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1. Morimoto R, Satoh F, Murakami O, Suzuki T, Abe T, Tanemoto M, Abe M, Uruno A, Ishidoya S, Arai Y, Takahashi K, Sasano H, Ito S: Immunohistochemistry of a proliferation marker Ki67/MIB1 in adrenocortical carcinomas: Ki67/MIB1 labeling index is a predictor for recurrence of adrenocortical carcinomas. Endocr J; 2008 Mar;55(1):49-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemistry of a proliferation marker Ki67/MIB1 in adrenocortical carcinomas: Ki67/MIB1 labeling index is a predictor for recurrence of adrenocortical carcinomas.
  • Adrenocortical carcinoma (ACC) is a rare, highly malignant tumor.
  • The aim of the present study is to evaluate the prognostic relevance of a proliferation marker Ki67/MIB1 by immunohistochemistry in 17 cases who underwent resections of the primary tumors and diagnosed to have ACC at Tohoku University Hospital based on the criteria of Weiss during the period from 1976 to 2005.
  • The median age at diagnosis was 46 years old, and the mean size of the primary tumors was 7.1 cm with the minimal of 3.5 cm.
  • Kaplan-Meier analysis revealed that patients with Ki67/MIB1LI of 7% or more were associated with significantly shortened disease-free survival (P = 0.0037).
  • The survival analysis with Weiss score showed that patients with the scores of 6 or more had both significantly shortened disease-free survival (P = 0.0001) and overall survival (P = 0.0063).
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenocortical Carcinoma / diagnosis. Biomarkers, Tumor / metabolism. Cell Proliferation. Ki-67 Antigen / metabolism. Ubiquitin-Protein Ligases / metabolism

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  • (PMID = 18187873.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; EC 6.3.2.19 / MIB1 ligase, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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2. Volante M, Sperone P, Bollito E, Frangipane E, Rosas R, Daffara F, Terzolo M, Berruti A, Papotti M: Matrix metalloproteinase type 2 expression in malignant adrenocortical tumors: Diagnostic and prognostic significance in a series of 50 adrenocortical carcinomas. Mod Pathol; 2006 Dec;19(12):1563-9
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  • [Title] Matrix metalloproteinase type 2 expression in malignant adrenocortical tumors: Diagnostic and prognostic significance in a series of 50 adrenocortical carcinomas.
  • The differential diagnosis of adrenocortical carcinoma from adrenocortical adenoma is based on different pathological parameters, usually incorporated in scoring systems, which unfortunately lack a 100% sensitivity and specificity.
  • Little is known on the molecular mechanisms leading to the malignant phenotype in adrenocortical tumors.
  • Among other molecules, metalloproteinases were demonstrated to be implicated in malignant progression and metastatization of solid tumors, including endocrine ones.
  • Therefore, we aimed to investigate metalloproteinases and their inhibitors expression in a series of 50 adrenocortical carcinomas and 50 control adrenocortical adenomas, diagnosed according to the Weiss histological criteria.
  • Metalloproteinase type 2 gave the most significant result, being detected in neoplastic cells in 1/50 adrenocortical adenomas (2%) and 37/50 adrenocortical carcinomas (74%) (P < 0.001), with a focal (score 1, <20% of positive cells--two-thirds of cases) or diffuse (score 2, >20% of positive cells--one-third of cases) pattern.
  • In addition, diffuse (score 2) metalloproteinase type 2 protein expression, as compared to focal or negative immunostaining, correlated with shorter survival (P < 0.02) and disease-free interval (P = 0.05).
  • Our data indicate that metalloproteinase type 2 immunohistochemical localization in tumor cells is significantly restricted to malignant adrenocortical tumors, with high specificity but low sensitivity.
  • In addition, a strong metalloproteinase type 2 expression in adrenocortical carcinoma was for the first time recognized as an unfavorable prognostic factor.
  • [MeSH-major] Adrenal Cortex Neoplasms / enzymology. Adrenocortical Adenoma / enzymology. Adrenocortical Carcinoma / enzymology. Matrix Metalloproteinase 2 / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Diagnosis, Differential. Female. Humans. Immunoenzyme Techniques. Male. Middle Aged. Prognosis. Reproducibility of Results. Sensitivity and Specificity. Survival Rate

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  • (PMID = 16980949.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 3.4.24.24 / Matrix Metalloproteinase 2
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3. Kotoula V, Sozopoulos E, Litsiou H, Fanourakis G, Koletsa T, Voutsinas G, Tseleni-Balafouta S, Mitsiades CS, Wellmann A, Mitsiades N: Mutational analysis of the BRAF, RAS and EGFR genes in human adrenocortical carcinomas. Endocr Relat Cancer; 2009 Jun;16(2):565-72
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  • [Title] Mutational analysis of the BRAF, RAS and EGFR genes in human adrenocortical carcinomas.
  • The serine/threonine kinase B-Raf plays a key role in the Ras/Raf/MEK/ERK pathway that relays extracellular signals for cell proliferation and survival.
  • EGFR inhibitors have produced objective responses in patients with non-small cell lung carcinomas harboring activating EGFR TK domain somatic mutations.
  • We evaluated the presence of mutations in BRAF (exons 11 and 15), KRAS (exons 1 and 2), NRAS (exons 1 and 2), and EGFR (exons 18-21) in adrenal carcinomas (35 tumor specimens and two cell lines) by DNA sequencing.
  • BRAF mutations were found in two carcinomas (5.7%).
  • Four carcinomas (11.4%) carried EGFR TK domain mutations.
  • No mutations were found in the two adrenocortical cell lines.
  • EGFR-mutant carcinomas exhibited increased phosphorylation of EGFR (Tyr 992) compared with wild-type carcinomas.
  • We conclude that BRAF, RAS, and EGFR mutations occur in a subset of human adrenocortical carcinomas.
  • Inhibitors of the Ras/Raf/MEK/ERK and EGFR pathways represent candidate targeted therapies for future clinical trials in carefully selected patients with adrenocortical carcinomas harboring respective activating mutations.
  • [MeSH-major] Adrenocortical Carcinoma / genetics. Genes, ras / genetics. Mutation / genetics. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins B-raf / genetics. Receptor, Epidermal Growth Factor / genetics. ras Proteins / genetics

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  • (PMID = 19190079.001).
  • [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 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 3.6.5.2 / ras Proteins
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4. 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.
  • 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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5. Szajerka A, Dziegiel P, Szajerka T, Zabel M, Winowski J, Grzebieniak Z: Immunohistochemical evaluation of metallothionein, Mcm-2 and Ki-67 antigen expression in tumors of the adrenal cortex. Anticancer Res; 2008 Sep-Oct;28(5B):2959-65

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  • [Title] Immunohistochemical evaluation of metallothionein, Mcm-2 and Ki-67 antigen expression in tumors of the adrenal cortex.
  • BACKGROUND: The aim of this study was to assess the metallothionein (MT), maintenance protein 2 (Mcm-2) and Ki-67 expressions in adrenocortical adenomas and carcinomas in comparison to normal tissue and evaluate the correlations between these markers of proliferation and between these markers and tumor diameter.
  • MATERIALS AND METHODS: The expression of MT, Mcm-2 and Ki-67 was assessed by immunochemistry in forty-eight adrenocortical adenomas, six adrenocortical carcinomas and eleven normal adrenal cortex tissue samples.
  • RESULTS: The expressions of MT, Mcm-2 and Ki-67 in the adrenocortical carcinomas were significantly higher than in the adenomas and normal tissue (p<0.05).
  • The levels of Mcm-2 were also higher in the adrenocortical adenomas compared to the normal tissue (p<0.05).
  • The Mcm-2 expression showed a positive correlation to the expression of MT in the adrenocortical carcinomas (r=0.773; p<0.05) and to the expression of Ki-67 in the adrenocortical adenomas (r=0.432; p<0.05).
  • The malignant tumor diameter was positively correlated with the MT and Mcm-2 expressions (r=0.766, p<0.05 and r=0.620, p<0.05, respectively).
  • CONCLUSION: The assessment of Mcm-2 expression seems to be of special importance as a marker of adrenocortical dysplasia and a reliable indicator of malignancy in suspicious masses of the adrenal cortex.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenocortical Adenoma / metabolism. Adrenocortical Carcinoma / metabolism. Biomarkers, Tumor / biosynthesis. Cell Cycle Proteins / biosynthesis. Ki-67 Antigen / biosynthesis. Metallothionein / biosynthesis. Nuclear Proteins / biosynthesis

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  • (PMID = 19031940.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / Ki-67 Antigen; 0 / Nuclear Proteins; 9038-94-2 / Metallothionein; EC 3.6.4.12 / MCM2 protein, human; EC 3.6.4.12 / Minichromosome Maintenance Complex Component 2
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6. De Martino MC, van Koetsveld PM, Pivonello R, Hofland LJ: Role of the mTOR pathway in normal and tumoral adrenal cells. Neuroendocrinology; 2010;92 Suppl 1:28-34
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  • [Title] Role of the mTOR pathway in normal and tumoral adrenal cells.
  • Presently, the role and functions of mTOR and its signaling pathway in the normal and pathological adrenal gland has not been clarified yet.
  • However, many growth factors and growth factor receptors, which are considered to play a role in the pathogenesis of adrenal tumors, can at least in part exert their effects through the activation of PI3K/AKT/mTOR pathway.
  • Dysregulation of AKT has been reported in adrenocortical carcinomas and adrenomedullary tumors, named pheochromocytomas.
  • Adrenocortical carcinomas and malignant pheochromocytomas are aggressive tumors with poor prognosis and scant treatment options.
  • On the basis of the current knowledge, mTOR could play a role in the pathogenesis of both adrenocortical carcinomas and pheochromocytomas.
  • Moreover, mTOR inhibitors, interfering with the activation of several mitogenic and angiogenic factors, could be considered as a novel treatment opportunity for the management of malignant adrenal tumors.
  • [MeSH-major] Adrenal Cortex / metabolism. Adrenal Cortex Neoplasms / metabolism. Signal Transduction / physiology. TOR Serine-Threonine Kinases / metabolism

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  • [Copyright] Copyright © 2010 S. Karger AG, Basel.
  • (PMID = 20829615.001).
  • [ISSN] 1423-0194
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 67763-96-6 / Insulin-Like Growth Factor I; EC 2.7.1.1 / TOR Serine-Threonine Kinases
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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

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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. van't Sant HP, Bouvy ND, Kazemier G, Bonjer HJ, Hop WC, Feelders RA, de Herder WW, de Krijger RR: The prognostic value of two different histopathological scoring systems for adrenocortical carcinomas. Histopathology; 2007 Aug;51(2):239-45

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The prognostic value of two different histopathological scoring systems for adrenocortical carcinomas.
  • AIMS: To compare two different multiparameter histopathological scoring indices and determine their prognostic value in patients presenting with adrenocortical carcinoma (ACC).
  • METHODS AND RESULTS: Seventy-nine adrenal cortical tumours were divided into adenomas (n = 17), non-metastatic carcinomas (n = 24) and carcinomas with metastatic disease and/or local recurrence during follow-up (n = 19) or at time of presentation (n = 19).
  • All cases were scored according to the Weiss revisited index (WRI) and the Van Slooten index (VSI).
  • Both scoring indices yielded a significantly different score (P < 0.005) between adenomas and carcinomas.
  • Non-metastasized carcinomas had a lower score with both indices compared with carcinomas with metastases at the time of presentation (VSI, P = 0.017; WRI, P = 0.019).
  • Cancer-specific survival in patients with metastasized ACC correlated with the scores for both indices (VSI, P = 0.0078; WRI, P = 0.0025).
  • Time from diagnosis of ACC to development of metastatic disease was correlated with the WRI (P = 0.036, r = -0.350).
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology
  • [MeSH-minor] Adenoma / pathology. Adolescent. Adult. Aged. Aged, 80 and over. Carcinoma / pathology. Carcinoma / secondary. Diagnosis, Differential. Disease-Free Survival. Female. Humans. Male. Middle Aged. Neoplasm Recurrence, Local / pathology. Prognosis

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  • (PMID = 17593212.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
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9. Soon PS, Sidhu SB: Molecular basis of adrenocortical carcinomas. Minerva Endocrinol; 2009 Jun;34(2):137-47
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular basis of adrenocortical carcinomas.
  • Adrenocortical carcinomas (ACCs) are rare tumors associated with poor prognosis.
  • Although surgery is the mainstay of treatment for this cancer, most patients will experience a recurrence of their tumor.
  • A better understanding of the molecular basis of this cancer is crucial to the development of newer and better treatment options.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Mutation. Neoplastic Syndromes, Hereditary / genetics

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  • (PMID = 19471238.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Number-of-references] 88
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10. Szolar DH, Korobkin M, Reittner P, Berghold A, Bauernhofer T, Trummer H, Schoellnast H, Preidler KW, Samonigg H: Adrenocortical carcinomas and adrenal pheochromocytomas: mass and enhancement loss evaluation at delayed contrast-enhanced CT. Radiology; 2005 Feb;234(2):479-85
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  • [Title] Adrenocortical carcinomas and adrenal pheochromocytomas: mass and enhancement loss evaluation at delayed contrast-enhanced CT.
  • PURPOSE: To retrospectively measure the adrenal gland attenuation and the percentage loss of adrenal gland enhancement at delayed contrast medium-enhanced computed tomography (CT) in patients with adrenocortical carcinomas and pheochromocytomas and to compare these data with those in patients with adenomas and metastases.
  • Eleven patients with proved adrenocortical carcinoma, 17 with proved pheochromocytoma, 23 with adrenal adenoma, and 16 with metastasis to the adrenal gland underwent helical CT.
  • RESULTS: The mean attenuation of adenomas (8 HU +/- 18 [standard deviation]) was significantly lower than those of adrenocortical carcinomas (39 HU +/- 14), pheochromocytomas (44 HU +/- 11), and metastases (34 HU +/- 11) on nonenhanced CT scans (P < .001).
  • Although the mean attenuation values for nonadenomas (ie, adrenocortical carcinomas, pheochromocytomas, and metastases) were significantly higher than the value for adenomas on the 1-minute contrast-enhanced CT scans (P < .001), there was more overlap in attenuation between adenomas and nonadenomas on contrast-enhanced scans than on nonenhanced scans.
  • On the 10-minute delayed contrast-enhanced scans, the mean attenuation of adenomas (32 HU +/- 17) was significantly lower than the mean attenuations of carcinomas (72 HU +/- 15), pheochromocytomas (83 HU +/- 14), and metastases (66 HU +/- 13) (P < .001).
  • At optimal threshold values of 50% for absolute percentage of enhancement loss and 40% for relative percentage of enhancement loss at 10 minutes, both the sensitivity and the specificity for the diagnosis of adenoma were 100% when adenomas were compared with carcinomas, pheochromocytomas, and metastases.
  • CONCLUSION: The enhancement loss in adrenocortical carcinomas and pheochromocytomas is similar to that in adrenal metastases but significantly less than that in adrenal adenomas.
  • The percentage change in contrast material washout is a useful adjunct to absolute CT attenuation values in differentiating adrenal adenomas from adrenocortical carcinomas and pheochromocytomas.
  • [MeSH-major] Adrenal Cortex Neoplasms / radiography. Adrenal Gland Neoplasms / radiography. Adrenocortical Carcinoma / radiography. Pheochromocytoma / radiography. Tomography, X-Ray Computed / methods

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  • [Copyright] (c) RSNA, 2005.
  • [CommentIn] Radiology. 2005 Sep;236(3):1112-3 [16118181.001]
  • [CommentIn] Radiology. 2006 Jan;238(1):373; author reply 373-4 [16373781.001]
  • (PMID = 15671003.001).
  • [ISSN] 0033-8419
  • [Journal-full-title] Radiology
  • [ISO-abbreviation] Radiology
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] United States
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11. Volante M, Bollito E, Sperone P, Tavaglione V, Daffara F, Porpiglia F, Terzolo M, Berruti A, Papotti M: Clinicopathological study of a series of 92 adrenocortical carcinomas: from a proposal of simplified diagnostic algorithm to prognostic stratification. Histopathology; 2009 Nov;55(5):535-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinicopathological study of a series of 92 adrenocortical carcinomas: from a proposal of simplified diagnostic algorithm to prognostic stratification.
  • AIMS: Pathological diagnosis of adrenocortical carcinoma relies on several microscopic features commonly used in combination in different scoring systems that are sometimes subjective and/or time consuming.
  • The aim was to investigate the impact of individual pathological parameters in the diagnosis and prognosis of adrenocortical carcinoma.
  • METHODS AND RESULTS: The series included 92 malignant cases and a control series of 47 adenomas, all classified according to Weiss score criteria.
  • The presence of disruption of the reticular network, as highlighted by histochemical staining, was present in all adrenocortical carcinomas and the inclusion of at least one of the three following additional parameters - mitotic index >5/50 high-power fields (HPF), presence of necrosis and presence of vascular invasion - gave an algorithm with 100% sensitivity and specificity to recognize malignant tumours according to the Weiss system, with easier and more practical applicability.
  • Moreover, on multivariate analysis, stage III/IV and mitotic count >9/50 HPF showed a strong adverse impact on disease-free and overall survival, leading to the identification of three risk groups affected by a significantly different prognosis.
  • CONCLUSIONS: We have defined an easy-to-perform and highly specific and sensitive algorithm for the diagnosis and prognostic categorization of adrenocortical tumours.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Algorithms
  • [MeSH-minor] Adenoma / pathology. Diagnosis, Differential. Disease-Free Survival. Humans. Prognosis. Proportional Hazards Models. Sensitivity and Specificity

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  • (PMID = 19912359.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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12. Nunes ML, Rault A, Teynie J, Valli N, Guyot M, Gaye D, Belleannee G, Tabarin A: 18F-FDG PET for the identification of adrenocortical carcinomas among indeterminate adrenal tumors at computed tomography scanning. World J Surg; 2010 Jul;34(7):1506-10
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  • [Title] 18F-FDG PET for the identification of adrenocortical carcinomas among indeterminate adrenal tumors at computed tomography scanning.
  • BACKGROUND: 18F-fluorodeoxyglucose positron emission tomography (18F-FDG PET) has been proposed for the evaluation of adrenal tumors.
  • However, only scarce data are available to evaluate its usefulness for the identification of primary adrenal carcinomas in patients with no previous history of cancer and equivocal tumors on computed tomography (CT) scan.
  • Twenty-three consecutive patients without previous history of cancer investigated for adrenal tumors without features of benign adrenocortical adenoma on CT scan but no obvious ACC underwent 18F-FDG PET.
  • The ratio of maxSUV adrenal tumor on maxSUV liver (adrenal/liver maxSUV ratio) during 18F-FDG PET was compared to Weiss pathological criteria.
  • RESULTS: Seventeen patients had an adrenal adenoma, 2 had small size adrenal carcinomas (<5 cm), 1 had an angiosarcoma, and 3 had noncortical benign lesions.
  • An adrenal/liver maxSUV ratio above 1.6 provided 100% sensitivity, 90% specificity, and 100% negative predictive value for the diagnosis of malignant tumor.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnostic imaging. Adrenal Gland Neoplasms / diagnostic imaging. Fluorodeoxyglucose F18. Positron-Emission Tomography. Radiopharmaceuticals. Tomography, X-Ray Computed
  • [MeSH-minor] Adrenocortical Adenoma / diagnostic imaging. Adult. Aged. Female. Humans. Male. Middle Aged. Retrospective Studies. Sensitivity and Specificity

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  • (PMID = 20396886.001).
  • [ISSN] 1432-2323
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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13. Jiménez Peláez M, Bouvy BM, Dupré GP: Laparoscopic adrenalectomy for treatment of unilateral adrenocortical carcinomas: technique, complications, and results in seven dogs. Vet Surg; 2008 Jul;37(5):444-53

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  • [Title] Laparoscopic adrenalectomy for treatment of unilateral adrenocortical carcinomas: technique, complications, and results in seven dogs.
  • OBJECTIVE: To investigate the feasibility of, and outcome after, laparoscopic adrenalectomy in dogs with unilateral adrenocortical carcinoma.
  • ANIMALS: Dogs (n=7) with Cushing's syndrome caused by unilateral adrenocortical carcinoma.
  • After dissection and hemostatic control of the phrenicoabdominal vein, the adrenal gland was carefully dissected or when there was capsule fragility, necrotic content was partially aspirated.
  • RESULTS: Dogs with unilateral adrenocortical carcinoma (3 right-sided, 4 left-sided) without invasion of the caudal vena cava were successfully operated by laparoscopic approach.
  • CONCLUSIONS: Laparoscopic adrenalectomy is feasible in dogs with either right- or left-sided adrenocortical carcinoma not involving the caudal vena cava.
  • CLINICAL RELEVANCE: When performed by experienced surgeons, laparoscopic adrenalectomy offers a minimally invasive alternative to open laparotomy or retroperitoneal surgery for the treatment of unilateral adrenocortical carcinoma in dogs.
  • [MeSH-major] Adrenal Cortex Neoplasms / veterinary. Adrenalectomy / veterinary. Adrenocortical Carcinoma / veterinary. Adrenocortical Hyperfunction / veterinary. Dog Diseases / surgery

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  • (PMID = 18986311.001).
  • [ISSN] 1532-950X
  • [Journal-full-title] Veterinary surgery : VS
  • [ISO-abbreviation] Vet Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Almeida MQ, Fragoso MC, Lotfi CF, Santos MG, Nishi MY, Costa MH, Lerario AM, Maciel CC, Mattos GE, Jorge AA, Mendonca BB, Latronico AC: Expression of insulin-like growth factor-II and its receptor in pediatric and adult adrenocortical tumors. J Clin Endocrinol Metab; 2008 Sep;93(9):3524-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of insulin-like growth factor-II and its receptor in pediatric and adult adrenocortical tumors.
  • BACKGROUND: Adrenocortical tumors are heterogeneous neoplasms with incompletely understood pathogenesis.
  • IGF-II overexpression has been consistently demonstrated in adult adrenocortical carcinomas.
  • OBJECTIVES: The objective of the study was to analyze expression of IGF-II and its receptor (IGF-IR) in pediatric and adult adrenocortical tumors and the effects of a selective IGF-IR kinase inhibitor (NVP-AEW541) on adrenocortical tumor cells.
  • PATIENTS: Fifty-seven adrenocortical tumors (37 adenomas and 20 carcinomas) from 23 children and 34 adults were studied.
  • Cell proliferation and apoptosis were analyzed in NCI H295 cells and a new cell line established from a pediatric adrenocortical adenoma.
  • RESULTS: IGF-II transcripts were overexpressed in both pediatric adrenocortical carcinomas and adenomas.
  • Otherwise, IGF-II was mainly overexpressed in adult adrenocortical carcinomas (270.5 +/- 130.2 vs. 16.1 +/- 13.3; P = 0.0001).
  • IGF-IR expression was significantly higher in pediatric adrenocortical carcinomas than adenomas (9.1 +/- 3.1 vs. 2.6 +/- 0.3; P = 0.0001), whereas its expression was similar in adult adrenocortical carcinomas and adenomas.
  • IGF-IR expression was a predictor of metastases in pediatric adrenocortical tumors in univariate analysis (hazard ratio 1.84; 95% confidence interval 1.28-2.66; P = 0.01).
  • Furthermore, NVP-AEW541 blocked cell proliferation in a dose- and time-dependent manner in both cell lines through a significant increase of apoptosis.
  • CONCLUSION: IGF-IR overexpression was a biomarker of pediatric adrenocortical carcinomas.
  • Additionally, a selective IGF-IR kinase inhibitor had antitumor effects in adult and pediatric adrenocortical tumor cell lines, suggesting that IGF-IR inhibitors represent a promising therapy for human adrenocortical carcinoma.
  • [MeSH-major] Adenoma / genetics. Adrenal Cortex Neoplasms / genetics. Carcinoma / genetics. Insulin-Like Growth Factor II / genetics. Receptor, IGF Type 2 / genetics

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  • (PMID = 18611974.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptor, IGF Type 2; 67763-97-7 / Insulin-Like Growth Factor II
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15. Menon V, Krishnamurthy SV: Adrenocortical carcinomas: a 12-year clinicopathologic study of 15 cases. Indian J Pathol Microbiol; 2006 Jan;49(1):7-11

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenocortical carcinomas: a 12-year clinicopathologic study of 15 cases.
  • Adrenal cortical carcinomas are rare neoplasms and the definitive diagnostic criteria are distant metastasis and / or local invasion.
  • Due to advances in imaging techniques, adrenal cortical neoplasms are discovered earlier and are smaller, increasing the need for more accurate diagnosis and pathologic indicators of prognosis.
  • A twelve year retrospective clinicopathologic analysis of 15 histopathologically proven cases of adrenocortical carcinomas was done.
  • Clinical details including radiologic findings, endocrine manifestations and gross finding were analysed.
  • Functional tumors showed a greater representation of mixed cell type.
  • It was concluded that Weiss criteria is easy to apply and that a combined evaluation of clinical features, size, weight and microscopic appearance seems necessary for the diagnosis of adrenocortical carcinomas.
  • [MeSH-major] Adrenal Cortex / pathology. Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology

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  • (PMID = 16625963.001).
  • [ISSN] 0377-4929
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
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16. Tissier F: [Pathology of adrenocortical tumors: review and recent data]. Ann Endocrinol (Paris); 2009 Jun;70(3):179-85

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Pathology of adrenocortical tumors: review and recent data].
  • [Transliterated title] Anatomie pathologique des tumeurs corticosurrénaliennes de l'adulte : état des lieux et données récentes.
  • Most adrenocortical tumors are benign; adrenocortical carcinomas are rare but their prognosis is poor and their therapeutic is sparse.
  • In most adrenocortical tumors, the morphological approach brings sufficient elements to establish the differential diagnosis between a benign and a malignant tumor but in few cases, it is insufficient.
  • Moreover, morphology is limited for predicting prognosis of adrenocortical carcinomas.
  • These genetics findings already have repercussions for the patients in the development of molecular markers for diagnosis and prognosis and in the future they could help in the development of new morphological approaches, in particular immunohistochemical approaches.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology

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  • (PMID = 19298951.001).
  • [ISSN] 0003-4266
  • [Journal-full-title] Annales d'endocrinologie
  • [ISO-abbreviation] Ann. Endocrinol. (Paris)
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Cyclin E; 0 / Tumor Suppressor Protein p53; 0 / beta Catenin; 67763-97-7 / Insulin-Like Growth Factor II
  • [Number-of-references] 77
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17. Mete O, Kapran Y, Güllüoğlu MG, Kiliçaslan I, Erbil Y, Senyürek YG, Dizdaroğlu F: Anti-CD10 (56C6) is expressed variably in adrenocortical tumors and cannot be used to discriminate clear cell renal cell carcinomas. Virchows Arch; 2010 May;456(5):515-21
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  • [Title] Anti-CD10 (56C6) is expressed variably in adrenocortical tumors and cannot be used to discriminate clear cell renal cell carcinomas.
  • In the evaluation of retroperitoneal masses, the practicing pathologist faces a dilemma when making a diagnosis based on histology given the often overlapping morphologic appearances of the adrenocortical carcinoma, renal cell carcinoma (RCC), and hepatocellular carcinoma (HCC).
  • CD10 is expressed in a membranous fashion in the vast majority of clear cell RCCs; therefore, it is widely used for distinction from its mimics.
  • However, its expression is not well-investigated in adrenal cortical tumors.
  • We examined CD10 expression in 47 surgically resected adrenocortical tumors (26 adenomas and 21 carcinomas) and compared with 20 clear cell RCCs and 25 HCCs.
  • Twenty HCCs (80%), 18 RCCs (90%), 11 adrenocortical carcinomas (52%), and 18 adrenocortical adenomas (69%) were positive for CD10.
  • HCCs were characterized by a canalicular staining, and clear cell RCCs exhibited membranous or mixed membranous-cytoplasmic staining.
  • Adrenocortical tumors displayed mainly cytoplasmic staining.
  • Four adrenocortical carcinomas and one adenoma also displayed the membranous staining pattern.
  • Despite the relatively small number of samples, our preliminary results revealed that adrenocortical tumors may express CD10 (Clone: 56C6).
  • The most important point from this paper is the fact that anti-CD10 expression has not been previously reported in adrenocortical carcinomas.
  • This suggests that CD10 does not seem to be a useful marker for discriminating clear cell RCCs from adrenocortical tumors since CD10 expression does not rule out the possibility of adrenocortical tumors.
  • This feature should be kept in mind when constructing an antibody panel for an epithelial tumor that involves the adrenal gland and kidney, especially in small biopsy specimens.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Carcinoma, Renal Cell / diagnosis. Kidney Neoplasms / diagnosis. Neprilysin / biosynthesis
  • [MeSH-minor] Adult. Antigens, Neoplasm / analysis. Carcinoma, Hepatocellular / diagnosis. Carcinoma, Hepatocellular / immunology. Female. Humans. Liver Neoplasms / diagnosis. Liver Neoplasms / immunology. Male. Middle Aged

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  • (PMID = 20390424.001).
  • [ISSN] 1432-2307
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; EC 3.4.24.11 / Neprilysin
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18. Takahashi K, Shoji I, Shibasaki A, Kato I, Hiraishi K, Yamamoto H, Kaneko K, Murakami O, Morimoto R, Satoh F, Ito S, Totsune K: Presence of kisspeptin-like immunoreactivity in human adrenal glands and adrenal tumors. J Mol Neurosci; 2010 May;41(1):138-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Presence of kisspeptin-like immunoreactivity in human adrenal glands and adrenal tumors.
  • Kisspeptins have also been reported to stimulate the aldosterone secretion from the adrenal cortex.
  • However, the expression of kisspeptins in human adrenal glands and adrenal tumors has not been clarified yet.
  • We, therefore, studied the presence of kisspeptin-like immunoreactivity (LI) in human adrenal glands and adrenal tumors (adrenocortical adenomas, adrenocortical carcinomas, and pheochromocytomas) by radioimmunoassay and immunocytochemistry.
  • Kisspeptin-LI was detected in all the tissues examined; normal portions of adrenal glands (3.0 +/- 2.3 pmol/g wet weight, n = 21, mean +/- SD), aldosterone-producing adenomas (4.6 +/- 3.3 pmol/g wet weight, n = 10), cortisol-producing adenomas (2.7 +/- 1.4 pmol/g wet weight, n = 14), adrenocortical carcinomas (1.7 +/- 0.2 pmol/g wet weight, n = 4), and pheochromocytomas (1.8 +/- 0.8 pmol/g wet weight, n = 6).
  • Immunocytochemistry showed positive kisspeptin-immunostaining in normal adrenal glands, with stronger immunostaining found in the medulla.
  • Furthermore, positive kisspeptin-immunostaining was found in all types of adrenal tumors examined; adrenocortical adenomas, adrenocortical carcinomas, and pheochromocytomas.
  • The intensity of kisspeptin-immunostaining in these adrenal tumors was, however, not so strong as that in normal adrenal medulla.
  • The present study has shown for the first time the presence of kisspeptin-LI in adrenal glands and adrenal tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / metabolism. Adrenal Glands / metabolism. Tumor Suppressor Proteins / metabolism

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  • (PMID = 19898965.001).
  • [ISSN] 1559-1166
  • [Journal-full-title] Journal of molecular neuroscience : MN
  • [ISO-abbreviation] J. Mol. Neurosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KISS1 protein, human; 0 / Kisspeptins; 0 / Tumor Suppressor Proteins
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19. Kazarian AM, Marangos IP, Røsok BI, Rosseland AR, Edwin B: [Laparoscopic resection of primary and metastatic malignant tumors of the adrenals]. Vestn Khir Im I I Grek; 2010;169(4):80-5
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  • [Title] [Laparoscopic resection of primary and metastatic malignant tumors of the adrenals].
  • An analysis was made of experience with treatment of 24 patients who underwent laparoscopic adrenalectomy for adrenocortical carcinomas (in 7 patients) and metastases in adrenals (in 17 cases).
  • The method can replace open operative intervention in the majority of patients with metastases to adrenals and primary cancer of the adrenals.
  • [MeSH-major] Adrenal Cortex Neoplasms / secondary. Adrenal Cortex Neoplasms / surgery. Adrenalectomy / methods. Adrenocortical Carcinoma / secondary. Adrenocortical Carcinoma / surgery. Laparoscopy / methods

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  • (PMID = 20973194.001).
  • [ISSN] 0042-4625
  • [Journal-full-title] Vestnik khirurgii imeni I. I. Grekova
  • [ISO-abbreviation] Vestn. Khir. Im. I. I. Grek.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
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20. Heye S, Woestenborghs H, Van Kerkhove F, Oyen R: Adrenocortical carcinoma with fat inclusion: case report. Abdom Imaging; 2005 Sep-Oct;30(5):641-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenocortical carcinoma with fat inclusion: case report.
  • Adrenocortical carcinoma is a rare tumor that arises from the adrenal cortex, with an estimated incidence of 0.5% to 2% per 1 million patients yearly.
  • Although some fat content can be expected in hormonally active adrenocortical carcinomas, areas of 100% fat are extremely rare.
  • We present a case of an adrenocortical carcinoma with a small focus of pure fat depicted on magnetic resonance imaging.
  • [MeSH-major] Adipose Tissue / pathology. Adrenal Cortex Neoplasms / diagnosis. Adrenocortical Carcinoma / diagnosis. Magnetic Resonance Imaging

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  • (PMID = 15688105.001).
  • [ISSN] 0942-8925
  • [Journal-full-title] Abdominal imaging
  • [ISO-abbreviation] Abdom Imaging
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
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21. Masi G, Lavezzo E, Iacobone M, Favia G, Palù G, Barzon L: Investigation of BRAF and CTNNB1 activating mutations in adrenocortical tumors. J Endocrinol Invest; 2009 Jul;32(7):597-600
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Investigation of BRAF and CTNNB1 activating mutations in adrenocortical tumors.
  • BACKGROUND: Activating mutations of the BRAF oncogene play a central role in the development of various cancer types, but their role in human adrenocortical tumors is unknown.
  • At variance, activating mutations of another oncogene, CTNNB1, which encodes beta-catenin, have been shown to be common events in both benign and malignant adrenocortical tumors.
  • AIM: To investigate the prevalence of BRAF and CTNNB1 activating mutations in sporadic adrenocortical tumors.
  • MATERIALS AND METHODS: Tissue samples from 15 adrenocortical carcinomas and 41 adrenocortical adenomas were investigated for the presence of BRAF and CTNNB1 activating mutations by PCR amplification and direct sequencing.
  • RESULTS: An advanced invasive non-functioning adrenocortical carcinoma carried a somatic heterozygous BRAF V600E mutation, while 4 functioning and 4 non-functioning adenomas and 3 functioning carcinomas carried different CTNNB1 activating mutations.
  • CONCLUSIONS: Activating BRAF somatic mutations may be occasionally found in advanced adrenocortical carcinomas, while CTNNB1 activating mutations are early and common events in adrenal tumorigenesis.
  • [MeSH-major] Adrenal Cortex Neoplasms. Cell Transformation, Neoplastic / genetics. Mutation. Proto-Oncogene Proteins B-raf / genetics. beta Catenin / genetics

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  • (PMID = 19498322.001).
  • [ISSN] 1720-8386
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / beta Catenin; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
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22. Lachenmayer A, Lichtenauer UD, Cox T, Schott M, Malendowicz LK, Goretzki PE, Cupisti K, Scherbaum WA, Bornstein SR, Willenberg HS: Nestin as a marker in the classification of adrenocortical tumors. Horm Metab Res; 2009 May;41(5):397-401
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  • [Title] Nestin as a marker in the classification of adrenocortical tumors.
  • Since adrenocortical carcinoma, a tumor entity still very difficult to classify, may gain the ability to aberrantly express neuroectodermal proteins including chromogranin A and synaptophysin, we asked the question whether nestin might also be detected in adrenocortical carcinomas, and if so, whether it might serve as a tool for clinical pathology.
  • Therefore, we studied the expression of nestin in normal adrenal glands, adrenocortical adenomas, and adrenocortical cancers using specific immunohistochemistry and semi-quantitative reverse transcriptase-polymerase chain reaction.
  • Immunostaining was nestin-positive in 1 out of 9 normal adrenal glands (11%), 2 out of 20 adrenocortical adenomas (10%), and 13 out of 16 adrenocortical carcinomas (81%).
  • We conclude that our findings provide further evidence that nestin, as a marker, is not restricted to neuronal stem cells and nestin expression is worth to be studied in adrenocortical tumors.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / classification. Adrenocortical Carcinoma / pathology. Biomarkers, Tumor / metabolism. Intermediate Filament Proteins / metabolism. Nerve Tissue Proteins / metabolism
  • [MeSH-minor] Adrenal Glands / metabolism. Adult. Aged. Aged, 80 and over. Female. Gene Expression. Humans. Male. Middle Aged. Nestin

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  • (PMID = 19294612.001).
  • [ISSN] 1439-4286
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin
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23. Crand A, Borson-Chazot F, Brue T: [Recent data in adrenocortical tumorigenesis]. Ann Endocrinol (Paris); 2009 Sep;70 Suppl 1:S20-5

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  • [Title] [Recent data in adrenocortical tumorigenesis].
  • [Transliterated title] Actualités dans la tumorigenèse surrénalienne.
  • Adrenocortical carcinomas are rare tumors characterized by an aggressive behaviour with a 5-year survival rate below 30%.
  • Until now, surgery is the only curative treatment for tumors confined to the adrenal gland and there is a lack of an effective medical treatment for invasive or metastatic tumors due to the poor knowledge of the mechanisms underlying adrenocortical malignancy.
  • Moreover, histopathology is sometimes insufficient to establish an accurate diagnosis between a benign and a malignant adrenal tumor and a poor indicator of prognosis.
  • In the last decade, the study of rare genetic syndromes associated with adrenocortical carcinomas and the identification of genetic alterations in adrenal tumors has improved our understanding of the pathogenesis of adrenal tumors.
  • The development of molecular predictors of malignancy and of survival could help for histological diagnosis and determination of prognosis.
  • These significant advances are essential to improve adrenocortical carcinoma management.
  • This review summarizes recent advances in the understanding and management of adrenocortical tumors.
  • [MeSH-major] Adrenal Cortex Neoplasms / etiology

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  • (PMID = 19878765.001).
  • [ISSN] 0003-4266
  • [Journal-full-title] Annales d'endocrinologie
  • [ISO-abbreviation] Ann. Endocrinol. (Paris)
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 34
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24. Schmitt A, Saremaslani P, Schmid S, Rousson V, Montani M, Schmid DM, Heitz PU, Komminoth P, Perren A: IGFII and MIB1 immunohistochemistry is helpful for the differentiation of benign from malignant adrenocortical tumours. Histopathology; 2006 Sep;49(3):298-307
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  • [Title] IGFII and MIB1 immunohistochemistry is helpful for the differentiation of benign from malignant adrenocortical tumours.
  • AIMS: The differentiation of adrenocortical carcinomas from adenomas may be difficult based on morphology alone.
  • METHODS AND RESULTS: We examined 22 benign and 17 malignant adrenocortical tumours and compared IGFII and CDK4 expression with known immunohistochemical as well as morphological criteria of malignancy.
  • Thirteen of 17 carcinomas showed immunohistochemical reactivity for IGFII, whereas all adenomas but one were negative.
  • Intense CDK4 expression was detected in 11 of 17 carcinomas but was present in only three of 22 adenomas.
  • The MIB1 index was >5% in 14 of 16 carcinomas and was <5% in all adenomas but one.
  • The combination of IGFII immunohistochemistry with MIB1 index led to high sensitivity and specificity in detecting adrenocortical carcinomas.
  • CONCLUSIONS: IGFII and MIB1 are helpful immunohistochemical markers to predict malignancy in adrenocortical neoplasms.
  • These markers can be used in addition to clinical, gross and morphological features to establish a diagnosis in difficult cases.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenocortical Adenoma / diagnosis. Adrenocortical Carcinoma / diagnosis. Insulin-Like Growth Factor Binding Protein 2 / biosynthesis. Ki-67 Antigen / biosynthesis
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / analysis. Cyclin-Dependent Kinase 4 / biosynthesis. Diagnosis, Differential. Golgi Apparatus / metabolism. Humans. Immunohistochemistry. Middle Aged. Sensitivity and Specificity. Tumor Suppressor Protein p53 / biosynthesis

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  • (PMID = 16918977.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Insulin-Like Growth Factor Binding Protein 2; 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53; EC 2.7.11.22 / Cyclin-Dependent Kinase 4
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25. Tissier F: [Sporadic adrenocortical tumors: genetics and perspectives for the pathologist]. Ann Pathol; 2008 Oct;28(5):409-16
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  • [Title] [Sporadic adrenocortical tumors: genetics and perspectives for the pathologist].
  • [Transliterated title] Tumeurs corticosurrénaliennes sporadiques de l'adulte : aspects génétiques et perspectives pour le pathologiste.
  • Most adrenocortical tumors are benign; adrenocortical carcinomas are rare but their prognosis is poor and few therapeutic options are available.
  • In most adrenocortical tumors, the morphological approach provides enough elements to establish the differential diagnosis between a benign and a malignant tumor but in few cases, it is insufficient.
  • Moreover, morphology is limited for predicting prognosis of adrenocortical carcinomas.
  • The comprehension of the genetic syndromes associated with adrenocortical tumors led to progress in the identification of genetic abnormalities involved in sporadic adrenocortical tumorigenesis.
  • Thus, in sporadic adrenocortical tumorigenesis, IGF-II overexpression and cyclin E overproduction have been associated with 11p15 alterations which are observed in Bethwith-Wiedemann syndrome and TP53 inactivating mutations and 17p13 locus abnormalities which are observed in Li-Fraumeni syndrome.
  • Activation of the Wnt/ss-catenin signaling pathway which is observed in familial adenomatous polyposis has been found in adrenocortical adenomas and carcinomas associated to mutations of CTNNB1, the gene coding ss-catenin, suggesting a central role for this pathway in adrenocortical tumorigenesis.
  • These genetics findings already have had repercussions for patients via the development of molecular markers for diagnosis and prognosis; in the future they should be helpful in the development of new therapeutics.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / pathology

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  • (PMID = 19068395.001).
  • [ISSN] 0242-6498
  • [Journal-full-title] Annales de pathologie
  • [ISO-abbreviation] Ann Pathol
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human; 67763-97-7 / Insulin-Like Growth Factor II; EC 3.1.4.- / Phosphoric Diester Hydrolases; EC 3.1.4.35 / PDE11A protein, human
  • [Number-of-references] 73
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26. Porterfield JR, Thompson GB, Young WF Jr, Chow JT, Fryrear RS, van Heerden JA, Farley DR, Atkinson JL, Meyer FB, Abboud CF, Nippoldt TB, Natt N, Erickson D, Vella A, Carpenter PC, Richards M, Carney JA, Larson D, Schleck C, Churchward M, Grant CS: Surgery for Cushing's syndrome: an historical review and recent ten-year experience. World J Surg; 2008 May;32(5):659-77
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  • BACKGROUND: Cushing's syndrome (CS), due to multiple etiologies, is a disorder associated with the ravages of cortisol excess.
  • The purpose of this review article is to provide a historical synopsis of surgery for CS, review a recent 10-year period of operative management at a tertiary care facility, and to outline a practical approach to diagnosis and management.
  • Fifty-four patients (18%) had cortisol-secreting adenomas, 10 patients (3%) had cortisol-producing adrenocortical carcinomas, and 1% had other causes.
  • Most benign adrenal processes could be managed laparoscopically.
  • Five-year survival rates (all causes) were 90%, 51%, and 23% for adrenocortical adenomas, ectopic ACTH syndrome, and adrenocortical carcinomas, respectively.
  • CONCLUSIONS: Surgery for CS is highly successful for pituitary-dependent CS and most ACTH-independent adrenal causes.
  • Unfortunately, to date, adrenocortical carcinomas are rarely cured.
  • Future successes with this disease will likely depend on a better understanding of tumor biology, more effective adjuvant therapies and earlier detection.

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  • (PMID = 18196319.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 139
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27. Ribeiro RC, Pinto EM, Zambetti GP: Familial predisposition to adrenocortical tumors: clinical and biological features and management strategies. Best Pract Res Clin Endocrinol Metab; 2010 Jun;24(3):477-90
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  • [Title] Familial predisposition to adrenocortical tumors: clinical and biological features and management strategies.
  • The incidence of adrenocortical tumors (ACTs) is increased in several familial cancer syndromes resulting from abnormalities in genes that encode transcription factors implicated in cell proliferation, differentiation, senescence, apoptosis, and genomic instability.
  • Adenomas are the most common ACTs, but adrenocortical carcinomas occur rarely as well.
  • The clinical manifestations of ACTs, which result from increased secretion of adrenocortical hormones, are similar in the familial and sporadic forms of the disease.
  • The analysis of gene expression profiles of ACTs in these constitutional syndromes have contributed to our understanding of adrenal tumorigenesis and revealed new molecular diagnostic and prognostic markers and candidate genes for targeted therapies.
  • This chapter summarizes the clinical and biological features, pathogenesis, and management strategies for ACTs that develop in patients with familial cancer syndrome.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Li-Fraumeni Syndrome / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Genes, p53. Genetic Predisposition to Disease. Humans. Male

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  • [Copyright] Copyright 2010. Published by Elsevier Ltd.
  • (PMID = 20833338.001).
  • [ISSN] 1878-1594
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
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28. Haase M, Willenberg HS: Adrenal cortical tumors and multiple endocrine neoplasia-related syndromes. Minerva Endocrinol; 2009 Jun;34(2):123-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenal cortical tumors and multiple endocrine neoplasia-related syndromes.
  • Relatively frequent, adrenal masses include a multitude of different tumor types: uni- or bilateral hyperplasias, adenomas, and the rare entity of adrenocortical carcinomas.
  • With significant progress in our appreciation of their underlying molecular pathomechanisms and from analysis of affected individuals and their families, a number of inherited diseases and tumor syndromes have been linked to adrenocortical tumorigenesis.
  • These syndromes and diseases include the Carney complex, the McCune-Albright syndrome, multiple endocrine neoplasia type 1, familial adenomatosis coli, congenital adrenal hyperplasia, familial forms of primary aldosteronism, the Beckwith-Wiedemann syndrome, and the Li-Fraumeni syndrome.
  • The key to successful management of these syndromes is identification of patients harboring adrenal tumors within the context of hereditary diseases, since diagnostic procedures, therapy and follow-up may significantly differ from the management of sporadic, isolated adrenal tumors.
  • This review explores the underlying genetic defects, diagnosis and therapy of the major heritable tumor syndromes associated with adrenocortical tumorigenesis.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Multiple Endocrine Neoplasia / genetics. Mutation
  • [MeSH-minor] Adenomatous Polyposis Coli / genetics. Adrenal Hyperplasia, Congenital / genetics. Beckwith-Wiedemann Syndrome / genetics. Fibrous Dysplasia, Polyostotic / genetics. Heart Neoplasms / genetics. Humans. Hyperaldosteronism / genetics. Li-Fraumeni Syndrome / genetics. Multiple Endocrine Neoplasia Type 1 / genetics. Myxoma / genetics. Pigmentation Disorders / genetics

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  • (PMID = 19471237.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Number-of-references] 100
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29. Gross MD, Korobkin M, Bou Assaly W, Dwamena B, Djekidel M: Contemporary imaging of incidentally discovered adrenal masses. Nat Rev Urol; 2009 Jul;6(7):363-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Contemporary imaging of incidentally discovered adrenal masses.
  • The incidental discovery of adrenal masses during modern diagnostic imaging is a common occurrence.
  • These masses form part of a long differential diagnostic list; most often, they are benign adrenal adenomas, but their discovery requires a clinical evaluation that is sufficiently broad to exclude clinically silent endocrine disease, metastases to the adrenal gland in patients with suspected or known malignancies, and rare adrenocortical carcinomas.
  • CT, MRI and nuclear medicine approaches have all been used to evaluate incidentally discovered adrenal masses.
  • Understanding of the modalities used to assess an unanticipated adrenal mass allows for more rapid diagnosis and cost avoidance in a condition that has been referred to as a 'disease' of modern imaging technology.
  • [MeSH-major] Adrenal Gland Diseases / diagnosis. Diagnostic Imaging. Incidental Findings
  • [MeSH-minor] Adrenal Gland Neoplasms / diagnosis. Adrenal Gland Neoplasms / etiology. Humans

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  • (PMID = 19506582.001).
  • [ISSN] 1759-4820
  • [Journal-full-title] Nature reviews. Urology
  • [ISO-abbreviation] Nat Rev Urol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 93
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30. 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.
  • 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

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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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31. Müssig K, Wehrmann M, Horger M, Maser-Gluth C, Häring HU, Overkamp D: Adrenocortical carcinoma producing 11-deoxycorticosterone: a rare cause of mineralocorticoid hypertension. J Endocrinol Invest; 2005 Jan;28(1):61-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenocortical carcinoma producing 11-deoxycorticosterone: a rare cause of mineralocorticoid hypertension.
  • Computed tomography (CT) scans showed a large right adrenal mass without signs of metastatic disease.
  • The tumor was removed by open laparotomy, and histology revealed an adrenocortical carcinoma.
  • Two yr after diagnosis, the patient is in good general condition and there is no sign of recurrence or metastatic disease, despite the large tumor size.
  • DOC producing adrenocortical carcinomas causing mineralocorticoid hypertension are very rare, so far only 10 cases have been described in the literature.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Desoxycorticosterone / biosynthesis. Hypertension / etiology. Hypertension / physiopathology. Mineralocorticoids / physiology. Pheochromocytoma / metabolism
  • [MeSH-minor] Adrenal Cortex Hormones / blood. Adrenal Cortex Hormones / urine. Adrenalectomy. Adult. Aldosterone / blood. Aldosterone / urine. Catecholamines / urine. Humans. Hypokalemia / etiology. Hypokalemia / physiopathology. Male. Renin / blood. Tomography, X-Ray Computed

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  • (PMID = 15816373.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Catecholamines; 0 / Mineralocorticoids; 40GP35YQ49 / Desoxycorticosterone; 4964P6T9RB / Aldosterone; EC 3.4.23.15 / Renin
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32. Ginat DT, Saad WE, Turba UC: Transcatheter renal artery embolization for management of renal and adrenal tumors. Tech Vasc Interv Radiol; 2010 Jun;13(2):75-88
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transcatheter renal artery embolization for management of renal and adrenal tumors.
  • Transcatheter arterial embolization is a minimally invasive procedure that is increasingly used for the management of angiomyolipomas and to augment and/or palliate the management of malignant renal and adrenal neoplasms.
  • The most common indications for renal artery embolization include (1) prenephrectomy and preradiofrequency ablation infarction of renal tumors, (2) management of renal angiomyolipomas, (3) palliations of unresectable renal malignancy, and (4) malignant renal hemorrhage (life-threatening or chronic debilitating hematuria).
  • The increasing use of renal artery embolization for these conditions reflects the procedure's effectiveness and safety.
  • Although there is less extensive literature available regarding the use of transcatheter embolization of adrenal tumors, this technique appears to be effective and safe for palliation and preadrenalectomy of adrenal metastatic disease, adrenocortical carcinomas, as well as treatment of symptomatic aldosteronomas.
  • This article reviews the indications and techniques involved in performing transcatheter arterial embolization for renal and adrenal tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / therapy. Catheterization. Embolization, Therapeutic. Kidney Neoplasms / therapy. Renal Artery

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20540917.001).
  • [ISSN] 1557-9808
  • [Journal-full-title] Techniques in vascular and interventional radiology
  • [ISO-abbreviation] Tech Vasc Interv Radiol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 31
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33. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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34. Aubert S, Buob D, Leroy X, Devos P, Carnaille B, Do Cao C, Wemeau JL, Leteurtre E: [Weiss system: a still in-use diagnostic tool for the assessment of adrenocortical malignancy]. Ann Pathol; 2005 Dec;25(6):545-54

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Weiss system: a still in-use diagnostic tool for the assessment of adrenocortical malignancy].
  • [Transliterated title] Le système de Weiss: un outil toujours d'actualité pour le diagnostic de malignité des tumeurs de la corticosurrenale.
  • Adrenocortical carcinomas are rare tumors.
  • In the absence of the gold standard that constitutes metastases, local invasion or recurrence, the diagnosis of malignancy may represent a great challenge for both clinicians and pathologists.
  • A more precise definition of the different microscopic criteria and the proposition of a modified Weiss system based on the most reliable criteria could help.
  • Besides, the Weiss system is of limited value for the diagnosis of malignancy in oxyphil tumors and children tumors of the adrenal cortex.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology

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  • (PMID = 16735978.001).
  • [ISSN] 0242-6498
  • [Journal-full-title] Annales de pathologie
  • [ISO-abbreviation] Ann Pathol
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 55
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35. Orlando R, Lirussi F: Development of mantle cell lymphoma in a patient with adrenocortical carcinoma and an 18-year survival after complete removal of the primary cancer and resection of local recurrences. Anticancer Res; 2006 Mar-Apr;26(2B):1563-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development of mantle cell lymphoma in a patient with adrenocortical carcinoma and an 18-year survival after complete removal of the primary cancer and resection of local recurrences.
  • The case of a patient with a non-functional and poorly-differentiated adrenocortical carcinoma, who had an unexpected long-term survival after a right adrenalectomy and subsequent removal of 2 local recurrences, is reported.
  • However, fifteen years after the complete resection of the primary neoplasm, the patient first developed an autoimmune thrombocytopenic purpura and later a mantle cell lymphoma located in the mediastinal lymph nodes.
  • This case confirms the possible growth of a second tumour in patients with adrenocortical carcinomas, especially if presenting a long survival after resection of the primary malignancy, and emphasises the need for the close follow-up of these patients.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenocortical Carcinoma / surgery. Lymphoma, Mantle-Cell / diagnosis. Neoplasm Recurrence, Local / surgery. Neoplasms, Second Primary / diagnosis

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  • (PMID = 16619572.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
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36. Mackie GC, Shulkin BL, Ribeiro RC, Worden FP, Gauger PG, Mody RJ, Connolly LP, Kunter G, Rodriguez-Galindo C, Wallis JW, Hurwitz CA, Schteingart DE: Use of [18F]fluorodeoxyglucose positron emission tomography in evaluating locally recurrent and metastatic adrenocortical carcinoma. J Clin Endocrinol Metab; 2006 Jul;91(7):2665-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Use of [18F]fluorodeoxyglucose positron emission tomography in evaluating locally recurrent and metastatic adrenocortical carcinoma.
  • CONTEXT: Adrenocortical carcinomas are uncommon, and their evaluation by [(18)F]fluorodeoxyglucose positron emission tomography (FDG PET) has not been well evaluated.
  • OBJECTIVE: The purpose of this study was to examine the potential utility of FDG PET in the detection of recurrent or metastatic adrenocortical carcinoma.
  • DESIGN: In patients with known adrenocortical carcinoma who underwent FDG-PET imaging for suspected recurrence or metastasis, FDG activity was compared with other imaging findings, clinical features, and the presence or absence of disease as confirmed by resection, biopsy, or clinical follow-up.
  • One patient with no abnormal FDG activity had a morphological abnormality subsequently proven to be a postoperative scar.
  • CONCLUSIONS: Most adrenocortical carcinomas accumulate and retain FDG and thus can be visualized by PET.
  • [MeSH-major] Adrenal Cortex Neoplasms / radionuclide imaging. Fluorodeoxyglucose F18. Neoplasm Metastasis / radionuclide imaging. Neoplasm Recurrence, Local / radionuclide imaging. Positron-Emission Tomography

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  • (PMID = 16621901.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5R25 CA23944; United States / NCI NIH HHS / CA / CA 21765; United States / NCI NIH HHS / CA / CA 54216; United States / NCRR NIH HHS / RR / M01-RR00042
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0Z5B2CJX4D / Fluorodeoxyglucose F18
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37. Costa MH, Latronico AC, Martin RM, Barbosa AS, Almeida MQ, Lotfi CF, Valassi HP, Nishi MY, Lucon AM, Siqueira SA, Zerbini MC, Carvalho LR, Mendonca BB, Fragoso MC: Expression profiles of the glucose-dependent insulinotropic peptide receptor and LHCGR in sporadic adrenocortical tumors. J Endocrinol; 2009 Feb;200(2):167-75

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression profiles of the glucose-dependent insulinotropic peptide receptor and LHCGR in sporadic adrenocortical tumors.
  • Aberrant expression of these receptors has rarely been demonstrated in adult sporadic adrenocortical tumors with a lack of data on pediatric tumors.
  • We quantified the GIPR and LHCGR expression in a large cohort of 55 patients (25 children and 30 adults) with functioning and non-functioning sporadic adrenocortical tumors.
  • Thirty-eight tumors were classified as adenomas whereas 17 were carcinomas.
  • Mean expression values were determined by fold increase in comparison with a normal adrenal pool.
  • GIPR mRNA levels were significantly higher in adrenocortical carcinomas than in adenomas from both pediatric and adult groups.
  • LHCGR expression was similar in both carcinomas and adenomas from the pediatric group but significantly lower in carcinomas than in adenomas from the adult group (median 0.06 and 2.3 respectively, P<0.001).
  • Staining and real-time PCR results correlated positively only when GIPR mRNA levels were increased at least two-fold in comparison with normal adrenal expression levels.
  • In conclusion, GIPR overexpression was observed in pediatric and adult adrenocortical tumors and very low levels of LHCGR expression were found in all adult adrenocortical carcinomas.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics. Adrenocortical Carcinoma / genetics. Gene Expression Regulation, Neoplastic / genetics. Receptors, Gastrointestinal Hormone / genetics

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  • (PMID = 18971217.001).
  • [ISSN] 1479-6805
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Gastrointestinal Hormone; 0 / Receptors, LH; 0 / gastric inhibitory polypeptide receptor
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38. Kiiveri S, Liu J, Arola J, Heikkilä P, Kuulasmaa T, Lehtonen E, Voutilainen R, Heikinheimo M: Transcription factors GATA-6, SF-1, and cell proliferation in human adrenocortical tumors. Mol Cell Endocrinol; 2005 Apr 15;233(1-2):47-56
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  • [Title] Transcription factors GATA-6, SF-1, and cell proliferation in human adrenocortical tumors.
  • Transcription factor GATA-6 is expressed in fetal and adult human adrenal cortex and has been suggested to have a role in adrenal androgen synthesis.
  • In other tissues GATA-6 has been linked to the cell cycle regulation and the dedifferentiation of carcinoma cells.
  • GATA-6 has been shown to be downregulated in mouse adrenocortical tumors, but has not been studied in human adrenocortical tumors in detail.
  • We have now analyzed GATA-6 expression in 20 human adrenocortical adenomas and 16 carcinomas using Northern blot analysis and immunohistochemistry.
  • GATA-6 mRNA and protein expression was remarkably diminished in adrenocortical carcinomas as compared to normal adrenal cortex and adenomas (p<0.05).
  • In opposite to other tumor types GATA-6 expression was, however, high in virilizing carcinomas.
  • Steroidogenic factor 1 (SF-1) has been functionally linked to GATA-6, and the expression of these two factors correlated in the adrenal tumors.
  • In contrast to GATA-6, we found upregulated cyclin-dependent kinase inhibitor p21 and proliferation marker Ki67 in adrenocortical carcinomas indicating that GATA-6 is not linked to cell proliferation in human adrenal tumors.
  • Taken together, the present and earlier results link GATA-6 to adrenocortical steroidogenesis and to the benign adrenocortical phenotype.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenocortical Adenoma / metabolism. Adrenocortical Carcinoma / metabolism. DNA-Binding Proteins / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Adrenal Glands / chemistry. Adrenal Glands / cytology. Adult. Aged. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Cell Cycle Proteins / genetics. Cell Cycle Proteins / metabolism. Cell Proliferation. Child. Child, Preschool. Cyclin-Dependent Kinase Inhibitor p21. Female. GATA6 Transcription Factor. Homeodomain Proteins. Humans. Infant. Ki-67 Antigen / genetics. Ki-67 Antigen / metabolism. Male. Middle Aged. RNA, Messenger / analysis. RNA, Messenger / metabolism. Receptors, Cytoplasmic and Nuclear. Steroidogenic Factor 1. Up-Regulation

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  • (PMID = 15767045.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDKN1A protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / DNA-Binding Proteins; 0 / GATA6 Transcription Factor; 0 / GATA6 protein, human; 0 / Homeodomain Proteins; 0 / Ki-67 Antigen; 0 / NR5A1 protein, human; 0 / RNA, Messenger; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Steroidogenic Factor 1; 0 / Transcription Factors; 0 / steroidogenic factor 1, mouse
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39. Remer EM, Motta-Ramirez GA, Shepardson LB, Hamrahian AH, Herts BR: CT histogram analysis in pathologically proven adrenal masses. AJR Am J Roentgenol; 2006 Jul;187(1):191-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CT histogram analysis in pathologically proven adrenal masses.
  • OBJECTIVE: The purpose of this article is to evaluate a histogram analysis method for distinguishing adrenal adenomas from metastases, pheochromocytomas, and adrenocortical carcinomas on CT.
  • CT images were available for retrospective review in 187 patients (93 males, 94 females; age range, 15-84 years; mean age, 55.2 years) with 208 adrenal masses.
  • This included 112 adenomas in 104 patients, 48 metastases in 39 patients, 40 pheochromocytomas in 36 patients, and eight adrenocortical carcinomas in eight patients.
  • Negative pixels were present in unenhanced and enhanced metastases, pheochromocytomas, and carcinomas.
  • CONCLUSION: Although specificity for the diagnosis of adenomas on enhanced CT scans with histogram analysis was high when a 10% negative pixel threshold was used, low sensitivity likely limits clinical usefulness.
  • [MeSH-major] Adrenal Gland Neoplasms / radiography. Tomography, X-Ray Computed
  • [MeSH-minor] Adenoma / radiography. Adolescent. Adrenocortical Carcinoma / radiography. Adult. Aged. Aged, 80 and over. Contrast Media. Female. Humans. Image Processing, Computer-Assisted. Male. Middle Aged. Pheochromocytoma / radiography. Sensitivity and Specificity

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  • (PMID = 16794176.001).
  • [ISSN] 1546-3141
  • [Journal-full-title] AJR. American journal of roentgenology
  • [ISO-abbreviation] AJR Am J Roentgenol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
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40. Liao CH, Chueh SC, Lai MK, Hsiao PJ, Chen J: Laparoscopic adrenalectomy for potentially malignant adrenal tumors greater than 5 centimeters. J Clin Endocrinol Metab; 2006 Aug;91(8):3080-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Laparoscopic adrenalectomy for potentially malignant adrenal tumors greater than 5 centimeters.
  • PURPOSE: Laparoscopic adrenalectomy (LA) is controversial for large, potentially malignant tumors.
  • We report a series of LA or hand-assisted LA for large (>5 cm) adrenal tumors.
  • PATIENTS AND METHODS: Among 210 LAs performed in 6 yr, 39 patients had potentially malignant tumors greater than 5 cm in diameter.
  • Final pathology revealed eight malignant (four adrenocortical carcinomas and four metastatic carcinomas) and 31 benign tumors (14 cortical adenomas, eight pheochromocytomas, six myelolipomas, and three ganglioneuromas).
  • Four patients (two adrenocortical carcinomas, one metastatic hepatoma, and one lymphoma) died 24, 10, 9, and 3 months after surgery, respectively.
  • CONCLUSIONS: LA is a reasonable option for selected large adrenal tumors when complete resection is technically feasible and there is no evidence of local invasion.
  • Hand-assisted LA is a good alternative to open conversion if a difficult dissection is encountered intraoperatively.
  • [MeSH-major] Adrenal Gland Neoplasms / pathology. Adrenal Gland Neoplasms / surgery. Adrenalectomy / methods. Laparoscopy

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  • [CommentIn] Nat Clin Pract Endocrinol Metab. 2007 Mar;3(3):210-1 [17262068.001]
  • (PMID = 16720665.001).
  • [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
  • [Publication-country] United States
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41. 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.
  • 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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42. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

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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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43. Tissier F: Classification of adrenal cortical tumors: what limits for the pathological approach? Best Pract Res Clin Endocrinol Metab; 2010 Dec;24(6):877-85

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Classification of adrenal cortical tumors: what limits for the pathological approach?
  • Most adrenocortical tumors are benign; adrenocortical carcinomas are rare but their prognosis is poor and their therapeutics are sparse.
  • In most adrenocortical tumors, the morphological approach in particular by Weiss system, brings sufficient elements to establish the differential diagnosis between a benign and a malignant tumor.
  • But some tumors of Weiss score of 2 or 3 can raise problems: are they benign, malignant or are they of uncertain malignant potential?
  • These genetics findings already have repercussions for the patients in the development of molecular markers for diagnosis and prognosis and in the future they could help in the development of new morphological approaches, in particular immunohistochemical approaches.
  • [MeSH-major] Adrenal Cortex Neoplasms / classification. Adrenal Cortex Neoplasms / pathology
  • [MeSH-minor] Adrenal Cortex / metabolism. Adrenal Cortex / pathology. Animals. Biomarkers, Tumor / metabolism. Diagnosis, Differential. Humans. Neoplasm Staging. Prognosis

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  • [Copyright] 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 21115156.001).
  • [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
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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44. Dehner LP, Hill DA: Adrenal cortical neoplasms in children: why so many carcinomas and yet so many survivors? Pediatr Dev Pathol; 2009 Jul-Aug;12(4):284-91

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenal cortical neoplasms in children: why so many carcinomas and yet so many survivors?
  • Adrenal cortical neoplasms in children are represented by a disproportionate number of cases that have been diagnosed pathologically as adrenocortical carcinomas (ACCs)-as many as 90% of all cortical tumors in some pediatric series.
  • A risk assessment system is proposed that incorporates tumor weight, localization of tumor to the gland without invasion into the surrounding tissues or organs, and absence of metastasis.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology

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  • (PMID = 19326954.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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45. Stratakis CA, Boikos SA: Genetics of adrenal tumors associated with Cushing's syndrome: a new classification for bilateral adrenocortical hyperplasias. Nat Clin Pract Endocrinol Metab; 2007 Nov;3(11):748-57
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetics of adrenal tumors associated with Cushing's syndrome: a new classification for bilateral adrenocortical hyperplasias.
  • Adrenocortical causes of Cushing's syndrome include the following: common cortisol-producing adenomas, which are usually isolated (without associated tumors) and sporadic (without a family history); rare, but often clinically devastating, adrenocortical carcinomas; and a spectrum of adrenocorticotropin-independent, and almost always bilateral, hyperplasias, which are not rare, and are the most recently recognized cause.
  • The majority of benign lesions of the adrenal cortex seem to be linked to abnormalities of the cyclic AMP signaling pathway, whereas cancer is linked to aberrant expression of insulin-like growth factor II, tumor protein p53 and related molecules.
  • In this article, we propose a new clinical classification and nomenclature for the various forms of adrenocorticotropin-independent adrenocortical hyperplasias that is based on their histologic and genetic features.
  • We also review the molecular genetics of adrenocortical tumors, including recent discoveries relating to the role of phosphodiesterase 11A.
  • [MeSH-major] Adrenal Gland Neoplasms / classification. Adrenal Gland Neoplasms / genetics. Cushing Syndrome / classification. Cushing Syndrome / genetics
  • [MeSH-minor] Adrenal Cortex Diseases / classification. Adrenal Cortex Diseases / complications. Adrenal Cortex Diseases / genetics. Adrenal Cortex Diseases / pathology. Adrenal Cortex Neoplasms / classification. Adrenal Cortex Neoplasms / complications. Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / pathology. Animals. Humans. Hyperplasia / classification. Hyperplasia / genetics. Hyperplasia / pathology

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  • (PMID = 17955016.001).
  • [ISSN] 1745-8374
  • [Journal-full-title] Nature clinical practice. Endocrinology & metabolism
  • [ISO-abbreviation] Nat Clin Pract Endocrinol Metab
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] England
  • [Number-of-references] 68
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46. Hantel C, Beuschlein F: Mouse models of adrenal tumorigenesis. Best Pract Res Clin Endocrinol Metab; 2010 Dec;24(6):865-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mouse models of adrenal tumorigenesis.
  • Adrenocortical carcinomas (ACCs) are heterogeneous tumors with a poor prognosis.
  • The rarity of this disorder causes a lack of treatment experience and material availability which is necessary to optimize existing treatments and to develop novel therapeutic strategies.
  • In recent years molecular characterization of surgical tumor specimen has aided in the understanding of disease mechanisms and definition of therapeutic targets also in adrenocortical carcinoma.
  • Here we give an overview on rodent models that have been described to either have adrenocortical tumors as part of their phenotype or have been utilized for therapeutic screens as adrenocortical tumor models.
  • [MeSH-major] Adrenal Cortex Neoplasms / therapy. Adrenal Gland Neoplasms / physiopathology. Adrenal Gland Neoplasms / therapy. Disease Models, Animal

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  • [Copyright] 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 21115155.001).
  • [ISSN] 1878-1594
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
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47. Karim RZ, Wills EJ, McCarthy SW, Scolyer RA: Myxoid variant of adrenocortical carcinoma: report of a unique case. Pathol Int; 2006 Feb;56(2):89-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myxoid variant of adrenocortical carcinoma: report of a unique case.
  • Myxoid variant of adrenocortical carcinomas (ACC) are rare, there being only 11 cases in the literature to date.
  • Reported herein are the findings of a case, which in contrast to all previously reported myxoid ACC, was devoid of typical non-myxoid areas.
  • The patient was a 61-year-old man in whom a left adrenal mass was detected during investigation of Cushing's syndrome.
  • The adrenal was replaced by malignant cells and expanses of myxoid material.
  • The ultrastructural features of the cells were typical of adrenal cortical differentiation.
  • The differential diagnosis of myxoid ACC includes extraskeletal myxoid chondrosarcoma, chordoma, myxoid adenocarcinoma, myxoma, lipomatous tumors, nerve sheath tumors, smooth muscle tumors, gastrointestinal stromal tumor and other sarcomas.
  • The presence of myxoid material in a retroperitoneal lesion raises a broad differential diagnosis in which myxoid adrenocortical neoplasms should be included.
  • Clinicoradiological correlation may be helpful, but special stains, immunohistochemistry and ultrastructural examination may be necessary to establish the diagnosis.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenocortical Carcinoma / diagnosis
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Antigens, Neoplasm. Chordoma / diagnosis. Chordoma / pathology. Diagnosis, Differential. Humans. Immunohistochemistry. MART-1 Antigen. Male. Microscopy, Electron. Middle Aged. Myxoma / diagnosis. Myxoma / pathology. Neoplasm Proteins / analysis. Nerve Sheath Neoplasms / diagnosis. Nerve Sheath Neoplasms / pathology. Retroperitoneal Neoplasms / diagnosis. Retroperitoneal Neoplasms / pathology. Synaptophysin / analysis. Vimentin / analysis

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  • (PMID = 16445821.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / MART-1 Antigen; 0 / MLANA protein, human; 0 / Neoplasm Proteins; 0 / Synaptophysin; 0 / Vimentin
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48. Papotti M, Volante M, Duregon E, Delsedime L, Terzolo M, Berruti A, Rosai J: Adrenocortical tumors with myxoid features: a distinct morphologic and phenotypical variant exhibiting malignant behavior. Am J Surg Pathol; 2010 Jul;34(7):973-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenocortical tumors with myxoid features: a distinct morphologic and phenotypical variant exhibiting malignant behavior.
  • Myxoid changes have been rarely reported both in adrenocortical adenomas and carcinomas.
  • The recent observation by our group of an adrenal myxoid tumor with morphologically borderline features, but aggressive clinical behavior prompted us to review a series of 196 adrenocortical lesions, comprising 122 carcinomas and 74 adenomas, to define the morphologic, phenotypical and clinical characteristics of adrenocortical tumors with myxoid features.
  • Fourteen cases, including 12 carcinomas and 2 borderline tumors, formed the basis of this report, and were characterized by a variably abundant myxoid component (from 5% to 90% of tumor) and 2 distinct cellular growth patterns: the first (10 cases), mostly associated with a predominant myxoid stromal component, was made of small cells with mild atypia arranged in cords and microcysts; the second (4 cases) was characterized by focal myxoid changes in tumors otherwise similar to conventional adrenocortical carcinoma, with large atypical cells having an eosinophilic cytoplasm and a diffuse or nodular architecture.
  • A peculiar reactivity to neurofilaments was seen, mostly associated to the presence of predominant rather that focal myxoid stromal changes, and in 40% of conventional adrenocortical carcinomas, thus representing an undescribed potential pitfall in the differential diagnosis of adrenal lesions.
  • Myxoid adrenocortical tumors probably represent a rare but histologically and phenotipically distinct entity and, although rare cases of benign lesions are on record, they seem to be generally associated to morphologic and clinical features of malignancy.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / pathology. Adrenocortical Carcinoma / secondary. Mucins / metabolism
  • [MeSH-minor] Adrenal Glands / embryology. Adrenal Glands / metabolism. Adult. Aged. Biomarkers, Tumor / metabolism. Fatal Outcome. Female. Fetal Development. Humans. Male. Middle Aged

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  • (PMID = 20534995.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Mucins
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49. Aiba M, Fujibayashi M: Histopathological diagnosis and prognostic factors in adrenocortical carcinoma. Endocr Pathol; 2005;16(1):13-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Histopathological diagnosis and prognostic factors in adrenocortical carcinoma.
  • A great majority of adrenocortical tumors are benign, and many adrenocortical carcinomas (ACC) are obviously malignant at presentation.
  • The histopathological diagnosis of ACC is occasionally difficult, particularly with stage I and stage II disease.
  • Histopathological prognostic factors of ACC have not been fully established because of the rarity of the disease.
  • These special type tumors include pediatric adrenocortical tumors, oncocytomas, and aldosterone-producing tumors of pure zona glomerulosa type.
  • Then we present three cases with unusual small adrenocortical tumors.
  • One patient had an unequivocal ACC showing metastatic disease.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenocortical Carcinoma / diagnosis
  • [MeSH-minor] Adenoma, Oxyphilic. Adult. Aged. Aged, 80 and over. Aldosterone / metabolism. Biomarkers, Tumor / metabolism. Cell Nucleus / pathology. Female. Humans. Immunohistochemistry. Infant. Insulin-Like Growth Factor II / metabolism. Male. Neoplasm Staging. Prognosis

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  • (PMID = 16000842.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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50. Russell-Swetek A, West AN, Mintern JE, Jenkins J, Rodriguez-Galindo C, Ribeiro R, Zambetti GP: Identification of a novel TP53 germline mutation E285V in a rare case of paediatric adrenocortical carcinoma and choroid plexus carcinoma. J Med Genet; 2008 Sep;45(9):603-6
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  • [Title] Identification of a novel TP53 germline mutation E285V in a rare case of paediatric adrenocortical carcinoma and choroid plexus carcinoma.
  • Paediatric choroid plexus carcinomas (CPC) and adrenocortical carcinomas (ACC) are exceedingly rare tumours, each occurring at an annual rate of 0.3 cases per million children or less.
  • We report here a young boy without a family history of cancer who presented with CPC and subsequently ACC.
  • Genetic testing revealed a novel de novo germline TP53 mutation (E285V).

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  • (PMID = 18762572.001).
  • [ISSN] 1468-6244
  • [Journal-full-title] Journal of medical genetics
  • [ISO-abbreviation] J. Med. Genet.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA63230; United States / NCI NIH HHS / CA / R25 CA023944; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / CA23944; United States / NCI NIH HHS / CA / R01 CA063230
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ NIHMS404658; NLM/ PMC3487594
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51. de Fraipont F, El Atifi M, Cherradi N, Le Moigne G, Defaye G, Houlgatte R, Bertherat J, Bertagna X, Plouin PF, Baudin E, Berger F, Gicquel C, Chabre O, Feige JJ: Gene expression profiling of human adrenocortical tumors using complementary deoxyribonucleic Acid microarrays identifies several candidate genes as markers of malignancy. J Clin Endocrinol Metab; 2005 Mar;90(3):1819-29

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression profiling of human adrenocortical tumors using complementary deoxyribonucleic Acid microarrays identifies several candidate genes as markers of malignancy.
  • The aim of this study was to identify predictor sets of genes whose over- or underexpression in human sporadic adrenocortical tumors would help to identify malignant vs. benign tumors and to predict postsurgical metastatic recurrence.
  • For this, we analyzed the expression of 230 candidate genes using cDNA microarrays in a series of 57 well-characterized human sporadic adrenocortical tumors (33 adenomas and 24 carcinomas).
  • The analysis of the population of carcinomas (13 tumors) for genes whose expression would be strongly different between recurring and nonrecurring tumors allowed identification of 14 genes meeting these criteria.
  • Taken together, these results show that the parallel analysis of the expression levels of a selected group of genes on microgram quantities of tumor RNA (a quantity that can be obtained from fine needle aspirations) appears as a complementary method to histopathology for the diagnosis and prognosis of evolution of adrenocortical carcinomas.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Gene Expression Profiling. Oligonucleotide Array Sequence Analysis
  • [MeSH-minor] Adolescent. Adult. Aged. Biomarkers, Tumor / genetics. Disease-Free Survival. Female. Gene Expression Regulation, Neoplastic. Genetic Markers. Humans. Male. Middle Aged. RNA, Messenger / analysis. Steroids / metabolism

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  • [CommentIn] J Clin Endocrinol Metab. 2005 Mar;90(3):1900-2 [15758065.001]
  • (PMID = 15613424.001).
  • [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 / Biomarkers, Tumor; 0 / Genetic Markers; 0 / RNA, Messenger; 0 / Steroids
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52. Velázquez-Fernández D, Laurell C, Geli J, Höög A, Odeberg J, Kjellman M, Lundeberg J, Hamberger B, Nilsson P, Bäckdahl M: Expression profiling of adrenocortical neoplasms suggests a molecular signature of malignancy. Surgery; 2005 Dec;138(6):1087-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression profiling of adrenocortical neoplasms suggests a molecular signature of malignancy.
  • BACKGROUND: Distinguishing between adrenocortical adenomas and carcinomas is often difficult.
  • Our aim was to investigate the differences in transcriptional profiles between benign and malignant adrenocortical neoplasms using complementary DNA microarray techniques.
  • METHODS: We studied 7 patients with adrenocortical carcinomas and 13 with adenomas.
  • RESULTS: Transcriptional profiles were homogeneous among adenomas, while carcinomas were much more heterogeneous.
  • Hierarchical clustering and self-organizing maps could separate clearly carcinomas from adenomas.
  • Among genes that were most significantly upregulated in carcinomas were 2 ubiquitin-related genes (USP4 and UFD1L) and several insulinlike growth factor-related genes (IGF2, IGF2R, IGFBP3 and IGFBP6).
  • Among genes that were most significantly downregulated in carcinomas were a cytokine gene (CXCL10), several genes related to cell metabolism (RARRES2, ALDH1A1, CYBRD1 and GSTA4), and the cadherin 2 gene (CDH2).
  • CONCLUSIONS: Through the use of cDNA arrays, adrenocortical adenomas and carcinomas appear to be clearly distinguishable on the basis of their specific molecular signature.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics. Adrenocortical Carcinoma / genetics

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  • (PMID = 16360395.001).
  • [ISSN] 0039-6060
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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53. Willatt JM, Francis IR: Radiologic evaluation of incidentally discovered adrenal masses. Am Fam Physician; 2010 Jun 1;81(11):1361-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Radiologic evaluation of incidentally discovered adrenal masses.
  • The increasing use of cross-sectional imaging has led to an increase in the incidental discovery of adrenal masses (adrenal incidentalomas).
  • Before creating a management plan, the physician should determine if the lesion is benign or malignant and if the lesion is functioning or nonfunctioning.
  • Incidentally discovered adrenal masses usually are benign adenomas; however, myelolipomas, cysts, hemorrhage, pheochromocytomas, metastases, and adrenocortical carcinomas are also possible.
  • This article summarizes the American College of Radiology Appropriateness Criteria for the use of imaging modalities and biopsy to characterize incidentally discovered adrenal masses.
  • [MeSH-major] Adrenal Gland Diseases / radiography. Incidental Findings
  • [MeSH-minor] Adrenal Gland Neoplasms / pathology. Adrenal Gland Neoplasms / radiography. Adrenal Glands / pathology. Adrenal Glands / radiography. Biopsy. Diagnosis, Differential. Humans. Magnetic Resonance Imaging. Tomography, X-Ray Computed

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  • (PMID = 20521756.001).
  • [ISSN] 1532-0650
  • [Journal-full-title] American family physician
  • [ISO-abbreviation] Am Fam Physician
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 38
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54. Morimoto R, Satoh F, Murakami O, Totsune K, Arai Y, Suzuki T, Sasano H, Ito S, Takahashi K: Immunolocalization of urotensin II and its receptor in human adrenal tumors and attached non-neoplastic adrenal tissues. Peptides; 2008 May;29(5):873-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunolocalization of urotensin II and its receptor in human adrenal tumors and attached non-neoplastic adrenal tissues.
  • In addition to its vascular actions, UII has been shown to have mitogenic effects on tumor growth and some regulatory effects on adrenal steroidogenesis.
  • In the present study, we examined expression of UII and UT-R in human adrenal tumors and attached non-neoplastic adrenal tissues by immunohistochemistry.
  • Both UII and UT-R were immunolocalized in tumor cells of all adrenal tumors examined: 8 cases of cortisol-producing adenomas, 8 cases of aldosterone-producing adenomas, 2 cases of non-functioning adenomas, 17 cases of adrenocortical carcinomas, and 8 cases of pheochromocytomas.
  • In attached adrenals, immunoreactivity for UII was detected in medulla, but much weaker in the cortex than in cortical tumors, suggesting that expression of UII was up-regulated in neoplastic adrenocortical tissues.
  • No significant differences were found in the degree of immunoreactivity for UT-R between the tumors and the attached adrenal tissues.
  • The present study showed that both UII and UT-R were expressed in the adrenal tumors and attached non-neoplastic adrenal tissues, and suggests possible roles of UII and UT-R in tumor growth and/or secretory activities of these tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / metabolism. Adrenal Glands / metabolism. Receptors, G-Protein-Coupled / metabolism. Urotensins / metabolism

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  • (PMID = 17686550.001).
  • [ISSN] 0196-9781
  • [Journal-full-title] Peptides
  • [ISO-abbreviation] Peptides
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, G-Protein-Coupled; 0 / UTS2R protein, human; 0 / Urotensins; 9047-55-6 / urotensin II
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55. Abadie C, Bernard F, Netchine I, Sanlaville D, Roque A, Rossignol S, Coupier I: Acute lymphocytic leukaemia in a child with Beckwith-Wiedemann syndrome harbouring a CDKN1C mutation. Eur J Med Genet; 2010 Nov-Dec;53(6):400-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This syndrome is a multigenic disorder caused by dysregulation of imprinted growth regulatory genes in the 11p15.5 region.
  • The most commonly reported tumours in this syndrome are tumours of embryologic origin such as Wilms tumours, hepatoblastomas, neuroblastomas, rhabdomyosarcomas and adrenocortical carcinomas.
  • We report the case of a 10-year-old patient diagnosed with BWS, harbouring a CDKN1C (p57(KIP2)) mutation, who developed a T-type acute lymphoblastic leukaemia.
  • We discuss the possibility of a link between BWS and leukaemia via one of the few known negative regulator of hematopoiesis, the transforming growth factor beta pathway, depending upon the up-regulation of CDKN1C.
  • [MeSH-major] Beckwith-Wiedemann Syndrome / genetics. Cyclin-Dependent Kinase Inhibitor p57 / genetics. Mutation. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Copyright] Copyright © 2010 Elsevier Masson SAS. All rights reserved.
  • (PMID = 20826236.001).
  • [ISSN] 1878-0849
  • [Journal-full-title] European journal of medical genetics
  • [ISO-abbreviation] Eur J Med Genet
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / CDKN1C protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p57
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56. Gross BA, Mindea SA, Pick AJ, Chandler JP, Batjer HH: Medical management of Cushing disease. Neurosurg Focus; 2007;23(3):E10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Medical management of Cushing disease.
  • Although transsphenoidal excision of the adrenocorticotropic hormone (ACTH)-producing neoplasm is often the treatment of choice in patients with Cushing disease, medical management is itself a useful preoperative temporizing measure, an option for long-term management in nonsurgical candidates, and an option for patients in whom surgery and/or radiotherapy have failed.
  • Three pathophysiologically based approaches exist in the research literature--neuro-modulation to limit ACTH levels, adrenal enzyme inhibition, and glucocorticoid receptor antagonism.
  • Adrenal enzyme inhibitors, however, offer substantial future promise in the management of Cushing disease but are limited by the potential need to use them indefinitely and by dose-tolerance effects.
  • Although etomidate is a potential intravenous alternative for acute cortisol level control, ketoconazole has shown efficacy in the long-term treatment of patients with the disease.
  • If success is still not achieved, the potent adrenolytic agent often used for adrenocortical carcinomas, mitotane, is another alternative.

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  • (PMID = 17961023.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Hormone Antagonists; 0 / Neurotransmitter Agents; 0 / Receptors, Glucocorticoid
  • [Number-of-references] 32
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57. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • Cell growth as measured by the MTT and 5-bromo-2'-deoxyuridine incorporation assays is inhibited, and cell cycle analysis has revealed a slight induction of apoptosis.
  • [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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58. Walz MK, Petersenn S, Koch JA, Mann K, Neumann HP, Schmid KW: Endoscopic treatment of large primary adrenal tumours. Br J Surg; 2005 Jun;92(6):719-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Endoscopic treatment of large primary adrenal tumours.
  • BACKGROUND: Endoscopic adrenalectomy has become the treatment of choice for small benign adrenal tumours but should not be used for malignant lesions.
  • It is debatable whether large and therefore potentially malignant primary adrenal tumours should be removed by minimally invasive techniques.
  • METHODS: Three hundred and eighty primary adrenal tumours in 368 patients (142 male and 226 female; mean(s.d.) age 48.9(14.4) years) were excised by laparoscopic or retroperitoneoscopic adrenalectomy.
  • Adrenal neoplasias exceeded 6 cm in diameter (range 6-13 cm) in 33 patients (18 male and 15 female; age 42.6(14.2) years).
  • Six malignant tumours were identified (diameter 4-10 cm; four phaeochromocytomas and two adrenocortical carcinomas).
  • Local recurrence developed in two patients and distant metastasis occurred in all six patients with malignant lesions.
  • [MeSH-major] Adrenal Gland Neoplasms / surgery. Adrenalectomy / methods. Adrenocortical Carcinoma / surgery. Endoscopy / methods. Pheochromocytoma / surgery

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  • [Copyright] Copyright (c) 2005 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd.
  • (PMID = 15856491.001).
  • [ISSN] 0007-1323
  • [Journal-full-title] The British journal of surgery
  • [ISO-abbreviation] Br J Surg
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
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59. Cardoso CC, Bornstein SR, Hornsby PJ: New methods for investigating experimental human adrenal tumorigenesis. Mol Cell Endocrinol; 2009 Mar 5;300(1-2):175-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New methods for investigating experimental human adrenal tumorigenesis.
  • Adenomas and nodules of the human adrenal cortex are common, whereas adrenocortical carcinomas are rare.
  • Genes such as IGF2 have been suggested to be important in human adrenocortical tumorigenesis but their role has not been directly investigated.
  • We describe here elements of a system in which hypotheses concerning the molecular basis for the formation of benign and malignant adrenocortical lesions can be experimentally tested.
  • Various viral vectors have been employed in the study of adrenocortical cell biology.
  • Because of the low proliferative rate of primary human adrenocortical (pHAC) cells, a lentiviral system is ideal for transducing these cells with genes that may alter their characteristics or cause them to acquire benign or malignant tumorigenicity.
  • For tumorigenesis studies of genetically modified adrenocortical cells, we use RAG2(-/-), gammac(-/-) mice.
  • Using this immunodeficient mouse model, we established an orthotopic intra-adrenal cell transplantation technique for adrenocortical cells that should be of value for future studies of the experimental conversion of human adrenocortical cells to a benign or malignant tumorigenic state.

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  • (PMID = 19047010.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / AG012287-14; United States / NIA NIH HHS / AG / P01 AG020752-020006; United States / NIA NIH HHS / AG / AG020752-020006; United States / NIA NIH HHS / AG / P01 AG020752; United States / NIA NIH HHS / AG / R37 AG012287-14; United States / NIA NIH HHS / AG / R37 AG012287
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Number-of-references] 37
  • [Other-IDs] NLM/ NIHMS99076; NLM/ PMC2676229
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60. West AN, Neale GA, Pounds S, Figueredo BC, Rodriguez Galindo C, Pianovski MA, Oliveira Filho AG, Malkin D, Lalli E, Ribeiro R, Zambetti GP: Gene expression profiling of childhood adrenocortical tumors. Cancer Res; 2007 Jan 15;67(2):600-8
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  • [Title] Gene expression profiling of childhood adrenocortical tumors.
  • Pediatric adrenocortical tumors (ACT) are rare and often fatal malignancies; little is known regarding their etiology and biology.
  • To provide additional insight into the nature of ACT, we determined the gene expression profiles of 24 pediatric tumors (five adenomas, 18 carcinomas, and one undetermined) and seven normal adrenal glands.
  • Distinct patterns of gene expression, validated by quantitative real-time PCR and Western blot analysis, were identified that distinguish normal adrenal cortex from tumor.
  • Differences in gene expression were also identified between adrenocortical adenomas and carcinomas.
  • In addition, pediatric adrenocortical carcinomas were found to share similar patterns of gene expression when compared with those published for adult ACT.
  • Our findings lay the groundwork for establishing gene expression profiles that may aid in the diagnosis and prognosis of pediatric ACT, and in the identification of signaling pathways that contribute to this disease.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics. Adrenocortical Carcinoma / genetics

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  • (PMID = 17234769.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / CA63230; United States / NCI NIH HHS / CA / CA71907
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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61. Bielinska M, Parviainen H, Kiiveri S, Heikinheimo M, Wilson DB: Review paper: origin and molecular pathology of adrenocortical neoplasms. Vet Pathol; 2009 Mar;46(2):194-210
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Review paper: origin and molecular pathology of adrenocortical neoplasms.
  • Neoplastic adrenocortical lesions are common in humans and several species of domestic animals.
  • Although there are unanswered questions about the origin and evolution of adrenocortical neoplasms, analysis of human tumor specimens and animal models indicates that adrenocortical tumorigenesis involves both genetic and epigenetic alterations.
  • Epigenetic changes serve to expand the size of the uncommitted adrenal progenitor population, modulate their phenotypic plasticity (i.e., responsiveness to extracellular signals), and increase the likelihood of subsequent genetic alterations.
  • Analyses of heritable and spontaneous types of human adrenocortical tumors documented alterations in either cell surface receptors or their downstream effectors that impact neoplastic transformation.
  • Many of the mutations associated with benign human adrenocortical tumors result in dysregulated cyclic adenosine monophosphate signaling, whereas key factors and/or signaling pathways associated with adrenocortical carcinomas include dysregulated expression of the IGF2 gene cluster, activation of the Wnt/beta-catenin pathway, and inactivation of the p53 tumor suppressor.
  • A better understanding of the factors and signaling pathways involved in adrenal tumorigenesis is necessary to develop targeted pharmacologic and genetic therapies.

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  • (PMID = 19261630.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK075618-02; United States / NIDDK NIH HHS / DK / R01 DK075618-02; United States / NIDDK NIH HHS / DK / DK52574; United States / NIDDK NIH HHS / DK / DK075618; United States / NIDDK NIH HHS / DK / P30 DK052574; United States / NIDDK NIH HHS / DK / R01 DK075618; United States / NIDDK NIH HHS / DK / P30 DK052574-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 165
  • [Other-IDs] NLM/ NIHMS85359; NLM/ PMC2811968
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62. Palmero EI, Schüler-Faccini L, Caleffi M, Achatz MI, Olivier M, Martel-Planche G, Marcel V, Aguiar E, Giacomazzi J, Ewald IP, Giugliani R, Hainaut P, Ashton-Prolla P: Detection of R337H, a germline TP53 mutation predisposing to multiple cancers, in asymptomatic women participating in a breast cancer screening program in Southern Brazil. Cancer Lett; 2008 Mar 8;261(1):21-5
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  • [Title] Detection of R337H, a germline TP53 mutation predisposing to multiple cancers, in asymptomatic women participating in a breast cancer screening program in Southern Brazil.
  • Germline TP53 mutations predispose to a rare familial cancer syndrome, the Li-Fraumeni Syndrome (LFS), characterized by the early onset of multiple cancers including childhood adrenocortical carcinomas, sarcomas and brain tumors, and breast and colon cancer in young adults.
  • An identical germline mutation at codon 337 in TP53 (R337H) has been shown to be causally related to an increased risk of multiple cancers in unrelated subjects with familial cancer risk in Southern Brazil.
  • Here we have assessed the prevalence of R337H in 750 healthy women participating in a community-based breast cancer screening program in the area of Porto Alegre.
  • The mutant was detected in two participants (0.3%) who were fourth-degree relatives and reported a familial history of cancer at multiple sites that did not match classical criteria for LFS and its variants.
  • Testing in additional family members detected the mutation in three subjects, one of whom developed breast cancer at the age of 36.
  • [MeSH-major] Genes, p53. Genetic Predisposition to Disease. Germ-Line Mutation. Neoplasms / genetics
  • [MeSH-minor] Adult. Aged. Brazil. Breast Neoplasms / diagnosis. Female. Genetic Testing. Humans. Li-Fraumeni Syndrome / genetics. Middle Aged. Pedigree

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  • (PMID = 18248785.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
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63. Barzon L, Maffei P, Sonino N, Pilon C, Baldazzi L, Balsamo A, Del Maschio O, Masi G, Trevisan M, Pacenti M, Fallo F: The role of 21-hydroxylase in the pathogenesis of adrenal masses: review of the literature and focus on our own experience. J Endocrinol Invest; 2007 Jul-Aug;30(7):615-23
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  • [Title] The role of 21-hydroxylase in the pathogenesis of adrenal masses: review of the literature and focus on our own experience.
  • An exaggerated response of 17- hydroxyprogesterone (17-OHP) to exogenous ACTH stimulation has been found in 30 to 70% of patients with incidentally discovered adrenal tumors, supporting the concept that congenital 21- hydroxylase deficiency may be a predisposing factor for adrenocortical tumorigenesis.
  • Decreased expression of 21-hydroxylase gene has been observed in sporadic non-functioning adrenocortical adenomas and adrenocortical carcinomas, in agreement with the reduced steroidogenic activity found in these types of tumors.
  • Screening studies for the presence of mutations in CYP21A2 gene, encoding 21-hydroxylase, in patients with sporadic adrenocortical tumors yielded discordant results.
  • Overall, a higher frequency of germline 21-hydroxylase mutation carriers has been found among patients with adrenal tumors, including incidentalomas, than in the general population.
  • However, the presence of mutations did not correlate with endocrine test results and tumor mass features, suggesting that 21-hydroxylase deficiency does not represent a relevant mechanism in adrenal tumorigenesis.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Adrenal Hyperplasia, Congenital / genetics. Adrenocortical Carcinoma / genetics. Steroid 21-Hydroxylase / physiology

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  • (PMID = 17848847.001).
  • [ISSN] 1720-8386
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Glucocorticoids; 68-96-2 / 17-alpha-Hydroxyprogesterone; EC 1.14.14.16 / Steroid 21-Hydroxylase
  • [Number-of-references] 64
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64. Weismann D, Briese J, Niemann J, Grüneberger M, Adam P, Hahner S, Johanssen S, Liu W, Ezzat S, Saeger W, Bamberger AM, Fassnacht M, Schulte HM, Asa SL, Allolio B, Bamberger CM: Osteopontin stimulates invasion of NCI-h295 cells but is not associated with survival in adrenocortical carcinoma. J Pathol; 2009 Jun;218(2):232-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Osteopontin stimulates invasion of NCI-h295 cells but is not associated with survival in adrenocortical carcinoma.
  • Gene array studies indicated that osteopontin (OPN) mRNA is highly expressed in adrenocortical carcinomas (ACCs).
  • OPN enhances invasiveness, proliferation, and metastasis formation, and is associated with poor survival in some malignant diseases.
  • In this study, we demonstrated OPN and integrin alphavbeta3 expression in normal adrenal glands and benign adenomas, with staining seen exclusively in adrenocortical cells as well as even stronger staining in ACC.
  • In conclusion, our in vitro data indicate that OPN and integrin alphavbeta3 may act as a functional complex facilitating the invasiveness of adrenocortical tumours.
  • This relationship remains of relevance to our understanding of carcinogenesis, but further studies are needed to address the physiological and pathological function of OPN in adrenal tissue.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenocortical Carcinoma / metabolism. Osteopontin / analysis
  • [MeSH-minor] Adenoma / chemistry. Adrenal Glands / chemistry. Blotting, Western / methods. Cell Line, Tumor. Gene Expression Profiling. Humans. Immunohistochemistry. Integrin alphaVbeta3 / analysis. Integrin alphaVbeta3 / genetics. Integrin alphaVbeta3 / metabolism. Kaplan-Meier Estimate. Neoplasm Invasiveness. Oligonucleotide Array Sequence Analysis. Reverse Transcriptase Polymerase Chain Reaction. Statistics, Nonparametric. Transfection / methods

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  • (PMID = 19326399.001).
  • [ISSN] 1096-9896
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Integrin alphaVbeta3; 106441-73-0 / Osteopontin
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65. Coli A, Di Giorgio A, Castri F, Destito C, Marin AW, Bigotti G: Sarcomatoid carcinoma of the adrenal gland: A case report and review of literature. Pathol Res Pract; 2010 Jan 15;206(1):59-65
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  • [Title] Sarcomatoid carcinoma of the adrenal gland: A case report and review of literature.
  • Reports about adrenocortical carcinomas (AC) mixed with sarcomatous areas are very rare.
  • Herein, we report a case of sarcomatoid carcinoma of the adrenal gland in a 75-year-old woman who presented with left abdominal pain of one month's standing.
  • The results of abdominal ultrasonography and computed tomography (CT) showed the presence of a large heterogeneous adrenal mass.
  • Histologically, the neoplasm showed areas of adrenocortical carcinoma and areas of sarcomatoid spindle cell proliferation.
  • Twelve months after removal of the primary tumor, the patient died of her disease.
  • To the best of our knowledge, only seven cases of adrenal sarcomatoid carcinoma have been reported in the medical literature.
  • We review the reported cases according to the 2004 classification of the World Health Organization (WHO) of lung tumors, and highlight the histogenesis, diagnosis, and clinical course of this very aggressive tumor.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Carcinosarcoma / secondary. Liver Neoplasms / secondary

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  • [Copyright] Copyright 2009 Elsevier GmbH. All rights reserved.
  • (PMID = 19369012.001).
  • [ISSN] 1618-0631
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Neoplasm Proteins
  • [Number-of-references] 16
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66. Gruschwitz T, Breza J, Wunderlich H, Junker K: Improvement of histopathological classification of adrenal gland tumors by genetic differentiation. World J Urol; 2010 Jun;28(3):329-34

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  • [Title] Improvement of histopathological classification of adrenal gland tumors by genetic differentiation.
  • PURPOSE: There are often problems in differentiating between benign and malignant adrenal gland tumors by imaging and histopathology.
  • On account of considerable differences in the therapy and aftercare of benign and malignant adrenal tumors, correct classification of tumor type is of greatest importance.
  • The purpose of this study was to define specific genetic alterations differentiating between adenomas and carcinomas.
  • Retrospectively, 26 (16 adenomas and 10 carcinomas) tumors of the adrenal cortex were analyzed.
  • RESULTS: Genetic alterations were found in 5/16 adenomas (31.25%) and in all adrenocortical carcinomas.
  • The mean number of genetic changes per tumor was 8.7 (range 6-12) in carcinomas.
  • The benign cortical tumors present 1.6 changes (range 0-3) per tumor.
  • Furthermore, specific chromosomal alterations of carcinomas were identified.
  • CONCLUSIONS: Genetic evaluation facilitates differentiation between adrenal gland tumors.
  • Genetic tests should be used in routine diagnostics of adrenal specimens.
  • Potentially, fine-needle biopsy can be established as standard diagnostics of adrenal tumors with unknown genesis.
  • [MeSH-major] Adenoma / classification. Adenoma / genetics. Adrenal Cortex Neoplasms / classification. Adrenal Cortex Neoplasms / genetics. Carcinoma / genetics

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  • (PMID = 20364258.001).
  • [ISSN] 1433-8726
  • [Journal-full-title] World journal of urology
  • [ISO-abbreviation] World J Urol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
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67. Kim AC, Barlaskar FM, Heaton JH, Else T, Kelly VR, Krill KT, Scheys JO, Simon DP, Trovato A, Yang WH, Hammer GD: In search of adrenocortical stem and progenitor cells. Endocr Rev; 2009 May;30(3):241-63
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  • [Title] In search of adrenocortical stem and progenitor cells.
  • The theory that adrenocortical organ homeostasis is maintained by undifferentiated stem or progenitor cells can be traced back nearly a century.
  • Similar to other organ systems, it is widely believed that these rare cells of the adrenal cortex remain relatively undifferentiated and quiescent until needed to replenish the organ, at which time they undergo proliferation and terminal differentiation.
  • Historical studies examining cell cycle activation by label retention assays and regenerative potential by organ transplantation experiments suggested that the adrenocortical progenitors reside in the outer periphery of the adrenal gland.
  • Over the past decade, the Hammer laboratory, building on this hypothesis and these observations, has endeavored to understand the mechanisms of adrenocortical development and organ maintenance.
  • In this review, we summarize the current knowledge of adrenal organogenesis.
  • We present evidence for the existence and location of adrenocortical stem/progenitor cells and their potential contribution to adrenocortical carcinomas.
  • Together, the work provides a framework for the emerging somatic stem cell field as it relates to the adrenal gland.
  • [MeSH-major] Adrenal Cortex / cytology. Stem Cells / cytology
  • [MeSH-minor] Animals. Cell Differentiation / physiology. Clone Cells / cytology. Clone Cells / physiology. Humans. Organogenesis / physiology

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  • (PMID = 19403887.001).
  • [ISSN] 1945-7189
  • [Journal-full-title] Endocrine reviews
  • [ISO-abbreviation] Endocr. Rev.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA134606
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 225
  • [Other-IDs] NLM/ PMC2726842
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68. de Cremoux P, Rosenberg D, Goussard J, Brémont-Weil C, Tissier F, Tran-Perennou C, Groussin L, Bertagna X, Bertherat J, Raffin-Sanson ML: Expression of progesterone and estradiol receptors in normal adrenal cortex, adrenocortical tumors, and primary pigmented nodular adrenocortical disease. Endocr Relat Cancer; 2008 Jun;15(2):465-74

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of progesterone and estradiol receptors in normal adrenal cortex, adrenocortical tumors, and primary pigmented nodular adrenocortical disease.
  • Adrenal tumors occur more frequently in women and are the leading cause of Cushing's syndrome during pregnancy.
  • We aimed to evaluate the potential role of sex steroids in the susceptibility of women to adrenocortical tumors.
  • We evaluated the presence of the progesterone receptor (PR), estradiol receptors (ERs), and aromatase in 5 patients with primary pigmented nodular adrenal disease (PPNAD), 15 adrenocortical adenomas (ACAs) and adjacent normal tissues, 12 adrenocortical carcinomas (ACCs), and 3 normal adrenal glands (NA).
  • ERalpha concentrations were low in NA, in adrenal tissues adjacent to ACA (51+/-33), in ACC (53+/-78), and lower in ACA (11+/-11 fmol/mg DNA).
  • Conversely, PR concentrations were high in NA and adrenal tissues adjacent to ACA, at 307+/-216 fmol/mg DNA, and were even higher in tumors - 726+/-706 fmol/mg DNA in ACA and 1154+/-1586 fmol/mg DNA in ACC - and in isolated PPNAD nodules.
  • PR and ERbeta are clearly present in normal adrenal glands and adrenal tumors.
  • Further studies may shed light on the possible pathogenic role of these receptors in adrenal proliferation.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics. Estrogen Receptor alpha / genetics. Estrogen Receptor beta / genetics. Receptors, Progesterone / genetics
  • [MeSH-minor] Adolescent. Adrenal Cortex / pathology. Adrenal Cortex / physiology. Adrenal Cortex Diseases / genetics. Adrenal Cortex Diseases / metabolism. Adrenal Cortex Diseases / pathology. Adult. Aged. Aged, 80 and over. Aromatase / metabolism. Child. Cytosol / metabolism. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. RNA, Messenger / metabolism

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  • (PMID = 18508999.001).
  • [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 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / RNA, Messenger; 0 / Receptors, Progesterone; EC 1.14.14.1 / Aromatase
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69. Soon PS, Yeh MW, Delbridge LW, Bambach CP, Sywak MS, Robinson BG, Sidhu SB: Laparoscopic surgery is safe for large adrenal lesions. Eur J Surg Oncol; 2008 Jan;34(1):67-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Laparoscopic surgery is safe for large adrenal lesions.
  • INTRODUCTION: Laparoscopic adrenalectomy has surpassed open adrenalectomy as the gold standard for excision of benign adrenal lesions.
  • The size threshold for offering laparoscopic adrenalectomy is controversial as the prevalence of adrenocortical carcinoma increases with increasing tumour size.
  • The aim of this paper was to assess the safety of laparoscopic adrenalectomy for large adrenal tumours (tumours > or = 60 mm).
  • There were 8 adrenocortical carcinomas in the group with tumours > or = 60 mm in size.
  • Four of the patients undergoing open adrenalectomy died of their disease while 1 is alive with recurrence 3 years later.
  • The 3 patients who underwent either laparoscopic or laparoscopic converted to open adrenalectomy are alive without evidence of disease after 18 months follow up.
  • These findings are concordant with the growing body of literature supporting laparoscopic adrenalectomy for potentially malignant tumours > or = 60 mm in size without preoperative or intraoperative features of malignancy.
  • [MeSH-major] Adrenal Gland Neoplasms / surgery. Laparoscopy / methods
  • [MeSH-minor] Adrenal Cortex Neoplasms / surgery. Adrenalectomy. Adrenocortical Carcinoma / surgery. Female. Humans. Male. Middle Aged. Postoperative Complications. Time Factors

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  • (PMID = 17532597.001).
  • [ISSN] 1532-2157
  • [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
  • [Publication-country] England
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70. Gockel I, Heintz A, Domeyer M, Trinh TT, Dünschede F, Junginger T: [Indications for conventional adrenalectomy]. Zentralbl Chir; 2008 Jun;133(3):255-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: Indications for conventional adrenalectomy were - as compared with the minimally invasive procedure - significantly more frequent adrenocortical carcinomas (ACC), especially in the context of multivisceral resections, as well as adrenal metastases (synchronous and metachronous).
  • In contrast, adrenal Cushing's disease (including 19 patients with bilateral tumours), pheochromocytoma, incidentaloma and Conn's syndrome constituted a more frequent indication for minimally invasive adrenalectomy.
  • Conventionally operated adrenal pathologies with on average 6.0 (range: 1.2-19.0) cm diameter were significantly larger than the endoscopically removed tumours with on average 3.3 (range: 0.2-9.2) cm diameter (p < 0.0001).
  • The side localisation and the frequency of bilateral adrenal tumours did not differ significantly in the two groups.
  • CONCLUSION: Since the establishment of the minimally invasive technique in 1994, conventional adrenalectomy has been selected for 26 % of all resected adrenal pathologies at our clinic and, therefore, still plays an important role even in the era of laparoscopic surgery.
  • The benefit of the laparoscopic procedure in the case of malignant pheochromocytoma, adrenocortical carcinoma, and isolated adrenal metastases at a locally confined stage is still unclear and requires prospective, randomised studies.
  • [MeSH-major] Adrenal Gland Neoplasms / surgery. Adrenalectomy / utilization. Minimally Invasive Surgical Procedures / utilization
  • [MeSH-minor] Adrenal Cortex Neoplasms / pathology. Adrenal Cortex Neoplasms / surgery. Adrenal Glands / pathology. Adult. Aged. Aged, 80 and over. Cushing Syndrome / pathology. Cushing Syndrome / surgery. Female. Humans. Hyperaldosteronism / pathology. Hyperaldosteronism / surgery. Male. Mathematical Computing. Middle Aged. Pheochromocytoma / pathology. Pheochromocytoma / surgery. Utilization Review / statistics & numerical data

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  • (PMID = 18563692.001).
  • [ISSN] 0044-409X
  • [Journal-full-title] Zentralblatt für Chirurgie
  • [ISO-abbreviation] Zentralbl Chir
  • [Language] ger
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Germany
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71. Blanes A, Diaz-Cano SJ: DNA and kinetic heterogeneity during the clonal evolution of adrenocortical proliferative lesions. Hum Pathol; 2006 Oct;37(10):1295-303

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DNA and kinetic heterogeneity during the clonal evolution of adrenocortical proliferative lesions.
  • Monoclonal adrenocortical lesions show inverse correlation between proliferation and apoptosis, with proliferation being the single most important criterion of malignancy in adrenal lesions.
  • No study yet has evaluated the variability of proliferation regarding the clonal pattern and diagnosis in adrenocortical nodular hyperplasias (ACNHs), adrenocortical adenomas (ACAs), and adrenocortical carcinomas (ACCs).
  • Statistics included analysis of variance/Student t tests regarding the clonal patterns and diagnosis.
  • Cell kinetic heterogeneity is the hallmark of adrenocortical neoplasms: tetraploid/hypertetraploid cell accumulation characterizes monoclonal lesions (suggesting nondisjunctional mitoses), whereas heterogeneously distributed mitotic figures and decreased diploid percentage define ACCs.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics. Adrenocortical Carcinoma / genetics. DNA, Neoplasm / analysis
  • [MeSH-minor] Apoptosis. Cell Nucleus / genetics. Cell Nucleus / pathology. Cell Proliferation. Clone Cells. Disease Progression. Flow Cytometry. Humans. Hyperplasia. Image Cytometry. Ki-67 Antigen / metabolism. Kinetics. Mitotic Index. Polyploidy. X Chromosome Inactivation / genetics

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  • (PMID = 16949934.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Ki-67 Antigen
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72. Sticchi D, Fassina A, Ganzaroli C, Pasqualetto C, Pessina AC, Nussdorfer GG, Rossi GP: Expression of telomerase (hTERT) in aldosterone-producing adrenocortical tumors. Int J Mol Med; 2006 Mar;17(3):469-74

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of telomerase (hTERT) in aldosterone-producing adrenocortical tumors.
  • Telomerase was found in cancers and immortalized cell lines, but only occasionally in normal tissues, thus suggesting that measurement of its hTERT subunit might help distinguishing benign from malignant tumors.
  • Data on hTERT expression in adrenocortical tumors are scant and mostly confined to non-functioning tumors.
  • Therefore, we investigated whether hTERT expression may predict malignancy in aldosterone producing adrenocortical tumors.
  • We also studied two rare aldosterone-producing carcinomas (APCs), eight adrenocortical carcinomas (ACs), twelve normal adrenal cortexes, and two malignant cell lines (NCI-295H and SW-13).
  • Of interest, we detected hTERT mRNA in 58% of APAs at levels similar to those of malignant tumors, which all consistently showed hTERT expression.
  • No hTERT expression was found in the normal adrenocortical tissue.
  • In conclusion, RT-PCR measurement of hTERT mRNA is a hallmark of malignant adrenocortical tumors, but identifies also a subset of hTERT-expressing APAs that might show metastatic spread at long-term follow-up.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / secretion. Aldosterone / secretion. Telomerase / genetics
  • [MeSH-minor] Aged. Anthropometry. Cell Nucleus / metabolism. Gene Expression Regulation, Neoplastic. Humans. Middle Aged. Protein Transport. RNA, Messenger / genetics. RNA, Messenger / metabolism

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  • (PMID = 16465394.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / RNA, Messenger; 4964P6T9RB / Aldosterone; EC 2.7.7.49 / Telomerase
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73. Hofland J, Timmerman MA, de Herder WW, van Schaik RH, de Krijger RR, de Jong FH: Expression of activin and inhibin subunits, receptors and binding proteins in human adrenocortical neoplasms. Clin Endocrinol (Oxf); 2006 Dec;65(6):792-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of activin and inhibin subunits, receptors and binding proteins in human adrenocortical neoplasms.
  • OBJECTIVE: The growth and differentiation factors activin and inhibin can affect tumour formation and steroid production in the adrenal cortex.
  • Expression of these activin-related mRNAs was measured in different types of adrenocortical tissues and tumours to study the relationship with tumorigenesis.
  • DESIGN: Quantitative expression of activin-related mRNAs was investigated in patient adrenocortical samples.
  • PATIENTS: Twenty-eight human adrenocortical samples from normal and hyperplastic adrenals and from adrenocortical adenomas and carcinomas were collected after surgery for study purposes.
  • MEASUREMENTS: Using quantitative reverse transcription polymerase chain reaction (RT-PCR), we investigated the expression of inhibin alpha-, betaA- and betaB-subunits, follistatin, betaglycan, ActRIIA, ActRIIB and Alk-4 in the adrenocortical tissues.
  • RESULTS: All genes studied were expressed in all tissues, with the exception of the inhibin alpha-subunit in one hyperplastic adrenal and three adrenocortical carcinomas.
  • Expression of inhibin betaA-subunit, follistatin, betaglycan, ActRIIA, ActRIIB and CYP17 differed between nontumorous adrenals and carcinomas.
  • We conclude that the expression of activin and inhibin subunits, receptors and binding proteins is affected by tumour formation in the adrenal gland and may play a role in tumorigenesis.
  • [MeSH-major] Activins / metabolism. Adrenal Cortex Neoplasms / metabolism. Adrenocortical Adenoma / metabolism. Adrenocortical Carcinoma / metabolism. Inhibins / metabolism
  • [MeSH-minor] Activin Receptors, Type II / genetics. Activin Receptors, Type II / metabolism. Adrenal Cortex / metabolism. Adrenal Cortex / pathology. Adult. Carrier Proteins / genetics. Carrier Proteins / metabolism. Female. Follistatin / genetics. Follistatin / metabolism. Gene Expression. Humans. Hyperplasia. Inhibin-beta Subunits / genetics. Inhibin-beta Subunits / metabolism. Male. Middle Aged. Proteoglycans / genetics. Proteoglycans / metabolism. Receptors, Transforming Growth Factor beta / genetics. Receptors, Transforming Growth Factor beta / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Statistics, Nonparametric. Steroid 17-alpha-Hydroxylase / genetics. Steroid 17-alpha-Hydroxylase / metabolism

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  • (PMID = 17121532.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Follistatin; 0 / Proteoglycans; 0 / Receptors, Transforming Growth Factor beta; 0 / inhibin beta A subunit; 0 / inhibin-alpha subunit; 104625-48-1 / Activins; 145170-29-2 / betaglycan; 57285-09-3 / Inhibins; 93443-12-0 / Inhibin-beta Subunits; EC 1.14.99.9 / Steroid 17-alpha-Hydroxylase; EC 2.7.11.30 / Activin Receptors, Type II
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74. Soon PS, Gill AJ, Benn DE, Clarkson A, Robinson BG, McDonald KL, Sidhu SB: Microarray gene expression and immunohistochemistry analyses of adrenocortical tumors identify IGF2 and Ki-67 as useful in differentiating carcinomas from adenomas. Endocr Relat Cancer; 2009 Jun;16(2):573-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Microarray gene expression and immunohistochemistry analyses of adrenocortical tumors identify IGF2 and Ki-67 as useful in differentiating carcinomas from adenomas.
  • The management of adrenocortical tumors (ACTs) is complex.
  • The Weiss score is the present most widely used system for ACT diagnosis.
  • However, ACTs with a score of 3 can be phenotypically benign or malignant.
  • Our objective is to use microarray profiling of a cohort of adrenocortical carcinomas (ACCs) and adrenocortical adenomas (ACAs) to identify discriminatory genes that could be used as an adjunct to the Weiss score.
  • [MeSH-major] Adrenocortical Adenoma / genetics. Adrenocortical Carcinoma / genetics. Biomarkers, Tumor / genetics. Gene Expression Profiling. Insulin-Like Growth Factor II / genetics. Ki-67 Antigen / genetics
  • [MeSH-minor] Adolescent. Adrenal Cortex / metabolism. Adrenal Cortex / pathology. Adult. Aged. Female. Humans. Immunoenzyme Techniques. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Sensitivity and Specificity. Young Adult

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  • (PMID = 19218281.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / IGF2 protein, human; 0 / Ki-67 Antigen; 0 / RNA, Messenger; 67763-97-7 / Insulin-Like Growth Factor II
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75. Tömböl Z, Szabó PM, Molnár V, Wiener Z, Tölgyesi G, Horányi J, Riesz P, Reismann P, Patócs A, Likó I, Gaillard RC, Falus A, Rácz K, Igaz P: Integrative molecular bioinformatics study of human adrenocortical tumors: microRNA, tissue-specific target prediction, and pathway analysis. Endocr Relat Cancer; 2009 Sep;16(3):895-906
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Integrative molecular bioinformatics study of human adrenocortical tumors: microRNA, tissue-specific target prediction, and pathway analysis.
  • MicroRNAs (miRs) are involved in the pathogenesis of several neoplasms; however, there are no data on their expression patterns and possible roles in adrenocortical tumors.
  • Our objective was to study adrenocortical tumors by an integrative bioinformatics analysis involving miR and transcriptomics profiling, pathway analysis, and a novel, tissue-specific miR target prediction approach.
  • Thirty-six tissue samples including normal adrenocortical tissues, benign adenomas, and adrenocortical carcinomas (ACC) were studied by simultaneous miR and mRNA profiling.
  • To our knowledge, this is the first report describing miR expression patterns and pathway analysis in sporadic adrenocortical tumors. miR biomarkers may be helpful for the diagnosis of adrenocortical malignancy.
  • [MeSH-major] Adenoma / genetics. Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Computational Biology / methods. Gene Expression Profiling / methods. MicroRNAs / genetics. Signal Transduction / genetics

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  • (PMID = 19546168.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MicroRNAs
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76. Tomkova K, Tomka M, Zajac V: Contribution of p53, p63, and p73 to the developmental diseases and cancer. Neoplasma; 2008;55(3):177-81
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  • [Title] Contribution of p53, p63, and p73 to the developmental diseases and cancer.
  • This syndrome is characterized by the early onset of different types of cancers including soft-tissue sarcomas, breast and brain cancers, leukemias, lung, laryngeal cancers, and adrenocortical carcinomas.

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  • (PMID = 18348649.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / CKAP4 protein, human; 0 / DNA-Binding Proteins; 0 / Membrane Proteins; 0 / Nuclear Proteins; 0 / Tumor Suppressor Proteins
  • [Number-of-references] 63
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77. Achatz MI, Hainaut P, Ashton-Prolla P: Highly prevalent TP53 mutation predisposing to many cancers in the Brazilian population: a case for newborn screening? Lancet Oncol; 2009 Sep;10(9):920-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The unusually high population frequency of a germline TP53 mutation (R337H) predisposing to early cancer has led to mass newborn testing for this mutation in the State of Paraná, southern Brazil.
  • Newborn screening for inherited cancer risk is complex and controversial.
  • R337H has been identified in Brazilian families with Li-Fraumeni or related syndromes predisposing to cancers in childhood (ie, brain, renal, and adrenocortical carcinomas), adolescence (ie, soft tissue and bone sarcomas), and young adulthood (ie, breast cancer).
  • R337H has also been detected in children with adrenocortical carcinoma without a documented family history of cancer.
  • The mutation is estimated to occur in about 0.3% of the population in southern Brazil and is associated with increased cancer risk throughout life.
  • Cancer patterns in families positive for R337H suggest strong genetic modifying effects, making it difficult to predict individual risk.
  • Because protocols for cancer-risk management in Li-Fraumeni or related syndromes are debatable, extreme care should prevail in predictive testing of children for R337H.
  • [MeSH-minor] Brazil / epidemiology. Genetic Predisposition to Disease / epidemiology. Genetic Predisposition to Disease / genetics. Humans. Infant, Newborn. Prevalence


78. Sone M, Shibata H, Homma K, Tamura N, Akahira J, Hamada S, Yahata M, Fukui N, Itoh H, Sasano H, Nakao K: Close examination of steroidogenesis disorders in a DOC- and progesterone-producing adrenocortical carcinoma. Endocrine; 2009 Feb;35(1):25-33
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  • [Title] Close examination of steroidogenesis disorders in a DOC- and progesterone-producing adrenocortical carcinoma.
  • We report a case of hypertension, hypokalemia, and amenorrhea accompanying an adrenocortical carcinoma.
  • A 27-year-old woman was admitted to our hospital because of a left adrenal incidentaloma.
  • After the tumor was removed, levels of all adrenal steroids were normalized.
  • Based on the Weiss criteria, the tumor was diagnosed as an adrenocortical carcinoma, and immunohistochemical analysis of steroidogenic enzymes revealed disorganized steroidogenesis in the tumor tissue.
  • With adrenocortical carcinomas, heterogeneity of individual steroid producing enzymes within tumor cells can lead to hypersecretion of various steroid intermediates, even when steroid end products are within the normal range.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenocortical Carcinoma / diagnosis. Desoxycorticosterone / metabolism. Endocrine System Diseases / etiology. Progesterone / metabolism
  • [MeSH-minor] Adult. Female. Humans. Hypertension / diagnosis. Incidental Findings. Models, Biological. Physical Examination. Steroids / biosynthesis

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  • (PMID = 18985457.001).
  • [ISSN] 1355-008X
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Steroids; 40GP35YQ49 / Desoxycorticosterone; 4G7DS2Q64Y / Progesterone
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79. Yan BC, Gong C, Song J, Krausz T, Tretiakova M, Hyjek E, Al-Ahmadie H, Alves V, Xiao SY, Anders RA, Hart JA: Arginase-1: a new immunohistochemical marker of hepatocytes and hepatocellular neoplasms. Am J Surg Pathol; 2010 Aug;34(8):1147-54
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  • The distinction of hepatocellular carcinoma (HCC) from metastatic tumor in the liver often presents a diagnostic challenge that carries significant impact on prognostication and therapy.
  • We also examined Arg-1 expression in nonhepatocellular tumors, including many that are potential mimics of HCC (renal cell carcinomas, neuroendocrine tumors, melanomas, gastric adenocarcinomas, and adrenocortical carcinomas) and found that only 2 non-HCC tumors were reactive for Arg-1.
  • Arg-1 represents a sensitive and specific marker of benign and malignant hepatocytes that may ultimately prove to be a useful diagnostic tool in routine surgical pathology practice.
  • [MeSH-major] Arginase / analysis. Biomarkers, Tumor / analysis. Carcinoma, Hepatocellular / enzymology. Hepatocytes / enzymology. Immunohistochemistry. Liver Neoplasms / enzymology
  • [MeSH-minor] Brazil. Cell Differentiation. Humans. Predictive Value of Tests. Sensitivity and Specificity. Tissue Array Analysis. United States

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  • (PMID = 20661013.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK081417; United States / NIDDK NIH HHS / DK / R01 DK081417-01; United States / NIDDK NIH HHS / DK / R01 DK081417-02
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 3.5.3.1 / Arginase
  • [Other-IDs] NLM/ NIHMS316258; NLM/ PMC3160135
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80. Achatz MI, Olivier M, Le Calvez F, Martel-Planche G, Lopes A, Rossi BM, Ashton-Prolla P, Giugliani R, Palmero EI, Vargas FR, Da Rocha JC, Vettore AL, Hainaut P: The TP53 mutation, R337H, is associated with Li-Fraumeni and Li-Fraumeni-like syndromes in Brazilian families. Cancer Lett; 2007 Jan 8;245(1-2):96-102
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  • A TP53 germline mutation, R337H, has been previously described in children from southern Brazil with adrenocortical tumours but no documented familial history of other cancers.
  • Families with the R337H mutation presented a wide spectrum of tumours, including breast cancers (30.4%), brain cancers (10.7%), soft tissue sarcomas (10.7%) and adrenocortical carcinomas (8.9%).
  • Testing of 53 Brazilian subjects with no cancer history showed that R337H was not a common polymorphism in that population.
  • Moreover, loss of heterozygocity with retention of the R337H allele was observed in a breast adenocarcinoma, supporting a role for this mutation in breast tumorigenesis.
  • [MeSH-minor] Base Sequence. Brazil. DNA Mutational Analysis. Female. Genetic Predisposition to Disease / genetics. Humans. Male. Mutation, Missense. Neoplastic Syndromes, Hereditary / genetics. Neoplastic Syndromes, Hereditary / pathology

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  • [CommentIn] Cancer Lett. 2007 Mar 18;247(2):353-5; author reply 356-8 [16750598.001]
  • (PMID = 16494995.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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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. Fassnacht M, Weismann D, Ebert S, Adam P, Zink M, Beuschlein F, Hahner S, Allolio B: AKT is highly phosphorylated in pheochromocytomas but not in benign adrenocortical tumors. J Clin Endocrinol Metab; 2005 Jul;90(7):4366-70
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  • [Title] AKT is highly phosphorylated in pheochromocytomas but not in benign adrenocortical tumors.
  • OBJECTIVE: The objective of this study was the investigation of the role of AKT in the pathogenesis of pheochromocytomas and adrenocortical tumors.
  • DESIGN, SETTING, AND PARTICIPANTS: Total AKT and phosphorylated AKT (pAKT) in 15 pheochromocytomas, nine aldosterone-producing adenomas, nine cortisol-producing adenomas, eight adrenocortical carcinomas (ACC), and 15 normal adrenals were investigated by Western blot analysis.
  • Immunohistochemistry for total AKT and pAKT was performed in pheochromocytomas (n = 8), ACC (n = 4), and normal adrenal glands (n = 2).
  • MAIN OUTCOME MEASURES: Determination of pAKT/total AKT ratio in adrenal tissues was the main outcome.
  • CONCLUSION: Our findings provide evidence for increased activation of AKT in pheochromocytomas but not in adrenocortical adenomas.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenal Gland Neoplasms / metabolism. Pheochromocytoma / metabolism. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins / metabolism

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  • (PMID = 15855265.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Proteins; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
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83. Peppa M, Pikounis V, Papaxoinis G, Macheras A, Economopoulos T, Raptis SA, Hadjidakis D: Adrenocortical carcinoma secreting cortisol, androgens and aldosterone: a case report. Cases J; 2009;2:8951

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenocortical carcinoma secreting cortisol, androgens and aldosterone: a case report.
  • INTRODUCTION: Adrenocortical carcinoma is a rare malignancy with a poor prognosis and presents with mass effects and less often with signs of hormone excess (approximately 60% of all adrenocortical carcinoma's).
  • Hormonally active adrenocortical carcinomas most commonly secrete cortisol while the co-secretion of multiple steroid hormones is rare.
  • CASE PRESENTATION: We report the case of a 59 year-old woman with a medical history of hyperaldosteronism due to a right adrenal adenoma.
  • During follow up, she showed symptoms of hypercortisolism and hyperandrogenemia and a rapid growth of the adrenal mass.
  • She underwent right adrenalectomy and the histology revealed the presence of an adrenocortical carcinoma.
  • Six months post-operatively being on treatment with mitotane, she was diagnosed of metastatic disease to the liver.
  • CONCLUSION: The hormonal status should be carefully investigated in all cases of suspected adrenocortical carcinoma, as the pattern of hormone secretion may be a clue to the malignancy of an adrenal lesion.
  • In addition, more data are needed to clarify the clinical and prognostic significance of the combined production of all adrenocortical hormones affecting either the survival or the quality of life of adrenocortical carcinoma patients.

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  • (PMID = 20181215.001).
  • [ISSN] 1757-1626
  • [Journal-full-title] Cases journal
  • [ISO-abbreviation] Cases J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2827070
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84. de Reyniès A, Assié G, Rickman DS, Tissier F, Groussin L, René-Corail F, Dousset B, Bertagna X, Clauser E, Bertherat J: Gene expression profiling reveals a new classification of adrenocortical tumors and identifies molecular predictors of malignancy and survival. J Clin Oncol; 2009 Mar 1;27(7):1108-15
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  • [Title] Gene expression profiling reveals a new classification of adrenocortical tumors and identifies molecular predictors of malignancy and survival.
  • PURPOSE: Adrenocortical tumors, especially cancers, remain challenging both for their diagnosis and prognosis assessment.
  • PATIENTS AND METHODS: One hundred fifty-three unilateral adrenocortical tumors were studied by microarray (n = 92) or reverse transcription quantitative polymerase chain reaction (n = 148).
  • A two-gene predictor of malignancy was built using the disease-free survival as the end point in a training cohort (n = 47), then validated in an independent validation cohort (n = 104).
  • Similarly, for malignant tumors, a two-gene predictor of survival was built using the overall survival as the end point in a training cohort (n = 23), then tested in an independent validation cohort (n = 35).
  • RESULTS: Unsupervised clustering analysis discriminated robustly the malignant and benign tumors, and identified two groups of malignant tumors with very different outcome.
  • The combined expression of DLG7 and PINK1 was the best predictor of disease-free survival (log-rank P approximately 10(-12)), could overcome the uncertainties of intermediate pathological Weiss scores, and remained significant after adjustment to the Weiss score (P < 1.3 x 10(-2)).
  • Among the malignant tumors, the combined expression of BUB1B and PINK1 was the best predictor of overall survival (P < 2 x 10(-6)), and remained significant after adjusting for MacFarlane staging (P < .005).
  • CONCLUSION: Gene expression analysis unravels two distinct groups of adrenocortical carcinomas.
  • These original tools should provide important improvements for adrenal tumors management.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Biomarkers, Tumor / genetics. Neoplasm Proteins / genetics. Protein Kinases / genetics. Protein-Serine-Threonine Kinases / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cluster Analysis. Diagnosis, Differential. Disease-Free Survival. Female. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Proportional Hazards Models. Prospective Studies. Reproducibility of Results. Survival Analysis

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  • (PMID = 19139432.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DLGAP5 protein, human; 0 / Neoplasm Proteins; EC 2.7.- / Protein Kinases; EC 2.7.11.1 / Bub1 spindle checkpoint protein; EC 2.7.11.1 / PTEN-induced putative kinase; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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85. Soon PS, Libe R, Benn DE, Gill A, Shaw J, Sywak MS, Groussin L, Bertagna X, Gicquel C, Bertherat J, McDonald KL, Sidhu SB, Robinson BG: Loss of heterozygosity of 17p13, with possible involvement of ACADVL and ALOX15B, in the pathogenesis of adrenocortical tumors. Ann Surg; 2008 Jan;247(1):157-64
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  • [Title] Loss of heterozygosity of 17p13, with possible involvement of ACADVL and ALOX15B, in the pathogenesis of adrenocortical tumors.
  • OBJECTIVE: To determine the minimal common region of loss on 17p13 in a cohort of adrenocortical carcinomas (ACCs) (defined by a Weiss score > or =3) and adrenocortical adenomas (ACAs) (defined by a Weiss score <3) and subsequently to assess 3 genes in this region that could be involved in adrenocortical tumorigenesis.
  • METHODS: Using 12 microsatellite markers across 17p13, LOH analysis was performed on 37 paired blood and adrenocortical tumor samples (23 ACC and 14 ACA samples) to determine the minimal common region of loss for ACCs and ACAs.
  • [MeSH-major] Acyl-CoA Dehydrogenases / genetics. Adrenal Cortex Neoplasms / genetics. Arachidonate 12-Lipoxygenase / genetics. Chromosomes, Human, Pair 17. Genes, Tumor Suppressor. Loss of Heterozygosity

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  • (PMID = 18156936.001).
  • [ISSN] 0003-4932
  • [Journal-full-title] Annals of surgery
  • [ISO-abbreviation] Ann. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers; EC 1.13.11.31 / Arachidonate 12-Lipoxygenase; EC 1.3.- / Acyl-CoA Dehydrogenases
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86. Advani A, Johnson SJ, Nicol MR, Papacleovoulou G, Evans DB, Vaikkakara S, Mason JI, Quinton R: Adult-onset hypogonadotropic hypogonadism caused by aberrant expression of aromatase in an adrenocortical adenocarcinoma. Endocr J; 2010;57(7):651-6
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  • [Title] Adult-onset hypogonadotropic hypogonadism caused by aberrant expression of aromatase in an adrenocortical adenocarcinoma.
  • Estrogen-secreting adrenal cancers are extremely rare, with feminizing symptoms attributed to aromatase expression in the adrenal tumor.
  • We describe a case of hypogonadotropic hypogonadism as a consequence of aberrant aromatase expression in a patient with adrenocortical adenocarcinoma.
  • A right adrenal mass was identified on CT scanning and the patient underwent an open adrenalectomy.
  • Immunohistochemistry of the adrenal cancer confirmed aberrant expression of aromatase in most, although not all, carcinoma cells.
  • This case highlights that clinical features of feminizing adrenocortical carcinomas can be secondary to estrogen production by aberrantly transcribed and translated aromatase within the tumor.
  • The diagnosis of adrenocortical adenocarcinoma should be considered in men presenting with low testosterone and gonadotropins, particularly in the presence of feminizing features.
  • [MeSH-major] Adenocarcinoma / genetics. Adrenal Cortex Neoplasms / genetics. Aromatase / genetics. Hypogonadism / genetics
  • [MeSH-minor] Adult. Age of Onset. Gene Expression Regulation, Enzymologic / physiology. Gene Expression Regulation, Neoplastic / physiology. Genetic Predisposition to Disease. Humans. Male. Middle Aged

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  • (PMID = 20467160.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] EC 1.14.14.1 / Aromatase
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87. 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.
  • 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.
  • Western blot analysis showed that TZDs increased the expression of the cell cycle inhibitors p21 and p27 and reduced the expression of cyclin D1.
  • 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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88. Laurell C, Velázquez-Fernández D, Lindsten K, Juhlin C, Enberg U, Geli J, Höög A, Kjellman M, Lundeberg J, Hamberger B, Larsson C, Nilsson P, Bäckdahl M: Transcriptional profiling enables molecular classification of adrenocortical tumours. Eur J Endocrinol; 2009 Jul;161(1):141-52
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  • [Title] Transcriptional profiling enables molecular classification of adrenocortical tumours.
  • Adrenocortical tumours are often associated with altered hormone production with a variety of clinical symptoms.
  • The aggressiveness of carcinomas together with the high frequency of adenomas calls for a deeper understanding of the underlying biological mechanisms and an improvement of the diagnostic possibilities.
  • The sample set consisted of 17 adenomas, 11 carcinomas and 4 histological normal adrenocortexes.
  • RESULTS: Unsupervised clustering to reveal relationships between samples based on the entire gene expression profile resulted in two subclusters; carcinomas and non-cancer specimens.
  • A large number of genes were accordingly found to be differentially expressed comparing carcinomas to adenomas.
  • Moreover, two subgroups of carcinomas were identified with different survival outcome, suggesting that survival prediction can be made on the basis of gene expression profiles.
  • CONCLUSIONS: Adrenocortical carcinomas are associated with a distinct molecular signature apparent in their gene expression profiles.

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  • (PMID = 19411298.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.1.2.15 / USP4 protein, human; EC 3.1.2.15 / Ubiquitin Thiolesterase
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89. Sturgeon C, Shen WT, Clark OH, Duh QY, Kebebew E: Risk assessment in 457 adrenal cortical carcinomas: how much does tumor size predict the likelihood of malignancy? J Am Coll Surg; 2006 Mar;202(3):423-30
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  • [Title] Risk assessment in 457 adrenal cortical carcinomas: how much does tumor size predict the likelihood of malignancy?
  • STUDY DESIGN: Adrenocortical carcinomas (ACC) recorded in the Surveillance, Epidemiology, and End Results (SEER) database (1988 to 2000) were compared with benign functional or nonfunctional adrenal cortical adenomas (excluding aldosteronomas) operated on at our institution between January 1, 1993, and July 1, 2003.
  • RESULTS: We identified 457 patients with ACC and 47 patients with adrenal cortical adenomas; 376 and 44 neoplasms, respectively, had tumor size data available.
  • For ACC presenting with local disease, the sensitivity, specificity, and likelihood ratios of tumor size to predict malignancy were 96%, 52%, and 2.0, respectively, for tumors > or = 4 cm; 90%, 80%, and 4.4 for tumors > or = 6 cm; 77%, 95%, and 16.9 for tumors > or = 8 cm; and 55%, 98%, and 24.4 for tumors > or = 10 cm.
  • Assuming a pretest probability of malignancy of 5%, the likelihood ratios derived from this study yield a posttest probability of 10%, 19%, and 47% for cancer in adrenal cortical tumors > or = 4 cm, > or = 6 cm, and > or = 8 cm, respectively.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Diagnosis, Differential. Female. Humans. Infant. Infant, Newborn. Male. Middle Aged. Neoplasm Staging. Prevalence. Probability. Prognosis. Retrospective Studies. Risk Assessment. SEER Program / statistics & numerical data. Severity of Illness Index

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  • (PMID = 16500246.001).
  • [ISSN] 1072-7515
  • [Journal-full-title] Journal of the American College of Surgeons
  • [ISO-abbreviation] J. Am. Coll. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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90. Pradeep PV, Mishra AK, Aggarwal V, Bhargav PR, Gupta SK, Agarwal A: Adrenal cysts: an institutional experience. World J Surg; 2006 Oct;30(10):1817-20
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  • [Title] Adrenal cysts: an institutional experience.
  • INTRODUCTION: Adrenal cysts are rare clinical entities.
  • We report our institutional experience with adrenal cysts and also assess various management options.
  • MATERIAL AND METHODS: Over the past 15 years the Department of Endocrine Surgery, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India, has had seven cases of adrenal cysts, of which two were functional: one patient had Cushing's syndrome and the other patient had pheochromocytoma.
  • It is generally agreed that a hormonal work-up is necessary in all cases of adrenal cysts to rule out a sub-clinical disease.
  • Adrenal neoplasms, including adrenocortical carcinomas, can be associated with cysts that are benign in appearance.
  • However, surgical excision provides a definite histopathological diagnosis and also removes the fear of future complications such as hemorrhage into the cyst and local pressure effects due to the tumor.
  • CONCLUSIONS: Given that the adrenals are a vascular gland and taking into consideration the possibilities of bleeding and complications in the cyst, our treatment of choice is the elective excision of adrenal cysts.
  • [MeSH-major] Academies and Institutes / statistics & numerical data. Adrenal Gland Diseases / diagnosis. Adrenal Gland Diseases / surgery. Adrenalectomy / methods. Cysts / diagnosis. Cysts / surgery
  • [MeSH-minor] Adult. Diagnosis, Differential. Female. Follow-Up Studies. Humans. India. Laparoscopy. Middle Aged. Retrospective Studies. Tomography, X-Ray Computed

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  • [Cites] J Urol. 2005 Mar;173(3):915-7 [15711326.001]
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  • (PMID = 16983481.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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91. Han SJ, Kim TS, Jeon SW, Jeong SJ, Yun M, Rhee Y, Kang ES, Cha BS, Lee EJ, Lee HC, Lim SK: Analysis of adrenal masses by 18F-FDG positron emission tomography scanning. Int J Clin Pract; 2007 May;61(5):802-9
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  • [Title] Analysis of adrenal masses by 18F-FDG positron emission tomography scanning.
  • This study aimed to analyse the characteristics of adrenal masses visible in the computerised tomography (CT) scans which have been also evaluated by 2-[18F]fluoro-2-deoxy-D-glucose positron emission tomography (18F-FDG PET), and to characterise the features of 18F-FDG PET scans associated with various adrenal endocrine tumours, especially benign functional tumours.
  • 18F-FDG PET scans of 105 patients with adrenal masses on the CT scan were analysed.
  • Positive uptakes in the 18F-FDG PET scans were seen in 60 malignant tumours (54 metastasic lesions, six primary adrenal cancers) and seven benign tumours.
  • The positive predictive value of 18F-FDG PET imaging to characterise an adrenal mass as a malignant tumour was 90%; the corresponding negative predictive value to rule out malignancy was also 90%.
  • Benign adrenal tumours were smaller than that of malignant lesions (p<0.05).
  • The mean standardised uptake value max (SUVmax) of the metastatic lesions [8.4+/-6.5 (microCi/g)/microCi/kg] was significantly higher than that of the benign adrenal tumours [2.4+/-1.2 (microCi/g)/microCi/kg, p<0.001].
  • Examination of only the primary adrenal lesions revealed that all adrenocortical carcinomas, two of three cases of pheochromocytomas, three of five neuroblastomas and two of four cases of primary aldosteronism showed positive 18F-FDG uptake.
  • In conclusion, for patients presenting adrenal masses with a high probability of malignancy, 18F-FDG PET can be used to differentiate malignant from benign adrenal lesions.
  • This study suggests that 18F-FDG PET scanning can offer supporting data to localise and characterise adrenal tumours.
  • [MeSH-major] Adrenal Gland Neoplasms / radionuclide imaging. Fluorodeoxyglucose F18. Positron-Emission Tomography / methods. Radiopharmaceuticals

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  • (PMID = 17343665.001).
  • [ISSN] 1368-5031
  • [Journal-full-title] International journal of clinical practice
  • [ISO-abbreviation] Int. J. Clin. Pract.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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92. Terzolo M, Angeli A, Fassnacht M, Daffara F, Tauchmanova L, Conton PA, Rossetto R, Buci L, Sperone P, Grossrubatscher E, Reimondo G, Bollito E, Papotti M, Saeger W, Hahner S, Koschker AC, Arvat E, Ambrosi B, Loli P, Lombardi G, Mannelli M, Bruzzi P, Mantero F, Allolio B, Dogliotti L, Berruti A: Adjuvant mitotane treatment for adrenocortical carcinoma. N Engl J Med; 2007 Jun 7;356(23):2372-80
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  • [Title] Adjuvant mitotane treatment for adrenocortical carcinoma.
  • BACKGROUND: Adrenocortical carcinoma is a rare neoplasm characterized by a high risk of recurrence after radical resection.
  • METHODS: We performed a retrospective analysis involving 177 patients with adrenocortical cancer who had undergone radical surgery at 8 centers in Italy and 47 centers in Germany between 1985 and 2005.
  • RESULTS: Baseline features in the mitotane group and the control group from Italy were similar; the German patients were significantly older (P=0.03) and had more stage I or II adrenocortical carcinomas (P=0.02) than did patients in the mitotane group.
  • CONCLUSIONS: Adjuvant mitotane may prolong recurrence-free survival in patients with radically resected adrenocortical carcinoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Adrenocortical Carcinoma / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Mitotane / therapeutic use


93. Gaujoux S, Pinson S, Gimenez-Roqueplo AP, Amar L, Ragazzon B, Launay P, Meatchi T, Libé R, Bertagna X, Audebourg A, Zucman-Rossi J, Tissier F, Bertherat J: Inactivation of the APC gene is constant in adrenocortical tumors from patients with familial adenomatous polyposis but not frequent in sporadic adrenocortical cancers. Clin Cancer Res; 2010 Nov 1;16(21):5133-41
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  • [Title] Inactivation of the APC gene is constant in adrenocortical tumors from patients with familial adenomatous polyposis but not frequent in sporadic adrenocortical cancers.
  • PURPOSE: In adrenocortical tumors (ACT), Wnt/β-catenin pathway activation can be explained by β-catenin somatic mutations only in a subset of tumors.
  • EXPERIMENTAL DESIGN: ACTs from patients with FAP and sporadic adrenocortical carcinomas (ACC) with abnormal β-catenin localization on immunohistochemistry but no somatic β-catenin mutations were studied.
  • RESULTS: Four ACTs were observed in three patients with FAP and were ACC, adrenocortical adenoma, and bilateral macronodular adrenocortical hyperplasia, all with abnormal β-catenin localization.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Gene Silencing. Genes, APC

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  • [Copyright] ©2010 AACR.
  • (PMID = 20978149.001).
  • [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 / AMER1 protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / Adenomatous Polyposis Coli Protein; 0 / Tumor Suppressor Proteins; 0 / beta Catenin
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94. Lumachi F, Borsato S, Tregnaghi A, Marino F, Fassina A, Zucchetta P, Marzola MC, Cecchin D, Bui F, Iacobone M, Favia G: High risk of malignancy in patients with incidentally discovered adrenal masses: accuracy of adrenal imaging and image-guided fine-needle aspiration cytology. Tumori; 2007 May-Jun;93(3):269-74
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  • [Title] High risk of malignancy in patients with incidentally discovered adrenal masses: accuracy of adrenal imaging and image-guided fine-needle aspiration cytology.
  • AIMS AND BACKGROUND: The incidental finding of nonfunctioning adrenal masses (incidentalomas) is common, but no reliable criteria in differentiating between benign and malignant adrenal masses have been defined.
  • The aim of this preliminary study was to assess the usefulness of adrenal imaging and image-guided fine-needle aspiration cytology in patients with nonfunctioning adrenal incidentalomas with the aim of excluding or confirming malignancy before surgery.
  • METHODS: Forty-two consecutive patients (18 men and 24 women; median age, 54 years; range, 25-75 years) with incidentally discovered adrenal masses of 3 cm or more in the greatest diameter were prospectively enrolled in the study.
  • RESULTS: The revised final pathology showed 30 (71.4%) benign (26 adrenocortical adenomas, of which 3 were atypical, 2 ganglioneuromas, and 2 nonfunctioning benign pheochromocytomas) and 12 (28.6%, 95% CI = 15-42) adrenal malignancies (8 adrenocortical carcinomas and 4 unsuspected adrenal metastases).
  • The definitive diagnosis of adrenocortical carcinoma was made according to Weiss criteria and confirmed on the basis of local invasion at surgery or metastases.
  • CONCLUSIONS: With the aim of selecting for surgery patients with a non-functioning adrenal incidentaloma of 3 cm or more in diameter, the combination of magnetic resonance imaging and fine-needle aspiration cytology should be considered the strategy of choice.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis. Biopsy, Fine-Needle. Incidental Findings. Magnetic Resonance Imaging
  • [MeSH-minor] 19-Iodocholesterol / analogs & derivatives. Adrenal Gland Diseases / diagnosis. Adrenal Gland Diseases / metabolism. Adrenal Gland Diseases / pathology. Adrenal Gland Diseases / radiography. Adrenal Gland Diseases / surgery. Adrenalectomy. Adrenocortical Adenoma / diagnosis. Adrenocortical Adenoma / metabolism. Adrenocortical Adenoma / pathology. Adrenocortical Adenoma / radiography. Adrenocortical Adenoma / surgery. Adrenocortical Carcinoma / diagnosis. Adrenocortical Carcinoma / metabolism. Adrenocortical Carcinoma / pathology. Adrenocortical Carcinoma / radiography. Adrenocortical Carcinoma / surgery. Adult. Aged. Aldosterone / blood. Epinephrine / urine. Female. Ganglioneuroma / diagnosis. Ganglioneuroma / metabolism. Ganglioneuroma / pathology. Ganglioneuroma / radiography. Ganglioneuroma / surgery. Humans. Hydrocortisone / blood. Iodine Radioisotopes. Laparoscopy. Male. Middle Aged. Norepinephrine / urine. Pheochromocytoma / diagnosis. Pheochromocytoma / metabolism. Pheochromocytoma / pathology. Pheochromocytoma / radiography. Pheochromocytoma / surgery. Predictive Value of Tests. Prospective Studies. Radiography, Abdominal. Renin / blood. Sensitivity and Specificity. Tomography, X-Ray Computed

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  • (PMID = 17679462.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Iodine Radioisotopes; 30461-91-7 / 19-Iodocholesterol; 4964P6T9RB / Aldosterone; 68232-36-0 / 6-iodomethylcholesterol; EC 3.4.23.15 / Renin; WI4X0X7BPJ / Hydrocortisone; X4W3ENH1CV / Norepinephrine; YKH834O4BH / Epinephrine
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95. Waldmann J, Bartsch DK, Kann PH, Fendrich V, Rothmund M, Langer P: Adrenal involvement in multiple endocrine neoplasia type 1: results of 7 years prospective screening. Langenbecks Arch Surg; 2007 Jul;392(4):437-43
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  • [Title] Adrenal involvement in multiple endocrine neoplasia type 1: results of 7 years prospective screening.
  • BACKGROUND: Adrenal tumors are a common manifestation of the multiple endocrine neoplasia type 1 (MEN-1) syndrome.
  • A genotype-phenotype correlation has been described as well as the development of adrenocortical carcinomas.
  • Adrenal glands have been screened by biochemical analysis and either by endoscopic ultrasound (EUS) or computed tomography (CT) or both.
  • Age at diagnosis of MEN-1, type of adrenal tumor, genotype, therapy, and clinical characteristics have been analyzed.
  • RESULTS: In 21 (55%) patients, adrenal involvement of the disease was detected.
  • Adrenal lesions were detected in average 6.9 years after the initial diagnosis of MEN-1.
  • Twelve patients had unilateral while nine had bilateral adrenal lesions.
  • EUS detected all adrenal tumors, whereas CT failed in seven cases.
  • In three patients, functioning tumors (one pheochromocytoma, one bilateral Cushing adenoma, and one adrenocortical carcinoma) and one nonfunctioning adenoma were diagnosed by histology and biochemical assessment.
  • Nonfunctioning adrenal lesions, not characterized by histology yet, were found in 18 patients.
  • There was no statistical difference with regard to adrenal involvement between patients with germline mutations in exons 2 and 10 (12/21) and those with mutations in exons 3-9 (6/11).
  • CONCLUSION: MEN-1-associated adrenal tumors are mostly small, benign, and nonfunctioning and much more common than previously reported.
  • [MeSH-major] Adrenal Gland Neoplasms. Multiple Endocrine Neoplasia Type 1

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  • (PMID = 17235589.001).
  • [ISSN] 1435-2443
  • [Journal-full-title] Langenbeck's archives of surgery
  • [ISO-abbreviation] Langenbecks Arch Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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96. Kazaryan AM, Marangos IP, Rosseland AR, Røsok BI, Villanger O, Pinjo E, Pfeffer PF, Edwin B: Laparoscopic adrenalectomy: Norwegian single-center experience of 242 procedures. J Laparoendosc Adv Surg Tech A; 2009 Apr;19(2):181-9
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  • BACKGROUND: The last 15 years have been characterized by a rapid expansion of minimally invasive surgery as treatment for adrenal diseases.
  • Of these, 192 patients were operated on for benign lesions, 23 for malignant lesions, and in 5 cases "en bloc" adrenalectomies were performed.
  • Benign lesions included 136 hormonally active lesions (41 pheochromocytomas, 48 Conn adenomas, 25 Cushing adenomas, and 18 patients with Cushing's disease) and 56 with hormonally inactive lesions (among them, 47 nonfunctional adenomas).
  • Malignant lesions included 16 adrenal metastases and 7 adrenocortical carcinomas.
  • The number of complications did not differ between the types of adrenal pathology.
  • Per- and postoperative parameters were homogeneous among patients with different adrenal lesions.
  • The patients with adrenocortical carcinoma had a distinctive intraoperative course with an evidently longer operative time and higher blood loss.
  • Hospital stay was the only postoperative parameter where a difference was found between patients with different adrenal lesions.
  • The patients with carcinoma, pheochromocytoma, and Cushing's disease had the longest median postoperative stay, respectively, 5 (range, 2-6), 3 (range, 1-15), and 3 (range, 2-6) days.
  • CONCLUSIONS: Laparoscopic adrenalectomy is a safe, effective procedure providing improved fast and uncomplicated patient recovery independent of the type of adrenal lesion.
  • [MeSH-major] Adrenal Gland Diseases / surgery. Adrenalectomy / methods. Laparoscopy / methods

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  • (PMID = 19216698.001).
  • [ISSN] 1092-6429
  • [Journal-full-title] Journal of laparoendoscopic & advanced surgical techniques. Part A
  • [ISO-abbreviation] J Laparoendosc Adv Surg Tech A
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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97. 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.
  • DESIGN AND SETTING: This study is a descriptive and multivariate analysis of a cohort from a single endocrinology center.
  • 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

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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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98. Rizk-Rabin M, Assie G, Rene-Corail F, Perlemoine K, Hamzaoui H, Tissier F, Lieberherr M, Bertagna X, Bertherat J, Bouizar Z: Differential expression of parathyroid hormone-related protein in adrenocortical tumors: autocrine/paracrine effects on the growth and signaling pathways in H295R cells. Cancer Epidemiol Biomarkers Prev; 2008 Sep;17(9):2275-85
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  • [Title] Differential expression of parathyroid hormone-related protein in adrenocortical tumors: autocrine/paracrine effects on the growth and signaling pathways in H295R cells.
  • Adrenocortical tumors (ACT) are rare and heterogeneous, but their pathogenesis is unclear.
  • We monitored the synthesis of PTHrP and PTH-R1 in a series of 25 ACT: 12 adrenocortical carcinomas (ACC) and 13 adrenocortical adenomas (ACA), and investigated the effects of PTHrP(1-34) on H295R cells derived from an ACC.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Parathyroid Hormone-Related Protein / metabolism. Receptor, Parathyroid Hormone, Type 1 / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Apoptosis. Blotting, Western. Calcium / metabolism. Cell Cycle. Cell Line, Tumor. Cyclic AMP-Dependent Protein Kinases / metabolism. Female. Humans. Male. Middle Aged. Prognosis. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction

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  • (PMID = 18768493.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Parathyroid Hormone-Related Protein; 0 / RNA, Messenger; 0 / Receptor, Parathyroid Hormone, Type 1; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; SY7Q814VUP / Calcium
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99. Faria JF, Goldman SM, Szejnfeld J, Melo H, Kater C, Kenney P, Huayllas MP, Demarchi G, Francisco VV, Andreoni C, Srougi M, Ortiz V, Abdalla N: Adrenal masses: characterization with in vivo proton MR spectroscopy--initial experience. Radiology; 2007 Dec;245(3):788-97
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  • [Title] Adrenal masses: characterization with in vivo proton MR spectroscopy--initial experience.
  • PURPOSE: To prospectively determine the accuracy of in vivo proton ((1)H) magnetic resonance (MR) spectroscopy in distinguishing adrenal adenomas, pheochromocytomas, adrenocortical carcinomas, and metastases, with histologic or computed tomographic findings and follow-up data as the reference standards.
  • Sixty consecutive patients (24 male and 36 female patients; mean age, 53 years) harboring adrenal tumors larger than 2 cm in diameter (mean diameter, 4.6 cm +/- 3.4 [standard deviation]) entered the study and were examined with a 1.5-T MR imaging system and point-resolved multivoxel (1)H MR spectroscopy.
  • Thirty-eight patients had adenomas; 10, pheochromocytomas; five, carcinomas; and seven, metastases.
  • Metabolite ratios (choline-creatine, choline-lipid, lipid-creatine, and 4.0-4.3 ppm/creatine) and cutoff values (obtained by using receiver operating characteristic analyses) were obtained and compared for each type of adrenal mass, which was identified previously on the basis of clinical, hormonal, and pathologic evidence.
  • RESULTS: Cutoff values of 1.20 for the choline-creatine ratio (92% sensitivity, 96% specificity; P < .01), 0.38 for the choline-lipid ratio (92% sensitivity, 90% specificity; P < .01), and 2.10 for the lipid-creatine ratio (45% sensitivity, 100% specificity) enabled adenomas and pheochromocytomas to be distinguished from carcinomas and metastases.
  • A 4.0-4.3 ppm/creatine ratio greater than 1.50 enabled distinction of pheochromocytomas and carcinomas from adenomas and metastases (87% sensitivity, 98% specificity; P < .01).
  • CONCLUSION: (1)H MR spectroscopy can be used to characterize adrenal masses on the basis of spectral findings for benign adenomas, carcinomas, pheochromocytomas, and metastases.
  • [MeSH-major] Adenoma / diagnosis. Adrenal Gland Neoplasms / diagnosis. Adrenocortical Carcinoma / diagnosis. Magnetic Resonance Spectroscopy. Pheochromocytoma / diagnosis
  • [MeSH-minor] Adult. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Prospective Studies. Reproducibility of Results

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  • [Copyright] (c) RSNA, 2007.
  • [CommentIn] Radiology. 2009 Mar;250(3):955-6; author reply 955-6; discussion 956 [19244058.001]
  • (PMID = 18024453.001).
  • [ISSN] 1527-1315
  • [Journal-full-title] Radiology
  • [ISO-abbreviation] Radiology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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100. van Nederveen FH, de Krijger RR: Precursor lesions of the adrenal gland. Pathobiology; 2007;74(5):285-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Precursor lesions of the adrenal gland.
  • OBJECTIVE: To review the existing literature for evidence that adrenocortical and adrenomedullary tumours develop through a multistep process of carcinogenesis.
  • RESULTS: In the adrenal cortex hyperplasia and adenomas are frequently observed tumours or tumour-like conditions.
  • In contrast, adrenocortical carcinomas are rare.
  • Based on well-validated histopathological scoring systems, benign and malignant adrenocortical tumours can be separated, although a small subset of tumours remains hard to classify.
  • Although extensive follow-up studies might argue against multistep carcinogenesis, analysis of chromosomal imbalances and gene expression profiling studies in these tumours are inconclusive and could give support for both multistep pathogenesis or de novo genesis of carcinomas.
  • In the adrenal medulla, pheochromocytomas (PCC) are the most frequent tumours in adults, with an incidence of 8 per million.
  • They can be divided into benign and malignant PCC, but the distinction can only be made when metastases are present.
  • In contrast to cortical tumours, the frequent 1p and 3q loss as an early event in tumourigenesis of benign PCC is verified in multiple studies.
  • However, studies in malignant PCC yield divergent results, due to the small numbers analysed.
  • CONCLUSION: Taken together, there appears to be a relationship between cortical and medullary hyperplasia on the one hand and cortical adenomas and PCC on the other.
  • However, whether there is a transition from benign to malignant tumours, both cortical and medullary, remains to be determined.
  • [MeSH-major] Adenoma / pathology. Adrenal Gland Neoplasms / pathology. Carcinoma / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Adrenal Cortex / pathology. Adrenal Cortex / physiology. Adrenal Medulla / pathology. Adrenal Medulla / physiology. Disease Progression. Humans. Hyperplasia / pathology

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  • [Copyright] Copyright 2007 S. Karger AG, Basel.
  • (PMID = 17890895.001).
  • [ISSN] 1423-0291
  • [Journal-full-title] Pathobiology : journal of immunopathology, molecular and cellular biology
  • [ISO-abbreviation] Pathobiology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 44
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