Uchida E, Matsuda K, Hirayama K, Yoshii K, Takiguchi M, Taniyama H: Aldosterone-, corticosterone- and cortisol-secreting adrenocortical carcinoma in a dog: case report. J Vet Med Sci; 2008 Mar;70(3):317-20
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  • [Title] Aldosterone-, corticosterone- and cortisol-secreting adrenocortical carcinoma in a dog: case report.
  • Abdominal ultrasonography confirmed a mass in the left adrenal gland.
  • Diagnosis was a tumor of the adrenal cortex with metastases.
  • Pathological findings confirmed a diagnosis of adrenocortical carcinoma.

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  • (PMID = 18388437.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 08J2K08A3Y / Dihydrotestosterone; 4964P6T9RB / Aldosterone; L0FPV48Q5R / trilostane; W980KJ009P / Corticosterone; WI4X0X7BPJ / Hydrocortisone
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50. Cuevas C, Raske M, Bush WH, Takayama T, Maki JH, Kolokythas O, Meshberg E: Imaging primary and secondary tumor thrombus of the inferior vena cava: multi-detector computed tomography and magnetic resonance imaging. Curr Probl Diagn Radiol; 2006 May-Jun;35(3):90-101
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  • [Title] Imaging primary and secondary tumor thrombus of the inferior vena cava: multi-detector computed tomography and magnetic resonance imaging.
  • Tumor thrombus of the inferior vena cava (IVC) is a severe medical condition with very poor prognosis unless the patient is treated with surgical resection.
  • It can be caused by a primary leiomyosarcoma originating in the vessel wall or by intraluminal extension of tumor thrombus into the IVC from an adjacent organ.
  • We reviewed 21 cases of tumoral thrombus in the IVC including primary leiomyosarcoma of the IVC (2 cases), renal cell carcinoma (14 cases), adrenocortical carcinoma (2 cases), primary adrenocortical leiomyosarcoma (1 case), hepatocellular carcinoma (1 case), and retroperitoneal metastasis (1 case).
  • The most common findings of IVC tumor thrombus by multi-detector CT and magnetic resonance imaging will be discussed, including scanning protocols and the advantages and disadvantages of each method.
  • [MeSH-major] Adrenal Gland Neoplasms / complications. Kidney Neoplasms / complications. Liver Neoplasms / complications. Thrombosis / diagnosis. Vena Cava, Inferior / radiography


51. Harvey PW, Everett DJ, Springall CJ: Adrenal toxicology: a strategy for assessment of functional toxicity to the adrenal cortex and steroidogenesis. J Appl Toxicol; 2007 Mar-Apr;27(2):103-15
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  • [Title] Adrenal toxicology: a strategy for assessment of functional toxicity to the adrenal cortex and steroidogenesis.
  • The adrenal is the most common toxicological target organ in the endocrine system in vivo and yet it is neglected in regulatory endocrine disruption screening and testing.
  • There has been a recent marked increase in interest in adrenal toxicity, but there are no standardised approaches for assessment.
  • Consequently, a strategy is proposed to evaluate adrenocortical toxicity.
  • Human adrenal conditions are reviewed and adrenocortical suppression, known to have been iatrogenically induced leading to Addisonian crisis and death, is identified as the toxicological hazard of most concern.
  • The consequences of inhibition of key steroidogenic enzymes and the possible toxicological modulation of other adrenal conditions are also highlighted.
  • The proposed strategy involves an in vivo rodent adrenal competency test based on ACTH challenge to specifically examine adrenocortical suppression.
  • The H295R human adrenocortical carcinoma cell line is also proposed to identify molecular targets, and is useful for measuring steroids, enzymes or gene expression.
  • Hypothalamo-pituitary-adrenal endocrinology relevant to rodent and human toxicology is reviewed (with an emphasis on multi-endocrine axis effects on the adrenal and also how the adrenal affects a variety of other hormones) and the endocrinology of the H295R cell line is also described.
  • Chemicals known to induce adrenocortical toxicity are reviewed and over 60 examples of compounds and their confirmed steroidogenic targets are presented, with much of this work published very recently using H295R cell systems.
  • In proposing a strategy for adrenocortical toxicity assessment, the outlined techniques will provide hazard assessment data but it will be regulatory agencies that must consider the significance of such data in risk extrapolation models.
  • The cases of etomindate and aminoglutethimide induced adrenal suppression are clearly documented examples of iatrogenic adrenal toxicity in humans.
  • Environmentally, sentinel species, such as fish, have also shown evidence of adrenal endocrine disruption attributed to exposure to chemicals.
  • The extent of human sub-clinical adrenal effects from environmental chemical exposures is unknown, and the extent to which environmental chemicals may act as a contributory factor to human adrenal conditions following chronic low-level exposures will remain unknown unless purposefully studied.
  • [MeSH-major] Adrenal Cortex / drug effects. Adrenal Cortex Hormones / metabolism. Hormone Antagonists / toxicity. Toxicity Tests / methods. Xenobiotics / toxicity
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Hypothalamo-Hypophyseal System / physiology. Pituitary-Adrenal System / physiology. Rats

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  • (PMID = 17265431.001).
  • [ISSN] 0260-437X
  • [Journal-full-title] Journal of applied toxicology : JAT
  • [ISO-abbreviation] J Appl Toxicol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Hormone Antagonists; 0 / Xenobiotics
  • [Number-of-references] 121
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52. Vuorenoja S, Rivero-Muller A, Kiiveri S, Bielinska M, Heikinheimo M, Wilson DB, Huhtaniemi IT, Rahman NA: Adrenocortical tumorigenesis, luteinizing hormone receptor and transcription factors GATA-4 and GATA-6. Mol Cell Endocrinol; 2007 Apr 15;269(1-2):38-45
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  • [Title] Adrenocortical tumorigenesis, luteinizing hormone receptor and transcription factors GATA-4 and GATA-6.
  • Luteinizing hormone (LH/hCG) responsiveness of normal and pathological human adrenal glands as well as the possibility of constitutive expressions of luteinizing hormone receptor (LHR) in adrenal cortex has been reported.
  • Some recent studies showed a correlation between the LHR and abundant GATA-4 expression in both metastasizing and non-metastasizing human adrenocortical tumors, but not in normal adrenals, implicating the putative relevance of LHR and GATA-4 for adrenocortical pathophysiology.
  • However, the physio- and pathophysiological significance of LHR and GATA-4 in the mechanism of adrenocortical tumorigenesis remains unclear.
  • The paucity of suitable models for adrenal tumorigenesis makes the establishment of proper animal models highly important.
  • LHR expression in the murine adrenal gland is an exception and not found in wild-type (WT) animal.
  • We have previously shown that ectopic LHR expression in the murine adrenal gland can be induced by chronically elevated LH levels.
  • We have generated a gonadotropin-responsive adrenal tumor model in gonadectomized transgenic (TG) mice expressing the inhibin alpha promoter/Simian Virus 40 T antigen transgene (inhalpha/Tag).
  • Given the induction of expression and regulation of GATA-4 and GATA-6 zinc finger transcription factors in the gonads by gonadotropins, this review will explore their relationship to LHR expression and their role in adrenocortical tumorigenesis.
  • A functional link between LHR and GATA-4 actions in the adrenal pathophysiology is proposed.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Carcinoma / genetics. GATA4 Transcription Factor / physiology. GATA6 Transcription Factor / physiology. Receptors, LH / physiology
  • [MeSH-minor] Animals. Disease Models, Animal. Humans. Inhibins / genetics. Mice. Mice, Transgenic

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  • (PMID = 17337116.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / GATA4 Transcription Factor; 0 / GATA4 protein, human; 0 / GATA6 Transcription Factor; 0 / GATA6 protein, human; 0 / Receptors, LH; 0 / inhibin-alpha subunit; 57285-09-3 / Inhibins
  • [Number-of-references] 87
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53. Rizzardi C, Brollo A, Thomann B, Santirocco C, Melato M: Intra-abdominal ovarian-type mucinous cystadenoma associated with fallopian tube-like structure and aberrant epididymal tissue in a male patient. Hum Pathol; 2005 Aug;36(8):927-31
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  • Ovarian-type mucinous tumors may occasionally occur in the retroperitoneum, pancreas, and liver exclusively or almost exclusively in women.
  • In men, only few cases of such neoplasms arising within or around the testis have been reported.
  • We describe a unique case of an ovarian-type mucinous cystadenoma occurring in the peritoneal cavity of a 65-year-old male patient with secondary adrenocortical insufficiency and hypogonadism.
  • There was a typical fallopian tube enclosed in the capsule of the tumor.
  • We have interpreted this case as the result of a minor disorder of embryonic development involving structures of both müllerian and wolffian origin.
  • [MeSH-major] Cystadenoma, Mucinous / pathology. Peritoneal Neoplasms / pathology

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  • (PMID = 16112012.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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54. Jain SH, Sadow PM, Nosé V, Dluhy RG: A patient with ectopic cortisol production derived from malignant testicular masses. Nat Clin Pract Endocrinol Metab; 2008 Dec;4(12):695-700
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  • DIAGNOSIS: Cushing syndrome was diagnosed on the basis of a markedly elevated 24-hour urine free cortisol level and classic cushingoid features.
  • The etiology of Cushing syndrome was determined to be an adrenocortical carcinoma arising from testicular adrenal rest cells.
  • Nevertheless, the possibility of a malignant Leydig cell tumor with ectopic cortisol production could not be excluded.
  • Despite initial success with this regimen, the patient died as a result of tumor progression and complications of poorly controlled hypercortisolism.
  • [MeSH-major] Adrenal Rest Tumor / complications. Cushing Syndrome / diagnosis. Cushing Syndrome / drug therapy. Hydrocortisone / blood. Testicular Neoplasms / complications
  • [MeSH-minor] Adrenocortical Carcinoma / blood. Adrenocortical Carcinoma / diagnosis. Adrenocortical Carcinoma / pathology. Adrenocorticotropic Hormone / blood. Aged. Humans. Male. Metyrapone / therapeutic use. Mitotane / therapeutic use

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  • (PMID = 18941436.001).
  • [ISSN] 1745-8374
  • [Journal-full-title] Nature clinical practice. Endocrinology & metabolism
  • [ISO-abbreviation] Nat Clin Pract Endocrinol Metab
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 78E4J5IB5J / Mitotane; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone; ZS9KD92H6V / Metyrapone
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55. 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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  • [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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56. Tian L, Guo Y, Wu YP, Liu LZ: [CT features of adrenal cortical adenoma: a report of 109 cases]. Ai Zheng; 2008 Jan;27(1):66-70
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  • [Title] [CT features of adrenal cortical adenoma: a report of 109 cases].
  • BACKGROUND & OBJECTIVE: Adrenal cortical adenoma (ACA) is a common disease, and can be diagnosed easily with CT examination.
  • The maximal diameter of the tumor was <5 cm in 95 patients.
  • The maximal diameter of the tumor was > 5 cm in 14 patients.
  • [MeSH-major] Adrenal Cortex Neoplasms / radiography. Adrenocortical Adenoma / radiography. Radiographic Image Enhancement / methods. Tomography, Spiral Computed / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Diagnosis, Differential. Female. Humans. Infant. Male. Middle Aged. Neoplasm Recurrence, Local. Tumor Burden. Young Adult

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  • (PMID = 18184467.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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57. Almeida MQ, Fragoso MC, Lotfi CF, Santos MG, Nishi MY, Costa MH, Lerario AM, Maciel CC, Mattos GE, Jorge AA, Mendonca BB, Latronico AC: Expression of insulin-like growth factor-II and its receptor in pediatric and adult adrenocortical tumors. J Clin Endocrinol Metab; 2008 Sep;93(9):3524-31
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  • [Title] Expression of insulin-like growth factor-II and its receptor in pediatric and adult adrenocortical tumors.
  • BACKGROUND: Adrenocortical tumors are heterogeneous neoplasms with incompletely understood pathogenesis.
  • IGF-II overexpression has been consistently demonstrated in adult adrenocortical carcinomas.
  • OBJECTIVES: The objective of the study was to analyze expression of IGF-II and its receptor (IGF-IR) in pediatric and adult adrenocortical tumors and the effects of a selective IGF-IR kinase inhibitor (NVP-AEW541) on adrenocortical tumor cells.
  • PATIENTS: Fifty-seven adrenocortical tumors (37 adenomas and 20 carcinomas) from 23 children and 34 adults were studied.
  • Cell proliferation and apoptosis were analyzed in NCI H295 cells and a new cell line established from a pediatric adrenocortical adenoma.
  • RESULTS: IGF-II transcripts were overexpressed in both pediatric adrenocortical carcinomas and adenomas.
  • Otherwise, IGF-II was mainly overexpressed in adult adrenocortical carcinomas (270.5 +/- 130.2 vs. 16.1 +/- 13.3; P = 0.0001).
  • IGF-IR expression was significantly higher in pediatric adrenocortical carcinomas than adenomas (9.1 +/- 3.1 vs. 2.6 +/- 0.3; P = 0.0001), whereas its expression was similar in adult adrenocortical carcinomas and adenomas.
  • IGF-IR expression was a predictor of metastases in pediatric adrenocortical tumors in univariate analysis (hazard ratio 1.84; 95% confidence interval 1.28-2.66; P = 0.01).
  • CONCLUSION: IGF-IR overexpression was a biomarker of pediatric adrenocortical carcinomas.
  • Additionally, a selective IGF-IR kinase inhibitor had antitumor effects in adult and pediatric adrenocortical tumor cell lines, suggesting that IGF-IR inhibitors represent a promising therapy for human adrenocortical carcinoma.
  • [MeSH-major] Adenoma / genetics. Adrenal Cortex Neoplasms / genetics. Carcinoma / genetics. Insulin-Like Growth Factor II / genetics. Receptor, IGF Type 2 / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Female. Gene Expression Regulation, Neoplastic. Humans. Infant. Male. Middle Aged. Neoplasm Metastasis. Tumor Cells, Cultured

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  • (PMID = 18611974.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptor, IGF Type 2; 67763-97-7 / Insulin-Like Growth Factor II
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58. Suyama K, Beppu T, Isiko T, Sugiyama S, Matsumoto K, Doi K, Masuda T, Ohara C, Takamori H, Kanemitsu K, Hirota M, Baba H: Spontaneous rupture of adrenocortical carcinoma. Am J Surg; 2007 Jul;194(1):77-8
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  • [Title] Spontaneous rupture of adrenocortical carcinoma.
  • Massive hemorrhage from an adrenocortical carcinoma seldom occurs in the retroperitoneal or abdominal cavity.
  • We report a case of spontaneous rupture of primary adrenocortical carcinoma occurring in an adolescent.
  • A right adrenalectomy with complete removal of the tumor was performed successfully.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenocortical Carcinoma / surgery

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  • (PMID = 17560914.001).
  • [ISSN] 1879-1883
  • [Journal-full-title] American journal of surgery
  • [ISO-abbreviation] Am. J. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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59. Xu Y, Yu RM, Zhang X, Murphy MB, Giesy JP, Lam MH, Lam PK, Wu RS, Yu H: Effects of PCBs and MeSO2-PCBs on adrenocortical steroidogenesis in H295R human adrenocortical carcinoma cells. Chemosphere; 2006 May;63(5):772-84
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  • [Title] Effects of PCBs and MeSO2-PCBs on adrenocortical steroidogenesis in H295R human adrenocortical carcinoma cells.
  • In this study, the potential effects of four selected polychlorinated biphenyl (PCB) congeners (PCB101, PCB110, PCB126 and PCB149) as well as several of their environmentally-relevant methylsulfonyl-(MeSO(2)-) PCB metabolites (3'-MeSO(2)-CB101, 4'-MeSO(2)-CB101, 4'-MeSO(2)-CB110, 3'-MeSO(2)-CB149 and 4'-MeSO(2)-CB149) on adrenocortical steroidogenesis were evaluated by in vitro bioassay based on the human adrenocortical carcinoma H295R cell line.
  • Overall, these findings suggest that PCBs and PCB metabolites can affect regulation of adrenocortical steroidogenesis.
  • [MeSH-major] Adrenocortical Carcinoma / metabolism. Cytochrome P-450 Enzyme System / biosynthesis. Hydroxysteroid Dehydrogenases / drug effects. Polychlorinated Biphenyls / toxicity. Steroids / biosynthesis
  • [MeSH-minor] Enzyme Activation / drug effects. Humans. Tumor Cells, Cultured

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  • (PMID = 16216300.001).
  • [ISSN] 0045-6535
  • [Journal-full-title] Chemosphere
  • [ISO-abbreviation] Chemosphere
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Steroids; 9035-51-2 / Cytochrome P-450 Enzyme System; DFC2HB4I0K / Polychlorinated Biphenyls; EC 1.1.- / Hydroxysteroid Dehydrogenases
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60. Watanabe M, Noda M, Nakajin S: Effect of epidermal growth factor and prostaglandin on the expression of aromatase (CYP19) in human adrenocortical carcinoma cell line NCI-H295R cells. J Endocrinol; 2006 Jan;188(1):59-68
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  • [Title] Effect of epidermal growth factor and prostaglandin on the expression of aromatase (CYP19) in human adrenocortical carcinoma cell line NCI-H295R cells.
  • We investigated the effects of epidermal growth factor (EGF) and prostaglandins (PG) on the expression of aromatase (CYP19) in human adrenocortical carcinoma cell line NCI-H295R cells.
  • [MeSH-major] Adrenal Cortex Neoplasms / enzymology. Aromatase / metabolism. Epidermal Growth Factor / pharmacology. Prostaglandins / pharmacology
  • [MeSH-minor] Alprostadil / analogs & derivatives. Alprostadil / pharmacology. Benzylamines / pharmacology. Cell Line, Tumor. Dinoprost / pharmacology. Dinoprostone / analogs & derivatives. Dinoprostone / pharmacology. Exons. Flavonoids / pharmacology. Humans. Isoquinolines / pharmacology. Promoter Regions, Genetic. Prostaglandins A / pharmacology. Prostaglandins E / analysis. Prostaglandins E / pharmacology. Protein Kinase Inhibitors / pharmacology. RNA, Messenger / analysis. Receptors, Prostaglandin E / agonists. Receptors, Prostaglandin E, EP1 Subtype. Receptors, Prostaglandin E, EP2 Subtype. Reverse Transcriptase Polymerase Chain Reaction. Stimulation, Chemical. Sulfonamides / pharmacology

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  • (PMID = 16394175.001).
  • [ISSN] 0022-0795
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / 9-deoxy-9-chloro-15-deoxy-16-hydroxy-17,17-trimethylene-19,20-didehydroprostaglandin E2; 0 / Benzylamines; 0 / Flavonoids; 0 / Isoquinolines; 0 / ONO-DI-004; 0 / PTGER1 protein, human; 0 / PTGER2 protein, human; 0 / Prostaglandins; 0 / Prostaglandins A; 0 / Prostaglandins E; 0 / Protein Kinase Inhibitors; 0 / RNA, Messenger; 0 / Receptors, Prostaglandin E; 0 / Receptors, Prostaglandin E, EP1 Subtype; 0 / Receptors, Prostaglandin E, EP2 Subtype; 0 / Sulfonamides; 127243-85-0 / N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide; 139298-40-1 / KN 93; 62229-50-9 / Epidermal Growth Factor; B7IN85G1HY / Dinoprost; EC 1.14.14.1 / Aromatase; F5TD010360 / Alprostadil; K7Q1JQR04M / Dinoprostone; VYR271N44P / prostaglandin A1
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61. Zografos GN, Vasiliadis G, Farfaras AN, Aggeli C, Digalakis M: Laparoscopic surgery for malignant adrenal tumors. JSLS; 2009 Apr-Jun;13(2):196-202
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  • [Title] Laparoscopic surgery for malignant adrenal tumors.
  • Advances in imaging have improved early detection of primary and metastatic adrenal tumors.
  • The laparoscopic approach, the gold standard for benign adrenal diseases, is controversial for malignant adrenal tumors.
  • A prospective randomized study of the role of laparoscopic surgery in adrenal cancer is not feasible because of the rarity of the disease.
  • A review of the literature demonstrates the safety and efficacy of laparoscopic adrenalectomy for solitary adrenal tumors.
  • In primary adrenal malignancies, the laparoscopic approach should be considered cautiously, only when it can achieve complete tumor resection with an intact adrenal capsule.
  • Conversion to an open procedure should be an early decision, prior to tumor morcellation or fracture of the tumor capsule.
  • Patients who have local invasion, tumors that are too large, or require organ resection require an open procedure.

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  • (PMID = 19660215.001).
  • [ISSN] 1086-8089
  • [Journal-full-title] JSLS : Journal of the Society of Laparoendoscopic Surgeons
  • [ISO-abbreviation] JSLS
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 63
  • [Other-IDs] NLM/ PMC3015945
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62. Karim RZ, Wills EJ, McCarthy SW, Scolyer RA: Myxoid variant of adrenocortical carcinoma: report of a unique case. Pathol Int; 2006 Feb;56(2):89-94
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  • [Title] Myxoid variant of adrenocortical carcinoma: report of a unique case.
  • Myxoid variant of adrenocortical carcinomas (ACC) are rare, there being only 11 cases in the literature to date.
  • Reported herein are the findings of a case, which in contrast to all previously reported myxoid ACC, was devoid of typical non-myxoid areas.
  • The patient was a 61-year-old man in whom a left adrenal mass was detected during investigation of Cushing's syndrome.
  • The adrenal was replaced by malignant cells and expanses of myxoid material.
  • The ultrastructural features of the cells were typical of adrenal cortical differentiation.
  • The differential diagnosis of myxoid ACC includes extraskeletal myxoid chondrosarcoma, chordoma, myxoid adenocarcinoma, myxoma, lipomatous tumors, nerve sheath tumors, smooth muscle tumors, gastrointestinal stromal tumor and other sarcomas.
  • The presence of myxoid material in a retroperitoneal lesion raises a broad differential diagnosis in which myxoid adrenocortical neoplasms should be included.
  • Clinicoradiological correlation may be helpful, but special stains, immunohistochemistry and ultrastructural examination may be necessary to establish the diagnosis.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenocortical Carcinoma / diagnosis
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Antigens, Neoplasm. Chordoma / diagnosis. Chordoma / pathology. Diagnosis, Differential. Humans. Immunohistochemistry. MART-1 Antigen. Male. Microscopy, Electron. Middle Aged. Myxoma / diagnosis. Myxoma / pathology. Neoplasm Proteins / analysis. Nerve Sheath Neoplasms / diagnosis. Nerve Sheath Neoplasms / pathology. Retroperitoneal Neoplasms / diagnosis. Retroperitoneal Neoplasms / pathology. Synaptophysin / analysis. Vimentin / analysis

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  • (PMID = 16445821.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / MART-1 Antigen; 0 / MLANA protein, human; 0 / Neoplasm Proteins; 0 / Synaptophysin; 0 / Vimentin
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63. Mete O, Kapran Y, Güllüoğlu MG, Kiliçaslan I, Erbil Y, Senyürek YG, Dizdaroğlu F: Anti-CD10 (56C6) is expressed variably in adrenocortical tumors and cannot be used to discriminate clear cell renal cell carcinomas. Virchows Arch; 2010 May;456(5):515-21
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  • [Title] Anti-CD10 (56C6) is expressed variably in adrenocortical tumors and cannot be used to discriminate clear cell renal cell carcinomas.
  • In the evaluation of retroperitoneal masses, the practicing pathologist faces a dilemma when making a diagnosis based on histology given the often overlapping morphologic appearances of the adrenocortical carcinoma, renal cell carcinoma (RCC), and hepatocellular carcinoma (HCC).
  • However, its expression is not well-investigated in adrenal cortical tumors.
  • We examined CD10 expression in 47 surgically resected adrenocortical tumors (26 adenomas and 21 carcinomas) and compared with 20 clear cell RCCs and 25 HCCs.
  • Twenty HCCs (80%), 18 RCCs (90%), 11 adrenocortical carcinomas (52%), and 18 adrenocortical adenomas (69%) were positive for CD10.
  • Adrenocortical tumors displayed mainly cytoplasmic staining.
  • Four adrenocortical carcinomas and one adenoma also displayed the membranous staining pattern.
  • Despite the relatively small number of samples, our preliminary results revealed that adrenocortical tumors may express CD10 (Clone: 56C6).
  • The most important point from this paper is the fact that anti-CD10 expression has not been previously reported in adrenocortical carcinomas.
  • This suggests that CD10 does not seem to be a useful marker for discriminating clear cell RCCs from adrenocortical tumors since CD10 expression does not rule out the possibility of adrenocortical tumors.
  • This feature should be kept in mind when constructing an antibody panel for an epithelial tumor that involves the adrenal gland and kidney, especially in small biopsy specimens.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Carcinoma, Renal Cell / diagnosis. Kidney Neoplasms / diagnosis. Neprilysin / biosynthesis
  • [MeSH-minor] Adult. Antigens, Neoplasm / analysis. Carcinoma, Hepatocellular / diagnosis. Carcinoma, Hepatocellular / immunology. Female. Humans. Liver Neoplasms / diagnosis. Liver Neoplasms / immunology. Male. Middle Aged

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  • (PMID = 20390424.001).
  • [ISSN] 1432-2307
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; EC 3.4.24.11 / Neprilysin
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64. Bielinska M, Kiiveri S, Parviainen H, Mannisto S, Heikinheimo M, Wilson DB: Gonadectomy-induced adrenocortical neoplasia in the domestic ferret (Mustela putorius furo) and laboratory mouse. Vet Pathol; 2006 Mar;43(2):97-117
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  • [Title] Gonadectomy-induced adrenocortical neoplasia in the domestic ferret (Mustela putorius furo) and laboratory mouse.
  • Sex steroid-producing adrenocortical adenomas and carcinomas occur frequently in neutered ferrets, but the molecular events underlying tumor development are not well understood.
  • Prepubertal gonadectomy elicits similar tumors in certain inbred or genetically engineered strains of mice, and these mouse models shed light on tumorigenesis in ferrets.
  • In mice and ferrets, the neoplastic adrenocortical cells, which functionally resemble gonadal steroidogenic cells, arise from progenitors in the subcapsular or juxtamedullary region.
  • Tumorigenesis in mice is influenced by the inherent susceptibility of adrenal tissue to gonadectomy-induced hormonal changes.
  • Gonadectomy alters the plasma or local concentrations of steroid hormones and other factors that affect adrenocortical tumor development, including inhibins, activins, and Müllerian inhibiting substance.
  • Cases of human adrenocortical neoplasia have been linked to precocious expression of hormone receptors and to mutations that alter the activity of G-proteins or downstream effectors.
  • Whether such genetic changes contribute to tissue susceptibility to neoplasia in neutered ferrets and mice awaits further study.
  • [MeSH-major] Adrenal Cortex Neoplasms / veterinary. Castration / veterinary. Ferrets

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  • (PMID = 16537928.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK52574; United States / NHLBI NIH HHS / HL / HL61006
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 135
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65. Wang FF, Chang YH, Pan CC, Tu DG, Won JG: Unusual visualization of an adrenal carcinoma on NP-59 scintiscan. J Formos Med Assoc; 2006 Apr;105(4):340-5
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  • [Title] Unusual visualization of an adrenal carcinoma on NP-59 scintiscan.
  • [Iodine-131]6-beta-iodomethylnorcholesterol (NP-59) visualization of adrenocortical carcinoma is unusual.
  • Magnetic resonance imaging disclosed a 9-cm right adrenal mass.
  • NP-59 adrenal scanning displayed unilateral uptake of tracer and no visualization of the contralateral adrenal gland.
  • Exploratory laparotomy revealed adrenocortical carcinoma.
  • Subsequent immunohistochemical studies confirmed that the tumor was capable of producing a mixture of steroids, including testosterone, DHEAS and aldosterone.
  • Visualization of an adrenal tumor on NP-59 scintiscan is an unusual finding, which cannot exclude the possibility of malignancy.

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  • (PMID = 16618615.001).
  • [ISSN] 0929-6646
  • [Journal-full-title] Journal of the Formosan Medical Association = Taiwan yi zhi
  • [ISO-abbreviation] J. Formos. Med. Assoc.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Singapore
  • [Chemical-registry-number] 3XMK78S47O / Testosterone; 4964P6T9RB / Aldosterone; 55623-03-5 / Adosterol; 57B09Q7FJR / Dehydroepiandrosterone Sulfate
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66. Heyerdahl SL, Boikos S, Horvath A, Giatzakis C, Bossis I, Stratakis CA: Protein kinase A subunit expression is altered in Bloom syndrome fibroblasts and the BLM protein is increased in adrenocortical hyperplasias: inverse findings for BLM and PRKAR1A. Horm Metab Res; 2008 Jun;40(6):391-7
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  • [Title] Protein kinase A subunit expression is altered in Bloom syndrome fibroblasts and the BLM protein is increased in adrenocortical hyperplasias: inverse findings for BLM and PRKAR1A.
  • Bloom syndrome is a genetic disorder associated with chromosomal instability and a predisposition to tumors that is caused by germline mutations of the BLM gene, a RecQ helicase.
  • Benign adrenocortical tumors display a degree of chromosomal instability that is more significant than benign tumors of other tissues.
  • Cortisol-producing hyperplasias, such as primary pigmented nodular adrenocortical disease (PPNAD), which has been associated with protein kinase A (PKA) abnormalities and/or PRKAR1A mutations, also show genomic instability.
  • In this study, we have investigated the PRKAR1A expression in primary human Bloom syndrome cell lines with known BLM mutations and examined the BLM gene expression in PPNAD and other adrenal tumor tissues.
  • The BLM protein was upregulated in PPNAD and other hyperplasias, compared to samples from normal adrenals and normal cortex, as well as samples from cortisol- and aldosterone-producing adenomas (in which BLM was largely absent).
  • These data reveal an inverse relationship between BLM and PRKAR1A: BLM deficiency is associated with a relative excess of PRKAR1A in fibroblasts compared to other PKA subunits; and PRKAR1A deficiency is associated with increased BLM protein in adrenal hyperplasias.
  • [MeSH-major] Adrenal Cortex Diseases / metabolism. Bloom Syndrome / metabolism. Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / metabolism. DNA Helicases / metabolism. Fibroblasts / metabolism
  • [MeSH-minor] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / metabolism. Adrenal Cortex Neoplasms / pathology. Adrenal Glands / metabolism. Adrenal Glands / pathology. Cell Line. Gene Expression Regulation. Humans. Hyperplasia. Immunohistochemistry. Pigmentation Disorders / complications. Pigmentation Disorders / genetics. Pigmentation Disorders / metabolism. Pigmentation Disorders / pathology. RNA, Messenger / analysis. RecQ Helicases

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  • (PMID = 18401830.001).
  • [ISSN] 0018-5043
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human; 0 / RNA, Messenger; EC 3.6.1.- / Bloom syndrome protein; EC 3.6.4.- / DNA Helicases; EC 3.6.4.12 / RecQ Helicases
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67. Tissier F: [Pathology of adrenocortical tumors: review and recent data]. Ann Endocrinol (Paris); 2009 Jun;70(3):179-85
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  • [Title] [Pathology of adrenocortical tumors: review and recent data].
  • [Transliterated title] Anatomie pathologique des tumeurs corticosurrénaliennes de l'adulte : état des lieux et données récentes.
  • Most adrenocortical tumors are benign; adrenocortical carcinomas are rare but their prognosis is poor and their therapeutic is sparse.
  • In most adrenocortical tumors, the morphological approach brings sufficient 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.
  • These genetics findings already have repercussions for the patients in the development of molecular markers for diagnosis and prognosis and in the future they could help in the development of new morphological approaches, in particular immunohistochemical approaches.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology
  • [MeSH-minor] Cyclin E / genetics. Gene Expression Regulation, Neoplastic. Insulin-Like Growth Factor II / genetics. Mitosis. Mutation. Necrosis / pathology. Neoplasm Metastasis / pathology. Pheochromocytoma / genetics. Pheochromocytoma / pathology. Prognosis. Tumor Suppressor Protein p53 / genetics. beta Catenin / genetics

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  • (PMID = 19298951.001).
  • [ISSN] 0003-4266
  • [Journal-full-title] Annales d'endocrinologie
  • [ISO-abbreviation] Ann. Endocrinol. (Paris)
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Cyclin E; 0 / Tumor Suppressor Protein p53; 0 / beta Catenin; 67763-97-7 / Insulin-Like Growth Factor II
  • [Number-of-references] 77
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68. Jaroenporn S, Furuta C, Nagaoka K, Watanabe G, Taya K: Comparative effects of prolactin versus ACTH, estradiol, progesterone, testosterone, and dihydrotestosterone on cortisol release and proliferation of the adrenocortical carcinoma cell line H295R. Endocrine; 2008 Apr;33(2):205-9
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  • [Title] Comparative effects of prolactin versus ACTH, estradiol, progesterone, testosterone, and dihydrotestosterone on cortisol release and proliferation of the adrenocortical carcinoma cell line H295R.
  • In this study, using the H295R cell line as a model system, we investigated the role of prolactin (PRL) and steroid hormones in the growth regulation and cortisol release of adrenocortical cells.
  • Taken together, these results indicate that steroid hormones exert differential effects on adrenocortical function.
  • Additionally, the present study demonstrates that PRL had biphasic actions in regulating adrenocortical function.
  • PRL may form a novel regulatory system for steroid hormone secretion and cell proliferation in the adrenal cortex.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Cell Proliferation / drug effects. Gonadal Steroid Hormones / pharmacology. Hydrocortisone / metabolism. Prolactin / pharmacology
  • [MeSH-minor] Adrenocorticotropic Hormone / pharmacology. Cell Line, Tumor. Dihydrotestosterone / pharmacology. Dose-Response Relationship, Drug. Estradiol / pharmacology. Humans. Progesterone / pharmacology. Radioimmunoassay. Testosterone / pharmacology

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  • (PMID = 18484195.001).
  • [ISSN] 1355-008X
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gonadal Steroid Hormones; 08J2K08A3Y / Dihydrotestosterone; 3XMK78S47O / Testosterone; 4G7DS2Q64Y / Progesterone; 4TI98Z838E / Estradiol; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin; WI4X0X7BPJ / Hydrocortisone
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69. Abidi P, Zhang H, Zaidi SM, Shen WJ, Leers-Sucheta S, Cortez Y, Han J, Azhar S: Oxidative stress-induced inhibition of adrenal steroidogenesis requires participation of p38 mitogen-activated protein kinase signaling pathway. J Endocrinol; 2008 Jul;198(1):193-207
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  • [Title] Oxidative stress-induced inhibition of adrenal steroidogenesis requires participation of p38 mitogen-activated protein kinase signaling pathway.
  • To accomplish these studies, we employed a highly responsive mouse adrenocortical cell line, Y1-BS1 cells that secrete large quantities of steroids when stimulated with lipoprotein plus hormone.
  • Inhibition of p38 MAPK with SB203580 or SB202190 upregulated the basal steroid production and also prevented the oxidant-mediated inhibition of steroid production. mRNA measurements by qPCR indicated that Y1-BS1 adrenal cells predominantly express p38 MAPKalpha isoform, along with relatively low-level expression of p38 MAPKgamma.
  • These results indicate that activated p38 MAPK mediates oxidant (excessive oxidative stress)-induced inhibition of adrenal steroidogenesis.
  • [MeSH-major] 20-alpha-Dihydroprogesterone / biosynthesis. Adrenal Glands / metabolism. MAP Kinase Signaling System. Oxidative Stress. p38 Mitogen-Activated Protein Kinases / physiology
  • [MeSH-minor] Adrenocorticotropic Hormone / pharmacology. Animals. Cell Line, Tumor. Cyclic CMP / analogs & derivatives. Cyclic CMP / pharmacology. MAP Kinase Kinase 3 / physiology. MAP Kinase Kinase 6 / physiology. Mice. Phosphoproteins / genetics. Phosphorylation. Superoxides / metabolism

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  • (PMID = 18417530.001).
  • [ISSN] 1479-6805
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK56339
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Phosphoproteins; 0 / steroidogenic acute regulatory protein; 11062-77-4 / Superoxides; 145-14-2 / 20-alpha-Dihydroprogesterone; 3616-08-8 / Cyclic CMP; 64649-87-2 / dibutyryl cyclic-3',5'-cytidine monophosphate; 9002-60-2 / Adrenocorticotropic Hormone; EC 2.7.1.- / Map2k3 protein, mouse; EC 2.7.1.- / Map2k6 protein, mouse; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 2.7.12.2 / MAP Kinase Kinase 3; EC 2.7.12.2 / MAP Kinase Kinase 6
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70. Miyoshi Y, Oue T, Oowari M, Soh H, Tachibana M, Kimura S, Kiyohara Y, Yamada H, Bessyo K, Mushiake S, Homma K, Hasegawa T, Sasano H, Ozono K: A case of pediatric virilizing adrenocortical tumor resulting in hypothalamic-pituitary activation and central precocious puberty following surgical removal. Endocr J; 2009;56(8):975-82
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  • [Title] A case of pediatric virilizing adrenocortical tumor resulting in hypothalamic-pituitary activation and central precocious puberty following surgical removal.
  • We present a 6-year-old boy with a virilizing adrenocortical tumor who initially presented with peripheral precocious puberty.
  • Both serum and urinary levels of adrenal androgens were elevated.
  • The histological diagnosis was adrenocortical carcinoma according to the criteria of Weiss.
  • Following surgical removal of the androgen-producing tumor, the patient subsequently developed hypothalamic-pituitary activation and demonstrated central precocious puberty.
  • Clinical follow-up of potential secondary effects of excess hormone secretion after removal is important in some pediatric patients with virilizing adrenocortical tumor.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenal Cortex Neoplasms / surgery. Adrenocortical Carcinoma / complications. Adrenocortical Carcinoma / surgery. Hypothalamo-Hypophyseal System / physiopathology. Puberty, Precocious / etiology

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  • (PMID = 19671995.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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71. Fassnacht M, Johanssen S, Quinkler M, Bucsky P, Willenberg HS, Beuschlein F, Terzolo M, Mueller HH, Hahner S, Allolio B, German Adrenocortical Carcinoma Registry Group, European Network for the Study of Adrenal Tumors: Limited prognostic value of the 2004 International Union Against Cancer staging classification for adrenocortical carcinoma: proposal for a Revised TNM Classification. Cancer; 2009 Jan 15;115(2):243-50
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  • [Title] Limited prognostic value of the 2004 International Union Against Cancer staging classification for adrenocortical carcinoma: proposal for a Revised TNM Classification.
  • BACKGROUND: Adrenocortical carcinoma (ACC) is a rare malignancy, and it was only in 2004 that the International Union Against Cancer (UICC) defined TNM criteria and published the first staging classification.
  • METHODS: The German ACC Registry comprising 492 patients was searched for patients who were diagnosed between 1986 and 2007 with detailed information on primary diagnosis and a minimum follow-up of 6 months.
  • Patients were assigned to UICC tumor stage, and disease-specific survival (DSS) was assessed.
  • Furthermore, patients who had stage IV ACC without distant metastases had an improved DSS compared with patients who had metastatic disease (P=.004).
  • An analysis of different potential risk factors for defining stage III ACC revealed important roles in DSS for tumor infiltration in surrounding tissue, venous tumor thrombus (VTT), and positive lymph nodes; whereas tumor invasion in adjacent organs carried a prognosis similar to that of infiltration in surrounding tissue only.
  • On the basis of the current analysis, a revised classification with superior prognostic accuracy is proposed (the European Network for the Study of Adrenal Tumors classification).
  • [MeSH-major] Adrenocortical Carcinoma / pathology. Neoplasm Staging / classification
  • [MeSH-minor] Humans. Lymphatic Metastasis. Neoplasm Invasiveness. Neoplasm Metastasis. Prognosis. Risk Factors

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  • [Copyright] Copyright (c) 2009 American Cancer Society.
  • [CommentIn] Cancer. 2009 Dec 15;115(24):5847; author reply 5848 [19827149.001]
  • (PMID = 19025987.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Investigator] Allolio B; Behrend M; Bucsky P; Brauckhoff M; Fasanacht M; Fottner C; Haaf M; Hahner S; Johanssen S; Koschker AC; Langer P; Laubner K; Linden T; Maeder U; Morcos M; Oelkers W; Quinkler M; Reincke M; Reisch N; Saeger W; Weismann D; Willenberg HS; Wortmann S; Baudin E; Bertherat J; Beuschlein F; Mannelli M; Terzolo M
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72. Rosenkrantz AB, Do RK, Hajdu CH: Imaging appearance of bulk fat within an oncocytic adrenocortical neoplasm, a rare and potentially malignant tumour. Br J Radiol; 2010 Oct;83(994):e204-7
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  • [Title] Imaging appearance of bulk fat within an oncocytic adrenocortical neoplasm, a rare and potentially malignant tumour.
  • Oncocytic adrenocortical neoplasm is a rare adrenal tumour that usually follows a benign clinical course.
  • In some cases, however, these tumours have exhibited malignant behaviour.
  • Here, we present the first published case showing bulk fat within an oncocytic adrenocortical neoplasm on CT and MRI, a finding that mimics fat within an adrenal myelolipoma.
  • The distinction between these entities is important, as the current suggested management of an oncocytic adrenocortical neoplasm is resection with subsequent imaging surveillance.
  • [MeSH-major] Adenoma, Oxyphilic / diagnosis. Adrenal Cortex Neoplasms / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Proteins / metabolism. Tomography, X-Ray Computed

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  • (PMID = 20846977.001).
  • [ISSN] 1748-880X
  • [Journal-full-title] The British journal of radiology
  • [ISO-abbreviation] Br J Radiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neoplasm Proteins
  • [Other-IDs] NLM/ PMC3473746
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73. Fassnacht M, Weismann D, Ebert S, Adam P, Zink M, Beuschlein F, Hahner S, Allolio B: AKT is highly phosphorylated in pheochromocytomas but not in benign adrenocortical tumors. J Clin Endocrinol Metab; 2005 Jul;90(7):4366-70
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  • [Title] AKT is highly phosphorylated in pheochromocytomas but not in benign adrenocortical tumors.
  • CONTEXT: Activation of AKT plays a major role in a variety of human neoplasias.
  • OBJECTIVE: The objective of this study was the investigation of the role of AKT in the pathogenesis of pheochromocytomas and adrenocortical tumors.
  • DESIGN, SETTING, AND PARTICIPANTS: Total AKT and phosphorylated AKT (pAKT) in 15 pheochromocytomas, nine aldosterone-producing adenomas, nine cortisol-producing adenomas, eight adrenocortical carcinomas (ACC), and 15 normal adrenals were investigated by Western blot analysis.
  • Immunohistochemistry for total AKT and pAKT was performed in pheochromocytomas (n = 8), ACC (n = 4), and normal adrenal glands (n = 2).
  • MAIN OUTCOME MEASURES: Determination of pAKT/total AKT ratio in adrenal tissues was the main outcome.
  • CONCLUSION: Our findings provide evidence for increased activation of AKT in pheochromocytomas but not in adrenocortical adenomas.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenal Gland Neoplasms / metabolism. Pheochromocytoma / metabolism. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins / metabolism
  • [MeSH-minor] Adult. Aged. Female. Humans. Immunohistochemistry. Male. Middle Aged. PTEN Phosphohydrolase. Phosphatidylinositol 3-Kinases / physiology. Phosphoric Monoester Hydrolases / analysis. Phosphorylation. Proto-Oncogene Proteins c-akt. Tumor Suppressor Proteins / analysis

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  • (PMID = 15855265.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Proteins; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
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74. Mazzuco TL, Chabre O, Feige JJ, Thomas M: Aberrant expression of human luteinizing hormone receptor by adrenocortical cells is sufficient to provoke both hyperplasia and Cushing's syndrome features. J Clin Endocrinol Metab; 2006 Jan;91(1):196-203
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  • [Title] Aberrant expression of human luteinizing hormone receptor by adrenocortical cells is sufficient to provoke both hyperplasia and Cushing's syndrome features.
  • CONTEXT: Aberrant expression of LH/human chorionic gonadotropin (hCG) receptor has been suggested in several cases of bilateral macronodular adrenal hyperplasia with Cushing's syndrome.
  • OBJECTIVE: The aim of this study was to explore the action of LH/hCG receptor on the development of adrenal hyperplasia.
  • RESULTS: The ectopic expression of this single nonmutated gene transduced into bovine adrenocortical cells was sufficient to induce not only the aberrant cortisol secretion but also hyperproliferation and benign transformation.
  • CONCLUSIONS: These results demonstrate that a single genetic event such as the inappropriate expression of the nonmutated LH/hCG receptor gene is sufficient to initiate the phenotypic changes that cause the development of a benign adrenocortical tumor.
  • [MeSH-major] Adrenal Cortex / metabolism. Adrenal Hyperplasia, Congenital / genetics. Cushing Syndrome / genetics. Receptors, LH / biosynthesis

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  • (PMID = 16249277.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / DNA-Binding Proteins; 0 / Rag2 protein, mouse; 0 / Receptors, LH
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75. Venkatesan AM, Locklin J, Dupuy DE, Wood BJ: Percutaneous ablation of adrenal tumors. Tech Vasc Interv Radiol; 2010 Jun;13(2):89-99
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  • [Title] Percutaneous ablation of adrenal tumors.
  • Adrenal tumors comprise a broad spectrum of benign and malignant neoplasms and include functional adrenal adenomas, pheochromocytomas, primary adrenocortical carcinoma, and adrenal metastases.
  • Percutaneous ablative approaches that have been described and used in the treatment of adrenal tumors include percutaneous radiofrequency ablation, cryoablation, microwave ablation, and chemical ablation.
  • Local tumor ablation in the adrenal gland presents unique challenges, secondary to the adrenal gland's unique anatomic and physiological features.
  • The results of clinical series employing percutaneous ablative techniques in the treatment of adrenal tumors are reviewed in this article.
  • Clinical and technical considerations unique to ablation in the adrenal gland are presented, including approaches commonly used in our practices, and risks and potential complications are discussed.
  • [MeSH-major] Adrenal Gland Neoplasms / surgery. Catheter Ablation

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  • [Copyright] Published by Elsevier Inc.
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  • (PMID = 20540918.001).
  • [ISSN] 1557-9808
  • [Journal-full-title] Techniques in vascular and interventional radiology
  • [ISO-abbreviation] Tech Vasc Interv Radiol
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 CL999999
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 3K9958V90M / Ethanol
  • [Number-of-references] 69
  • [Other-IDs] NLM/ NIHMS199588; NLM/ PMC2886030
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76. Gumy-Pause F, Bongiovanni M, Wildhaber B, Jenkins JJ, Chardot C, Ozsahin H: Adrenocortical oncocytoma in a child. Pediatr Blood Cancer; 2008 Mar;50(3):718-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenocortical oncocytoma in a child.
  • Adrenocortical oncocytoma is a rare epithelial tumor only described in adults.
  • We report the case of a 12-year-old female who presented a left adrenal mass with abdominal pain, fatigue, acne vulgaris, and elevation of the androstenedione and total testosterone.
  • A diagnosis of adrenocortical oncocytoma was made after detailed histological, immunohistochemical, and ultrastructural studies.
  • [MeSH-major] Adenoma, Oxyphilic / pathology. Adrenal Cortex Neoplasms / pathology
  • [MeSH-minor] Acne Vulgaris / etiology. Adrenalectomy. Androstenedione / secretion. Child. Female. Humans. Neoplasm Proteins / analysis. Testosterone / secretion

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17091483.001).
  • [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 / Neoplasm Proteins; 3XMK78S47O / Testosterone; 409J2J96VR / Androstenedione
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77. Duenschede F, Bittinger F, Heintz A, Musholt T, Korenkov M, Kann P, Ewald P, Gockel I, Junginger T: Malignant and unclear histological findings in incidentalomas. Eur Surg Res; 2008;40(2):235-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: The management of incidentalomas with tumor size 3 cm and larger is still under controversial discussion.
  • Indications for surgery were tumor size equal and larger than 3 cm, recurrent pain, hormone status and patients' fear of malignancy.
  • There were 9 cases of adrenal hyperplasia, and two cysts and two hematomas were found in 4 patients.
  • In 3 patients, a primary adrenocortical carcinoma of 3.4, 4.0, and 5.0 cm in diameter, respectively, was identified.
  • In 1 patient, an adrenal cortical carcinoma of 10.0 cm in diameter was operated.
  • CONCLUSION: Hormonal activity should be determined independent of the size, and lesions with hormonal activity should be resected; in the presence of hormonally inactive masses, removal of tumors of 3 cm and larger in size is recommended.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis. Adrenal Gland Neoplasms / surgery. Adrenalectomy. Incidental Findings
  • [MeSH-minor] Diagnostic Techniques, Endocrine. Female. Hormones / metabolism. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Staging. Tomography, X-Ray Computed. Ultrasonography

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  • [Copyright] Copyright 2008 S. Karger AG, Basel.
  • (PMID = 18032908.001).
  • [ISSN] 1421-9921
  • [Journal-full-title] European surgical research. Europäische chirurgische Forschung. Recherches chirurgicales européennes
  • [ISO-abbreviation] Eur Surg Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Hormones
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78. Hishiki T, Kazukawa I, Saito T, Terui K, Mitsunaga T, Nakata M, Matsuura G, Minagawa M, Kohno Y, Yoshida H: Diagnosis of adrenocortical tumor in a neonate by detection of elevated blood 17-hydroxyprogesterone measured as a routine neonatal screening for congenital adrenal hyperplasia: a case report. J Pediatr Surg; 2008 Oct;43(10):e19-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnosis of adrenocortical tumor in a neonate by detection of elevated blood 17-hydroxyprogesterone measured as a routine neonatal screening for congenital adrenal hyperplasia: a case report.
  • We report herein a case of prenatally detected neonatal adrenocortical tumor (ACT).
  • Computed tomography and ultrasonography after birth revealed a round solid tumor 40 mm in diameter in the right suprarenal area.
  • The precise diagnosis of ACT was unexpectedly obtained based on results from the Japanese neonatal mass screening program.
  • Blood 17-hydroxyprogesterone is routinely measured as a part of this program for early detection of congenital adrenal hyperplasia in Japan.
  • Abnormally elevated level of 17-hydroxyprogesterone was reported in the patient and, thus, led to the diagnosis of ACT.
  • Adrenocortical tumors are extremely rare in childhood, particularly in the neonatal period.
  • Some of these tumors secrete abnormally high levels of cortisol, suppressing function of the contralateral adrenal gland and, thus, leading to life-threatening postoperative adrenal insufficiency.
  • Adrenocortical tumor should always be considered among the differential diagnoses for neonatal suprarenal mass because precise diagnosis will enable the physician to develop appropriate treatment strategies.
  • [MeSH-major] 17-alpha-Hydroxyprogesterone / blood. Adrenal Cortex Neoplasms / diagnosis. Adrenal Hyperplasia, Congenital / diagnosis. Carcinoma / diagnosis. Fetal Blood / chemistry. Neonatal Screening
  • [MeSH-minor] Adrenal Insufficiency / prevention & control. Adrenalectomy. Aldosterone / blood. Dehydroepiandrosterone Sulfate / blood. Early Diagnosis. Female. Humans. Hydrocortisone / administration & dosage. Hydrocortisone / therapeutic use. Infant, Newborn. Postoperative Complications / prevention & control. Premedication. Testosterone / blood. Tomography, X-Ray Computed. Ultrasonography, Prenatal


79. Bovio S, Reimondo G, Daffara F, Allasino B, Angeli A, Terzolo M: [Subclinical Cushing's syndrome in adrenal incidentalomas]. Recenti Prog Med; 2006 Jan;97(1):6-15
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  • [Title] [Subclinical Cushing's syndrome in adrenal incidentalomas].
  • [Transliterated title] La sindrome di Cushing subclinica nei pazienti con incidentaloma surrenalico.
  • In the heyday of high-tech medicine, the incidental discovery of an adrenal mass is a frequent event owing to the routine use of sophisticated radiological techniques.
  • The potential harm to health associated with incidentally discovered cortical adenoma, the most frequent tumor among adrenal incidentalomas, is unclear at present.
  • Incidentally discovered adrenal adenoma may secrete cortisol autonomously, in a way that is no longer under close control by pituitary feedback, in 5 to 20% of cases.
  • At present, data are insufficient to indicate the superiority of a surgical or nonsurgical approach to manage patients with subclinical hyperfunctioning adrenal cortical adenoma.
  • It is of the utmost importance to establish collaborative prospective studies with clearly defined entry criteria and standardized evaluation protocols and treatment modalities to appraise the natural history and long-term morbidity of clinically inapparent adrenal adenoma and subclinical Cushing's syndrome.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications. Cushing Syndrome

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  • (PMID = 16535924.001).
  • [ISSN] 0034-1193
  • [Journal-full-title] Recenti progressi in medicina
  • [ISO-abbreviation] Recenti Prog Med
  • [Language] ita
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] WI4X0X7BPJ / Hydrocortisone
  • [Number-of-references] 87
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80. Nakamura Y, Aoki S, Xing Y, Sasano H, Rainey WE: Metastin stimulates aldosterone synthesis in human adrenal cells. Reprod Sci; 2007 Dec;14(8):836-45
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  • [Title] Metastin stimulates aldosterone synthesis in human adrenal cells.
  • In addition, they examine the effects of metastin on steroidogenesis and steroidogenic enzyme mRNA levels in fetal adrenal cells and in the H295R adrenocortical cell line using enzyme immunoassay and RT-PCR techniques.
  • Metastin increases aldosterone production (approximately 2-fold) in both fetal neocortex adrenal cells and H295R adrenal cells, with a maximal increase seen at 100 nM.
  • These results suggest that the high fetal/maternal levels of metastin seen during pregnancy may affect adrenal production of aldosterone.
  • [MeSH-major] Adrenal Glands / metabolism. Aldosterone / biosynthesis. Receptors, G-Protein-Coupled / metabolism. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cytochrome P-450 CYP11B2 / genetics. Cytochrome P-450 CYP11B2 / metabolism. Female. Fetus. Humans. Hydrocortisone / metabolism. Kisspeptins. Pregnancy. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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  • (PMID = 18089602.001).
  • [ISSN] 1933-7205
  • [Journal-full-title] Reproductive sciences (Thousand Oaks, Calif.)
  • [ISO-abbreviation] Reprod Sci
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK43140; United States / NICHD NIH HHS / HD / HD11149
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KISS1 protein, human; 0 / KISS1R protein, human; 0 / Kisspeptins; 0 / RNA, Messenger; 0 / Receptors, G-Protein-Coupled; 0 / Tumor Suppressor Proteins; 4964P6T9RB / Aldosterone; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; WI4X0X7BPJ / Hydrocortisone
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81. Betz MJ, Shapiro I, Fassnacht M, Hahner S, Reincke M, Beuschlein F, German and Austrian Adrenal Network: Peroxisome proliferator-activated receptor-gamma agonists suppress adrenocortical tumor cell proliferation and induce differentiation. J Clin Endocrinol Metab; 2005 Jul;90(7):3886-96
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  • [Title] Peroxisome proliferator-activated receptor-gamma agonists suppress adrenocortical tumor cell proliferation and induce differentiation.
  • Moreover, recent evidence has suggested that TZDs might have favorable effects in the treatment of a variety of tumors as differentiation-inducing agents.
  • Adrenocortical carcinoma (ACC) is a rare tumor entity with poor prognosis due to its highly malignant phenotype and lack of effective treatment options.
  • OBJECTIVE: The purpose of this study was to investigate effects of TZDs on adrenocortical cancer cells.
  • RESULTS: PPARgamma mRNA expression was detectable in all adrenocortical tumors including ACCs at similar levels.
  • Furthermore, incubation of the adrenocortical tumor cell line NCI h295 with the PPARgamma agonist rosiglitazone led to a decrease in cell viability, a decrease of cellular proliferation, and an increase in apoptosis as well as steroidogenesis.
  • On the molecular level, NCI h295 cells expressed higher levels of ACTH receptor (melanocortin receptor-2) mRNA upon treatment, whereas cyclin E mRNA was reduced, thus reflecting a shift toward an expression pattern found in less aggressive adrenocortical tumors in vivo.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. PPAR gamma / agonists. Thiazolidinediones / pharmacology
  • [MeSH-minor] Adult. Aged. Anilides / pharmacology. Apoptosis / drug effects. Cell Differentiation. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin E / genetics. Dose-Response Relationship, Drug. Female. Humans. Insulin-Like Growth Factor II / genetics. Male. Middle Aged. Promoter Regions, Genetic. RNA, Messenger / analysis. Receptor, Melanocortin, Type 2 / genetics

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  • (PMID = 15886257.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-chloro-5-nitrobenzanilide; 0 / Anilides; 0 / Cyclin E; 0 / PPAR gamma; 0 / RNA, Messenger; 0 / Receptor, Melanocortin, Type 2; 0 / Thiazolidinediones; 05V02F2KDG / rosiglitazone; 67763-97-7 / Insulin-Like Growth Factor II
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82. Mattos GE, Lotfi CF: Differences between the growth regulatory pathways in primary rat adrenal cells and mouse tumor cell line. Mol Cell Endocrinol; 2005 Dec 21;245(1-2):31-42
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  • [Title] Differences between the growth regulatory pathways in primary rat adrenal cells and mouse tumor cell line.
  • In this study, DNA synthesis, phosphorylation of ERK1/2 and CREB proteins, as well as induction of c-Fos protein, were examined in rat adrenocortical, glomerulosa and fasciculata/reticularis cells, as well as in the Y1 cell line.
  • We found that FGF2 was mitogenic only in glomerulosa cells and although ACTH did not activate ERK1/2, it did activate CREB protein, indicating efficient transduction of signals initiated in the ACTH receptors of rat adrenocortical cells.
  • The FGF2 activated ERK1/2 in rat adrenal cells by a mechanism that might be modulated by upstream PKA pathway phosphorylation of MEK and despite the nonmitogenic effect of ACTH on rat adrenal cells it effectively induces c-Fos protein.
  • The results presented herein describe distinct differences between the ACTH and FGF2 signal transduction mechanisms seen in adrenocortical cells and those observed in the Y1 cell line, indicating that, in vitro, ACTH blockage of the mitogenic effect occurs in normal adrenal cells after induction of c-Fos protein.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Cell Proliferation. Zona Fasciculata / cytology. Zona Glomerulosa / cytology. Zona Reticularis / cytology
  • [MeSH-minor] Adrenocorticotropic Hormone / pharmacology. Animals. Cell Cycle / physiology. Cell Line, Tumor. Cell Survival. Cells, Cultured. Cyclic AMP Response Element-Binding Protein / metabolism. Cyclic AMP-Dependent Protein Kinases / physiology. Cytochrome P-450 CYP11B2 / genetics. Cytochrome P-450 CYP11B2 / metabolism. Enzyme Activation. Extracellular Signal-Regulated MAP Kinases / metabolism. Fibroblast Growth Factor 2 / pharmacology. Gene Expression Regulation. Male. Mice. Phosphorylation. Proto-Oncogene Proteins c-fos / metabolism. Rats. Rats, Wistar. Signal Transduction

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  • (PMID = 16289304.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Cyclic AMP Response Element-Binding Protein; 0 / Proto-Oncogene Proteins c-fos; 103107-01-3 / Fibroblast Growth Factor 2; 9002-60-2 / Adrenocorticotropic Hormone; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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83. Owecki M, Majewska KA, Stawny B, Nikisch E, Drews M, Sowiński J: [Adrenal tumours in a selected 10-years surgical material]. Pol Merkur Lekarski; 2006 Jun;20(120):678-81
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  • [Title] [Adrenal tumours in a selected 10-years surgical material].
  • The aim of the study was to analyze the number and proportions of different adrenal tumours resected during the last 10 years in our centre.
  • Besides, we seek correlations between the size of tumours and the age and body mass indexes (BMI) of the examined patients.
  • MATERIAL AND METHODS: The tumours where measured on CT and MRI before surgery, and on pathological examination after resection.
  • In 45 (65.22%) cases the right adrenal was affected, in 21 (30.43%)--the left, in 3 (4.35%)--both.
  • RESULTS: 12 adrenocortical cancers, 20 phaeochromocytomas, 9 cortisol-secreting adenomas, 4 aldosteronomas, 18 hormonally inactive adenomas, 6 miscellaneous tumours were found.
  • Malignant tumours where significantly larger than benign (12.20 +/- 6.81 vs 6.71 +/- 5.62 cm, p < 0.005).
  • We observed no correlation between the age and preoperative tumor size (p = 0.1756), between the age and pathological tumor size (p = 0.3601), and between BMI and the preoperative and histopathologic size (p = 0.4204, and p = 0.6478, respectively).
  • CONCLUSIONS: The most common tumour was phaeochromocytoma.
  • Most tumours where found in the right adrenal.
  • The malignant tumours where larger than benign ones.
  • No correlations between age and BMI, and tumour size where demonstrated.
  • [MeSH-major] Adrenal Gland Neoplasms / surgery
  • [MeSH-minor] Aged. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Staging. Time Factors. Tomography, X-Ray Computed

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  • (PMID = 17007266.001).
  • [ISSN] 1426-9686
  • [Journal-full-title] Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego
  • [ISO-abbreviation] Pol. Merkur. Lekarski
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
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84. Mann MW, Ellis SS, Mallory SB: Infantile acne as the initial sign of an adrenocortical tumor. J Am Acad Dermatol; 2007 Feb;56(2 Suppl):S15-8
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  • [Title] Infantile acne as the initial sign of an adrenocortical tumor.
  • Ultrasound and abdominal computed tomographic scan revealed a large adrenal mass consistent with an adrenocortical tumor.
  • The patient underwent surgical excision of the well-encapsulated tumor with normalization of his hormones and no subsequent recurrence.
  • Although rare, childhood adrenocortical tumors have a poor prognosis, with the majority of tumors having regional and metastatic disease.
  • Because early diagnosis and complete surgical excision improve prognosis, children with refractory infantile acne should be evaluated for signs of virilization and accelerated growth.
  • Elevated levels of DHEA and DHEA-S should prompt an aggressive diagnostic evaluation for an adrenocortical tumor.
  • [MeSH-major] Acne Vulgaris / etiology. Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications

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  • (PMID = 17097383.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 3XMK78S47O / Testosterone; 459AG36T1B / Dehydroepiandrosterone
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85. Zhang L, Liu M, Merling R, Giam CZ: Versatile reporter systems show that transactivation by human T-cell leukemia virus type 1 Tax occurs independently of chromatin remodeling factor BRG1. J Virol; 2006 Aug;80(15):7459-68
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  • Using an easily transduced and chromosomally integrated reporter system derived from a self-inactivating lentivirus vector, we showed in a BRG1- and BRM1-deficient adrenal carcinoma cell line, SW-13, that Tax- and 21-bp repeat-mediated transactivation does not require BRG1 or BRM1 and is not enhanced by BRG1.
  • With a similar reporter system, we further demonstrated that Tax- and tumor necrosis factor alpha-induced NF-kappaB activation occurs readily in SW-13 cells in the absence of BRG1 and BRM1.

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  • (PMID = 16840326.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / F32 GM075688; United States / NCI NIH HHS / CA / R01 CA048709; United States / NCI NIH HHS / CA / R01 CA 48709; United States / NCI NIH HHS / CA / R01 CA/GM 75688
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Activating Transcription Factors; 0 / CREB1 protein, human; 0 / Chromatin; 0 / Cyclic AMP Response Element-Binding Protein; 0 / Gene Products, tax; 0 / Histones; 0 / NF-kappa B; 0 / Nuclear Proteins; 0 / SMARCA2 protein, human; 0 / Transcription Factors; 0 / Tumor Necrosis Factor-alpha; 0 / enhanced green fluorescent protein; 147336-22-9 / Green Fluorescent Proteins; EC 3.6.1.- / SMARCA4 protein, human; EC 3.6.4.- / DNA Helicases
  • [Other-IDs] NLM/ PMC1563696
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86. Luconi M, Mangoni M, Gelmini S, Poli G, Nesi G, Francalanci M, Pratesi N, Cantini G, Lombardi A, Pepi M, Ercolino T, Serio M, Orlando C, Mannelli M: Rosiglitazone impairs proliferation of human adrenocortical cancer: preclinical study in a xenograft mouse model. Endocr Relat Cancer; 2010 Mar;17(1):169-77
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  • [Title] Rosiglitazone impairs proliferation of human adrenocortical cancer: preclinical study in a xenograft mouse model.
  • Adrenocortical carcinoma (ACC) is a rare aggressive tumor with a poor prognosis.
  • The lack of a specific and effective medical treatment is due to the poor knowledge of the mechanisms underlying tumor growth.
  • Research on potential drugs able to specifically interfere with tumor proliferation is essential to develop more efficacious therapies.
  • We evaluated for the first time the in vivo effect of rosiglitazone (RGZ), an anti-diabetic drug with in vitro anti-tumor properties, on ACC proliferation in a xenograft model obtained by s.c. injection of human ACC H295R cells in athymic mice.
  • When the tumor size reached 5 mm, animals were allocated to 5 mg/kg RGZ- or water-treated groups.
  • Tumor volume was measured twice a week.
  • A significant reduction of tumor growth in RGZ versus control (control) group was observed and was already maximal following 17 day treatment (1-T/C=75.4% (43.7-93.8%)).
  • After 31 days of treatment, mice were killed and tumor analyzed.
  • Tumor histological evaluation revealed characteristics of invasiveness, richness in small vessels and mitotic figures in control group, while RGZ group tumors presented non infiltrating borders, few vessels, and many apoptotic bodies.
  • Tumor immunohistochemistry showed that Ki-67 was reduced in RGZ versus control group.
  • Quantitative real-time RT-PCR demonstrated a significant reduction in the expression of angiogenic (VEGF), vascular (CD31), proliferation (BMI-1), and anti-apoptotic (Bcl-2) genes in RGZ versus control group tumors.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Carcinoma / pathology. Cell Proliferation / drug effects. Thiazolidinediones / pharmacology
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Cell Line, Tumor. Female. Gene Expression Regulation, Neoplastic / drug effects. Humans. Hypoglycemic Agents / pharmacology. Hypoglycemic Agents / therapeutic use. Mice. Mice, Nude. Tumor Burden / drug effects. Xenograft Model Antitumor Assays

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  • (PMID = 19955217.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hypoglycemic Agents; 0 / Thiazolidinediones; 05V02F2KDG / rosiglitazone
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87. Cheng MF, Wu YW, Tzen KY, Yen RF: F-18 FDG PET/CT illustrating tumor invasion in the IVC from adrenocortical carcinoma. Clin Nucl Med; 2007 Nov;32(11):891-2
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  • [Title] F-18 FDG PET/CT illustrating tumor invasion in the IVC from adrenocortical carcinoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Fluorodeoxyglucose F18. Positron-Emission Tomography. Tomography, X-Ray Computed. Vena Cava, Inferior / pathology. Vena Cava, Inferior / radionuclide imaging
  • [MeSH-minor] Female. Humans. Middle Aged. Neoplasm Invasiveness

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  • (PMID = 18075433.001).
  • [ISSN] 0363-9762
  • [Journal-full-title] Clinical nuclear medicine
  • [ISO-abbreviation] Clin Nucl Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0Z5B2CJX4D / Fluorodeoxyglucose F18
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88. Weber CC, Kressmann S, Ott M, Fricker G, Müller WE: Inhibition of P-glycoprotein function by several antidepressants may not contribute to clinical efficacy. Pharmacopsychiatry; 2005 Nov;38(6):293-300
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  • INTRODUCTION: In many depressive patients the negative feedback mechanism of the HPA (hypothalamic-pituitary-adrenocortical) axis is impaired.
  • [MeSH-minor] Adenosine Triphosphate / metabolism. Animals. Antipsychotic Agents / pharmacology. Blood-Brain Barrier / drug effects. Capillaries / cytology. Capillaries / drug effects. Capillaries / metabolism. Cell Line, Tumor. Drug Resistance, Multiple. Endothelial Cells / drug effects. Endothelial Cells / metabolism. Fluoresceins. Fluorescent Dyes. Humans. Hydrogen Peroxide / pharmacology. Oxidants / pharmacology. Serotonin Uptake Inhibitors / pharmacology. Swine

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  • (PMID = 16342001.001).
  • [ISSN] 0176-3679
  • [Journal-full-title] Pharmacopsychiatry
  • [ISO-abbreviation] Pharmacopsychiatry
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antidepressive Agents; 0 / Antipsychotic Agents; 0 / Fluoresceins; 0 / Fluorescent Dyes; 0 / Oxidants; 0 / P-Glycoprotein; 0 / Serotonin Uptake Inhibitors; 148504-34-1 / calcein AM; 8L70Q75FXE / Adenosine Triphosphate; BBX060AN9V / Hydrogen Peroxide
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89. Hamamatsu A, Arai T, Iwamoto M, Kato T, Sawabe M: Adenomatoid tumor of the adrenal gland: case report with immunohistochemical study. Pathol Int; 2005 Oct;55(10):665-9
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  • [Title] Adenomatoid tumor of the adrenal gland: case report with immunohistochemical study.
  • Adrenal adenomatoid tumor (AT) is a recently recognized disease with marked male predominance.
  • Herein is presented a case of adrenal AT incidentally found in a 30-year-old man and results of immunohistochemical examination of the tumor.
  • The left adrenal gland, weighing 17 g, contained a mass measuring 3 x 2.5 x 2.5 cm in the cortical tissue.
  • Cut surface showed a relatively well-circumscribed firm tumor with a white solid appearance.
  • Histologically, the tumor had the typical appearance of AT described in the genital tract.
  • Immunohistochemically, the tumor cells were positive for calretinin, D2-40, WT1, mesothelial cell antigen, CA125, thrombomodulin, vimentin and cytokeratins (stained by AE1 + AE3, OV-TL 12/30, CAM5.2 and MNF116), and negative for endothelial markers (CD31, CD34 and factor VIII-related antigen) and CD56.
  • CD56-positive adrenocortical cells were diffusely scattered in the tumor, especially in its periphery.
  • These findings confirm mesothelial origin of the tumor and suggest that this tumor has little relation to sex hormone despite male predominance.
  • [MeSH-major] Adrenal Gland Neoplasms / pathology. Adrenocortical Adenoma / pathology
  • [MeSH-minor] Adult. Biomarkers, Tumor / analysis. Coronary Thrombosis / mortality. Coronary Thrombosis / pathology. Fatal Outcome. Humans. Immunoenzyme Techniques. Male

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  • (PMID = 16185299.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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90. Botsios D, Blouhos K, Vasiliadis K, Asimaki A, Tsalis K, Betsis D: Adrenocortical oncocytoma -- a rare tumor of undefined malignant potential: report of a case. Surg Today; 2007;37(7):612-7
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  • [Title] Adrenocortical oncocytoma -- a rare tumor of undefined malignant potential: report of a case.
  • Adrenocortical oncocytomas are exceptionally rare.
  • We report a case of adrenocortical oncocytoma diagnosed by pathological examination of an extirpated right adrenal mass in a young woman.
  • [MeSH-major] Adenoma, Oxyphilic / diagnosis. Adrenal Cortex Neoplasms / diagnosis

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  • (PMID = 17593485.001).
  • [ISSN] 0941-1291
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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91. Hirose A, Okada Y, Fukushima A, Tanaka Y: [A rare case of primary aldosteronism caused by bilateral functioning adrenocortical adenomas with renal cell carcinoma]. J UOEH; 2005 Dec 1;27(4):315-23
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  • [Title] [A rare case of primary aldosteronism caused by bilateral functioning adrenocortical adenomas with renal cell carcinoma].
  • Abdominal CT and MRI revealed tumor masses in both adrenal glands, and a large left renal mass.
  • The preoperative diagnosis was primary aldosteronism due to bilateral functioning adrenocortical adenomas and left renal cell carcinoma.
  • The Pathological diagnosis was left renal cell carcinoma and bilateral functioning adrenocortical adenomas.
  • Primary aldosteronism due to bilateral functioning adrenocortical adenomas is relatively rare and its complication with renal cell carcinoma is an extremely rare case.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications. Carcinoma, Renal Cell / complications. Hyperaldosteronism / etiology. Kidney Neoplasms / complications


92. Park BK, Kim CK, Jung BC, Suh YL: Cortical adenoma in adrenohepatic fusion tissue: clue to making a correct diagnosis at preoperative computed tomography examination. Eur Urol; 2009 Dec;56(6):1082-5
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  • [Title] Cortical adenoma in adrenohepatic fusion tissue: clue to making a correct diagnosis at preoperative computed tomography examination.
  • A 45-yr-old woman was admitted to excise a solid hepatic tumor which was incidentally detected at ultrasound examination for an unrelated reason.
  • Preoperative differential diagnoses included primary or secondary malignant hepatic tumors or adrenal cortical carcinoma due to aggressive imaging features.
  • The tumor proved to be an adrenal cortical adenoma arising from the adrenohepatic fusion tissue and consisted of adenoma cells with lipid-rich cytoplasm.
  • Retrospective review of preoperative computed tomography (CT) images demonstrated that the tumor measured 6 Hounsfield units in mean CT number and was continuous with a medial limb of the right adrenal gland.
  • [MeSH-major] Adrenal Cortex Neoplasms / radiography. Adrenocortical Adenoma / radiography. Liver Neoplasms / radiography. Tomography, X-Ray Computed
  • [MeSH-minor] Diagnosis, Differential. Female. Humans. Middle Aged. Preoperative Care. Ultrasonography

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  • (PMID = 19447543.001).
  • [ISSN] 1873-7560
  • [Journal-full-title] European urology
  • [ISO-abbreviation] Eur. Urol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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93. Lacroix A: Approach to the patient with adrenocortical carcinoma. J Clin Endocrinol Metab; 2010 Nov;95(11):4812-22
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  • [Title] Approach to the patient with adrenocortical carcinoma.
  • Adrenocortical cancer (ACC) is a rare and often aggressive malignancy that requires multidisciplinary expertise for optimal management.
  • Thorough imaging and endocrine evaluations can identify the majority of ACCs amongst adrenal tumors; however, some smaller ACCs are better identified using fluorodeoxyglucose-positron emission tomography/computed tomography scan.
  • Complete resection by an expert surgeon is the only potentially curative treatment for ACC, and tumor spillage should be avoided.
  • Histopathology is important for diagnosis, but immunohistochemistry markers and gene profiling of the resected tumor may become superior to current staging systems to stratify prognosis.
  • Despite complete resection in stage I-III tumors, approximately 40% of patients develop metastasis within 2 yr.
  • Some retrospective studies indicate that adjuvant mitotane therapy prolongs disease-free survival, leading several centers to recommend its administration; prospective studies are under way to provide future evidence-based recommendations.
  • Careful replacement of glucocorticoid and mineralocorticoid deficiency after surgery or mitotane therapy is important; steroid excess from remaining tumor burden should also be controlled to avoid its morbidities.
  • For metastatic disease, combination chemotherapy should be administered, if possible, in the context of multicenter collaborative research protocols.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenocortical Carcinoma / surgery
  • [MeSH-minor] Disease Progression. Female. Humans. Prognosis. Treatment Outcome. Young Adult

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  • (PMID = 21051577.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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94. Gonzalez KD, Noltner KA, Buzin CH, Gu D, Wen-Fong CY, Nguyen VQ, Han JH, Lowstuter K, Longmate J, Sommer SS, Weitzel JN: Beyond Li Fraumeni Syndrome: clinical characteristics of families with p53 germline mutations. J Clin Oncol; 2009 Mar 10;27(8):1250-6
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  • PURPOSE: A clinical testing cohort was used to gain a broader understanding of the spectrum of tumors associated with germline p53 mutations to aid clinicians in identifying high-risk families.
  • All families with a p53 mutation had at least one family member with a sarcoma, breast, brain, or adrenocortical carcinoma (ACC).
  • Every individual with a choroid plexus tumor (eight of eight) and 14 of 21 individuals with a childhood ACC had a mutation regardless of family history.
  • CONCLUSION: This is, to our knowledge, the largest single report of diagnostic testing for germline p53 mutations, yielding practical mutation prevalence tables and suggesting clinical utility of classic LFS and Chompret criteria for identifying a subset of cancer-prone families with p53 germline mutations, with important implications for diagnosis and management.
  • [MeSH-minor] Adolescent. Adrenal Cortex Neoplasms / genetics. Adult. Age of Onset. Breast Neoplasms / genetics. Child. Child, Preschool. Female. Genotype. Humans. Infant. Male. Middle Aged


95. Kuwada M, Hosokawa Y, Takada S, Kumamoto H, Hayashi Y, Fujimoto K, Hirao Y: [Adrenocortical carcinoma with intratumoral hemorrhage detected from chest and back pain: a case report]. Hinyokika Kiyo; 2009 Oct;55(10):599-602
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  • [Title] [Adrenocortical carcinoma with intratumoral hemorrhage detected from chest and back pain: a case report].
  • Computed tomography (CT) showed left retroperitoneal tumor, which was 6 cm in diameter with intratumoral hemorrhage.
  • Based on abdominal CT, magnetic resonance imaging and blood tests, preoperative diagnosis was adrenocortical carcinoma.
  • En bloc resection of the tumor and the left kidney was performed.
  • The histological diagnosis was adrenocortical carcinoma.
  • The patient died three months after operation because of disease progression.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Back Pain / etiology. Carcinoma / diagnosis. Chest Pain / etiology. Hemorrhage / etiology


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

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  • (PMID = 16444357.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] por
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Brazil
  • [Number-of-references] 36
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97. Cartier D, Jégou S, Parmentier F, Lihrmann I, Louiset E, Kuhn JM, Bastard C, Plouin PF, Godin M, Vaudry H, Lefebvre H: Expression profile of serotonin4 (5-HT4) receptors in adrenocortical aldosterone-producing adenomas. Eur J Endocrinol; 2005 Dec;153(6):939-47
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  • [Title] Expression profile of serotonin4 (5-HT4) receptors in adrenocortical aldosterone-producing adenomas.
  • OBJECTIVE: We aimed to investigate the expression profile of serotonin4 (5-HT4) receptors in adrenocortical aldosterone-producing adenoma (APA) tissues in comparison with normal adrenal cortex.
  • DESIGN AND METHODS: Total 5-HT4 receptor mRNAs were quantified by real-time quantitative polymerase chain reaction (PCR) assay, and the mRNAs encoding the 5-HT4 receptor isoforms were characterized by reverse transcription (RT)-PCR in seven normal adrenal cortices and 11 APA tissues.
  • The distribution of 5-HT4 receptor mRNAs was investigated by in situ hybridization in both normal adrenal and APA tissues, and the presence of 5-HT in APA tissues was studied by immunohistochemistry.
  • In situ hybridization studies showed that 5-HT4 receptor mRNAs were expressed in both zona glomerulosa and zona fasciculata/reticularis of the normal cortex and in groups of APA steroidogenic cells disseminated in the tumor tissues.
  • Isoforms (a) and (b) were not expressed in any APA but were present in the majority of normal adrenocortical tissues.
  • CONCLUSION: Our results show overexpression and different splicing of the 5-HT4 receptor in APA tissues in comparison with normal adrenocortical tissue.
  • They also demonstrate the presence of 5-HT in both mast cells and tumor steroidogenic cells, providing evidence for a possible autocrine/paracrine activation of aldosterone secretion within adenoma tissues.

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  • (PMID = 16322401.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Isoforms; 158165-40-3 / Receptors, Serotonin, 5-HT4; 4964P6T9RB / Aldosterone
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98. Cohade C, Broussaud S, Louiset E, Bennet A, Huyghe E, Caron P: Ectopic Cushing's syndrome due to a pheochromocytoma: a new case in the post-partum and review of literature. Gynecol Endocrinol; 2009 Sep;25(9):624-7
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  • We report the case of a 30-year-old woman who presented 3 months after delivery acute psychiatric signs and rapid progressive features of Cushing's syndrome.
  • A computed tomography scan revealed a 25 x 30 mm tumoral mass in the left adrenal gland and octreoscan scintigraphy showed only an uptake of the radiolabelled octreotide by the adrenal tumor.
  • Histological examination revealed a 3.5 x 2.5 cm adrenal tumor consistent with a pheochromocytoma without signs of malignancy.
  • The tumor cells immunostained for ACTH and diffuse hyperplasia of adrenocortical cells was observed.
  • [MeSH-major] Adrenal Gland Neoplasms / complications. Cushing Syndrome / diagnosis. Pheochromocytoma / complications


99. Powell AC, Stratakis CA, Patronas NJ, Steinberg SM, Batista D, Alexander HR, Pingpank JF, Keil M, Bartlett DL, Libutti SK: Operative management of Cushing syndrome secondary to micronodular adrenal hyperplasia. Surgery; 2008 Jun;143(6):750-8
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  • [Title] Operative management of Cushing syndrome secondary to micronodular adrenal hyperplasia.
  • BACKGROUND: We reviewed our experience with micronodular adrenal hyperplasia (MAH), its pigmented variant primary pigmented nodular adrenocortical disease (PPNAD), and the association with Carney's complex (CNC) to better characterize these disorders.
  • CONCLUSION: Cushing syndrome due to MAH and PPNAD may be cured by bilateral adrenal resection.
  • All patients should be screened for manifestations of CNC at the time of adrenal diagnosis with particular attention to cardiac disease.

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  • (PMID = 18549891.001).
  • [ISSN] 1532-7361
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / / NIH0012762233; United States / NICHD NIH HHS / HD / Z01 HD000642; United States / NICHD NIH HHS / HD / Z01HD000642-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS56801; NLM/ PMC2601697
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100. Budziszewska B, Basta-Kaim A, Kubera M, Jaworska L, Leśkiewicz M, Tetich M, Otczyk M, Zajicova A, Holan V, Lasoń W: Effect of lipopolysaccharide and antidepressant drugs on glucocorticoid receptor-mediated gene transcription. Pharmacol Rep; 2005 Jul-Aug;57(4):540-4
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  • It has been hypothesized that pro-inflammatory response and hyperactivity of hypothalamic-pituitary-adrenocortical axis (HPA) are involved in the pathogenesis of depression.
  • In order to study a role of some mediators of pro-inflammatory response in this process, presently, we investigated the effect of lipopolysaccharide (LPS) on imipramine- or fluoxetine-induced inhibition of GR-mediated gene transcription in fibroblast cells, stably transfected with mouse mammary tumor virus promoter (LMCAT cells).
  • [MeSH-minor] Animals. Cell Line, Tumor. Corticosterone / pharmacology. Fibroblasts / drug effects. Fibroblasts / metabolism. Hypothalamo-Hypophyseal System / drug effects. Hypothalamo-Hypophyseal System / metabolism. Interleukin-6 / metabolism. Mice. Pituitary-Adrenal System / drug effects. Pituitary-Adrenal System / metabolism

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  • (PMID = 16129923.001).
  • [ISSN] 1734-1140
  • [Journal-full-title] Pharmacological reports : PR
  • [ISO-abbreviation] Pharmacol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antidepressive Agents; 0 / Interleukin-6; 0 / Lipopolysaccharides; 0 / Receptors, Glucocorticoid; 01K63SUP8D / Fluoxetine; OGG85SX4E4 / Imipramine; W980KJ009P / Corticosterone
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