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1. Daffara F, De Francia S, Reimondo G, Zaggia B, Aroasio E, Porpiglia F, Volante M, Termine A, Di Carlo F, Dogliotti L, Angeli A, Berruti A, Terzolo M: Prospective evaluation of mitotane toxicity in adrenocortical cancer patients treated adjuvantly. Endocr Relat Cancer; 2008 Dec;15(4):1043-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prospective evaluation of mitotane toxicity in adrenocortical cancer patients treated adjuvantly.
  • Seventeen consecutive patients who were treated with mitotane after radical resection of adrenocortical cancer (ACC) from 1999 to 2005 underwent physical examination, routine laboratory evaluation, monitoring of mitotane concentrations, and a hormonal work-up at baseline and every 3 months till ACC relapse or study end (December 2007).
  • Mitotane affected adrenal steroidogenesis with a more remarkable inhibition of cortisol and DHEAS than aldosterone.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Mitotane / therapeutic use
  • [MeSH-minor] Adult. Chemotherapy, Adjuvant. Chromatography, High Pressure Liquid. Female. Humans. Hydrocortisone / metabolism. Hypothyroidism / etiology. Male. Middle Aged. Neoplasm Staging. Prospective Studies. Survival Rate. Testosterone / metabolism. Young Adult

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  • (PMID = 18824557.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 3XMK78S47O / Testosterone; 78E4J5IB5J / Mitotane; WI4X0X7BPJ / Hydrocortisone
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2. Libè R, Fratticci A, Bertherat J: Adrenocortical cancer: pathophysiology and clinical management. Endocr Relat Cancer; 2007 Mar;14(1):13-28
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenocortical cancer: pathophysiology and clinical management.
  • Adrenocortical cancer (ACC) is a rare tumor with a poor prognosis.
  • By contrast, benign adrenocortical tumors are frequent, underlying the importance of a correct diagnosis of malignancy of such tumors.
  • ACC can be diagnosed by the investigation of endocrine signs of steroid excess, symptoms due to tumor growth or an adrenal incidentaloma.
  • Imaging by CT-scan or MRI shows a large heterogeneous tumor with a low fat content.
  • Careful pathological investigation with the assessment of the Weiss score is important for the diagnosis of malignancy.
  • Tumors localized to the adrenal gland (McFarlane stages 1 and 2) have a better outcome than invasive and metastatic tumors (stages 3 and 4).
  • Tumor removal by a specialized team is crucial for treatment and should always aim at complete removal.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / therapy
  • [MeSH-minor] Genes, Tumor Suppressor. Humans. Oncogenes / genetics

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  • (PMID = 17395972.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 127
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3. Soon PS, McDonald KL, Robinson BG, Sidhu SB: Molecular markers and the pathogenesis of adrenocortical cancer. Oncologist; 2008 May;13(5):548-61
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  • [Title] Molecular markers and the pathogenesis of adrenocortical cancer.
  • Adrenal tumors are common, with an estimated incidence of 7.3% in autopsy cases, while adrenocortical carcinomas (ACCs) are rare, with an estimated prevalence of 4-12 per million population.
  • Because the prognoses for adrenocortical adenomas (ACAs) and ACCs are vastly different, it is important to be able to accurately differentiate the two tumor types.
  • Advancement in the understanding of the pathophysiology of ACCs is essential for the development of more sensitive means of diagnosis and treatment, resulting in better clinical outcome.
  • Adrenocortical tumors (ACTs) occur as a component of several hereditary tumor syndromes, which include the Li-Fraumeni syndrome, Beckwith-Wiedemann syndrome, multiple endocrine neoplasia 1, Carney complex, and congenital adrenal hyperplasia.
  • The adrenocorticotropic hormone-cAMP-protein kinase A and Wnt pathways are also implicated in adrenocortical tumorigenesis.
  • The aim of this review is to summarize the current knowledge on the molecular mechanisms involved in adrenocortical tumorigenesis, including results of comparative genomic hybridization, loss of heterozygosity, and microarray gene-expression profiling studies.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics. Adrenocortical Carcinoma / genetics. Neoplastic Syndromes, Hereditary / genetics
  • [MeSH-minor] Adrenocorticotropic Hormone / genetics. Adrenocorticotropic Hormone / metabolism. Animals. Gene Expression Profiling. Genes, Tumor Suppressor. Humans. Loss of Heterozygosity. Molecular Biology

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  • (PMID = 18515740.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
  • [Number-of-references] 135
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4. Libè R, Groussin L, Tissier F, Elie C, René-Corail F, Fratticci A, Jullian E, Beck-Peccoz P, Bertagna X, Gicquel C, Bertherat J: Somatic TP53 mutations are relatively rare among adrenocortical cancers with the frequent 17p13 loss of heterozygosity. Clin Cancer Res; 2007 Feb 1;13(3):844-50
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  • [Title] Somatic TP53 mutations are relatively rare among adrenocortical cancers with the frequent 17p13 loss of heterozygosity.
  • PURPOSE: Allelic losses [loss of heterozygosity (LOH)] at the 17p13 locus are frequent (85%) in adrenocortical cancers.
  • The tumor suppressor gene TP53 is located at 17p13.
  • The aim of the study was to determine the frequency of TP53 somatic inactivating mutations in adrenocortical tumors with 17p13 LOH and their clinico-biological correlations.
  • EXPERIMENTAL DESIGN: TP53 somatic mutations, intragenic LOH (VNTR1 marker), and p53 overexpression were studied in 36 adrenocortical tumors with 17p13 LOH determined by Southern blot.
  • TP53-mutant tumors were significantly larger than wild-type TP53 tumors (median tumor weight: 640 versus 185 g; P=0.02), were associated with a more advanced stage of tumor progression (MacFarlane stage IV; P=0.01), and had a shorter disease-free survival (P=0.03).
  • CONCLUSIONS: The finding that only a minority of adrenocortical tumors with 17p13 LOH had either a VNTR1 LOH or a TP53 mutation indicates that TP53 might not be the only or major tumor suppressor gene at 17p13 involved in adrenocortical cancer progression.
  • We suggest that a genetic instability of the 17p13 region, occurring early in adrenocortical cancer development, involves various genes located in this region.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Chromosomes, Human, Pair 17. Genes, p53. Loss of Heterozygosity. Minisatellite Repeats / genetics. Mutation
  • [MeSH-minor] Adult. Alleles. Disease Progression. Female. Humans. Immunohistochemistry. Male. Middle Aged. RNA, Neoplasm / chemistry

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  • (PMID = 17289876.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Neoplasm
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5. Szabó D, Zsippai A, Bendes M, Tömböl Z, Szabó PM, Rácz K, Igaz P: [Pathogenesis of adrenocortical cancer]. Orv Hetil; 2010 Jul 18;151(29):1163-70
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  • [Title] [Pathogenesis of adrenocortical cancer].
  • [Transliterated title] A mellékvesekéreg-carcinoma molekuláris patogenezise.
  • Adrenocortical cancer is a rare tumor with poor prognosis.
  • Whereas most cases occur in a sporadic setting, there are very rare hereditary forms that are important for the understanding of tumor pathogenesis.
  • The hereditary syndromes associated with adrenocortical cancer are: Li-Fraumeni's syndrome, Beckwith-Wiedemann's syndrome and familial adenomatous polyposis, whereas multiple endocrine neoplasia type 1, Carney's complex and McCune-Albright's syndrome mostly predispose to benign adrenocortical tumors.
  • Options for medical treatment of adrenocortical cancer are rather limited.
  • In this study, the pathogenesis of hereditary tumor syndromes, the alterations in sporadic tumors and the most recent molecular-bioinformatical observations are discussed.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / metabolism
  • [MeSH-minor] Adenomatous Polyposis Coli / genetics. Beckwith-Wiedemann Syndrome / genetics. Carney Complex / genetics. Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / metabolism. Fibrous Dysplasia, Polyostotic / genetics. Gene Expression Regulation, Neoplastic. Genes, p53. Genetic Predisposition to Disease. Humans. Insulin-Like Growth Factor II / metabolism. Li-Fraumeni Syndrome / genetics. Multiple Endocrine Neoplasia Type 1 / genetics. Mutation. Proto-Oncogene Proteins / genetics. Signal Transduction. Up-Regulation. Wnt Proteins / metabolism. beta Catenin / metabolism

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  • (PMID = 20591784.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Wnt Proteins; 0 / beta Catenin; 67763-97-7 / Insulin-Like Growth Factor II
  • [Number-of-references] 37
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6. 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.
  • [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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7. Aspinall SR, Imisairi AH, Bliss RD, Scott-Coombes D, Harrison BJ, Lennard TW: How is adrenocortical cancer being managed in the UK? Ann R Coll Surg Engl; 2009 Sep;91(6):489-93
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  • [Title] How is adrenocortical cancer being managed in the UK?
  • INTRODUCTION: Adrenocortical carcinomas are rare.
  • This case series is reported to give an overview of how adrenocortical carcinoma is currently managed in the UK.
  • PATIENTS AND METHODS: A retrospective review was made of case notes from patients with adrenocortical carcinomas presenting to the authors (TWJL, RDB, BJH, and DS-C) over the past 10 years in Newcastle, Sheffield and Cardiff.
  • CONCLUSIONS: The size of tumour, stage and mode of presentation, age and overall survival of patients in this study are comparable to published series of adrenocortical carcinomas from major endocrine surgical centres world-wide.
  • The exact role of adjuvant therapy in the management of adrenocortical carcinoma is not as well established as for other more common malignancies.
  • Establishing a database for adrenocortical carcinomas in the UK would contribute to our understanding of the management of this disease.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Adrenocortical Carcinoma / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Mitotane / therapeutic use
  • [MeSH-minor] Adrenalectomy / methods. Antineoplastic Combined Chemotherapy Protocols. Chemotherapy, Adjuvant. Cytotoxins / therapeutic use. Great Britain. Humans. Neoplasm Recurrence, Local. Retrospective Studies. Survival Analysis

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  • (PMID = 19558758.001).
  • [ISSN] 1478-7083
  • [Journal-full-title] Annals of the Royal College of Surgeons of England
  • [ISO-abbreviation] Ann R Coll Surg Engl
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Cytotoxins; 78E4J5IB5J / Mitotane
  • [Other-IDs] NLM/ PMC2966201
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8. Cantini G, Lombardi A, Piscitelli E, Poli G, Ceni E, Marchiani S, Ercolino T, Galli A, Serio M, Mannelli M, Luconi M: Rosiglitazone inhibits adrenocortical cancer cell proliferation by interfering with the IGF-IR intracellular signaling. PPAR Res; 2008;2008:904041
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  • [Title] Rosiglitazone inhibits adrenocortical cancer cell proliferation by interfering with the IGF-IR intracellular signaling.
  • We investigated RGZ effect on cell proliferation in two cell line models (SW13 and H295R) of human adrenocortical carcinoma (ACC) and its interaction with the signaling pathways of the activated IGF-I receptor (IGF-IR).

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  • (PMID = 18670617.001).
  • [ISSN] 1687-4757
  • [Journal-full-title] PPAR research
  • [ISO-abbreviation] PPAR Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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9. Bertherat J, Bertagna X: Pathogenesis of adrenocortical cancer. Best Pract Res Clin Endocrinol Metab; 2009 Apr;23(2):261-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pathogenesis of adrenocortical cancer.
  • The study of the clonality of adrenocortical tumours (ACTs) has shown that adrenocortical cancers (ACCs) are of monoclonal origin.
  • Numerous chromosomal alterations have been observed in ACCs, and they are much more frequent than in adrenocortical adenomas.
  • Somatic mutations of the tumour suppressor gene TP53 are observed in a third of ACCs.
  • This recent progress in the molecular genetics of ACC has led to the development of new molecular markers for the diagnosis of malignancy; these might also help to identify prognostic markers of ACC and may ultimately lead to novel therapeutic approaches.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology

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  • (PMID = 19500768.001).
  • [ISSN] 1878-1594
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 67
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10. Balasubramaniam S, Fojo T: Practical considerations in the evaluation and management of adrenocortical cancer. Semin Oncol; 2010 Dec;37(6):619-26
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  • [Title] Practical considerations in the evaluation and management of adrenocortical cancer.
  • Adrenocortical cancer (ACC) is a rare, challenging disease with a broad range of clinical presentations.
  • Often presenting in an advanced stage with a large, locally invasive primary tumor or with Cushing's syndrome, it requires a multidisciplinary approach to treatment.
  • Biopsies should be performed only when metastatic disease is present and a primary tumor has not been clearly established.
  • [MeSH-major] Adrenocortical Carcinoma / pathology. Adrenocortical Carcinoma / therapy

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  • [Copyright] Published by Elsevier Inc.
  • (PMID = 21167380.001).
  • [ISSN] 1532-8708
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 5W494URQ81 / Streptozocin; 78E4J5IB5J / Mitotane
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11. Patalano A, Brancato V, Mantero F: Adrenocortical cancer treatment. Horm Res; 2009 Jan;71 Suppl 1:99-104
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenocortical cancer treatment.
  • BACKGROUND: With a reported incidence of 1 to 2 cases per million, adrenocortical cancer (ACC) is a rare disease with poor prognosis.
  • In sporadic ACC, some molecular modifications are commonly observed (i.e., overexpression of insulin-like growth factor II or vascular endothelial growth factor and somatic mutations of tumor protein 53).
  • When surgical resection of the tumor is impossible or ineffective, chemotherapy with etoposide, doxorubicin and cisplatin plus mitotane or with streptozotocin plus mitotane is frequently used; however, the overall survival rates are disappointing.
  • New treatments, such as insulin-like growth factor I receptor antibodies, tyrosine kinase inhibitors and other antiangiogenic compounds, are now being intensively investigated to identify better therapies for this extremely severe malignant neoplasia.
  • [MeSH-major] Adrenal Cortex Neoplasms / therapy. Adrenocortical Carcinoma / therapy

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19153517.001).
  • [ISSN] 1423-0046
  • [Journal-full-title] Hormone research
  • [ISO-abbreviation] Horm. Res.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 5W494URQ81 / Streptozocin; 78E4J5IB5J / Mitotane
  • [Number-of-references] 29
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12. Ignaszak-Szczepaniak M, Horst-Sikorska W, Sawicka J, Kaczmarek M, Slomski R: The TP53 codon 72 polymorphism and predisposition to adrenocortical cancer in Polish patients. Oncol Rep; 2006 Jul;16(1):65-71
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  • [Title] The TP53 codon 72 polymorphism and predisposition to adrenocortical cancer in Polish patients.
  • The association between this common polymorphism and risk of different cancers has been extensive studied, however various reports are controversial.
  • We have analyzed the 72Pro polymorphic variant in patients with adrenocortical tumors to evaluate whether 72G--> C substitution at codon 72 of TP53 gene may be associated with increased risk for malignancy in adrenal cortex in comparison to the control group.
  • DNA extracted from peripheral leucocytes of 46 Polish patients with adrenocortical tumors (17 malignant and 29 benign) and 50 controls was examined by PCR-HD method followed by direct sequencing.
  • The genotype Arg/Arg, Arg/Pro and Pro/Pro distribution was respectively 53%/35%/12% for cancers, 72%/28%/0% for benign tumors and 76%/24%/0% for controls.
  • High frequency of 72Pro allele in patients with carcinoma (29%) in comparison to the benign tumors (14%) and controls (12%) was statistically analyzed.
  • Our results suggest that the TP53 codon 72 polymorphism could be associated with susceptibility for adrenocortical cancer in the examined Polish patients.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Genetic Predisposition to Disease. Polymorphism, Genetic. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 16786124.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Codon; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53
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13. Loncarevic IF, Hering A, Posorski N, Linden T, Hoyer H, Bucsky P: Number of genomic imbalances correlates with the overall survival for adrenocortical cancer in childhood. Pediatr Blood Cancer; 2008 Sep;51(3):356-62
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  • [Title] Number of genomic imbalances correlates with the overall survival for adrenocortical cancer in childhood.
  • BACKGROUND: Adrenocortical tumours (ACT) in children are rare and, if malignant, often associated with poor prognosis.
  • PROCEDURES: We analysed 14 adrenocortical cancers (ACC) of children by comparative genomic hybridisation (CGH).
  • RESULTS: The total number of genomic imbalances ranged from 1 to 17 in individual tumour samples.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / mortality. Chromosome Aberrations

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18478573.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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14. Frederiks WM, Kümmerlin IP, Bosch KS, Vreeling-Sindelárová H, Jonker A, Van Noorden CJ: NADPH production by the pentose phosphate pathway in the zona fasciculata of rat adrenal gland. J Histochem Cytochem; 2007 Sep;55(9):975-80
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  • [Title] NADPH production by the pentose phosphate pathway in the zona fasciculata of rat adrenal gland.
  • Biosynthesis of steroid hormones in the cortex of the adrenal gland takes place in smooth endoplasmic reticulum and mitochondria and requires NADPH.
  • However, the contribution of each enzyme to NADPH production in the cortex of adrenal gland has not been established.
  • Therefore, activity of G6PD, PGD, MDH, and ICDH was localized and quantified in rat adrenocortical tissue using metabolic mapping, image analysis, and electron microscopy.
  • The four enzymes have similar localization patterns in adrenal gland with highest activities in the zona fasciculata of the cortex.
  • It is concluded that G6PD and PGD provide the major part of NADPH in adrenocortical cells.

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  • (PMID = 17533217.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0U46U6E8UK / NAD; C24W7J5D5R / Androsterone; EC 1.1.1.37 / Malate Dehydrogenase; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.43 / Phosphogluconate Dehydrogenase; EC 1.1.1.49 / Glucosephosphate Dehydrogenase
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15. Lindhe O, Skogseid B: Mitotane effects in a H295R xenograft model of adjuvant treatment of adrenocortical cancer. Horm Metab Res; 2010 Sep;42(10):725-30
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  • [Title] Mitotane effects in a H295R xenograft model of adjuvant treatment of adrenocortical cancer.
  • Adrenocortical cancer is one of the most aggressive endocrine malignancies.
  • Growth through the capsule or accidental release of cancer cells during surgery frequently results in metastatic disease.
  • We investigated the antitumoral effect of 2 adrenocorticolytic compounds, O, P'-DDD and MeSO2-DDE, in the adrenocortical cell line H295R both in vitro and as a xenograft model in vivo.
  • Tumor growth was significantly inhibited when O, P'-DDD was given at the same time as injection of tumor cells.
  • We suggest that FLT may be a potential PET biomarker when assessing adrenocortical cancer treatment with O,P'-DDD.
  • [MeSH-major] Adjuvants, Pharmaceutic / therapeutic use. Adrenal Cortex Neoplasms / drug therapy. Mitotane / therapeutic use. Xenograft Model Antitumor Assays
  • [MeSH-minor] Animals. Cell Aggregation / drug effects. Cell Count. Cell Proliferation / drug effects. Female. Humans. Mice. Positron-Emission Tomography. Radioactive Tracers. Spheroids, Cellular / drug effects. Spheroids, Cellular / pathology. Time Factors. Tumor Burden / drug effects. Tumor Cells, Cultured

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  • (PMID = 20665429.001).
  • [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
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Adjuvants, Pharmaceutic; 0 / Radioactive Tracers; 78E4J5IB5J / Mitotane
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16. Kvacheniuk AN: [Surgical treatment of adrenocortical cancer: significance of systematic lymphodissection]. Klin Khir; 2008 Mar;(3):34-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Surgical treatment of adrenocortical cancer: significance of systematic lymphodissection].
  • Comparative efficacy of radical methods of surgical intervention for adrenocortical cancer (ACC) with lymphodissection (LD) and without it was studied.
  • Adrenalectomy (AE) with en bloc excision of tumor and systematic lymph nodes dissection (paranephral, left-side paraaortal and the right-side paracaval collectors) constitutes the optimal surgical procedure.
  • AE with the tumor en bloc excision without performance of LD may give the same expected efficacy only for I-II stages tumor, when it is impossible to confirm malignancy intraoperatively.

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  • (PMID = 18680995.001).
  • [ISSN] 0023-2130
  • [Journal-full-title] Klinichna khirurhiia
  • [ISO-abbreviation] Klin Khir
  • [Language] RUS
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Ukraine
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17. Porpiglia F, Fiori C, Daffara F, Zaggia B, Bollito E, Volante M, Berruti A, Terzolo M: Retrospective evaluation of the outcome of open versus laparoscopic adrenalectomy for stage I and II adrenocortical cancer. Eur Urol; 2010 May;57(5):873-8
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  • [Title] Retrospective evaluation of the outcome of open versus laparoscopic adrenalectomy for stage I and II adrenocortical cancer.
  • BACKGROUND: Although there is consensus that laparoscopy is the standard of care for the resection of benign adrenal tumours, there is controversy regarding the role of laparoscopy for the resection of adrenocortical cancer (ACC).
  • OBJECTIVE: The aim of the present study was to review the ACC database of the San Luigi Hospital to compare the oncologic effectiveness of open adrenalectomy (OA) versus laparoscopic adrenalectomy (LA) in the treatment of patients with stage I and II ACC.
  • The "open group" consisted of patients treated with OA; the "lap group" consisted of patients treated with LA.
  • MEASUREMENTS: Oncologic effectiveness of the procedures was tested comparing the recurrence-free survival of patients treated with OA versus LA.
  • CONCLUSIONS: The present findings provide interesting evidence that OA and LA may be comparable in terms of recurrence-free survival for patients with stage I and II ACC when the principles of surgical oncology are respected.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenal Cortex Neoplasms / surgery. Adrenalectomy / methods. Laparoscopy
  • [MeSH-minor] Adult. Aged. Female. Humans. Male. Middle Aged. Neoplasm Staging. Retrospective Studies. Treatment Outcome. Young Adult

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  • [Copyright] Copyright © 2010 European Association of Urology. Published by Elsevier B.V. All rights reserved.
  • (PMID = 20137850.001).
  • [ISSN] 1873-7560
  • [Journal-full-title] European urology
  • [ISO-abbreviation] Eur. Urol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
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18. Wandoloski M, Bussey KJ, Demeure MJ: Adrenocortical cancer. Surg Clin North Am; 2009 Oct;89(5):1255-67
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  • [Title] Adrenocortical cancer.
  • Adrenocortical carcinoma (ACC) is a rare endocrine malignancy causing up to 0.2% of all cancer deaths This article reviews the incidence, presentation, and pathology of ACC.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Combined Modality Therapy. Diagnosis, Differential. Diagnostic Imaging. Genetic Predisposition to Disease. Humans. Mitotane / therapeutic use

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  • (PMID = 19836496.001).
  • [ISSN] 1558-3171
  • [Journal-full-title] The Surgical clinics of North America
  • [ISO-abbreviation] Surg. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 78E4J5IB5J / Mitotane
  • [Number-of-references] 51
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19. Cerquetti L, Sampaoli C, Amendola D, Bucci B, Misiti S, Raza G, De Paula U, Marchese R, Brunetti E, Toscano V, Stigliano A: Mitotane sensitizes adrenocortical cancer cells to ionizing radiations by involvement of the cyclin B1/CDK complex in G2 arrest and mismatch repair enzymes modulation. Int J Oncol; 2010 Aug;37(2):493-501
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  • [Title] Mitotane sensitizes adrenocortical cancer cells to ionizing radiations by involvement of the cyclin B1/CDK complex in G2 arrest and mismatch repair enzymes modulation.
  • It also has a cytotoxic effect on the adrenocortical cells and represents a primary drug used in the adrenocortical carcinoma (ACC).
  • H295R and SW13 cell lines were treated with mitotane 10(-5) M and ionizing radiations (IR) in combination therapy, inducing an irreversible inhibition of cell growth in both adrenocortical cancer cells.
  • [MeSH-major] Adrenal Cortex Neoplasms / radiotherapy. Adrenocortical Carcinoma / radiotherapy. Cyclin B / metabolism. Cyclin-Dependent Kinases / metabolism. DNA Repair Enzymes / metabolism. Mitotane / pharmacology
  • [MeSH-minor] Cell Proliferation / drug effects. Cell Proliferation / radiation effects. DNA Mismatch Repair / drug effects. DNA Mismatch Repair / physiology. Drug Evaluation, Preclinical. G2 Phase / drug effects. G2 Phase / physiology. Humans. Multiprotein Complexes / metabolism. Protein Kinase Inhibitors / pharmacology. Purines / pharmacology. Radiation, Ionizing. Radiation-Sensitizing Agents / pharmacology. Tumor Cells, Cultured

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  • (PMID = 20596677.001).
  • [ISSN] 1791-2423
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / 6-((3-chloro)anilino)-2-(isopropyl-2-hydroxyethylamino)-9-isopropylpurine; 0 / Cyclin B; 0 / Multiprotein Complexes; 0 / Protein Kinase Inhibitors; 0 / Purines; 0 / Radiation-Sensitizing Agents; 78E4J5IB5J / Mitotane; EC 2.7.11.22 / Cyclin-Dependent Kinases; EC 6.5.1.- / DNA Repair Enzymes
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20. Przybylik-Mazurek E, Darczuk A, Huszno B, Budzyński A, Rembiasz K, Gałazka K, Wierzchowski W, Giza A, Jurczak W, Skotnicki AB, Sztuk S, Urbanik A: [Primary adrenal lymphoma in incidentally discovered adrenal tumour]. Przegl Lek; 2006;63(8):701-5
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  • [Title] [Primary adrenal lymphoma in incidentally discovered adrenal tumour].
  • The new imaging techniques used during the last several years: ultrasound, computed tomography and magnetic resonance imaging have improved detection of non-functional adrenal tumours s.c. "incidentaloma".
  • Incidence of adrenal incidentaloma is not very low.
  • In most of cases incidentaloma are benign and gave no clinical signs; however primary adrenal cortex cancer and metastases of different cancers are not uncommon.
  • The primary adrenal lymphoma is an extremely rare disease.
  • Most frequently both adrenal glands are affected and signs of adrenal insufficiency (despite weakness, fever and loss of weight) are present.
  • Hormonal examinations were normal, but the tumour size was indication for surgery treatment.
  • The diagnosis was made by histological examination and adjuvant chemotherapy was administrated.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis. Adrenal Gland Neoplasms / surgery. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Non-Hodgkin / diagnosis. Lymphoma, Non-Hodgkin / surgery

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  • (PMID = 17441388.001).
  • [ISSN] 0033-2240
  • [Journal-full-title] Przegla̧d lekarski
  • [ISO-abbreviation] Prz. Lek.
  • [Language] pol
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide
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21. Bauditz J, Quinkler M, Beyersdorff D, Wermke W: Improved detection of hepatic metastases of adrenocortical cancer by contrast-enhanced ultrasound. Oncol Rep; 2008 May;19(5):1135-9
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  • [Title] Improved detection of hepatic metastases of adrenocortical cancer by contrast-enhanced ultrasound.
  • Adrenocortical carcinoma (ACC) is a rare and heterogeneous malignancy whose pathogenesis and poor prognosis is poorly understood.
  • Computerized tomography (CT) and magnetic resonance imaging (MRI) are routinely performed for the imaging of the adrenal mass and for standard staging of the chest and abdomen as the lung and liver are the primary organs for metastasis in ACC.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Contrast Media / pharmacology. Liver Neoplasms / secondary. Liver Neoplasms / ultrasonography. Ultrasonography / methods
  • [MeSH-minor] Adult. Aged. Female. Humans. Magnetic Resonance Imaging / methods. Male. Middle Aged. Neoplasm Metastasis. Retrospective Studies. Sensitivity and Specificity. Tomography, X-Ray Computed / methods

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  • (PMID = 18425368.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Contrast Media
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22. Drelicharz L, Mikita J, Chabielska E, Chłopicki S: [Endothelial action of aldosterone--therapeutic implications from basic and clinical research]. Kardiol Pol; 2005 Oct;63(4 Suppl 2):S409-19
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  • It is produced and secreted by zona glomerulosa of the adrenal gland cortex, cardiomyocytes as well as by cells of the blood vessel wall.

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  • (PMID = 20527396.001).
  • [ISSN] 0022-9032
  • [Journal-full-title] Kardiologia polska
  • [ISO-abbreviation] Kardiol Pol
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Mineralocorticoid Receptor Antagonists; 0 / Receptors, Mineralocorticoid; 31C4KY9ESH / Nitric Oxide; 4964P6T9RB / Aldosterone
  • [Number-of-references] 120
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23. Kanczkowski W, Morawietz H, Ziegler CG, Funk RH, Schmitz G, Zacharowski K, Mohn CE, Ehrhart-Bornstein M, Bornstein SR: Pam3CSK4 and LTA-TLRs ligands associated with microdomains induce IL8 production in human adrenocortical cancer cells. Horm Metab Res; 2007 Jun;39(6):457-60

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pam3CSK4 and LTA-TLRs ligands associated with microdomains induce IL8 production in human adrenocortical cancer cells.
  • Bacterially derived ligands, Pam3CSK4 and LPS, can directly impact adrenal glands steroidogenesis through microdomain-related TLR1/2 and 4, respectively, and indirectly via immune cell-derived cytokines.
  • CXC chemokine-dependent immune cell infiltration into adrenocortical carcinomas (ACC), which correlates with poor prognosis, is a common phenomenon.
  • Recently, IL8 was identified in ACC and NCI-H295R cells, and was found to contribute to ACC tumour growth.
  • This is the first study to demonstrate the expression of several TLRs including TLR1, 3, 6, 7 and 9 in human adrenocortical cells by using the RT-PCR approach.
  • Our data suggest that gram-positive bacteria-related TLR1/2/6 ligands might contribute to adrenal gland tumorigenesis via IL8 production.
  • [MeSH-major] Adrenal Cortex Neoplasms / immunology. Interleukin-8 / biosynthesis. Lipopolysaccharides / pharmacology. Peptides / pharmacology. Teichoic Acids / pharmacology. Toll-Like Receptors / physiology

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  • (PMID = 17578764.001).
  • [ISSN] 0018-5043
  • [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 / Interleukin-8; 0 / Ligands; 0 / Lipopeptides; 0 / Lipopolysaccharides; 0 / Pam(3)CSK(4) peptide; 0 / Peptides; 0 / Teichoic Acids; 0 / Toll-Like Receptors; 56411-57-5 / lipoteichoic acid
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24. Ferruzzi P, Ceni E, Tarocchi M, Grappone C, Milani S, Galli A, Fiorelli G, Serio M, Mannelli M: Thiazolidinediones inhibit growth and invasiveness of the human adrenocortical cancer cell line H295R. J Clin Endocrinol Metab; 2005 Mar;90(3):1332-9
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  • [Title] Thiazolidinediones inhibit growth and invasiveness of the human adrenocortical cancer cell line H295R.
  • Thiazolidinediones (TZDs) are a new class of antidiabetic drugs that have also been shown to possess antitumoral properties in different human cancers.
  • In the present study, we evaluated PPARgamma mRNA and protein expression in tissue samples of human adrenocortical carcinomas (ACCs), normal adrenal glands, and the human ACC cell line H295R.
  • PPARgamma mRNA was expressed in six of eight ACC, two of three normal adrenal glands and the H295R cells.
  • These data suggest that TZDs reduce the malignant potential of the H295R ACC cell line and, therefore, might potentially constitute a novel tool in the medical treatment of human ACCs.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Hypoglycemic Agents / pharmacology. Thiazolidinediones / pharmacology
  • [MeSH-minor] Adrenal Glands / cytology. Adrenal Glands / pathology. Adult. Aged. Cell Division / drug effects. Cell Line, Tumor. Female. Humans. Matrix Metalloproteinase 2 / metabolism. Middle Aged. Neoplasm Invasiveness. PPAR gamma / genetics. PPAR gamma / metabolism. RNA, Messenger / analysis. Tumor Cells, Cultured

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  • (PMID = 15585569.001).
  • [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 / Hypoglycemic Agents; 0 / PPAR gamma; 0 / RNA, Messenger; 0 / Thiazolidinediones; 05V02F2KDG / rosiglitazone; EC 3.4.24.24 / Matrix Metalloproteinase 2; X4OV71U42S / pioglitazone
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25. van Merkesteyn JP, Gortzak RA, Allard RH: [Using corticosteroids to prevent postoperative oedema]. Ned Tijdschr Tandheelkd; 2005 Sep;112(9):322-4
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  • [Transliterated title] Gebruik van corticosteroïden ter preventie van postoperatief oedeem.
  • Corticosteroids are produced in the adrenal gland cortex and are subdivided in mineralocorticosteroids and glucocorticosteroids.
  • Usually, corticosteroids are prescribed as drugs to replace natural corticosteroids in case of insufficient functioning adrenal glands and in numerous diseases because of their anti-inflammatory and immunosuppressive effects.
  • [MeSH-major] Adrenal Cortex Hormones / therapeutic use. Edema / prevention & control. Oral Surgical Procedures. Postoperative Complications / prevention & control

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  • (PMID = 16184907.001).
  • [ISSN] 0028-2200
  • [Journal-full-title] Nederlands tijdschrift voor tandheelkunde
  • [ISO-abbreviation] Ned Tijdschr Tandheelkd
  • [Language] dut
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
  • [Number-of-references] 23
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26. Strosberg JR, Hammer GD, Doherty GM: Management of adrenocortical carcinoma. J Natl Compr Canc Netw; 2009 Jul;7(7):752-8; quiz 759
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  • [Title] Management of adrenocortical carcinoma.
  • Adrenocortical carcinomas (ACCs) are rare tumors that arise from the cortex of the adrenal gland with an incidence 1 to 2 per million.
  • The rarity of this tumor translates into a paucity of experience in managing patients in most medical centers.
  • This article describes the basic diagnostic and prognostic issues in adrenal cancer management, and presents detailed rationales for therapeutic management.
  • [MeSH-major] Adrenal Cortex Neoplasms / therapy. Adrenocortical Carcinoma / therapy
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Catecholamines / analysis. Chemotherapy, Adjuvant. Cushing Syndrome / drug therapy. Cushing Syndrome / etiology. Diagnostic Imaging. Humans. Hydrocortisone / analysis. Metanephrine / analysis. Mitotane / therapeutic use. Neoplasm Metastasis. Neoplasm Staging. Prognosis

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  • (PMID = 19635227.001).
  • [ISSN] 1540-1405
  • [Journal-full-title] Journal of the National Comprehensive Cancer Network : JNCCN
  • [ISO-abbreviation] J Natl Compr Canc Netw
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Catecholamines; 5001-33-2 / Metanephrine; 78E4J5IB5J / Mitotane; WI4X0X7BPJ / Hydrocortisone
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27. Treska V, Wirthová M, Hadravská S, Mukensnábl P, Kuntscher V, Kreuzberg B, Lisá L, Kozák K: [Giant bilateral adrenal myelolipoma associated with congenital adrenal hyperplasia]. Zentralbl Chir; 2006 Feb;131(1):80-3
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  • [Title] [Giant bilateral adrenal myelolipoma associated with congenital adrenal hyperplasia].
  • [Transliterated title] Ein bilaterales Riesenmyelolipom der Nebennieren in Kombination mit kongenitaler adrenaler Hyperplasie.
  • BACKGROUND: Myelolipoma is a rare benign tumor formed by mature fat tissue with strata of haematopoiesis.
  • It is usually localized in the region of the adrenal gland.
  • PATIENT AND METHODS: The authors present a rare case of a giant bilateral myelolipoma emerging out of the adrenal gland cortex in a congenital adrenal hyperplasia, with steroid 21-hydroxylase deficiency, in a woman with pronounced virilism.
  • CONCLUSIONS: The coincidence of myelolipoma and congenital disorder with subsequent overproduction of the adrenocorticotropin hormone and androgens, might be explained by the incipient of myelolipoma through chronic hormonal stimulation of the adrenal gland cortex.
  • [MeSH-major] Adrenal Gland Neoplasms / complications. Adrenal Gland Neoplasms / surgery. Adrenal Hyperplasia, Congenital / complications. Adrenal Hyperplasia, Congenital / surgery. Myelolipoma / complications. Myelolipoma / surgery. Neoplasms, Multiple Primary / complications. Neoplasms, Multiple Primary / surgery
  • [MeSH-minor] Adrenal Glands / pathology. Adrenalectomy. Female. Humans. Middle Aged. Steroid 21-Hydroxylase / blood. Tomography, X-Ray Computed


28. Konoplia EF, Banetskaia NV, Popov EG, Rubchenia IN: [The role of initial state of adrenal cortex in external irradiation effects upon its structure, function and androgen-receptor interactions]. Radiats Biol Radioecol; 2005 Jan-Feb;45(1):46-50
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  • [Title] [The role of initial state of adrenal cortex in external irradiation effects upon its structure, function and androgen-receptor interactions].
  • We studied morphological-biochemical time-course reactions of adrenal cortex and hormonal function of testicles after combined or separate actions of external radiation exposure (1.0 Gy at 7.8 x 10(-4) Gy/sec) and prolonged (12-, 32 days) subcutaneous corticosterone injections (10 mg/kg/animal) in 2-3-month old male rats.
  • Both variants with exogenous hormone depressed endogenous glucocorticoid production and evolved acute structure-functional adrenal gland cortex deficiency.
  • Radiocensitivity of the gland at the experimental conditions was increased.
  • Simultaneously the aggravation of adrenal cortex functional activity accompanied with hypogonadism and depressed reproductive potential of male rats, accessed by means of androgen status and androgenspecific (transporting and receptional) proteins characteristics as sensitive molecular markers of an animal possible fecundity.

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  • (PMID = 15810521.001).
  • [ISSN] 0869-8031
  • [Journal-full-title] Radiatsionnaia biologiia, radioecologiia
  • [ISO-abbreviation] Radiats Biol Radioecol
  • [Language] RUS
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Androgens; 0 / Glucocorticoids; 0 / Receptors, Androgen; 3XMK78S47O / Testosterone; W980KJ009P / Corticosterone
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29. Abiven G, Coste J, Groussin L, Anract P, Tissier F, Legmann P, Dousset B, Bertagna X, Bertherat J: Clinical and biological features in the prognosis of adrenocortical cancer: poor outcome of cortisol-secreting tumors in a series of 202 consecutive patients. J Clin Endocrinol Metab; 2006 Jul;91(7):2650-5
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  • [Title] Clinical and biological features in the prognosis of adrenocortical cancer: poor outcome of cortisol-secreting tumors in a series of 202 consecutive patients.
  • CONTEXT: Adrenocortical carcinomas (ACC) are rare tumors with a poor prognosis.
  • Mean age at diagnosis was 44 +/- 16 yr (range, 11-88 yr).
  • We found that 154 patients (76%) had hypersecreting tumors [mostly cortisol and androgens (47%), cortisol alone (27%), or androgens alone (6%)] and 43 patients (21%) had metastases at diagnosis.
  • Multivariate analysis identified the following independent prognostic factors associated with shorter survival: older age at diagnosis [hazard ratio (HR), 1.03; P < 0.0001], initial MacFarlane extension stages 3 (HR, 4.42; P = 0.005) and 4 (HR, 7.93; P < 0.0001), and cortisol hypersecretion (HR, 3.90; P < 0.0001).
  • [MeSH-major] Adrenal Cortex Neoplasms / secretion. Hydrocortisone / secretion
  • [MeSH-minor] Adult. Analysis of Variance. Androgens / secretion. Antineoplastic Agents, Hormonal / therapeutic use. Bone Neoplasms / secondary. Chemotherapy, Adjuvant. Female. Humans. Liver Neoplasms / secondary. Lung Neoplasms / secondary. Male. Middle Aged. Mitotane / therapeutic use. Neoplasm Staging. Prognosis. Survival Rate

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  • (PMID = 16670169.001).
  • [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 / Androgens; 0 / Antineoplastic Agents, Hormonal; 78E4J5IB5J / Mitotane; WI4X0X7BPJ / Hydrocortisone
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30. Hein J, Wrase J, Heinz A: [Alcohol-related disorders: etiopathology and therapeutic considerations]. Fortschr Neurol Psychiatr; 2007 Jan;75(1):10-7
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  • Disturbances of the hpa-axis (hypothalamus-pituitary gland-adrenal cortex) were also shown to play a role in alcohol dependence.

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  • (PMID = 17230311.001).
  • [ISSN] 0720-4299
  • [Journal-full-title] Fortschritte der Neurologie-Psychiatrie
  • [ISO-abbreviation] Fortschr Neurol Psychiatr
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 333DO1RDJY / Serotonin; 56-12-2 / gamma-Aminobutyric Acid; VTD58H1Z2X / Dopamine
  • [Number-of-references] 125
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31. Sieber-Ruckstuhl NS, Meli ML, Boretti FS, Gönczi E, Lutz H, Reusch CE: Quantitative real-time PCR for the measurement of 11beta-HSD1 and 11beta-HSD2 mRNA levels in tissues of healthy dogs. Horm Metab Res; 2007 Aug;39(8):548-54

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  • Highest 11beta-HSD1 mRNA expression was seen in liver, lung, and renal medulla; highest 11beta-HSD2 mRNA expression in renal cortex, adrenal gland, and renal medulla.
  • Higher 11beta-HSD1 than 11beta-HSD2 mRNA levels were found in all tissues except adrenal gland, colon, and rectum.

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  • (PMID = 17712718.001).
  • [ISSN] 0018-5043
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / DNA Primers; 0 / RNA, Messenger; EC 1.1.1.146 / 11-beta-Hydroxysteroid Dehydrogenase Type 1; EC 1.1.1.146 / 11-beta-Hydroxysteroid Dehydrogenase Type 2
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32. Britvin TA, Kazantseva IA, Kalinin AP, Kushlinskii NE: Vascular endothelium growth factor in the sera of patients with adrenal tumors. Bull Exp Biol Med; 2005 Aug;140(2):228-30
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  • [Title] Vascular endothelium growth factor in the sera of patients with adrenal tumors.
  • Serum levels of vascular endothelium growth factor were measured in 43 patients with adrenal tumors and 25 healthy subjects.
  • The mean blood levels of the factor in patients with adrenal tumors significantly surpassed the control.
  • The levels of this factor were maximum in patients with adrenocortical cancer, but its mean level differed negligibly from that in other morphological variants of tumors.
  • The level of vascular endothelium growth factor tended to increase with increasing the stage of adrenocortical cancer.
  • A direct correlation was revealed between the level of vascular endothelium growth factor and tumor size in adrenocortical cancer and aldosterone-producing adenoma.
  • Presumably, vascular endothelium growth factor is involved into mechanisms of growth, invasion, and metastatic growth of adrenocortical cancer.
  • [MeSH-major] Adrenal Gland Neoplasms / blood. Gene Expression Regulation, Neoplastic. Vascular Endothelial Growth Factor A / blood
  • [MeSH-minor] Adult. Aged. Case-Control Studies. Female. Humans. Male. Middle Aged. Neoplasm Metastasis

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  • (PMID = 16283008.001).
  • [ISSN] 0007-4888
  • [Journal-full-title] Bulletin of experimental biology and medicine
  • [ISO-abbreviation] Bull. Exp. Biol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A
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33. Dickmeis T: Glucocorticoids and the circadian clock. J Endocrinol; 2009 Jan;200(1):3-22
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  • Glucocorticoids, hormones produced by the adrenal gland cortex, perform numerous functions in body homeostasis and the response of the organism to external stressors.
  • Circadian control of glucocorticoid production and secretion involves a central pacemaker in the hypothalamus, the suprachiasmatic nucleus, as well as a circadian clock in the adrenal gland itself.
  • Central circadian regulation is mediated via the hypothalamic-pituitary-adrenal axis and the autonomic nervous system, while the adrenal gland clock appears to control sensitivity of the gland to the adrenocorticopic hormone (ACTH).
  • [MeSH-minor] Adrenal Glands / physiology. Animals. Gene Expression Regulation. Humans. Hypothalamus / physiology. Neurosecretory Systems / physiology

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  • (PMID = 18971218.001).
  • [ISSN] 1479-6805
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Glucocorticoids
  • [Number-of-references] 164
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34. Calender A: [Pathogenic patterns of genetic predisposition to endocrine tumors]. Nephrol Ther; 2006 Jan;2 Suppl 2:S127-36
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  • [Transliterated title] Les modèles pathogèniques de la prèdisposition génétique aux tumeurs endocrines.
  • Multiple endocrine neoplasia (MEN) are major predisposition syndromes to endocrine tumours and are characterised by an autosomal dominant disorder and full penetrance.
  • MEN-1 is a major form of hyperparathyroidism associated with a high prevalence of endocrine tumours of the pancreas, pituitary gland, adrenal cortex and the lymphoid and bronchial endocrine tissues.
  • MEN-2 is the familial syndrome of medullary thyroid carcinoma, associated with pheochromocytoma and hyperparathyroidism.
  • Apart from the clinical expression of their allelic variants, both syndromes are different in their physiopathogenesis, in that MEN-2 is related to the constitutional activation of the proto-oncogene RET that encodes a putative tyrosine kinase receptor, while MEN-1 is a tumour suppressor gene model, related to mutations in the menin adapter-protein of multiple intracellular functions.
  • These hereditary models of endocrine cancer contribute as much to further physiopathogenic knowledge as to the therapeutic recommendations for managing these syndromes.
  • [MeSH-major] Endocrine Gland Neoplasms / genetics. Genetic Predisposition to Disease. Multiple Endocrine Neoplasia / genetics
  • [MeSH-minor] Humans. Multiple Endocrine Neoplasia Type 1 / genetics. Multiple Endocrine Neoplasia Type 2a / genetics

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  • (PMID = 17373213.001).
  • [ISSN] 1769-7255
  • [Journal-full-title] Néphrologie & thérapeutique
  • [ISO-abbreviation] Nephrol. Ther.
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 35
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35. Hiasa M, Matsumoto T, Komatsu T, Moriyama Y: Wide variety of locations for rodent MATE1, a transporter protein that mediates the final excretion step for toxic organic cations. Am J Physiol Cell Physiol; 2006 Oct;291(4):C678-86
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  • Immunological techniques with specific antibodies against mMATE1 combined with RT-PCR revealed that mMATE1 is also expressed in various cells, including brain glia-like cells and capillaries, pancreatic duct cells, urinary bladder epithelium, adrenal gland cortex, alpha cells of the islets of Langerhans, Leydig cells, and vitamin A-storing Ito cells.

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  • (PMID = 16641166.001).
  • [ISSN] 0363-6143
  • [Journal-full-title] American journal of physiology. Cell physiology
  • [ISO-abbreviation] Am. J. Physiol., Cell Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MATE1 protein, mouse; 0 / Organic Cation Transport Proteins; 0 / Protons; 66-40-0 / Tetraethylammonium
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36. Bayne S, Jones ME, Li H, Pinto AR, Simpson ER, Liu JP: Estrogen deficiency leads to telomerase inhibition, telomere shortening and reduced cell proliferation in the adrenal gland of mice. Cell Res; 2008 Nov;18(11):1141-50

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Estrogen deficiency leads to telomerase inhibition, telomere shortening and reduced cell proliferation in the adrenal gland of mice.
  • We report here that estrogen deficiency caused by targeted disruption of aromatase in mice results in significant inhibition of telomerase activity in the adrenal gland in vivo.
  • Gene expression analysis showed that, in the absence of estrogen, telomerase reverse transcriptase (TERT) gene expression is reduced in association with compromised cell proliferation in the adrenal gland cortex and adrenal atrophy.
  • Stem cells positive in c-kit are identified to populate in the parenchyma of adrenal cortex.
  • Analysis of telomeres revealed that estrogen deficiency results in significantly shorter telomeres in the adrenal cortex than that in wild-type (WT) control mice.
  • Thus, our data show for the first time that estrogen deficiency causes inhibitions of TERT gene expression, telomerase activity, telomere maintenance, and cell proliferation in the adrenal gland of mice in vivo, suggesting that telomerase inhibition and telomere shortening may mediate cell proliferation arrest in the adrenal gland, thus contributing to estrogen deficiency-induced aging under physiological conditions.
  • [MeSH-minor] Adrenal Cortex / metabolism. Adrenal Glands / growth & development. Adrenal Glands / metabolism. Animals. Cell Aging / genetics. Female. Gene Expression. Mice. Mice, Transgenic

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  • (PMID = 18936784.001).
  • [ISSN] 1748-7838
  • [Journal-full-title] Cell research
  • [ISO-abbreviation] Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Estrogens; EC 2.7.7.49 / Telomerase
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37. Pietilä I, Vainio S: The embryonic aorta-gonad-mesonephros region as a generator of haematopoietic stem cells. APMIS; 2005 Nov-Dec;113(11-12):804-12
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  • During mammalian embryonic development the definitive haematopoietic stem cells (HSCs) may arise either in the extra-embryonic mesoderm or in the aorta-gonad-mesonephros (AGM) region that forms in close proximity to the assembling urogenital system, generating the gonad, cortex of the adrenal gland and metanephros.

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  • (PMID = 16480451.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Denmark
  • [Number-of-references] 50
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38. Liao M, Shen J, Zhang Y, Li SH, Li XJ, Li H: Immunohistochemical localization of huntingtin-associated protein 1 in endocrine system of the rat. J Histochem Cytochem; 2005 Dec;53(12):1517-24
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  • HAP1-immunoreactive cells are widely distributed in the anterior lobe of the pituitary, scattered in the wall of the thyroid follicles, or clustered in the interfollicular space of the thyroid gland, exclusively but diffusely distributed in the medullae of adrenal glands, and selectively located in the pancreas islets.
  • However, no HAP1-immunoreactive cell was found in the cortex of the adrenal gland, the testis, and the ovary.
  • HAP1-immunoreactive stigmoid bodies were also found in the cytoplasm of endocrine cells in the thyroid gland, the medullae of adrenal gland, the pancreas islets, the stomach, and small intestine.
  • [MeSH-minor] Adrenal Medulla / metabolism. Animals. Enteroendocrine Cells / metabolism. Female. Gastric Mucosa / metabolism. Immunohistochemistry. Intestinal Mucosa / metabolism. Intestine, Small / metabolism. Islets of Langerhans / metabolism. Male. Organ Specificity. Pituitary Gland / metabolism. Rats. Rats, Sprague-Dawley. Thyroid Gland / metabolism

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  • (PMID = 16087704.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hap1 protein, rat; 0 / Nerve Tissue Proteins
  • [Other-IDs] NLM/ PMC3957544
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39. Bertherat J, Groussin L, Bertagna X: Mechanisms of disease: adrenocortical tumors--molecular advances and clinical perspectives. Nat Clin Pract Endocrinol Metab; 2006 Nov;2(11):632-41
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  • [Title] Mechanisms of disease: adrenocortical tumors--molecular advances and clinical perspectives.
  • Most adrenocortical tumors are benign, unilateral, adrenocortical adenomas that are often discovered incidentally.
  • Adrenocortical cancer is rare.
  • Exceptionally, adrenocortical tumors can be bilateral.
  • Although most adrenocortical tumors occur sporadically, they may also feature in congenital and/or familial disease.
  • The identification of germline genetic defects in familial diseases associated with adrenocortical tumors helped to define the somatic alterations in sporadic disease: for example, overexpression of insulin-like growth factor 2 and alterations at the 11p15 locus (observed in Beckwith-Wiedemann syndrome) are also found in most adrenocortical cancers.
  • Similarly, inactivating mutations of the TP53 gene, located at 17p13 (observed in Li-Fraumeni syndrome), can also be found at the somatic level in sporadic adrenocortical cancers, as can 17p13 allelic losses.
  • Components of the cyclic AMP signaling pathway--for example, adrenocorticotropic hormone receptors and other membrane receptors, Gs proteins and protein kinase A--can be altered to various degrees in adrenocortical tumors.
  • More recently, gene profiling and genetic studies have shown that the Wnt-beta-catenin signaling pathway is frequently activated in adrenocortical tumors.
  • These research findings already have profound implications for clinical management of patients with adrenocortical tumors, for example in unraveling the genetic origin of the disease in some patients, and in the development of molecular markers for diagnosis and prognosis.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics

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  • (PMID = 17082810.001).
  • [ISSN] 1745-8366
  • [Journal-full-title] Nature clinical practice. Endocrinology & metabolism
  • [ISO-abbreviation] Nat Clin Pract Endocrinol Metab
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 54
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40. Fuchs LF, Guimarães CR, Maganhin CC, Simões RS, Baracat MC, Soares Júnior JM, Baracat EC: [Melatonin action in apoptosis and vascular endothelial growth factor in adrenal cortex of pinealectomized female rats]. Rev Bras Ginecol Obstet; 2010 Aug;32(8):374-80
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  • [Title] [Melatonin action in apoptosis and vascular endothelial growth factor in adrenal cortex of pinealectomized female rats].
  • [Transliterated title] Ação da melatonina sobre a apoptose e fator de crescimento endotelial vascular no córtex da adrenal de ratas pinealectomizadas.
  • PURPOSE: to evaluate the reactivity of VEGF-A and cleaved caspase-3 in the adrenal gland cortex of female pinealectomized rats treated with melatonin.
  • After 60 days of treatment, all animals were anesthetized, and the adrenal glands were removed and fixed in 10% formaldehyde (phosphate buffered) for histological processing and paraffin embedding.
  • Sections (5 µm thick) were collected on silanized slides and submitted to imunnohistochemical methods for the detection of cleaved caspase-3 (apoptosis) and of vascular endothelial growth factor (VEGF-A) in the adrenal cortex.
  • RESULTS: reactivity to cleaved Caspase-3 was noted in the zona glomerulosa of the adrenal glands in all studied groups.
  • CONCLUSIONS: the pineal gland affects the arrangement of the zona glomerulosa and reticularis of the adrenal glands, which are related to the production of sex hormones.
  • [MeSH-major] Adrenal Cortex / drug effects. Adrenal Cortex / physiology. Apoptosis / drug effects. Melatonin / pharmacology. Vascular Endothelial Growth Factor A / drug effects
  • [MeSH-minor] Animals. Female. Pineal Gland / surgery. Rats

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  • (PMID = 21180873.001).
  • [ISSN] 1806-9339
  • [Journal-full-title] Revista brasileira de ginecologia e obstetrícia : revista da Federação Brasileira das Sociedades de Ginecologia e Obstetrícia
  • [ISO-abbreviation] Rev Bras Ginecol Obstet
  • [Language] por
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A; JL5DK93RCL / Melatonin
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41. López L, Aller MA, Miranda R, Sánchez-Patán F, Nava MP, Arias J, Arias JL: Prehepatic portal hypertension induces alterations in cytochrome oxidase activity in the rat adrenal gland. J Invest Surg; 2006 Mar-Apr;19(2):79-86

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  • [Title] Prehepatic portal hypertension induces alterations in cytochrome oxidase activity in the rat adrenal gland.
  • One approach to assess neuroendocrine response to portal hypertension in short-term portal vein-stenosed rats consists in studying metabolic and functional activity patterns in adrenal glands using mitochondrial enzyme cytochrome c oxidase (COX) as a histochemical marker.
  • In TPVS rats, COX activity in the adrenal gland cortex is lower than in control rats and affects the fascicular (52.30, 47.16-60.98, vs. 67.12, 60.31-73.89, p = .002), glomerular (49.68, 46.19-53.56 vs. 70.47, 64.64-73.51, p < .001), and reticular (47.35, 35.63-54.39, vs. 55.37, 49.76-58.97; p < .05) layers.
  • In contrast, COX activity in the adrenal gland medulla is similar in TPVS rats and in control rats (29.91, 29.54-31.18, vs. 29.67, 28.95-30.23).
  • The changes in adrenocortical COX activity in short-term-TPVS rats could constitute a pathogenic factor for both splanchnic and systemic hyperdynamic circulations, described in this experimental model of prehepatic portal hypertension.
  • [MeSH-major] Adrenal Glands / enzymology. Electron Transport Complex IV / metabolism. Hypertension, Portal / enzymology

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  • (PMID = 16531365.001).
  • [ISSN] 0894-1939
  • [Journal-full-title] Journal of investigative surgery : the official journal of the Academy of Surgical Research
  • [ISO-abbreviation] J Invest Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; EC 1.9.3.1 / Electron Transport Complex IV
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42. Dehghani F, Zabolizadeh J, Noorafshan A, Panjehshahin MR, Karbalay-Doust S: Protective effect of Brewer's yeast on methimazole-induced-adrenal atrophy (a stereological study). Tokai J Exp Clin Med; 2010 Apr;35(1):34-9
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  • [Title] Protective effect of Brewer's yeast on methimazole-induced-adrenal atrophy (a stereological study).
  • Induction of hypothyroidism by thioamide drugs will cause adrenal gland atrophy and decrease in its hormones.
  • To prevent side effect on the adrenal gland, brewer's yeast, a natural product rich in vitamins and minerals was used.
  • Serological techniques were applied to measure the volume of adrenal gland.
  • After 30 days, all the animals were anesthetized and their adrenal glands were removed, fixed, embedded and stained.
  • The volume of different zones of the adrenal glands was estimated by Cavalieri principle and point counting methods. statistical analysis was performed using Mann-Withney test and p < 0.05 was considered as statistically significant.
  • The results indicated that methimazole decreased the volume of fasciculata zone in the cortex of the adrenal gland and also decreased the blood cortisol level.
  • In conclusion, it seems that the use of brewer's yeast could prevent methimazole-induced atrophy of the adrenal gland.
  • [MeSH-major] Adrenal Cortex Diseases / pathology. Adrenal Glands / drug effects. Adrenal Glands / pathology. Antithyroid Agents / pharmacology. Methimazole / pharmacology. Saccharomyces cerevisiae

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  • (PMID = 21319024.001).
  • [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] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antithyroid Agents; 554Z48XN5E / Methimazole
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43. Murgia C, Devirgiliis C, Mancini E, Donadel G, Zalewski P, Perozzi G: Diabetes-linked zinc transporter ZnT8 is a homodimeric protein expressed by distinct rodent endocrine cell types in the pancreas and other glands. Nutr Metab Cardiovasc Dis; 2009 Jul;19(6):431-9
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  • Moreover, we show that ZnT8 is also expressed in other secretory cell types, namely the cubical epithelium that lines thyroid follicles and the cortex of the adrenal gland, suggesting a more widespread role in endocrine secretion.
  • [MeSH-minor] Adrenal Cortex / metabolism. Animals. COS Cells. Caco-2 Cells. Cell Membrane / metabolism. Cercopithecus aethiops. Dogs. Humans. Mice. Protein Multimerization. Rats. Thyroid Gland / metabolism. Transfection


44. Lindblom P, Rafter I, Copley C, Andersson U, Hedberg JJ, Berg AL, Samuelsson A, Hellmold H, Cotgreave I, Glinghammar B: Isoforms of alanine aminotransferases in human tissues and serum--differential tissue expression using novel antibodies. Arch Biochem Biophys; 2007 Oct 1;466(1):66-77
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  • Using immunohistochemistry, strong ALT1 reactivity was found in hepatocytes, renaltubular epithelial cells and in salivary gland epithelial cells, while ALT2 was expressed in adrenal gland cortex, neuronal cell bodies, cardiac myocytes, skeletal muscle fibers and endocrine pancreas.


45. Tadros SF, Frisina ST, Mapes F, Frisina DR, Frisina RD: Higher serum aldosterone correlates with lower hearing thresholds: a possible protective hormone against presbycusis. Hear Res; 2005 Nov;209(1-2):10-8
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  • Aldosterone hormone is a mineralocorticoid secreted by adrenal gland cortex and controls serum sodium (Na(+)) and potassium (K(+)) levels.

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  • (PMID = 16039078.001).
  • [ISSN] 0378-5955
  • [Journal-full-title] Hearing research
  • [ISO-abbreviation] Hear. Res.
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / P01 AG09524; United States / NIDCD NIH HHS / DC / P30 DC05409
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Mineralocorticoids; 4964P6T9RB / Aldosterone
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46. Toni García M, Anda Apiñániz E, Pablo J, de Esteban M, Munárriz Alcuaz P, Goñi Iriarte MJ, Forga Llenas L: An unusual association: pheochromocytoma on an atrophied adrenal gland due to addison's disease. Endocrinol Nutr; 2008 Dec;55(10):510-3
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  • [Title] An unusual association: pheochromocytoma on an atrophied adrenal gland due to addison's disease.
  • APS-II is defined by the development of two or more of the following entities: primary adrenal insufficiency (Addison's disease), Graves' disease, type 1A diabetes mellitus, autoimmune thyroiditis, primary hypogonadism, celiac disease, and myasthenia gravis.
  • Primary adrenal insufficiency in these patients affects the adrenal cortex, which is destroyed by autoantibodies against 21-hydroxylase.
  • Unlike other causes of adrenal insufficiency (infectious diseases, infiltrative diseases, bleeding, tumors), the adrenal medulla is not involved.
  • Pheochromocytomas are tumors arising from the chromaffin cells of the sympathetic nervous system in the adrenal medulla.
  • In this patient, the adrenal gland cortex was atrophied and the tumor was attached to the adrenal medulla.

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  • [Copyright] Copyright © 2008 Sociedad Española de Endocrinología y Nutrición. Published by Elsevier Espana. All rights reserved.
  • (PMID = 22980466.001).
  • [ISSN] 1575-0922
  • [Journal-full-title] Endocrinología y nutrición : órgano de la Sociedad Española de Endocrinología y Nutrición
  • [ISO-abbreviation] Endocrinol Nutr
  • [Language] eng; spa
  • [Publication-type] Journal Article
  • [Publication-country] Spain
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47. Nesher M, Dvela M, Igbokwe VU, Rosen H, Lichtstein D: Physiological roles of endogenous ouabain in normal rats. Am J Physiol Heart Circ Physiol; 2009 Dec;297(6):H2026-34
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  • Endogenous ouabain (EO)-like compounds are synthesized in and released from the adrenal gland.
  • The adrenal gland cortex was enlarged in the antiouabain antibody-treated rats.
  • These findings show for the first time that circulatory ouabain plausibly originating in the adrenal has physiological roles controlling vasculature tone and sodium homeostasis in normal rats.
  • [MeSH-major] Adrenal Cortex / metabolism. Aorta, Thoracic / metabolism. Cardenolides / blood. Kidney / metabolism. Natriuresis. Saponins / blood. Vasoconstriction. Vasodilation

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  • [CommentIn] Am J Physiol Heart Circ Physiol. 2009 Dec;297(6):H1972-3 [19855053.001]
  • (PMID = 19837951.001).
  • [ISSN] 1522-1539
  • [Journal-full-title] American journal of physiology. Heart and circulatory physiology
  • [ISO-abbreviation] Am. J. Physiol. Heart Circ. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Cardenolides; 0 / Saponins; 0 / Vasoconstrictor Agents; 0 / digoxin-like factors; 1WS297W6MV / Phenylephrine; 4964P6T9RB / Aldosterone; 85637-73-6 / Atrial Natriuretic Factor; 9NEZ333N27 / Sodium; EC 3.6.3.9 / Sodium-Potassium-Exchanging ATPase; W980KJ009P / Corticosterone
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48. Seki M, Kageyama H, Takenoya F, Hirayama M, Kintaka Y, Inoue S, Matsuno R, Itabashi K, Date Y, Nakazato M, Shioda S: Neuropeptide W is expressed in the noradrenalin-containing cells in the rat adrenal medulla. Regul Pept; 2008 Jan 10;145(1-3):147-52
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  • [Title] Neuropeptide W is expressed in the noradrenalin-containing cells in the rat adrenal medulla.
  • NPW plays an important role in the regulation of both feeding and energy metabolism, and is also implicated in modulating responses to an acute inflammatory pain through activation of the hypothalamus-pituitary-adrenal axis.
  • GPR7 mRNA has been shown to be expressed in the hypothalamus, pituitary gland and adrenal cortex.
  • Similarly, NPW expression has been demonstrated in the brain and pituitary gland.
  • However, the precise distribution of NPW-producing cells in the adrenal gland remains unknown.
  • The aim of this study was to explore the distribution and localization of NPW immunoreactivity in the rat adrenal gland.
  • Total RNA was prepared from the hypothalamus, pituitary gland and adrenal gland.
  • RT-PCR revealed the expression of NPW mRNA in these tissues, while in situ hybridization demonstrated the presence of NPW mRNA in the adrenal medulla.
  • When immunohistochemistry was performed on sections of adrenal gland, NPW-like immunoreactivity (NPW-LI) was observed in the medulla but not in the cortex.
  • The finding that NPW is expressed in noradrenalin-containing cells in the adrenal medulla suggests that it may play an important role in endocrine function in the adrenal gland.
  • [MeSH-major] Adrenal Medulla / metabolism. Gene Expression Regulation. Neuropeptides / genetics. Norepinephrine / metabolism

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  • (PMID = 17870191.001).
  • [ISSN] 0167-0115
  • [Journal-full-title] Regulatory peptides
  • [ISO-abbreviation] Regul. Pept.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Neuropeptides; 0 / RNA, Messenger; 0 / neuropeptide W, rat; X4W3ENH1CV / Norepinephrine
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49. Abbasova SG, Vysotskii MM, Ovchinnikova LK, Obusheva MN, Digaeva MA, Britvin TA, Bahoeva KA, Karabekova ZK, Kazantzeva IA, Mamedov UR, Manuchin IB, Davidov MI: Cancer and soluble FAS. Bull Exp Biol Med; 2009 Oct;148(4):638-42
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  • [Title] Cancer and soluble FAS.
  • A test system developed by the authors was used to measure serum concentrations of soluble Fas in patients with malignant and benign tumors of different location and morphology.
  • Relationships between soluble Fas levels and the main clinical and morphological characteristics of cancer were evaluated.
  • No appreciable differences in the concentrations of soluble Fas were detected in malignant and benign tumors of the mammary gland, bones, ovaries, and adrenals.
  • In thyroid cancer, soluble Fas levels were higher than in benign and hyperplastic processes in this organ.
  • High level of soluble Fas is associated with late stages of the disease (ovarian cancer, cancer of the corpus uteri, adrenocortical and colorectal cancer) and with poor differentiation of the tumor (ovarian cancer and cancer of the corpus uteri), with local metastases (colorectal and adrenocortical cancer), and with tumor invasion into the myometrial tissue, intestinal wall, and adjacent tissues (cancer of the corpus uteri and colorectal cancer).
  • A significantly high level of soluble Fas was detected in colorectal and adrenocortical cancer in the presence of at least 2 local metastases.
  • Soluble Fas levels depended on tumor histogenesis in malignant and benign ovarian tumors.
  • High concentration of soluble Fas was detected in large tumors in patients with ovarian cancer, cancer of the corpus uteri, colorectal cancer, thyroid cancer and adenoma, and in adrenocortical cancer.
  • The overall 5-year survival of patients with low levels of soluble Fas is better in osteosarcoma, cancer of the corpus uteri, ovarian and adrenocortical cancer.

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  • (PMID = 20396760.001).
  • [ISSN] 1573-8221
  • [Journal-full-title] Bulletin of experimental biology and medicine
  • [ISO-abbreviation] Bull. Exp. Biol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95
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50. Sidhu S, Martin E, Gicquel C, Melki J, Clark SJ, Campbell P, Magarey CJ, Schulte KM, Röher HD, Delbridge L, Robinson BG: Mutation and methylation analysis of TP53 in adrenal carcinogenesis. Eur J Surg Oncol; 2005 Jun;31(5):549-54
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  • [Title] Mutation and methylation analysis of TP53 in adrenal carcinogenesis.
  • AIM: To investigate the role of coding region mutation and promoter hypermethylation of TP53 in adrenocortical cancer formation.
  • METHODS: Twenty sporadic adrenocortical cancers (ACCs) and five normal adrenal tissue samples were available for analysis.
  • In 10 ACCs and five normal adrenal tissue specimens, methylation of the 16 CpG sites within the TP53 promoter was examined using bisulphite methylation sequencing.
  • Four of 5 patients with a TP53 mutation had metastases at diagnosis or detected soon thereafter and 3 of 4 died of disease within 12 months of surgical resection.
  • No methylation was seen in the TP53 promoter in 10 ACC and the five normal adrenal tissues examined.
  • Promoter methylation of TP53 is not present in ACC as a mechanism for tumour suppressor gene (TSG) inactivation and, therefore, other genes in the 17p13 region are implicated in adrenal carcinogenesis.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Adrenal Gland Neoplasms / metabolism. DNA Methylation. Genes, p53. Mutation. Promoter Regions, Genetic

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  • (PMID = 15922892.001).
  • [ISSN] 0748-7983
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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51. Trifunovc S, Filipovic B, Ajdzanovic V, Sosic-Jurijevic B, Manojlovic-Stojanoski M, Nestorovic N, Ristic N, Sekulic M, Milosevic V: The effects of chronic SRIH-14 and octreotide administration on the pituitary-adrenal axis in adult male rats. Eur J Histochem; 2008 Jan-Mar;52(1):61-8
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  • [Title] The effects of chronic SRIH-14 and octreotide administration on the pituitary-adrenal axis in adult male rats.
  • The effects of chronic treatments with SRIH-14 and octreotide on pituitary corticotropes (ACTH cells) and on the adrenal cortex of male Wistar rats were examined.
  • The adrenal cortex was analyzed by histological and morphometric methods.
  • A significant (p<0.05) decrease in body weight and in the absolute weights of the pituitary and adrenal glands was observed in both treated groups.
  • The absolute volumes of the adrenal gland and adrenal cortex were significantly (p<0.05) decreased in both treated groups.
  • Together, these findings show that SRIH-14 and octreotide administration affected the morphological characteristics of the adrenal ZG in a similar manner, and brought about a decrease in plasma aldosterone concentration.
  • These treatments did not affect pituitary ACTH cells or adrenal ZF and ZR functioning.
  • [MeSH-major] Adrenal Cortex / drug effects. Adrenocorticotropic Hormone / blood. Aldosterone / blood. Corticotrophs / drug effects. Octreotide / administration & dosage. Pituitary-Adrenal System / drug effects. Somatostatin / administration & dosage

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  • (PMID = 18502724.001).
  • [ISSN] 1121-760X
  • [Journal-full-title] European journal of histochemistry : EJH
  • [ISO-abbreviation] Eur J Histochem
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone; 51110-01-1 / Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone; RWM8CCW8GP / Octreotide
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52. Libé R, Bertherat J: Molecular genetics of adrenocortical tumours, from familial to sporadic diseases. Eur J Endocrinol; 2005 Oct;153(4):477-87
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  • [Title] Molecular genetics of adrenocortical tumours, from familial to sporadic diseases.
  • Adrenal masses can be detected in up to 4% of the population, and are mostly of adrenocortical origin.
  • Adrenocortical tumours (ACTs) may be responsible for excess steroid production and, in the case of adrenocortical cancers, for morbidity or mortality due to tumour growth.
  • The familial diseases concerned are Li-Fraumeni syndrome, which may be due to germline mutation of the tumour-suppressor gene TP53 and Beckwith-Wiedemann syndrome, which is caused by dys-regulation of the imprinted IGF-II locus at 11p15.
  • ACTs also occur in type 1 multiple endocrine neoplasia (MEN 1), which is characterized by a germline mutation of the menin gene.
  • Cushing's syndrome due to primary pigmented nodular adrenocortical disease (PPNAD) has been observed in Carney complex patients presenting inactivating germline PRKAR1A mutations.
  • Interestingly, allelic losses at 17p13 and 11p15 have been demonstrated in sporadic adrenocortical cancer and somatic PRKAR1A mutations have been found in secreting adrenocortical adenomas.
  • The genetics of another group of adrenal diseases that can lead to adrenal nodular hyperplasia -- congenital adrenal hyperplasia (CAH) and glucocorticoid-remediable aldosteronism (GRA) -- have also been studied extensively.
  • This review summarizes recent advances in the genetics of ACTs, highlighting both improvements in our understanding of the pathophysiology and the diagnosis of these tumours.

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  • (PMID = 16189167.001).
  • [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; Review
  • [Publication-country] England
  • [Number-of-references] 97
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53. Ziegler CG, Brown JW, Schally AV, Erler A, Gebauer L, Treszl A, Young L, Fishman LM, Engel JB, Willenberg HS, Petersenn S, Eisenhofer G, Ehrhart-Bornstein M, Bornstein SR: Expression of neuropeptide hormone receptors in human adrenal tumors and cell lines: antiproliferative effects of peptide analogues. Proc Natl Acad Sci U S A; 2009 Sep 15;106(37):15879-84
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  • [Title] Expression of neuropeptide hormone receptors in human adrenal tumors and cell lines: antiproliferative effects of peptide analogues.
  • Peptide analogues targeting various neuropeptide receptors have been used effectively in cancer therapy.
  • A hallmark of adrenocortical tumor formation is the aberrant expression of peptide receptors relating to uncontrolled cell proliferation and hormone overproduction.
  • Our microarray results have also demonstrated a differential expression of neuropeptide hormone receptors in tumor subtypes of human pheochromocytoma.
  • In light of these findings, we performed a comprehensive analysis of relevant receptors in both human adrenomedullary and adrenocortical tumors and tested the antiproliferative effects of peptide analogues targeting these receptors.
  • Specifically, we examined the receptor expression of somatostatin-type-2 receptor, growth hormone-releasing hormone (GHRH) receptor or GHRH receptor splice variant-1 (SV-1) and luteinizing hormone-releasing hormone (LHRH) receptor at the mRNA and protein levels in normal human adrenal tissues, adrenocortical and adrenomedullary tumors, and cell lines.
  • Cytotoxic derivatives of somatostatin AN-238 and, to a lesser extent, AN-162, reduced cell numbers of uninduced and NGF-induced adrenomedullary pheochromocytoma cells and adrenocortical cancer cells.
  • Both the splice variant of GHRH receptor SV-1 and the LHRH receptor were also expressed in adrenocortical cancer cell lines but not in the pheochromocytoma cell line.
  • The GHRH receptor antagonist MZ-4-71 and LHRH antagonist Cetrorelix both significantly reduced cell growth in the adrenocortical cancer cell line.
  • In conclusion, the expression of receptors for somatostatin, GHRH, and LHRH in the normal human adrenal and in adrenal tumors, combined with the growth-inhibitory effects of the antitumor peptide analogues, may make possible improved treatment approaches to adrenal tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / drug therapy. Adrenal Gland Neoplasms / metabolism. Neuropeptides / pharmacology. Receptors, Neuropeptide / metabolism
  • [MeSH-minor] 2-Hydroxyphenethylamine / analogs & derivatives. 2-Hydroxyphenethylamine / pharmacology. Adrenal Glands / metabolism. Aniline Compounds / pharmacology. Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Cytostatic Agents / pharmacology. Doxorubicin / analogs & derivatives. Doxorubicin / pharmacology. Gene Expression. Humans. Oligonucleotide Array Sequence Analysis. PC12 Cells. Pyrroles / pharmacology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Receptors, LHRH / genetics. Receptors, LHRH / metabolism. Receptors, Somatostatin / genetics. Receptors, Somatostatin / metabolism. Somatostatin / analogs & derivatives. Somatostatin / pharmacology

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  • (PMID = 19717419.001).
  • [ISSN] 1091-6490
  • [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 / AN 238; 0 / Aniline Compounds; 0 / Cytostatic Agents; 0 / Neuropeptides; 0 / Pyrroles; 0 / RNA, Messenger; 0 / Receptors, LHRH; 0 / Receptors, Neuropeptide; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 2PK59M9GFF / vapreotide; 33189-65-0 / N-(2-diethylaminoethyl)-N-(2-hydroxy-2-phenylethyl)-2,5-dichloroaniline; 51110-01-1 / Somatostatin; 7568-93-6 / 2-Hydroxyphenethylamine; 80168379AG / Doxorubicin
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54. Gatta G, Ciccolallo L, Kunkler I, Capocaccia R, Berrino F, Coleman MP, De Angelis R, Faivre J, Lutz JM, Martinez C, Möller T, Sankila R, EUROCARE Working Group: Survival from rare cancer in adults: a population-based study. Lancet Oncol; 2006 Feb;7(2):132-40
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  • [Title] Survival from rare cancer in adults: a population-based study.
  • BACKGROUND: Rare cancers are a challenge to clinical practice, and treatment experience, even in major cancer centres to which rare cancers are usually referred, is often limited.
  • We aimed to study the epidemiology of rare cancers in a large population of several countries.
  • METHODS: We analysed survival by age, sex, subsite, and morphology in 57,144 adults with 14 selected rare cancers diagnosed 1983-94.
  • We also estimated the adjusted relative excess risk of death for every rare cancer.
  • FINDINGS: Overall 5-year relative survival was good (ie, >65%) for placental choriocarcinoma (85.4% [95% CI 81.4-89.5]), thyroid medullary carcinoma (72.4% [69.2-75.5]), ovarian germ-cell cancer (73.0% [70.0-76.0]), lung carcinoid (70.1% [67.3-72.9]), and cervical adenocarcinoma (65.5% [64.3-66.6]); intermediate (ie, 35-65%) for testicular cancer at age 65 years or older (64.0% [59.3-68.7]), sarcoma of extremities (60.0% [58.9-61.2]), digestive-system endocrine cancers (55.6% [54.9-56.3]), anal squamous-cell carcinoma (53.1% [51.5-54.8]), and uterine sarcoma (43.5% [42.0-44.9]); low for carcinoma of adrenal-gland cortex (32.7% [28.3-37.2]) and bladder squamous-cell carcinoma (20.4% [18.8-22.0]); and poor for angiosarcoma of liver (6.4% [1.8-11.0]) and mesothelioma (4.7% [4.3-5.2]).
  • Survival significantly improved over time for ovarian germ-cell cancer, sarcomas of extremities, digestive-system endocrine tumours, anal squamous-cell carcinoma, and angiosarcoma of liver.
  • Survival in northern Europe was higher than in the other geographic groupings for most cancers.
  • INTERPRETATION: Because effective treatments are available for several of the rare cancers we assessed, further research is needed to ascertain why survival is lower in some European countries than in others, particularly in older patients.
  • Audit of best practice for rare cancers with treatment protocols would be useful.

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  • (PMID = 16455477.001).
  • [ISSN] 1470-2045
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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55. Turner DJ, Miskulin J: Management of adrenal lesions. Curr Opin Oncol; 2009 Jan;21(1):34-40
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  • [Title] Management of adrenal lesions.
  • PURPOSE OF REVIEW: Adrenal lesions are commonly seen on modern imaging modalities, and although the majority are benign, potentially lethal entities necessitate exclusion.
  • The purpose of this review is to summarize recent advances in diagnosis and therapies for adrenal lesions.
  • RECENT FINDINGS: New tumor markers and genetic risk factors continue to be discovered, and improved diagnostic techniques have made adrenal incidentalomas more common than ever before.
  • Laparoscopic approaches for adrenal lesions continue to evolve for functional lesions, and also for lesions 12 cm and larger.
  • Open adrenalectomy continues to be the most appropriate for adrenocortical cancer.
  • SUMMARY: All adrenal lesions should prompt a functional hormonal assessment and additional imaging to determine malignancy employed.
  • [MeSH-major] Adrenal Gland Diseases / diagnosis. Adrenal Gland Diseases / surgery. Adrenal Gland Neoplasms / diagnosis. Adrenal Gland Neoplasms / surgery
  • [MeSH-minor] Biomarkers, Tumor / analysis. Humans

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  • (PMID = 19125016.001).
  • [ISSN] 1531-703X
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 41
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56. Bovio S, Porpiglia F, Bollito E, Allasino B, Reimondo G, Rovero E, Perazzolo L, Angeli A, Papotti M, Terzolo M: Adrenal pseudocyst mimicking cancer: a case report. J Endocrinol Invest; 2007 Mar;30(3):256-8
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  • [Title] Adrenal pseudocyst mimicking cancer: a case report.
  • Adrenal cysts are infrequently observed, since less than 500 cases have been reported in Western literature.
  • Adrenal cysts are conventionally divided into four categories: epithelial, parasitic, endothelial, and hemorrhagic.
  • We report herein the case of an adrenal hemorrhagic pseudocyst that simulated adrenocortical cancer and argue on the clinical clues for a differential diagnosis with other adrenal tumors.
  • [MeSH-major] Adrenal Gland Diseases / diagnosis. Adrenal Gland Neoplasms / diagnosis. Cysts / diagnosis
  • [MeSH-minor] Adrenal Glands / pathology. Adrenal Glands / surgery. Aged. Diagnosis, Differential. Female. Humans

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  • (PMID = 17505162.001).
  • [ISSN] 1720-8386
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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57. Tissier F, Cavard C, Groussin L, Perlemoine K, Fumey G, Hagneré AM, René-Corail F, Jullian E, Gicquel C, Bertagna X, Vacher-Lavenu MC, Perret C, Bertherat J: Mutations of beta-catenin in adrenocortical tumors: activation of the Wnt signaling pathway is a frequent event in both benign and malignant adrenocortical tumors. Cancer Res; 2005 Sep 1;65(17):7622-7
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  • [Title] Mutations of beta-catenin in adrenocortical tumors: activation of the Wnt signaling pathway is a frequent event in both benign and malignant adrenocortical tumors.
  • Adrenocortical cancer is a rare cancer with a very poor prognosis.
  • The genetic alterations identified to date in adrenocortical tumors are limited.
  • Activating mutations of the Wnt signaling pathway have been observed in more frequent cancers, particularly digestive tract tumors.
  • We investigated whether Wnt pathway activation is involved in adrenocortical tumorigenesis.
  • In a series of 39 adrenocortical tumors, immunohistochemistry revealed abnormal cytoplasmic and/or nuclear accumulation of beta-catenin in 10 of 26 adrenocortical adenomas and in 11 of 13 adrenocortical carcinomas.
  • An activating somatic mutation of the beta-catenin gene was shown in 7 of 26 adrenocortical adenomas and in 4 of 13 adrenocortical carcinomas; these mutations were observed only in adrenocortical tumors with abnormal beta-catenin accumulation and most were point mutations altering the Ser45 of exon 3 (in the consensus GSK3-beta/CK1 phosphorylation site).
  • Functional studies showed that the activating Ser45 beta-catenin mutation found in the adrenocortical cancer H295R cell line leads to constitutive activation of T-cell factor-dependent transcription.
  • This is the first molecular defect to be reported with the same prevalence in both benign (27%) and malignant (31%) adrenocortical tumors. beta-Catenin mutations are also the most frequent genetic defect currently known in adrenocortical adenomas.
  • In adrenocortical adenomas, beta-catenin alterations are more frequent in nonfunctioning tumors, suggesting that beta-catenin pathway activation might be mostly involved in the development of nonsecreting adrenocortical adenomas and adrenocortical carcinomas.
  • The very frequent and substantial accumulation of beta-catenin in adrenocortical carcinomas suggests that other alterations might also be involved.
  • This finding may contribute to new therapeutic approaches targeting the Wnt pathway in malignant adrenocortical tumors, for which limited medical therapy is available.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Cytoskeletal Proteins / genetics. Intercellular Signaling Peptides and Proteins / genetics. Trans-Activators / genetics
  • [MeSH-minor] Adult. Aged. Cell Line, Tumor. Female. Humans. Immunohistochemistry. Male. Middle Aged. Mutation. Signal Transduction. Wnt Proteins. beta Catenin

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  • (PMID = 16140927.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / Cytoskeletal Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Trans-Activators; 0 / Wnt Proteins; 0 / beta Catenin
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58. Saeger W, Fassnacht M: [Effects of drugs on the adrenal cortex and its tumors]. Pathologe; 2006 Feb;27(1):61-4
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  • [Title] [Effects of drugs on the adrenal cortex and its tumors].
  • [Transliterated title] Wirkungen von Medikamenten auf die Nebennierenrinde und ihre Tumoren.
  • The structure of the normal adrenal cortex is changed by stimulating hormones (ACTH) and inhibiting hormonal drugs (especially glucocorticoids).
  • In the therapy of patients with adrenocortical cancer, mitotane can cause an increase in of necrosis and fibrosis, but also in intracellular lipid.
  • [MeSH-major] Adrenal Cortex / pathology. Adrenal Cortex Neoplasms / drug therapy. Antineoplastic Agents / therapeutic use

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  • (PMID = 16320017.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Hormonal; 0O54ZQ14I9 / Aminoglutethimide; 9002-60-2 / Adrenocorticotropic Hormone
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59. Lee JA, Duh QY: Reoperation for adrenocortical neoplasms. Curr Treat Options Oncol; 2006 Jul;7(4):320-5
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  • [Title] Reoperation for adrenocortical neoplasms.
  • Adrenocortical cancer is a highly lethal malignancy.
  • Patients with widely metastatic disease or those with tumors not amenable to re-resection may benefit from tumor debulking to help control symptoms associated with oversecretion syndromes.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery

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  • (PMID = 16916492.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 35
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60. Terzolo M, Bovio S, Pia A, Reimondo G, Angeli A: Management of adrenal incidentaloma. Best Pract Res Clin Endocrinol Metab; 2009 Apr;23(2):233-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Management of adrenal incidentaloma.
  • Clinically inapparent adrenal masses, or adrenal incidentalomas, are discovered inadvertently in the course of work-up or treatment of unrelated disorders.
  • Cortical adenoma is the most frequent tumour detected incidentally, but adrenocortical cancer, phaeochromocytoma and metastasis are not rare.
  • Two critical questions should be answered before trying to outline the management of adrenal incidentaloma:.
  • (1) identify either primary (adrenocortical cancer) or secondary (adrenal metastasis) malignancy;.
  • Radiological evaluation is the key to the differential diagnosis of benign and malignant tumours.
  • Endocrine testing is necessary to exclude phaeochromocytoma in all patients with an adrenal incidentaloma because this tumour may remain undiagnosed after imaging studies.
  • The management of clinically inapparent adrenal adenomas may vary depending whether or not they are functioning.
  • [MeSH-major] Adrenal Gland Neoplasms / therapy
  • [MeSH-minor] Adenoma / diagnosis. Adenoma / drug therapy. Adenoma / therapy. Animals. Humans. Pheochromocytoma / diagnosis. Pheochromocytoma / therapy

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  • (PMID = 19500766.001).
  • [ISSN] 1878-1594
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 46
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61. Leboulleux S, Dromain C, Bonniaud G, Aupérin A, Caillou B, Lumbroso J, Sigal R, Baudin E, Schlumberger M: Diagnostic and prognostic value of 18-fluorodeoxyglucose positron emission tomography in adrenocortical carcinoma: a prospective comparison with computed tomography. J Clin Endocrinol Metab; 2006 Mar;91(3):920-5
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  • [Title] Diagnostic and prognostic value of 18-fluorodeoxyglucose positron emission tomography in adrenocortical carcinoma: a prospective comparison with computed tomography.
  • OBJECTIVE: Patients with adrenocortical cancer are submitted to multiple imaging procedures for diagnosis of recurrence and staging.
  • METHODS: Twenty-eight consecutive patients with adrenocortical cancer referred from November 2003 to December 2004 to the Institut Gustave Roussy were included.
  • The sensitivities for the detection of distinct lesions and the diagnosis of metastatic organs were 90 and 93% for PET/CT and 88 and 82% for TAP-CT, respectively.
  • Tumor size and mitotic rate were significantly associated with FDG uptake.
  • CONCLUSIONS: We show that FDG-PET/CT is complementary to TAP-CT and of special interest in the diagnosis of local relapses.
  • [MeSH-major] Adrenal Cortex Neoplasms / radiography. Adrenal Cortex Neoplasms / radionuclide imaging. Fluorodeoxyglucose F18
  • [MeSH-minor] Adult. Aged. Female. Humans. Image Processing, Computer-Assisted. Male. Middle Aged. Neoplasm Metastasis. Positron-Emission Tomography. Prognosis. Radiopharmaceuticals. Survival Analysis. Tomography, X-Ray Computed

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  • (PMID = 16368753.001).
  • [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 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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62. Bertherat J, Gimenez-Roqueplo AP: New insights in the genetics of adrenocortical tumors, pheochromocytomas and paragangliomas. Horm Metab Res; 2005 Jun;37(6):384-90
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  • [Title] New insights in the genetics of adrenocortical tumors, pheochromocytomas and paragangliomas.
  • Recent advances in the molecular genetic of adrenal tumors give new insights in the pathophysiology of these neoplasms in both hereditary and sporadic cases.
  • The practice of genetic counselling in patients with adrenal tumors have been recently changed by the identification and the understanding of new specific hereditary cancer susceptibility syndromes.
  • In the case of sporadic adrenocortical tumors these progress also offer new prognosis predictors.
  • The genetic predisposition to adrenocortical cancer in children has been well established in the Li-Fraumeni and Beckewith-Wiedeman syndromes due to germline p53 mutation located at 17p13 and dysregulation of the imprinted IGF-2 locus at 11p15, respectively.
  • Adrenocortical tumors are also observed in Multiple Endocrine Neoplasia type I syndrome.
  • Cushing's syndrome due to primary pigmented nodular adrenocortical disease have been observed in patients with germline PRKAR1A inactivating mutations.
  • Interestingly allelic loss at 17p13 and 11p15 have been observed in sporadic adrenocortical cancer and somatic PRKAR1A mutations in secreting adrenocortical adenomas.
  • The potential interest of these finding for the diagnosis of these tumors will be discussed.
  • Up to date, four diagnosis of familal disease (multiple endocrine neoplasia type II, von Hippel Lindau disease, neurofibromatosis type 1 and hereditary paraganglioma) should be discussed and causative mutations in six different phaechomocytoma susceptibility genes (RET, VHL, NF1, SDHB, SDHD, SDHC) could be identified.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Gene Expression Regulation, Neoplastic / genetics. Paraganglioma / genetics. Pheochromocytoma / genetics

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  • (PMID = 16001332.001).
  • [ISSN] 0018-5043
  • [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; Review
  • [Publication-country] Germany
  • [Number-of-references] 53
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63. Ide H, Terado Y, Tokiwa S, Nishio K, Saito K, Isotani S, Kamiyama Y, Muto S, Imamura T, Horie S: Novel germ line mutation p53-P177R in adult adrenocortical carcinoma producing neuron-specific enolase as a possible marker. Jpn J Clin Oncol; 2010 Aug;40(8):815-8
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  • [Title] Novel germ line mutation p53-P177R in adult adrenocortical carcinoma producing neuron-specific enolase as a possible marker.
  • Adrenocortical cancer (ACC) is a rare and aggressive endocrine tumor.
  • The patient presented with a large retroperitoneum tumor and lung metastases.
  • Removal of the adrenocortical tumor with part of the transverse colon and tail of the pancreas, spleen and kidney was successfully performed following chemotherapy.
  • Levels of serum neuron-specific enolase (NSE) were found to be markedly high before surgery and may be clinically useful markers for monitoring tumor status during management.
  • Immunohistochemical studies showed that the cancer cells were positive for NSE and overexpression of p53.
  • The genetic and biochemical data presented in this case confirm the importance of screening for p53 status in ACC with inherited cancer syndrome.
  • [MeSH-major] Adrenal Gland Neoplasms / enzymology. Adrenal Gland Neoplasms / genetics. Adrenocortical Carcinoma / enzymology. Adrenocortical Carcinoma / genetics. Biomarkers, Tumor / blood. Genes, p53 / genetics. Germ-Line Mutation. Phosphopyruvate Hydratase / blood

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  • (PMID = 20421238.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 4.2.1.11 / Phosphopyruvate Hydratase
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64. Cerquetti L, Bucci B, Marchese R, Misiti S, De Paula U, Miceli R, Muleti A, Amendola D, Piergrossi P, Brunetti E, Toscano V, Stigliano A: Mitotane increases the radiotherapy inhibitory effect and induces G2-arrest in combined treatment on both H295R and SW13 adrenocortical cell lines. Endocr Relat Cancer; 2008 Jun;15(2):623-34
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  • [Title] Mitotane increases the radiotherapy inhibitory effect and induces G2-arrest in combined treatment on both H295R and SW13 adrenocortical cell lines.
  • This drug and radiotherapy are used also in adrenal cancer treatment even if their biological action in this neoplasia remains unknown.
  • We investigated the effects of o,p'-DDD and ionizing radiations (IR) on cell growth inhibition and cell cycle perturbation in H295R and SW13 adrenocortical cancer cells.
  • This combination treatment induced an irreversible inhibition of cell growth in both adrenocortical cancer cells.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Antineoplastic Agents, Hormonal / pharmacology. Mitotane / pharmacology. Radiotherapy
  • [MeSH-minor] CDC2 Protein Kinase / metabolism. Cell Division / drug effects. Cell Division / radiation effects. Cell Line, Tumor. Cyclin B / metabolism. Cyclin B1. G2 Phase / drug effects. G2 Phase / radiation effects. Humans. RNA, Messenger / metabolism. Steroids / pharmacology. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 18509009.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / CCNB1 protein, human; 0 / Cyclin B; 0 / Cyclin B1; 0 / RNA, Messenger; 0 / Steroids; 0 / Tumor Suppressor Protein p53; 78E4J5IB5J / Mitotane; EC 2.7.11.22 / CDC2 Protein Kinase
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65. Mannelli M, Cantini G, Poli G, Mangoni M, Nesi G, Canu L, Rapizzi E, Borgogni E, Ercolino T, Piccini V, Luconi M: Role of the PPAR-γ system in normal and tumoral pituitary corticotropic cells and adrenal cells. Neuroendocrinology; 2010;92 Suppl 1:23-7
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  • [Title] Role of the PPAR-γ system in normal and tumoral pituitary corticotropic cells and adrenal cells.
  • In this minireview, we summarize the current knowledge on PPAR-γ in normal and tumoral corticotropic pituitary and adrenal cells.
  • The receptor expression has been shown in ACTH-secreting cells in both normal and adenomal pituitary as well as in normal and tumor adrenal cortex.
  • Preclinical studies conducted both in vitro on tumor cells and in vivo on xenograft tumor models obtained by subcutaneous injection of cancer cells have evidenced the anticancer properties of TZD, in particular rosiglitazone (RGZ) and pioglitazone (PIO).
  • In both pituitary and adrenocortical cancer, RGZ treatment results in inhibition of cell proliferation, through G0/G1 cell-cycle arrest and induction of cell apoptosis, leading to significant inhibition of tumor growth in the xenograft tumor models.
  • [MeSH-major] Adrenal Cortex / metabolism. Corticotrophs / metabolism. PPAR gamma / metabolism. Pituitary ACTH Hypersecretion / metabolism. Pituitary Gland / metabolism
  • [MeSH-minor] Adrenal Cortex Neoplasms / drug therapy. Adrenal Cortex Neoplasms / metabolism. Humans. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / metabolism. Thiazolidinediones / therapeutic use

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  • [Copyright] Copyright © 2010 S. Karger AG, Basel.
  • (PMID = 20829614.001).
  • [ISSN] 1423-0194
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / PPAR gamma; 0 / Thiazolidinediones; X4OV71U42S / pioglitazone
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66. Mitra S, Roy SG, Sur PK: Adrenocortical carcinoma with skeletal metastases in a postmenopausal woman. Indian J Med Paediatr Oncol; 2009 Jan;30(1):24-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenocortical carcinoma with skeletal metastases in a postmenopausal woman.
  • Adrenocortical cancer is a very rare tumor with a poor prognosis.
  • CT-guided fine-needle aspiration cytology of an abdominal mass revealed the presence of a carcinoma of the left adrenal cortex.

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  • [Cites] N Engl J Med. 2007 Jun 7;356(23):2372-80 [17554118.001]
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  • (PMID = 20668603.001).
  • [ISSN] 0975-2129
  • [Journal-full-title] Indian journal of medical and paediatric oncology : official journal of Indian Society of Medical & Paediatric Oncology
  • [ISO-abbreviation] Indian J Med Paediatr Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC2902211
  • [Keywords] NOTNLM ; Adrenocortical carcinoma / androgen secreting tumors / mitotane
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67. Nishikawa T, Saito J, Omura M: [Medical treatment for Cushing's syndrome]. Nihon Rinsho; 2008 Jan;66(1):186-91
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  • Thus, we should treat Cushing's syndrome as soon as possible, since many complications, including cardiovascular diseases and infections, will soon occur when the definite diagnosis is delayed.
  • Adrenalectomy is essential for treatment for Cushing's syndrome even in the patients with pituitary or ectopic ACTH-producing tumor.
  • Medical adrenalectomy is achieved by using with mitotane which is usually used for adrenocortical cancer.
  • We commonly treat the patients with Cushing's syndrome due to adrenal tumor and pituitary or ectopic ACTH producing tumor by using metyrapone which mainly inhibits 11-hydroxylase.
  • Replacement therapy with hydrocortisone should be considered if adrenal failure will occur during treatment with those drugs.

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  • (PMID = 18186263.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Aromatase Inhibitors; 0O54ZQ14I9 / Aminoglutethimide; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase; R9400W927I / Ketoconazole; ZS9KD92H6V / Metyrapone
  • [Number-of-references] 6
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68. Nychytaĭlo ME, Diachenko VV, Litvinenko AN, Gul'ko ON, Bulik II, Lukecha II: [Experience of performance of laparoscopic adrenalectomy using lateral transabdominal approach]. Klin Khir; 2008 Sep;(9):41-4
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  • In 2002-2008 yrs. in the Department of Laparoscopic Surgery and Cholelithiasis in 52 patients laparoscopic adrenalectomy (LA) was accomplished, performed for different diseases of suprarenal glands.
  • Incidentaloma was diagnosed in 8, fibroma--in 4, pheokhromocytoma--in 10, aldosteroma--in 11, adrenocortical cancer--in 3, corticosteroma--in 13, suprarenal gland cyst--in 3 patients.
  • The operation time in right-sided and left-sided LA had constituted accordingly 85 and 118 minutes.
  • In 1 (2.4%) observation hemoperitoneum had occurred as a result of traumatic damage of spleen during performance of left-sided LA.

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  • (PMID = 19278040.001).
  • [ISSN] 0023-2130
  • [Journal-full-title] Klinichna khirurhiia
  • [ISO-abbreviation] Klin Khir
  • [Language] RUS
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Ukraine
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69. Kanczkowski W, Zacharowski K, Wirth MP, Ehrhart-Bornstein M, Bornstein SR: Differential expression and action of Toll-like receptors in human adrenocortical cells. Mol Cell Endocrinol; 2009 Mar 5;300(1-2):57-65
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential expression and action of Toll-like receptors in human adrenocortical cells.
  • During sepsis, an intact adrenal gland glucocorticoid stress response is critical for survival.
  • However, the exact role which TLRs play in adrenal homeostasis and malfunction is not yet sufficiently known.
  • Using quantitative real-time PCR, confocal microscopy and the NF-kappaB reporter gene assay, we aimed to analyse both, expression and function of all relevant TLRs in the human adrenocortical cell line-NCI-H295R and adrenal cells in primary culture.
  • Our results demonstrate a differential expression pattern of TLR1-9 in human adrenocortical cells as compared to immune cells and adrenocortical cancer cells.
  • Therefore, Toll-like receptors expression and function is a novel feature of the adrenal stress system contributing to adrenal tissue homeostasis, regeneration and tumorigenesis.
  • [MeSH-major] Adrenal Cortex. Gene Expression Regulation. Protein Isoforms / metabolism. Toll-Like Receptors / metabolism
  • [MeSH-minor] Aged. Cells, Cultured. Female. Homeostasis. Humans. Interleukin-8 / metabolism. Male. Middle Aged. NF-kappa B / metabolism. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 19022344.001).
  • [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
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Interleukin-8; 0 / NF-kappa B; 0 / Protein Isoforms; 0 / Toll-Like Receptors; 0 / Tumor Necrosis Factor-alpha
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70. Szabó PM, Wiener Z, Tömböl Z, Kovács A, Pócza P, Horányi J, Kulka J, Riesz P, Tóth M, Patócs A, Gaillard RC, Falus A, Rácz K, Igaz P: Differences in the expression of histamine-related genes and proteins in normal human adrenal cortex and adrenocortical tumors. Virchows Arch; 2009 Aug;455(2):133-42
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  • [Title] Differences in the expression of histamine-related genes and proteins in normal human adrenal cortex and adrenocortical tumors.
  • Histamine is involved in the pathogenesis of several tumors; however, there are no data on its possible involvement in human adrenocortical tumorigenesis.
  • The expression of genes and proteins involved in the biosynthesis (histidine decarboxylase, HDC), action (histamine receptors: HRH1-HRH4), and metabolism of histamine is largely unknown both in the normal human adrenal cortex and in adrenocortical tumors.
  • In this study, we examined the expression of histamine-related genes and proteins and histamine content in normal adrenal cortex, benign adrenocortical adenomas, and malignant adrenocortical cancer (ACC).
  • We found that all proteins involved in histamine biosynthesis and action are present both in the normal adrenal cortex and in the tumors studied.
  • Adrenocortical tumorigenesis might, thus, be characterized by reduced histamine biosynthesis; furthermore, different adrenocortical tumor subtypes may show unique histamine receptor expression profiles.
  • [MeSH-major] Adrenal Cortex / metabolism. Adrenal Cortex Neoplasms / metabolism. Adrenocortical Adenoma / metabolism. Histamine / metabolism. Histidine Decarboxylase / metabolism. Receptors, Histamine / metabolism

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  • (PMID = 19568768.001).
  • [ISSN] 1432-2307
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / HRH4 protein, human; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Histamine; 0 / Receptors, Histamine H1; 0 / Receptors, Histamine H2; 0 / Receptors, Histamine H3; 820484N8I3 / Histamine; EC 4.1.1.22 / Histidine Decarboxylase
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71. Doghman M, El Wakil A, Cardinaud B, Thomas E, Wang J, Zhao W, Peralta-Del Valle MH, Figueiredo BC, Zambetti GP, Lalli E: Regulation of insulin-like growth factor-mammalian target of rapamycin signaling by microRNA in childhood adrenocortical tumors. Cancer Res; 2010 Jun 1;70(11):4666-75
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regulation of insulin-like growth factor-mammalian target of rapamycin signaling by microRNA in childhood adrenocortical tumors.
  • Here, we report the identification of a set of miRNAs that are differentially regulated in childhood adrenocortical tumors (ACT), including miR-99a and miR-100.
  • Pharmacologic inhibition of mTOR signaling by everolimus greatly reduces tumor cell growth in vitro and in vivo.
  • Our results reveal a novel mechanism of regulation of mTOR signaling by miRNAs, and they lay the groundwork for clinical evaluation of drugs inhibiting the mTOR pathway for treatment of adrenocortical cancer.

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  • [Copyright] Copyright 2010 AACR.
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  • (PMID = 20484036.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM083159; United States / NCI NIH HHS / CA / P01 CA071907; United States / NIGMS NIH HHS / GM / GM083159; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / CA071907-060006; United States / NCI NIH HHS / CA / P01 CA071907-060006
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / MicroRNAs; 0 / Somatomedins; 9HW64Q8G6G / Everolimus; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ NIHMS192514; NLM/ PMC2880211
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72. Yang WH, Heaton JH, Brevig H, Mukherjee S, Iñiguez-Lluhí JA, Hammer GD: SUMOylation inhibits SF-1 activity by reducing CDK7-mediated serine 203 phosphorylation. Mol Cell Biol; 2009 Feb;29(3):613-25
Hazardous Substances Data Bank. Corticotropin .

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  • Steroidogenic factor 1 (SF-1) is an orphan nuclear receptor selectively expressed in the adrenal cortex and gonads, where it mediates the hormonal stimulation of multiple genes involved in steroid hormone biosynthesis.
  • Based on these observations, we propose a coordinated modification model in which inhibition of SF-1-mediated transcription by SUMOylation in adrenocortical cancer cells is mediated through reduced CDK7-induced phosphorylation of SF-1.

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  • (PMID = 19015234.001).
  • [ISSN] 1098-5549
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK61656; United States / NIDDK NIH HHS / DK / R01 DK061656; United States / NIDDK NIH HHS / DK / P60 DK20572; United States / NIDDK NIH HHS / DK / DK62027; United States / NIDDK NIH HHS / DK / R56 DK061656; United States / NIDDK NIH HHS / DK / R01 DK062027; United States / NIDDK NIH HHS / DK / P60 DK020572; United States / NCI NIH HHS / CA / T32 CA009676
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Small Ubiquitin-Related Modifier Proteins; 0 / Steroidogenic Factor 1; 17885-08-4 / Phosphoserine; 9002-60-2 / Adrenocorticotropic Hormone; EC 2.7.11.22 / Cyclin-Dependent Kinases; EC 2.7.11.22 / cyclin-dependent kinase 7, mouse; K3Z4F929H6 / Lysine
  • [Other-IDs] NLM/ PMC2630698
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73. Shi Z, Henwood MJ, Bannerman P, Batista D, Horvath A, Guttenberg M, Stratakis CA, Grimberg A: Primary pigmented nodular adrenocortical disease reveals insulin-like growth factor binding protein-2 regulation by protein kinase A. Growth Horm IGF Res; 2007 Apr;17(2):113-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary pigmented nodular adrenocortical disease reveals insulin-like growth factor binding protein-2 regulation by protein kinase A.
  • OBJECTIVE: Primary pigmented nodular adrenocortical disease (PPNAD) can occur as an isolated trait or part of Carney complex, a familial lentiginosis-multiple endocrine neoplasia syndrome frequently caused by mutations in PRKAR1A, which encodes the 1alpha regulatory subunit of protein kinase A (PKA).
  • Because alterations in the insulin-like growth factor (IGF) axis, particularly IGF-II and IGF binding protein (IGFBP)-2 overexpression, have been implicated in sporadic adrenocortical tumors, we sought to examine the IGF axis in PPNAD.
  • NCI-H295R cells were used to study PKA and IGF axis signaling in adrenocortical cells in vitro.
  • Moreover, PKA inhibitors increased IGFBP-2 expression in NCI-H295R adrenocortical cells, and anti-IGFBP-2 antibody reduced their proliferation.
  • CONCLUSIONS: IGFBP-2 expression is increased in PPNAD caused by PRKAR1A mutations, and in adrenocortical cancer cells.
  • This is the first evidence for PKA-dependent regulation of IGFBP-2 expression in adrenocortical cells.

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  • (PMID = 17280861.001).
  • [ISSN] 1096-6374
  • [Journal-full-title] Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society
  • [ISO-abbreviation] Growth Horm. IGF Res.
  • [Language] ENG
  • [Databank-accession-numbers] OMIM/ 160980
  • [Grant] United States / NIDDK NIH HHS / DK / T32 DK63688; United States / NIDDK NIH HHS / DK / T32 DK063688; United States / NICHD NIH HHS / HD / Z01 HD000642-04; United States / NIDDK NIH HHS / DK / 5 K08 DK64352; United States / NICHD NIH HHS / HD / Z01 HD000642; United States / NIDDK NIH HHS / DK / K08 DK064352
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / Insulin-Like Growth Factor Binding Protein 2; 0 / PRKAR1A protein, human; 0 / Protein Kinase Inhibitors; 0 / RNA, Messenger; 67763-97-7 / Insulin-Like Growth Factor II; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
  • [Other-IDs] NLM/ NIHMS22924; NLM/ PMC2577759
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74. Nieman LK, Ilias I: Evaluation and treatment of Cushing's syndrome. Am J Med; 2005 Dec;118(12):1340-6
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  • Cushing's syndrome results from sustained pathologic hypercortisolism caused by excessive corticotropin (ACTH) secretion by tumors in the pituitary gland (Cushing's disease, 70%) or elsewhere (15%), or by ACTH-independent cortisol secretion from adrenal tumors (15%).
  • The diagnosis of Cushing's syndrome should be followed by the measurement of plasma ACTH concentration to determine whether the hypercortisolism is ACTH-independent.
  • Surgical resection of tumor is the optimal treatment for all forms of Cushing's syndrome; bilateral adrenalectomy, medical treatment, or radiotherapy are sought in inoperable or recurrent cases.
  • The prognosis is better for Cushing's disease and benign adrenal causes of Cushing's syndrome than adrenocortical cancer and malignant ACTH-producing tumors.
  • [MeSH-major] Adrenocorticotropic Hormone / blood. Cushing Syndrome / diagnosis. Cushing Syndrome / drug therapy
  • [MeSH-minor] Adrenalectomy. Adult. Antifungal Agents / therapeutic use. Child. Diagnosis, Differential. Humans. Ketoconazole / therapeutic use. Prognosis. Recurrence. Survival Analysis

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  • (PMID = 16378774.001).
  • [ISSN] 1555-7162
  • [Journal-full-title] The American journal of medicine
  • [ISO-abbreviation] Am. J. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 9002-60-2 / Adrenocorticotropic Hormone; R9400W927I / Ketoconazole
  • [Number-of-references] 100
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75. Doghman M, Madoux F, Hodder P, Lalli E: Identification and characterization of steroidogenic factor-1 inverse agonists. Methods Enzymol; 2010;485:3-23

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Furthermore, SF-1 is amplified and overexpressed in most cases of adrenocortical tumor occurring in children; studies performed in transgenic mice have shown that an increased SF-1 dosage triggers tumor formation in the adrenal cortex.
  • For these reasons, drugs interfering with SF-1 action would represent a promising tool to be added to the current pharmacological protocols in the therapy of adrenocortical cancer.
  • These compounds have the attributes to inhibit the increase in proliferation triggered by an augmented SF-1 dosage in adrenocortical tumor cells and to reduce their steroid production.
  • This latter property may also reveal beneficial for drugs used in the therapy of adrenocortical tumors to alleviate symptoms of virilization and Cushing often associated with tumor burden.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 21050908.001).
  • [ISSN] 1557-7988
  • [Journal-full-title] Methods in enzymology
  • [ISO-abbreviation] Meth. Enzymol.
  • [Language] ENG
  • [Grant] United States / NIMH NIH HHS / MH / U54 MH084512; United States / NIMH NIH HHS / MH / MH077624; United States / NIMH NIH HHS / MH / MH084512
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Isoquinolines; 0 / Steroidogenic Factor 1; 0 / Steroids
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76. 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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77. Hahner S, Stürmer A, Fassnacht M, Hartmann RW, Schewe K, Cochran S, Zink M, Schirbel A, Allolio B: Etomidate unmasks intraadrenal regulation of steroidogenesis and proliferation in adrenal cortical cell lines. Horm Metab Res; 2010 Jun;42(7):528-34
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  • [Title] Etomidate unmasks intraadrenal regulation of steroidogenesis and proliferation in adrenal cortical cell lines.
  • To characterize intraadrenal adaptations for inhibition of cortisol synthesis, we analyzed the effects of etomidate (ETO) on steroid hormone secretion and expression of key regulators of steroidogenesis and proliferation in human NCI-h295 adrenocortical cancer cells.
  • In summary, ETO exhibits pleiotropic effects on adrenal function in vitro.
  • These changes reflect adaptations to maintain steroidogenesis at the cost of adrenal proliferation.
  • [MeSH-major] Adrenal Cortex / cytology. Adrenal Cortex / metabolism. Cell Proliferation / drug effects. Etomidate / pharmacology. Steroids / biosynthesis

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  • [Copyright] Georg Thieme Verlag KG Stuttgart * New York.
  • (PMID = 20352599.001).
  • [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 / Steroids; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase; EC 1.14.15.6 / Cholesterol Side-Chain Cleavage Enzyme; Z22628B598 / Etomidate
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78. Johnsen IK, Kappler R, Auernhammer CJ, Beuschlein F: Bone morphogenetic proteins 2 and 5 are down-regulated in adrenocortical carcinoma and modulate adrenal cell proliferation and steroidogenesis. Cancer Res; 2009 Jul 15;69(14):5784-92
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  • [Title] Bone morphogenetic proteins 2 and 5 are down-regulated in adrenocortical carcinoma and modulate adrenal cell proliferation and steroidogenesis.
  • Quantitative PCR analysis revealed down-regulation of BMP2 and BMP5 in tissue samples from adrenocortical carcinoma and adrenocortical tumor cell lines compared with normal adrenal glands.
  • Taken together, we show that loss of expression of members of the BMP family of ligands is a common finding in adrenocortical tumors and we provide evidence that BMP-dependent pathways are likely to be involved in the modulation of the malignant and functional phenotype of adrenocortical cancer cells.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Bone Morphogenetic Protein 2 / genetics. Bone Morphogenetic Protein 5 / genetics
  • [MeSH-minor] Aldosterone / metabolism. Blotting, Western. Bone Morphogenetic Protein Receptors / genetics. Bone Morphogenetic Protein Receptors / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Colforsin / pharmacology. Dose-Response Relationship, Drug. Down-Regulation / drug effects. GATA6 Transcription Factor / genetics. GATA6 Transcription Factor / metabolism. Humans. Hydrocortisone / metabolism. Insulin-Like Growth Factor I / genetics. Insulin-Like Growth Factor I / pharmacology. Phosphorylation / drug effects. Proto-Oncogene Proteins c-akt / metabolism. Recombinant Proteins / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Steroid 17-alpha-Hydroxylase / genetics. Steroid 17-alpha-Hydroxylase / metabolism. Time Factors. Tretinoin / pharmacology. Tumor Cells, Cultured

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  • (PMID = 19584291.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bone Morphogenetic Protein 2; 0 / Bone Morphogenetic Protein 5; 0 / GATA6 Transcription Factor; 0 / GATA6 protein, human; 0 / Recombinant Proteins; 1F7A44V6OU / Colforsin; 4964P6T9RB / Aldosterone; 5688UTC01R / Tretinoin; 67763-96-6 / Insulin-Like Growth Factor I; EC 1.14.99.9 / Steroid 17-alpha-Hydroxylase; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.30 / Bone Morphogenetic Protein Receptors; WI4X0X7BPJ / Hydrocortisone
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79. Stratakis CA: Cushing syndrome caused by adrenocortical tumors and hyperplasias (corticotropin- independent Cushing syndrome). Endocr Dev; 2008;13:117-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cushing syndrome caused by adrenocortical tumors and hyperplasias (corticotropin- independent Cushing syndrome).
  • Endogenous Cushing syndrome (CS) is caused by excess adrenal glucocorticoid secretion that is adrenocorticotropin (ACTH)-dependent or independent; ACTH-independent adrenocortical causes of CS account for up to 20% of CS in adults, and 15% in children over age 7 years.
  • In both adults and children, adrenocortical lesions causing CS include the common, isolated and sporadic, solitary cortisol-producing adenoma, the rare adrenocortical cancer, and a spectrum of recently recognized, bilateral hyperplasias (bilateral adrenocortical hyperplasias, BAHs): micronodular adrenal disease and its pigmented variant, primary pigmented nodular adrenocortical disease are mostly genetic processes.
  • Macronodular BAHs, ACTH-independent macronodular hyperplasia or massive macronodular adrenocortical disease are less frequently genetic and almost never present in children (except in McCune-Albright syndrome); they present often with atypical CS in middle-aged or elderly adults.
  • The majority of benign adrenocortical tumors associated with CS are associated with defects of the cAMP signaling pathway, whereas adrenal cancer is linked to aberrant expression of growth factors and germline or somatic mutations of tumor suppressor genes such as TP53.
  • Adrenalectomy is the preferred mode of treatment for all adrenocortical causes of CS.
  • [MeSH-major] Adenoma / complications. Adrenal Cortex Neoplasms / complications. Adrenal Glands / pathology. Adrenocorticotropic Hormone / physiology. Cushing Syndrome / etiology
  • [MeSH-minor] Algorithms. Cyclic AMP / physiology. Humans. Hyperplasia / complications. Hyperplasia / diagnosis. Hyperplasia / genetics. Signal Transduction / physiology

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  • (PMID = 18493137.001).
  • [ISSN] 1421-7082
  • [Journal-full-title] Endocrine development
  • [ISO-abbreviation] Endocr Dev
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 HD000642-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; E0399OZS9N / Cyclic AMP
  • [Number-of-references] 33
  • [Other-IDs] NLM/ NIHMS307822; NLM/ PMC3132884
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80. Lacroix A: Approach to the patient with adrenocortical carcinoma. J Clin Endocrinol Metab; 2010 Nov;95(11):4812-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • 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.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenocortical Carcinoma / surgery

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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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81. Tadjine M, Lampron A, Ouadi L, Bourdeau I: Frequent mutations of beta-catenin gene in sporadic secreting adrenocortical adenomas. Clin Endocrinol (Oxf); 2008 Feb;68(2):264-70

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequent mutations of beta-catenin gene in sporadic secreting adrenocortical adenomas.
  • OBJECTIVE: Molecular alterations remain largely unknown in most sporadic adrenocortical tumours and hyperplasias.
  • In our previous work, we demonstrated the differential expression of several Wnt/beta-catenin signalling-related genes implicated in ACTH-independent macronodular adrenal hyperplasias (AIMAH).
  • To better understand the role of Wnt/beta-catenin signalling in adrenocortical tumours, we performed mutational analysis of the beta-catenin gene.
  • METHODS: We studied 53 human adrenocortical samples (33 adenomas, 4 carcinomas, 13 AIMAH, 3 ACTH-dependent adrenal hyperplasias) and the human adrenocortical cancer cell line NCI-H295R.
  • RESULTS: No mutations were detected in adrenocortical carcinomas, AIMAH and ACTH-dependent hyperplasias.
  • CONCLUSIONS: Activating mutations of exon 3 of the beta-catenin gene are frequent in adrenocortical adenomas, and further characterization of the Wnt/beta-catenin signalling pathway should lead to a better understanding of adrenal tumourigenesis.
  • [MeSH-major] Adrenocortical Adenoma / genetics. Adrenocortical Adenoma / metabolism. beta Catenin / genetics. beta Catenin / metabolism

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  • (PMID = 17854394.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / beta Catenin
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82. Hennings J, Lindhe O, Bergström M, Långström B, Sundin A, Hellman P: [11C]metomidate positron emission tomography of adrenocortical tumors in correlation with histopathological findings. J Clin Endocrinol Metab; 2006 Apr;91(4):1410-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [11C]metomidate positron emission tomography of adrenocortical tumors in correlation with histopathological findings.
  • CONTEXT: Adrenal incidentalomas are common findings necessitating extensive laboratory work-up and repetitive radiological examinations.
  • Positron emission tomography (PET) using (11)C-labeled metomidate (MTO) has previously been described as a tool for specific adrenocortical imaging.
  • OBJECTIVE: We evaluated 212 MTO-PET examinations in 173 patients to identify its role in the management of adrenal tumors.
  • PATIENTS: Patients who were operated or biopsied due to adrenal tumors had histopathological diagnoses of adrenocortical adenoma (n = 26), adrenocortical cancer (ACC; n = 13), adrenocortical hyperplasia (n = 8), pheochromocytoma (n = 6), metastasis (n = 3), and tumors of nonadrenal origin (n = 19).
  • The hypothesis that MTO-PET is of value in the management of adrenal tumors, especially incidentaloma, was stated before data collection.
  • RESULTS: Sensitivity was 0.89 and specificity was 0.96 for MTO-PET in proving adrenocortical origin of the lesions.
  • Pheochromocytomas, metastases to the adrenal gland, and nonadrenal masses were all MTO negative.
  • PET measurements using standardized uptake values (SUV) in pathological adrenocortical tissue could differentiate lesions larger than 1-1.5 cm from normal adrenocortical tissue.
  • SUV was higher in aldosterone-hypersecreting adenomas, and the SUV ratio between the tumor and the contralateral gland was significantly higher in all hormonally hypersecreting adenomas as well as in ACC.
  • CONCLUSION: MTO-PET is a specific and sensitive method for diagnosing adrenocortical tumors.
  • MTO-PET is useful in the imaging work-up of adrenal incidentalomas and may be beneficial for the examination of patients with primary aldosteronism or ACC.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenal Cortex Neoplasms / radionuclide imaging. Antineoplastic Agents. Etomidate / analogs & derivatives

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  • (PMID = 16403816.001).
  • [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 / Antineoplastic Agents; 0 / Radiopharmaceuticals; 5377-20-8 / metomidate; Z22628B598 / Etomidate
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83. Paramonova I, Haase M, Mülders-Opgenoorth B, Ansurudeen-Rafi I, Bornstein SR, Papewalis C, Schinner S, Schott M, Scherbaum WA, Willenberg HS: The effects of the endothelium on adrenal steroidogenesis and growth are mainly mediated by proteins other than endothelin-1. Horm Metab Res; 2010 Nov;42(12):840-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The effects of the endothelium on adrenal steroidogenesis and growth are mainly mediated by proteins other than endothelin-1.
  • The endothelium releases factors stimulating the adrenal cortex.
  • It is also known that endothelin-1 (ET-1) promotes generation of cortisol and aldosterone, and proliferation of adrenocortical cells.
  • The aim of the study was to find out whether the effect of the endothelium on adrenocortical cells is dominated by the action of ET-1.
  • The effects of endothelial cell-conditioned medium (ECCM), obtained during growth of human umbilical cord vein endothelial cells, on aldosterone and cortisol release by cells of the adrenocortical cancer cell-line NCI-H295R and the promoter activity of steroidogenic acute-regulatory protein (StAR) were studied.
  • The effect of ECCM on proliferation of human primary normal adrenocortical and NCI-H295R cells was also investigated.
  • In conclusion, the cultured endothelial cells secrete a protein that stimulates steroidogenesis in adrenal cells and their growth.
  • [MeSH-major] Adrenal Cortex / cytology. Aldosterone / metabolism. Cell Proliferation. Endothelial Cells / metabolism. Endothelin-1 / metabolism. Hydrocortisone / metabolism. Proteins / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cells, Cultured. Culture Media, Conditioned / metabolism. Humans. Phosphoproteins / genetics. Phosphoproteins / metabolism. Promoter Regions, Genetic

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  • [Copyright] © Georg Thieme Verlag KG Stuttgart · New York.
  • (PMID = 20839150.001).
  • [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 / Culture Media, Conditioned; 0 / Endothelin-1; 0 / Phosphoproteins; 0 / Proteins; 0 / steroidogenic acute regulatory protein; 4964P6T9RB / Aldosterone; WI4X0X7BPJ / Hydrocortisone
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84. Waldmann J, Feldmann G, Slater EP, Langer P, Buchholz M, Ramaswamy A, Saeger W, Rothmund M, Fendrich V: Expression of the zinc-finger transcription factor Snail in adrenocortical carcinoma is associated with decreased survival. Br J Cancer; 2008 Dec 2;99(11):1900-7
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  • [Title] Expression of the zinc-finger transcription factor Snail in adrenocortical carcinoma is associated with decreased survival.
  • In this study, we evaluate whether Snail is expressed in adrenocortical cancer (ACC) and if its expression is related to patient outcome.
  • Increasing evidence suggests that EMT plays a pivotal role in tumour progression and metastatic spread.
  • Seventeen of 26 (65%) ACC tumour samples expressed Snail when assessed by immunohistochemistry.
  • Snail expression was neither detected in normal adrenocortical tissue, nor in benign adrenocortical adenomas.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenocortical Carcinoma / metabolism. Biomarkers, Tumor / analysis. Transcription Factors / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Cadherins / biosynthesis. Female. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Ki-67 Antigen / biosynthesis. Male. Middle Aged. Neoplasm Staging. Prognosis. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19018264.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cadherins; 0 / Ki-67 Antigen; 0 / RNA, Messenger; 0 / Transcription Factors; 0 / snail family transcription factors
  • [Other-IDs] NLM/ PMC2600683
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85. Libé R, Fratticci A, Coste J, Tissier F, Horvath A, Ragazzon B, Rene-Corail F, Groussin L, Bertagna X, Raffin-Sanson ML, Stratakis CA, Bertherat J: Phosphodiesterase 11A (PDE11A) and genetic predisposition to adrenocortical tumors. Clin Cancer Res; 2008 Jun 15;14(12):4016-24

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phosphodiesterase 11A (PDE11A) and genetic predisposition to adrenocortical tumors.
  • PURPOSE: We have reported previously nonsense inactivating mutations of the phosphodiesterase 11A (PDE11A) gene in patients with micronodular adrenocortical hyperplasia and Cushing syndrome.
  • The aim of this study is to investigate the presence of somatic or germ-line PDE11A mutations in various types of adrenocortical tumors: ACTH-independent macronodular adrenocortical hyperplasia (AIMAH), adrenocortical adenoma (ACA), and adrenocortical cancer (ACC).
  • EXPERIMENTAL DESIGN: PDE11A was sequenced in 117 adrenocortical tumors and 192 controls subjects; immunohistochemistry for PDE11A and tumor cyclic AMP levels were studied in a subgroup of adrenocortical tumors.
  • RESULTS: One PDE11A inactivating mutation (R307X) was found in one ACA, 22 germ-line missense variants (18.8%) were found in adrenocortical tumors, and only 11 missense variants (5.7%) were found in controls.
  • By comparing the common mutations, a higher frequency of mutations in adrenocortical tumors than in age/sex-matched controls were observed [16% versus 10% in ACC, 19% versus 10% in ACA, and 24% versus 9% in AIMAH; odds ratio (OR), 3.53; P = 0.05].
  • Somatic DNA from adrenocortical tumors with missense variants showed a wild-type allelic loss.
  • In AIMAH/ACA, cyclic AMP levels were higher than in normal adrenals and decreased PDE11A immunostaining was present in adrenocortical tumors with PDE11A variants.
  • CONCLUSIONS: The present investigation of a large cohort of adrenocortical tumors suggests that PDE11A sequence defects predispose to a variety of lesions (beyond micronodular adrenocortical hyperplasia) and may contribute to the development of these tumors in the general population.

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  • (PMID = 18559625.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / Z01 HD000642; United States / Intramural NIH HHS / / ZIA HD000642-13
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.1.4.- / Phosphoric Diester Hydrolases; EC 3.1.4.35 / PDE11A protein, human
  • [Other-IDs] NLM/ NIHMS306040; NLM/ PMC3134879
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86. Haase M, Schott M, Bornstein SR, Malendowicz LK, Scherbaum WA, Willenberg HS: CITED2 is expressed in human adrenocortical cells and regulated by basic fibroblast growth factor. J Endocrinol; 2007 Feb;192(2):459-65
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  • [Title] CITED2 is expressed in human adrenocortical cells and regulated by basic fibroblast growth factor.
  • CITED2 gene deletion in mice leads to adrenal agenesis.
  • Therefore, we analyzed CITED2, a CBP/p300 interacting transactivator with transforming activity, in the human adrenal gland.
  • In this study, we examined CITED2 expression in human embryonic and adult adrenal glands as well as adrenocortical carcinomas.
  • As ACTH and basic fibroblast growth factor (bFGF) are connected to the physiology and growth of adrenocortical cells we studied the regulation of CITED2 by these factors in the NCI-H295R adrenocortical carcinoma cell line.
  • We found CITED2 expression in the adult adrenal cortex as well in adrenocortical carcinomas.
  • At an early stage of human adrenal organogenesis CITED2 could be located to the definitive zone of the developing adrenal gland using immunohistochemistry.
  • CITED2 is expressed in embryonic and adult human adrenal glands as well as in adrenocortical cancer.
  • This suggests a novel role for CITED2 in human adrenal growth and possibly in adrenal tumorigenesis.
  • [MeSH-major] Adrenal Cortex / metabolism. DNA-Binding Proteins / analysis. Fibroblast Growth Factor 2 / pharmacology. Gene Expression Regulation. Repressor Proteins / analysis. Trans-Activators / analysis
  • [MeSH-minor] Adrenocortical Carcinoma. Adrenocorticotropic Hormone / metabolism. Adrenocorticotropic Hormone / pharmacology. Adult. Cell Line, Tumor. Cells, Cultured. Colforsin / pharmacology. Dose-Response Relationship, Drug. Embryonic Development. Humans. Immunohistochemistry / methods. Microscopy, Fluorescence. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction / methods. Transfection / methods

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  • (PMID = 17283246.001).
  • [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 / CITED2 protein, human; 0 / DNA-Binding Proteins; 0 / RNA, Messenger; 0 / Repressor Proteins; 0 / Trans-Activators; 103107-01-3 / Fibroblast Growth Factor 2; 1F7A44V6OU / Colforsin; 9002-60-2 / Adrenocorticotropic Hormone
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87. Aumo L, Rusten M, Mellgren G, Bakke M, Lewis AE: Functional roles of protein kinase A (PKA) and exchange protein directly activated by 3',5'-cyclic adenosine 5'-monophosphate (cAMP) 2 (EPAC2) in cAMP-mediated actions in adrenocortical cells. Endocrinology; 2010 May;151(5):2151-61
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  • [Title] Functional roles of protein kinase A (PKA) and exchange protein directly activated by 3',5'-cyclic adenosine 5'-monophosphate (cAMP) 2 (EPAC2) in cAMP-mediated actions in adrenocortical cells.
  • In the adrenal cortex, the biosynthesis of steroid hormones is controlled by the pituitary-derived hormone ACTH.
  • In the present study, we demonstrate the occurrence of the EPAC2 splicing variant EPAC2B in adrenocortical cancer cells.
  • [MeSH-minor] Adrenal Cortex / metabolism. Adrenal Cortex / pathology. Aldosterone / biosynthesis. Alternative Splicing. Animals. Blotting, Western. COS Cells. Cell Line. Cell Line, Tumor. Cell Movement / drug effects. Cell Shape / drug effects. Cercopithecus aethiops. Cytoskeleton / drug effects. Cytoskeleton / metabolism. Humans. Hydrocortisone / biosynthesis. Immunohistochemistry. Microscopy, Confocal. Protein Isoforms / genetics. Protein Isoforms / metabolism. Protein Isoforms / physiology. Reverse Transcriptase Polymerase Chain Reaction. rap1 GTP-Binding Proteins / metabolism

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  • (PMID = 20233795.001).
  • [ISSN] 1945-7170
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Guanine Nucleotide Exchange Factors; 0 / Protein Isoforms; 0 / RAPGEF4 protein, human; 4964P6T9RB / Aldosterone; E0399OZS9N / Cyclic AMP; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 3.6.5.2 / rap1 GTP-Binding Proteins; WI4X0X7BPJ / Hydrocortisone
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88. Igaz P, Tömböl Z, Szabó PM, Likó I, Rácz K: Steroid biosynthesis inhibitors in the therapy of hypercortisolism: theory and practice. Curr Med Chem; 2008;15(26):2734-47
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  • A few drugs inhibiting single or multiple steps in adrenal steroid biosynthesis can be used in clinical practice.
  • Besides blocking multiple steps in adrenal steroid biosynthesis, the DDT (insecticide) analogue mitotane also has adrenolytic properties by inducing mitochondrial degeneration that renders it superior to other drugs in the treatment of adrenocortical cancer.

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  • (PMID = 18991633.001).
  • [ISSN] 0929-8673
  • [Journal-full-title] Current medicinal chemistry
  • [ISO-abbreviation] Curr. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Steroids
  • [Number-of-references] 153
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89. Gil J, Kalembkiewicz M, Polak E, Kostecka-Matyja M: [Disseminated adrenocortical carcinoma: case report]. Pol Arch Med Wewn; 2007 Jul;117(7):317-21
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  • [Title] [Disseminated adrenocortical carcinoma: case report].
  • Adrenocortical carcinoma is a rare neoplasm occurring with a frequency of 1-2 cases per million.
  • This type of a tumor is slightly more frequent in women (58.6%) than in men (41.4%).
  • Etiology of adrenocortical carcinoma is still unclear, but a role of genetic and environmental factors has been largely considered.
  • The tumor size is still the best single predictor of prognosis.
  • Histopathology specimen from biopsy or obtained during operation should be stained for Melan A, which can confirm the adrenal origin of the tumor.
  • The only method of treatment is a complete surgical excision of the carcinoma.
  • We presented the case of functioning adrenocortical cancer in 37-year-old patient who at time of diagnosis had 12 cm in diameter tumor of the left adrenal gland and metastases to the liver and lung.
  • In the article the symptoms associated with hormones produced by the carcinoma, diagnostics and treatment with regard to the progression of the disease have also been discussed.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Liver Neoplasms / secondary. Lung Neoplasms / secondary

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  • (PMID = 17966598.001).
  • [Journal-full-title] Polskie Archiwum Medycyny Wewnetrznej
  • [ISO-abbreviation] Pol. Arch. Med. Wewn.
  • [Language] pol
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Poland
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90. Bimpaki EI, Iliopoulos D, Moraitis A, Stratakis CA: MicroRNA signature in massive macronodular adrenocortical disease and implications for adrenocortical tumourigenesis. Clin Endocrinol (Oxf); 2010 Jun;72(6):744-51

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  • [Title] MicroRNA signature in massive macronodular adrenocortical disease and implications for adrenocortical tumourigenesis.
  • PURPOSE: Massive macronodular adrenocortical disease (MMAD) may be caused by aberrant microRNA expression.
  • To determine the microRNA profile in MMAD and identify putative microRNA-gene target pairs involved in adrenal tumourigenesis.
  • EXPERIMENTAL DESIGN: We performed microRNA microarray analysis in 10 patients with ACTH-independent Cushing syndrome caused by MMAD (ages 39-60 years) and four normal adrenal cortex samples were used as controls.
  • Interestingly, we detected miR-200b targeting directly Matrin 3 (MATR3) expression in an adrenocortical cancer cell line (H295R).

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  • (PMID = 19849700.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / Z01 HD000642; United States / Intramural NIH HHS / / Z01 HD000642-11; United States / NICHD NIH HHS / HD / Z01-HD-000642-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Validation Studies
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MicroRNAs
  • [Other-IDs] NLM/ NIHMS154316; NLM/ PMC3003432
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91. Miller BS, Ammori JB, Gauger PG, Broome JT, Hammer GD, Doherty GM: Laparoscopic resection is inappropriate in patients with known or suspected adrenocortical carcinoma. World J Surg; 2010 Jun;34(6):1380-5
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  • [Title] Laparoscopic resection is inappropriate in patients with known or suspected adrenocortical carcinoma.
  • BACKGROUND: Complete surgical resection is the mainstay of treatment for patients with adrenocortical cancer (ACC).
  • Seventeen patients underwent laparoscopic adrenalectomy (LA).
  • Median tumor size of those who underwent LA was 7.0 (range, 4-14) cm versus 12.3 (range, 5-27) cm for OR.
  • Mean time to first recurrence for those who underwent LA was 9.6 months (+/-14) versus 19.2 months (+/-37.5) in the open group (p < 0.005).
  • Fifty percent of patients who underwent LA had positive margins or notation of intraoperative tumor spill versus 18% of those who underwent OR (p = 0.01).
  • Although feasible in many cases and tempting, laparoscopic resection should not be attempted in patients with tumors suspicious for or known to be adrenocortical carcinoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenocortical Carcinoma / surgery. Laparoscopy / contraindications
  • [MeSH-minor] Adolescent. Adrenalectomy / methods. Adult. Aged. Aged, 80 and over. Chi-Square Distribution. Female. Humans. Male. Middle Aged. Neoplasm Recurrence, Local. Neoplasm Staging. Retrospective Studies. Treatment Outcome

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  • (PMID = 20372905.001).
  • [ISSN] 1432-2323
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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92. Leboulleux S, Deandreis D, Al Ghuzlan A, Aupérin A, Goéré D, Dromain C, Elias D, Caillou B, Travagli JP, De Baere T, Lumbroso J, Young J, Schlumberger M, Baudin E: Adrenocortical carcinoma: is the surgical approach a risk factor of peritoneal carcinomatosis? Eur J Endocrinol; 2010 Jun;162(6):1147-53
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  • [Title] Adrenocortical carcinoma: is the surgical approach a risk factor of peritoneal carcinomatosis?
  • CONTEXT: Peritoneal carcinomatosis (PC) is a rare site of distant metastases in patients with adrenocortical cancer (ACC).
  • One preliminary study suggests an increased risk of PC after laparoscopic adrenalectomy (LA) for ACC.
  • Mean tumor size was 132 mm.
  • It was present at initial diagnosis in three cases and occurred during follow-up in 15 cases.
  • The only risk factor of PC occurring during follow-up was the surgical approach with a 4-year rate of PC of 67% (95% confidence interval (CI), 30-90%) for LA and 27% (95% CI, 15-44%) for open adrenalectomy (P=0.016).
  • Neither tumor size, stage, functional status, completeness of surgery, nor plasma level of op'DDD was associated with the occurrence of PC.
  • CONCLUSION: We found an increased risk of PC after LA for ACC.

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  • (PMID = 20348273.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
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93. Willenberg HS, Ansurudeen I, Schebesta K, Haase M, Wess B, Schinner S, Raffel A, Schott M, Scherbaum WA: The endothelium secretes interleukin-6 (IL-6) and induces IL-6 and aldosterone generation by adrenocortical cells. Exp Clin Endocrinol Diabetes; 2008 Sep;116 Suppl 1:S70-4
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  • [Title] The endothelium secretes interleukin-6 (IL-6) and induces IL-6 and aldosterone generation by adrenocortical cells.
  • Endothelial cells have been shown to induce adrenal steroidogenesis and to enhance aldosterone secretion via angiotensin II and endothelin 1-independent mechanisms.
  • It has been demonstrated that endothelial cells and adrenocortical cells are capable of producing interleukin-6 (IL-6) and IL-6 is a factor known to stimulate adrenal cortisol secretion.
  • We therefore asked whether endothelial cells have an effect on adrenal IL-6 generation and whether IL-6 mediates biosynthesis of aldosterone as is observed after exposure of adrenocortical cells to endothelial cell-conditioned medium (ECCM).
  • Cells from the adrenocortical cancer cell line NCI-H295R were incubated with ECCM produced from human umbilical vein endothelial cells at increasing concentrations.
  • As detected by an enzyme-linked immunosorbent assay, pure ECCM significantly increased IL-6 protein secretion by cultured adrenocortical cells in a dose-dependent fashion, to a 18.0+/-2.0 pg/mL (mean+/-SEM).
  • Pure ECCM also induced aldosterone secretion by adrenocortical cells more than three times that of controls with serum-free medium.
  • These data suggest that endothelial cells secrete IL-6 and that endothelial cell-derived factors regulate adrenal IL-6 synthesis which does not alter adrenal aldosterone secretion.
  • Our findings support the hypothesis that the endothelium and the adrenal gland may play a role in the development of some forms of hypertension and - more speculative - inflammation.
  • [MeSH-major] Adrenal Cortex / metabolism. Aldosterone / biosynthesis. Endothelium, Vascular / secretion. Interleukin-6 / biosynthesis. Interleukin-6 / secretion

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  • (PMID = 18777460.001).
  • [ISSN] 0947-7349
  • [Journal-full-title] Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
  • [ISO-abbreviation] Exp. Clin. Endocrinol. Diabetes
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Interleukin-6; 4964P6T9RB / Aldosterone
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94. Shah MA, Kortmansky J, Motwani M, Drobnjak M, Gonen M, Yi S, Weyerbacher A, Cordon-Cardo C, Lefkowitz R, Brenner B, O'Reilly E, Saltz L, Tong W, Kelsen DP, Schwartz GK: A phase I clinical trial of the sequential combination of irinotecan followed by flavopiridol. Clin Cancer Res; 2005 May 15;11(10):3836-45
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  • PURPOSE: Flavopiridol potently enhances the effect of irinotecan with cures in colorectal cancer xenografts, and is associated with modulation of several molecular targets, including p21, Differentiation-related gene 1 (Drg1), and p53.
  • At the maximal tolerated dose, the pharmacokinetic analysis was expanded and pre- and posttreatment tumor biopsies were done.
  • We observed partial responses in three patients and prolonged stable disease (i.e., >6 months) in 36% of patients including adrenocortical cancer and hepatocellular cancer.
  • [MeSH-minor] Adult. Aged. Bilirubin / analysis. Cell Cycle Proteins / biosynthesis. Cyclin-Dependent Kinase Inhibitor p21. Drug Administration Schedule. Drug Interactions. Female. Flavonoids / administration & dosage. Flavonoids / adverse effects. Flavonoids / pharmacokinetics. Humans. Intracellular Signaling Peptides and Proteins. Male. Maximum Tolerated Dose. Middle Aged. Piperidines / administration & dosage. Piperidines / adverse effects. Piperidines / pharmacokinetics. Treatment Outcome. Tumor Suppressor Protein p53 / biosynthesis

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  • (PMID = 15897584.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 067819
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Flavonoids; 0 / Intracellular Signaling Peptides and Proteins; 0 / N-myc downstream-regulated gene 1 protein; 0 / Piperidines; 0 / Tumor Suppressor Protein p53; 45AD6X575G / alvocidib; 7673326042 / irinotecan; RFM9X3LJ49 / Bilirubin; XT3Z54Z28A / Camptothecin
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95. Else T, Giordano TJ, Hammer GD: Evaluation of telomere length maintenance mechanisms in adrenocortical carcinoma. J Clin Endocrinol Metab; 2008 Apr;93(4):1442-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of telomere length maintenance mechanisms in adrenocortical carcinoma.
  • CONTEXT: Adrenocortical cancer (ACC) is a rare disease with an often fatal outcome.
  • The clinical and pathological diagnosis of a malignant vs. benign adrenocortical tumor is sometimes challenging.
  • Telomere maintenance mechanisms (TMMs) are critical for the persistence of the malignant phenotype, but little is known about these mechanisms or their diagnostic value in adrenocortical lesions.
  • OBJECTIVE: Tissue samples of diagnostically known adrenocortical neoplasms were evaluated for parameters of known TMMs, telomerase activity (TA), and alternative telomere lengthening (ALT).
  • DESIGN: The study analyzed retrospectively collected frozen adrenocortical tissue samples from the University of Michigan Health System.
  • PATIENT SAMPLES: Samples included 24 ACCs, 11 adrenocortical adenomas (ACAs), and three normal adrenal tissues.
  • None of the normal adrenal tissues (none of three) or ACA (none of 11) samples had signs of an active TMM.
  • Determination of telomere maintenance mechanisms in diagnostically challenging adrenocortical tumors might be of additional diagnostic value in the pathological diagnosis of malignant vs. benign lesions.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Telomere

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  • (PMID = 18198226.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.7.49 / Telomerase
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96. Zancanella P, Pianovski MA, Oliveira BH, Ferman S, Piovezan GC, Lichtvan LL, Voss SZ, Stinghen ST, Callefe LG, Parise GA, Santana MH, Figueiredo BC: Mitotane associated with cisplatin, etoposide, and doxorubicin in advanced childhood adrenocortical carcinoma: mitotane monitoring and tumor regression. J Pediatr Hematol Oncol; 2006 Aug;28(8):513-24
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  • [Title] Mitotane associated with cisplatin, etoposide, and doxorubicin in advanced childhood adrenocortical carcinoma: mitotane monitoring and tumor regression.
  • PURPOSE: To define a mitotane dose for pediatric patients with adrenocortical cancer (ACC) that maintains therapeutic plasma levels (TL) between 14 and 20 microg/mL and to verify its antitumor efficacy in association with 8 cycles of cisplatin, etoposide, and doxorubicin (CED).
  • Minor to partial tumor remission was found in 5 patients (<1 y) and complete remission was found in 2 patients.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Adrenocortical Carcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cisplatin / administration & dosage. Doxorubicin / administration & dosage. Etoposide / administration & dosage. Mitotane / administration & dosage
  • [MeSH-minor] Administration, Oral. Child. Child, Preschool. Disease Progression. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug Monitoring / methods. Drug Therapy, Combination. Female. Follow-Up Studies. Humans. Male. Neoplasm Staging. Prospective Studies. Remission Induction. Survival Rate. Time Factors. Treatment Outcome

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  • (PMID = 16912591.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 6PLQ3CP4P3 / Etoposide; 78E4J5IB5J / Mitotane; 80168379AG / Doxorubicin; Q20Q21Q62J / Cisplatin
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97. Hong DS, Sebti SM, Newman RA, Blaskovich MA, Ye L, Gagel RF, Moulder S, Wheler JJ, Naing A, Tannir NM, Ng CS, Sherman SI, El Naggar AK, Khan R, Trent J, Wright JJ, Kurzrock R: Phase I trial of a combination of the multikinase inhibitor sorafenib and the farnesyltransferase inhibitor tipifarnib in advanced malignancies. Clin Cancer Res; 2009 Nov 15;15(22):7061-8
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  • Interestingly, six of eight patients with medullary thyroid cancer had durable stable disease (n = 3) or partial remissions (n = 3), lasting 12 to 26+ months.
  • Prolonged (> or =6 months) stable disease was also seen in nine patients as follows: papillary thyroid cancer (n = 4; 18+ to 27+ months), adrenocortical cancer (n = 2; 7 and 11 months), and one each of melanoma (platelet-derived growth factor receptor mutation positive; 14 months), renal (6 months), and pancreatic cancer (6 months).
  • Activity was seen, especially in patients with medullary thyroid cancer, a tumor characterized by RET mutations.

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  • (PMID = 19903778.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA062461-10; United States / NCI NIH HHS / CA / U01 CA062461; United States / NCI NIH HHS / CA / 5 U01 CA062461; United States / NCI NIH HHS / CA / U01 CA062461-10
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzenesulfonates; 0 / Phenylurea Compounds; 0 / Pyridines; 0 / Quinolones; 192185-72-1 / tipifarnib; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 2.5.1.29 / Farnesyltranstransferase; EC 2.7.10.1 / Proto-Oncogene Proteins c-ret; EC 2.7.10.1 / RET protein, human
  • [Other-IDs] NLM/ NIHMS140339; NLM/ PMC2784003
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98. Farnworth PG, Wang Y, Escalona R, Leembruggen P, Ooi GT, Findlay JK: Transforming growth factor-beta blocks inhibin binding to different target cell types in a context-dependent manner through dual mechanisms involving betaglycan. Endocrinology; 2007 Nov;148(11):5355-68

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • To clarify the nature and extent of interactions between inhibin and TGF-beta, we therefore examined 1) the mutual competition between these ligands for binding, 2) the regulation of endogenous betaglycan expression by inhibin and TGF-beta isoforms, and 3) the consequences of such betaglycan regulation for subsequent inhibin binding in mouse Leydig (TM3), Sertoli (TM4), adrenocortical cancer (AC), and gonadotroph (LbetaT2) cell lines, chosen to model cellular targets for local and endocrine actions of inhibin.

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  • (PMID = 17656464.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proteoglycans; 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta; 145170-29-2 / betaglycan; 57285-09-3 / Inhibins
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99. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Peroxisome proliferator-activated receptor-gamma agonists suppress adrenocortical tumor cell proliferation and induce differentiation.
  • 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

  • Hazardous Substances Data Bank. ROSIGLITAZONE .
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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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100. Wang Y, Nicholls PK, Stanton PG, Harrison CA, Sarraj M, Gilchrist RB, Findlay JK, Farnworth PG: Extra-ovarian expression and activity of growth differentiation factor 9. J Endocrinol; 2009 Sep;202(3):419-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The present studies confirm GDF9 expression in the mouse testis, pituitary gland and adrenocortical cancer (AC) cells, and establish its expression in L beta T2 gonadotrophs, and in mouse adrenal glands, particularly foetal and neonatal cortical cells.
  • Our findings show that GDF9 regulates the expression of R-SMAD2/3-responsive reporter genes through ALK4, 5 or 7 in extra-ovarian (adrenocortical and Sertoli) cells with similar potency and signalling pathway to its actions on granulosa cells, but suggest that expression of BMPRII, ALK5 (TGFBR1) and R-SMADs 2 and 3 may not be sufficient for a cell to respond to GDF9.
  • [MeSH-major] Adrenal Glands / physiology. Growth Differentiation Factor 9 / genetics. Leydig Cells / physiology. Pituitary Gland / physiology. Sertoli Cells / physiology

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  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
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  • (PMID = 19505950.001).
  • [ISSN] 1479-6805
  • [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 / 4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide; 0 / Benzamides; 0 / Dioxoles; 0 / GDF9 protein, human; 0 / Gdf9 protein, mouse; 0 / Gdf9 protein, rat; 0 / Growth Differentiation Factor 9; 9002-68-0 / Follicle Stimulating Hormone; EC 1.13.12.- / Luciferases
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