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1. Bezerra MG, Latronico AC, Fragoso MC: [Endocrine tumors associated to protein Gsalpha/Gi2alpha mutations]. Arq Bras Endocrinol Metabol; 2005 Oct;49(5):784-90

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The G proteins couple an array of seven transmembrane receptors at the cell surface with a variety of intracellular effectors, which produce second messenger molecules.
  • A subset of endocrine tumors, such as GH- or ACTH-secreting pituitary adenomas, functioning thyroid adenomas, adrenocortical and gonadal tumors were associated with somatic activating mutations in the highly conserved codons of the Gs (Arg201 and Gln227) and Gi (Arg179 and Gln205) proteins.
  • [MeSH-major] Endocrine Gland Neoplasms / genetics. GTP-Binding Protein alpha Subunits, Gi-Go / genetics. GTP-Binding Protein alpha Subunits, Gs / genetics. Mutation / genetics. Oncogenes / genetics

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  • (PMID = 16444361.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] por
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Brazil
  • [Chemical-registry-number] EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gi-Go; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
  • [Number-of-references] 64
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2. Shigematsu K, Nishida N, Sakai H, Igawa T, Toriyama K, Nakatani A, Takahara O, Kawai K: Synaptophysin immunoreactivity in adrenocortical adenomas: a correlation between synaptophysin and CYP17A1 expression. Eur J Endocrinol; 2009 Dec;161(6):939-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Synaptophysin immunoreactivity in adrenocortical adenomas: a correlation between synaptophysin and CYP17A1 expression.
  • DESIGN AND METHODS: The adrenal cortex is not considered to be an intrinsic part of the diffuse neuroendocrine system, but adrenocortical neoplasms possess neuroendocrine properties.
  • In this study, we examined synaptophysin (SYP) and neural cell adhesion molecule (NCAM) expression in adrenocortical adenomas in relation to adrenal function.
  • RESULTS: Immunohistochemical analysis showed that 50.7 and 98.6% of the cortical adenomas showed SYP and NCAM immunoreactivities respectively.
  • There was no apparent difference in NCAM immunoreactivity among the adenomas.
  • However, the immunostaining for SYP was significantly stronger in cortisol-producing adenomas (CPA) than in aldosterone-producing adenomas (APA), nonfunctioning adenomas (NFA), showing no clinical or endocrinological abnormality, or adenomas associated with preclinical Cushing's syndrome (preCS).
  • CONCLUSIONS: We propose that SYP expression in adrenocortical cells may be involved in some aspect of adrenal function such as transport or secretion of glucocorticoids.

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  • (PMID = 19755404.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neural Cell Adhesion Molecules; 0 / RNA, Messenger; 0 / Synaptophysin; EC 1.14.99.9 / CYP17A1 protein, human; EC 1.14.99.9 / Steroid 17-alpha-Hydroxylase
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3. Tan HS, Thai AC, Nga ME, Mukherjee JJ: Development of ipsilateral adrenocortical carcinoma sixteen years after resection of an adrenal tumour causing Cushing's syndrome. Ann Acad Med Singapore; 2005 Apr;34(3):271-4
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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 ipsilateral adrenocortical carcinoma sixteen years after resection of an adrenal tumour causing Cushing's syndrome.
  • INTRODUCTION: At times, it may be difficult to differentiate early stage, low-grade adrenocortical carcinoma from benign adrenal adenoma.
  • CLINICAL PICTURE: A 53-year-old lady underwent right adrenalectomy for a 4-cm adrenocortical tumour causing Cushing's syndrome.
  • Histology revealed an adrenocortical adenoma.
  • Sixteen years later, she presented with a 14-cm adrenal tumour, again on the right side.
  • Histology confirmed adrenocortical carcinoma.
  • OUTCOME: She died of metastatic disease 17 months later.
  • CONCLUSIONS: This case highlights the importance of long-term, systematic follow-up of patients treated for benign adrenal adenomas, especially if the tumour size exceeds 4 cm.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Cushing Syndrome / etiology. Neoplasm Recurrence, Local / pathology
  • [MeSH-minor] Adrenocortical Adenoma / pathology. Diagnosis, Differential. Fatal Outcome. Female. Humans. Middle Aged

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  • (PMID = 15902349.001).
  • [ISSN] 0304-4602
  • [Journal-full-title] Annals of the Academy of Medicine, Singapore
  • [ISO-abbreviation] Ann. Acad. Med. Singap.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Singapore
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4. Shigematsu K, Nakagaki T, Yamaguchi N, Kawai K, Sakai H, Takahara O: Analysis of mRNA expression for steroidogenic enzymes in the remaining adrenal cortices attached to adrenocortical adenomas. Eur J Endocrinol; 2008 Jun;158(6):867-78

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of mRNA expression for steroidogenic enzymes in the remaining adrenal cortices attached to adrenocortical adenomas.
  • DESIGN AND METHODS: We have recently demonstrated that the adrenal cortices attached to aldosterone-producing adenoma (APA) contained microscopic subcapsular micronodules suggestive of active aldosterone production.
  • In this study, we used in situ hybridization to investigate the mRNA expression of steroidogenic enzymes in the adrenal cortices attached to cortisol-producing adenoma (CPA) and clinically silent adenoma (non-functioning adenoma; NFA), in addition to APA.
  • Most of the cortical nodules in zona fasciculata to zona reticularis showed a suppressed steroidogenesis in the cortices attached to adenoma, but some expressed intensely all necessary steroidogenic enzyme mRNAs for cortisol synthesis.
  • CONCLUSIONS: It is thus necessary to keep in mind, on the occasion of subtotal adrenalectomy, that lesions with the potential to later develop into functional adrenocortical nodules may be present in other parts of the ipsilateral or contralateral adrenal cortices.

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  • (PMID = 18505908.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / RNA, Messenger; 0 / SPATA7 protein, human; EC 1.14.15.6 / Cholesterol Side-Chain Cleavage Enzyme; EC 1.14.99.9 / CYP17A1 protein, human; EC 1.14.99.9 / Steroid 17-alpha-Hydroxylase; EC 2.8.2.- / Sulfotransferases; EC 2.8.2.2 / alcohol sulfotransferase
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5. 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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6. 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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7. 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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8. Tadjine M, Lampron A, Ouadi L, Horvath A, Stratakis CA, Bourdeau I: Detection of somatic beta-catenin mutations in primary pigmented nodular adrenocortical disease (PPNAD). Clin Endocrinol (Oxf); 2008 Sep;69(3):367-73

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of somatic beta-catenin mutations in primary pigmented nodular adrenocortical disease (PPNAD).
  • BACKGROUND: Primary pigmented nodular adrenocortical disease (PPNAD) leads to Cushing syndrome (CS) and is often associated with Carney complex (CNC).
  • Recent studies have demonstrated that beta-catenin mutations are frequent in adrenocortical adenomas and carcinomas and that the Wnt-signalling pathway is involved in PPNAD tumorigenesis.
  • We hypothesized that adrenocortical adenomas that form in the context of PPNAD may harbour beta-catenin mutations.
  • Tumor DNA was extracted from pigmented adrenocortical adenoma and nodular adrenal hyperplasia.
  • In both cases, the mutations occurred in relatively large adenomas that had formed in the background of PPNAD.
  • Nuclear translocation of beta-catenin protein in the PPNAD adenoma suggests activation of the Wnt-beta-catenin pathway in PPNAD.
  • CONCLUSIONS: We report, for the first time, beta-catenin mutations in adenomas associated with PPNAD, further implicating Wnt-beta-catenin signalling in tumorigenesis linked to bilateral adrenal hyperplasias.
  • [MeSH-major] Adrenal Cortex Diseases / genetics. beta Catenin / genetics
  • [MeSH-minor] Adenoma / complications. Adenoma / genetics. Adenoma / pathology. Adolescent. Adrenal Cortex Neoplasms / complications. Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / pathology. Adult. Child. Child, Preschool. Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / genetics. DNA Mutational Analysis. Female. Genetic Testing. Humans. Male. Middle Aged. Mutation. Phosphoric Diester Hydrolases / genetics. Pigmentation Disorders / complications. Pigmentation Disorders / genetics. Young Adult

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  • (PMID = 18419788.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / ZIA HD000642-13
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human; 0 / beta Catenin; EC 3.1.4.- / Phosphoric Diester Hydrolases; EC 3.1.4.35 / PDE11A protein, human
  • [Other-IDs] NLM/ NIHMS307371; NLM/ PMC3138207
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9. Ziaja J, Cholewa K, Mazurek U, Cierpka L: [Molecular basics of aldosterone and cortisol synthesis in normal adrenals and adrenocortical adenomas]. Endokrynol Pol; 2008 Jul-Aug;59(4):330-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Molecular basics of aldosterone and cortisol synthesis in normal adrenals and adrenocortical adenomas].
  • [Transliterated title] Molekularne podstawy syntezy aldosteronu i kortyzolu w prawidlowych nadnerczach i w gruczolakach kory nadnerczy.
  • The aim of the study is to present genes encoding enzymatic proteins of aldosterone and cortisol synthesis pathway, methods of their transcriptional activity measurement, mRNA expression of the genes in normal adrenal cortex, in adrenocortical adenomas excised from patients with Conn and Cushing syndromes, as well as in adrenocortical adenomas excised from patients, in which hormonal activity of the tumour was not confirmed.
  • According to presented papers mRNA expression of analyzed genes is best known in tissue obtained from tumours excised from patients with Conn syndrome.
  • On the other hand transcriptional activity of the genes within the other adrenocortical adenomas is documented in lesser degree.
  • It concerns particularly analyses of tissue material obtained from patients, in which hormonal activity of adrenal tumours was not confirmed with biochemical tests.
  • It should be also considered, that the frame of reference for the majority of molecular analyses of adrenocortical tumour tissues was material obtained from little number of normal adrenals, what decreases in some degree credibility of obtained results.
  • Mentioned above remarks may be the basis for conduction of further investigations based on larger material, obtained both from normal adrenals and adrenocortical adenomas.
  • [MeSH-major] Adrenal Cortex Neoplasms / enzymology. Adrenal Glands / metabolism. Adrenocortical Adenoma / enzymology. Aldosterone / biosynthesis. Gene Expression Regulation, Enzymologic. Hydrocortisone / biosynthesis. Mixed Function Oxygenases / genetics
  • [MeSH-minor] Adrenal Cortex / metabolism. Cushing Syndrome / genetics. Cushing Syndrome / metabolism. Cytochrome P-450 CYP11B2 / genetics. Humans. Hyperaldosteronism / genetics. Hyperaldosteronism / metabolism. RNA, Messenger / analysis. Reference Values. Transcription, Genetic

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  • (PMID = 18777504.001).
  • [ISSN] 0423-104X
  • [Journal-full-title] Endokrynologia Polska
  • [ISO-abbreviation] Endokrynol Pol
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / RNA, Messenger; 4964P6T9RB / Aldosterone; EC 1.- / Mixed Function Oxygenases; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; WI4X0X7BPJ / Hydrocortisone
  • [Number-of-references] 76
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10. Inoue T, Ishiguro K, Suda T, Ito N, Suzuki Y, Taniguchi Y, Ohgi S: Laparoscopic bilateral partial adrenalectomy for adrenocortical adenomas causing Cushing's syndrome: report of a case. Surg Today; 2006;36(1):94-7
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  • [Title] Laparoscopic bilateral partial adrenalectomy for adrenocortical adenomas causing Cushing's syndrome: report of a case.
  • Laparoscopic total adrenalectomy has become a standard technique for small adrenal tumors; however, bilateral adrenalectomy results in postoperative adrenal insufficiency, necessitating lifelong steroid replacement.
  • To preserve adrenocortical function in a 41-year-old woman with bilateral adrenocortical adenoma (BAA) causing Cushing's syndrome, we performed laparoscopic bilateral partial adrenalectomy.
  • We based our preoperative diagnosis of bilateral adrenocortical tumors causing Cushing's syndrome on the results of endocrinological investigations and imaging findings.
  • Thus, we performed lateral transperitoneal laparoscopic bilateral partial adrenalectomy, preserving the adrenal glands, which were normal.
  • Pathological examination of both tumors confirmed the diagnosis of adrenocortical adenoma.
  • The patient had no postoperative complications, and her adrenocortical function was normal without steroid replacement at her 10-month follow-up.
  • This report shows that Cushing's syndrome resulting from bilateral adenomas can be effectively treated by laparoscopic bilateral partial adrenalectomy as a minimally invasive, adrenocortical-preserving operation.
  • [MeSH-major] Adrenalectomy / methods. Adrenocortical Adenoma / surgery. Cushing Syndrome / etiology. Laparoscopy

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  • (PMID = 16378204.001).
  • [ISSN] 0941-1291
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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11. Kamenicky P, Houdoin L, Ferlicot S, Salenave S, Brailly S, Droupy S, Meduri G, Sasano H, Suzuki T, Young J, Chanson P: Benign cortisol-secreting adrenocortical adenomas produce small amounts of androgens. Clin Endocrinol (Oxf); 2007 Jun;66(6):778-88
Hazardous Substances Data Bank. Corticotropin .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Benign cortisol-secreting adrenocortical adenomas produce small amounts of androgens.
  • BACKGROUND: Serum androgen levels are below normal in patients with benign cortisol-secreting adrenocortical adenomas, owing to ACTH suppression.
  • The objective of the study was to analyse the androgen-producing ability of cortisol-secreting adrenocortical adenomas.
  • METHODS: Dehydroepiandrosterone sulfate (DHEAS), Delta4androstenedione and testosterone concentrations were measured before and after adrenalectomy and then at 6-month intervals in 20 women (eight cortisol-secreting adrenocortical adenomas, six subclinical cortisol-secreting adrenocortical adenomas, and six nonfunctional adenomas).
  • RESULTS: Before adrenalectomy, serum androgen concentrations were measurable in all women with clinically apparent and subclinical cortisol-secreting adrenocortical adenomas.
  • Postoperatively, during adrenocortical insufficiency, DHEAS, Delta4androstenedione and testosterone concentrations fell to near the detection limit in all patients with cortisol-secreting adrenocortical adenomas (P = 0.008 for each marker) and showed a similar tendency to fall in all patients with subclinical cortisol-secreting adrenocortical adenomas.
  • Pre- and post-treatment androgen concentrations did not differ in patients with nonfunctional adenomas.
  • The intensity of CYP17 and SULT2A1 expression was stronger in cortisol-secreting adenomas than in their adjacent normal adrenal tissue.
  • CONCLUSION: Both clinically apparent and subclinical cortisol-secreting adrenocortical adenomas appear to show moderate autonomous androgen production.
  • Thus, weak androgen secretion in patients with adrenocortical tumours should not necessarily be considered as a sign of malignancy.
  • [MeSH-major] Adenoma / secretion. Adrenal Cortex Neoplasms / secretion. Androgens / secretion. Hydrocortisone / secretion

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  • (PMID = 17408424.001).
  • [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 / Androgens; 0 / Estrogens; 0 / Gonadotropins, Pituitary; 3XMK78S47O / Testosterone; 409J2J96VR / Androstenedione; 57B09Q7FJR / Dehydroepiandrosterone Sulfate; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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12. Hennings J, Sundin A, Hägg A, Hellman P: 11C-metomidate positron emission tomography after dexamethasone suppression for detection of small adrenocortical adenomas in primary aldosteronism. Langenbecks Arch Surg; 2010 Sep;395(7):963-7
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  • [Title] 11C-metomidate positron emission tomography after dexamethasone suppression for detection of small adrenocortical adenomas in primary aldosteronism.
  • PURPOSE: To evaluate whether dexamethasone suppression treatment can improve (11) C-metomidate positron emission tomography (MTO-PET) detection of small adrenocortical adenomas in primary aldosteronism (PA).
  • MATERIALS AND METHODS: Eleven patients with proven PA and two patients with non-hyperfunctioning adrenocortical incidentalomas and small adrenocortical tumours observed on CT underwent MTO-PET before and 3 days after administration of oral dexamethasone suppression treatment.
  • RESULTS: All tumours were detected and categorised as adrenocortical by MTO-PET.
  • SUVhs as well as SUVmax were higher in PA compared to nonfunctional adenomas.
  • Normal adrenal cortex was suppressed after dexamethasone (p < 0.05), but tumour SUV was not significantly decreased after suppression in either PA or nonfunctional tumours (p > 0.05).
  • However, these changes caused no significant increase in the tumour-to-normal adrenal ratio (p > 0.05).
  • CONCLUSION: MTO-PET is a highly sensitive method for detecting and categorising even small adrenocortical tumours in PA.
  • In this series, dexamethasone-suppressed MTO-PET was unable to increase the tumour-to-normal adrenal ratio to further facilitate detection of small adenomas in PA as an alternative to adrenal venous sampling.

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  • (PMID = 20644954.001).
  • [ISSN] 1435-2451
  • [Journal-full-title] Langenbeck's archives of surgery
  • [ISO-abbreviation] Langenbecks Arch Surg
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 5377-20-8 / metomidate; 7S5I7G3JQL / Dexamethasone; Z22628B598 / Etomidate
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13. Boyle B, Butz H, Liko I, Zalatnai A, Toth M, Feldman K, Horanyi J, Igaz P, Racz K, Patocs A: Expression of glucocorticoid receptor isoforms in human adrenocortical adenomas. Steroids; 2010 Oct;75(10):695-700

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of glucocorticoid receptor isoforms in human adrenocortical adenomas.
  • INTRODUCTION: Glucocorticoid receptor (GR) is expressed in the normal human adrenal gland, however, no study has been performed to evaluate the separate expression of alpha- and beta-isoforms (GRalpha and GRbeta) in normal human adrenals and in adrenocortical adenomas.
  • EXPERIMENTAL: GRalpha and GRbeta mRNA expression was examined by quantitative real-time PCR in 31 adrenal tissues including 19 non-functioning adenomas (NFA), 6 cortisol-producing adenomas (CPA) and 6 normal adrenocortical tissues.
  • In addition, the presence and cellular localization of GRalpha and GRbeta proteins in adrenal tissues were studied by immunohistochemistry.
  • RESULTS: Compared to normal adrenocortical tissues, both GRalpha and GRbeta mRNAs were significantly increased in CPA but not in NFA.
  • Using anti-GRalpha antibody a strong nuclear staining was observed in NFA and CPA, and a less remarkable immunoreactivity was detected in some nuclei of normal adrenocortical cells.
  • GRbeta immunostaining was absent in normal adrenal tissues and NFA, while a strong cytoplasmic and nuclear immunoreaction was found in CPA.
  • CONCLUSIONS: Altered expression of GRalpha and GRbeta in CPA raises their possible role in the pathophysiology of these adrenal tumors, although further studies are needed to elucidate the potential significance of these findings.
  • [MeSH-major] Adrenocortical Adenoma / metabolism. Protein Isoforms / metabolism. Receptors, Glucocorticoid / metabolism

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  • (PMID = 20438742.001).
  • [ISSN] 1878-5867
  • [Journal-full-title] Steroids
  • [ISO-abbreviation] Steroids
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / Receptors, Glucocorticoid
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14. Hirose A, Okada Y, Fukushima A, Tanaka Y: [A rare case of primary aldosteronism caused by bilateral functioning adrenocortical adenomas with renal cell carcinoma]. J UOEH; 2005 Dec 1;27(4):315-23
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  • [Title] [A rare case of primary aldosteronism caused by bilateral functioning adrenocortical adenomas with renal cell carcinoma].
  • We report a rare case of bilateral primary aldosteronism with renal cell carcinoma.
  • Abdominal CT and MRI revealed tumor masses in both adrenal glands, and a large left renal mass.
  • The preoperative diagnosis was primary aldosteronism due to bilateral functioning adrenocortical adenomas and left renal cell carcinoma.
  • The Pathological diagnosis was left renal cell carcinoma and bilateral functioning adrenocortical adenomas.
  • Primary aldosteronism due to bilateral functioning adrenocortical adenomas is relatively rare and its complication with renal cell carcinoma is an extremely rare case.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications. Carcinoma, Renal Cell / complications. Hyperaldosteronism / etiology. Kidney Neoplasms / complications


15. 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.
  • Genetic alterations were found in 5 (15%) out of 33 adenomas: three cortisol-secreting adenomas, one aldosterone-secreting adenoma and one nonfunctional adenoma.
  • In addition, cytoplasmic and/or nuclear accumulation of beta-catenin was observed in mutated adenomas by immunohistochemistry.
  • 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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16. Contesse V, Reznik Y, Louiset E, Duparc C, Cartier D, Sicard F, Laquerriere A, Parmentier F, Kuhn JM, Vaudry H, Lefebvre H: Abnormal sensitivity of cortisol-producing adrenocortical adenomas to serotonin: in vivo and in vitro studies. J Clin Endocrinol Metab; 2005 May;90(5):2843-50
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  • [Title] Abnormal sensitivity of cortisol-producing adrenocortical adenomas to serotonin: in vivo and in vitro studies.
  • Two patients with incidentally discovered adrenocortical adenomas underwent a series of pharmacological and physiological tests after pretreatment with dexamethasone.
  • In the two cases, 5-HT stimulated cortisol secretion from tumor cells with increased efficacy and/or potency to activate steroidogenesis by comparison with normal adrenocortical cells.
  • In the two adenoma tissues, immunohistochemical studies revealed the presence of 5-HT-like immunoreactivity within clusters of steroidogenic cells, suggesting that 5-HT acted through an autocrine/paracrine mechanism to stimulate steroidogenesis.
  • In conclusion, this study provides the first observation of adrenocortical cortisol-producing adenomas hypersensitive in vivo and in vitro to serotonergic agonists.
  • Our results also show that cortisol-producing adenomas can express simultaneously several illegitimate receptors.
  • [MeSH-major] Adenoma / metabolism. Adrenocortical Adenoma / metabolism. Hydrocortisone / secretion. Serotonin / pharmacology

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  • [CommentIn] Horm Metab Res. 2005 Aug;37(8):528-9 [16138268.001]
  • (PMID = 15705918.001).
  • [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] 158165-40-3 / Receptors, Serotonin, 5-HT4; 333DO1RDJY / Serotonin; WI4X0X7BPJ / Hydrocortisone
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17. Spinazzi R, Rucinski M, Neri G, Malendowicz LK, Nussdorfer GG: Preproorexin and orexin receptors are expressed in cortisol-secreting adrenocortical adenomas, and orexins stimulate in vitro cortisol secretion and growth of tumor cells. J Clin Endocrinol Metab; 2005 Jun;90(6):3544-9
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  • [Title] Preproorexin and orexin receptors are expressed in cortisol-secreting adrenocortical adenomas, and orexins stimulate in vitro cortisol secretion and growth of tumor cells.
  • We previously found that orexin-A, via the OX1-R, stimulates cortisol secretion from dispersed human adrenocortical cells.
  • In this study, we demonstrate that six of eight cortisol-secreting adenomas expressed preproorexin mRNA, and seven of 10 adenomas contained measurable amounts of orexin-A but not orexin-B.
  • Normal adrenal cortexes neither expressed preproorexin nor contained orexins.
  • All adenomas expressed OX1-R and OX2-R mRNAs, and real-time PCR showed that the expression of both receptors was up-regulated in adenomas, compared with normal adrenal cortex.
  • Orexin-A concentration-dependently raised basal cortisol secretion from freshly dispersed normal and adenomatous cells, minimal and maximal effective concentrations being 10(-10) and 10(-8) m, and the peptide efficacy (percent increase elicited by 10(-8) m orexin-A) was significantly higher in adenomas than in the normal adrenal cortex.
  • Collectively, our findings allow us to conclude that the orexin system is overexpressed in cortisol-secreting adenomas and suggest that orexin-A may act as an autocrine-paracrine regulator of the secretory activity and growth of some of these adrenal tumors.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics. Hydrocortisone / secretion. Receptors, Neuropeptide / genetics

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  • (PMID = 15797953.001).
  • [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
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA, Complementary; 0 / HCRT protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / Neuropeptides; 0 / Orexin Receptors; 0 / Orexins; 0 / RNA, Messenger; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Neuropeptide; WI4X0X7BPJ / Hydrocortisone
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18. Schittenhelm J, Ebner FH, Harter P, Bornemann A: Symptomatic intraspinal oncocytic adrenocortical adenoma. Endocr Pathol; 2009;20(1):73-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Symptomatic intraspinal oncocytic adrenocortical adenoma.
  • Benign epithelial tumors are rarely found at this site.
  • We here present the case of a 44-year-old woman with a lesion in the cauda equina that fulfilled the radiologic criteria of schwannoma and caused clinical symptoms for 3 years.
  • This immunoprofile indicated adrenocortical origin.
  • The diagnosis of an oncocytic adrenal cortical adenoma was made.
  • These extraadrenal tumors are thought to arise from heterotopic adrenocortical tissue in the spinal cavity.
  • Oncocytic tumors are rare neoplasms and they comprise non-functioning variants of adrenal cortical adenomas.
  • Immunohistochemistry excluded oncocytic paraganglioma, oncocytic meningioma, renal cell carcinoma, alveolar soft part sarcoma, and granular cell tumor.
  • [MeSH-major] Adenoma, Oxyphilic / pathology. Adrenocortical Adenoma / pathology. Spinal Cord Neoplasms / pathology

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  • (PMID = 19039533.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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19. Hosogi H, Nagayama S, Kanamoto N, Yoshizawa A, Suzuki T, Nakao K, Sakai Y: Biallelic APC inactivation was responsible for functional adrenocortical adenoma in familial adenomatous polyposis with novel germline mutation of the APC gene: report of a case. Jpn J Clin Oncol; 2009 Dec;39(12):837-46
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  • [Title] Biallelic APC inactivation was responsible for functional adrenocortical adenoma in familial adenomatous polyposis with novel germline mutation of the APC gene: report of a case.
  • Familial adenomatous polyposis (FAP) patients develop various extracolonic lesions, among which functional adrenocortical neoplasms are infrequent.
  • Furthermore, bilateral adrenocortical adenomas were detected, and functional analyses showed a hormonal secretion pattern consistent with Cushing's syndrome.
  • At 10 months post-operative with no detectable metastatic lesions, the residual colorectum and the larger, left adrenal gland were resected, and the hormonal hypersecretion was normalized.
  • Biallelic APC inactivation due to loss of the normal allele was evident in the adrenocortical adenoma.
  • Immunostaining for beta-catenin revealed diffuse cytoplasmic expression in resected tissues including adrenocortical adenoma.
  • Biallelic APC inactivation may play a role in developing cortisol-secreting adrenocortical adenoma in FAP patients.
  • [MeSH-major] Adenomatous Polyposis Coli / metabolism. Adenomatous Polyposis Coli Protein / genetics. Adrenocortical Adenoma / metabolism. Genes, APC / physiology

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  • (PMID = 19684041.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein
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20. Ouzounian S, Tissier F, Gouya H, Kujas M, Louvel A, Legmann P, Bertagna X: [Cushing's syndrome and adrenal adenoma. Two surprising associations]. Presse Med; 2005 Apr 09;34(7):511-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Cushing's syndrome and adrenal adenoma. Two surprising associations].
  • [Transliterated title] Maladie de Cushing et adénome cortico-surrénalien. Deux associations étonnantes.
  • CASES: In the first case, we describe the case of a patient with an adrenal adenoma 20 years before the occurrence of Cushing's disease related to the pineal gland.
  • In the second case, two members of the same family were diagnosed almost simultaneously with adrenal cortical adenoma (mother) and Cushing's disease (daughter).
  • [MeSH-major] Adenoma / complications. Adrenal Gland Neoplasms / complications. Cushing Syndrome / etiology

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  • (PMID = 15903005.001).
  • [ISSN] 0755-4982
  • [Journal-full-title] Presse medicale (Paris, France : 1983)
  • [ISO-abbreviation] Presse Med
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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21. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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
  • [MeSH-minor] Adenoma / radiography. Adolescent. Adult. Aged. Female. Humans. Male. Middle Aged. Sensitivity and Specificity

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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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22. Vezzosi D, Bertherat J, Groussin L: Pathogenesis of benign adrenocortical tumors. Best Pract Res Clin Endocrinol Metab; 2010 Dec;24(6):893-905

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pathogenesis of benign adrenocortical tumors.
  • Most adrenocortical tumors (ACT) are benign unilateral adrenocortical adenomas, often discovered incidentally.
  • The identification of the genetics of familial diseases associated with benign ACT has been helpful to define somatic alterations in sporadic ACT: for example, identification of PRKAR1A mutations in Carney complex or alterations of the Wnt/β-catenin pathway in Familial Adenomatous Polyposis Coli.
  • Components of the cAMP signaling pathway-for example, adrenocorticotropic-hormone receptors and other membrane receptors, Gs protein, phosphodiesterases and protein kinase A-can be altered to various degrees in benign cortisol-secreting ACT.
  • These progress have been important for the understanding of the pathogenesis of benign ACT, but already have profound implications for clinical management, for example in unraveling the genetic origin of disease in some patients with ACT.
  • [MeSH-major] Adrenal Cortex Neoplasms / etiology

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  • [Copyright] 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 21115158.001).
  • [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
  • [Publication-country] Netherlands
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23. Wu Z, Ni D, Yan Y, Li J, Wang B, Ouyang J, Zhang G, Ma X, Li H, Zhang X: Expression of angiotensin II receptors in aldosterone-producing adenoma of the adrenal gland and their clinical significance. J Huazhong Univ Sci Technolog Med Sci; 2010 Aug;30(4):486-9
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  • [Title] Expression of angiotensin II receptors in aldosterone-producing adenoma of the adrenal gland and their clinical significance.
  • The expression of angiotensin II type 1 receptor (AT1R) and angiotensin II type 2 receptor (AT2R) in aldosterone-producing adenoma (APA) of the adrenal gland was detected, and their relationship with clinical indexes of APA was analyzed.
  • The mRNA expression of AT1R and AT2R in 50 cases of APA and tissues adjacent to tumors and 12 cases of normal adrenal tissues was detected by using reverse transcriptase polymerase chain reaction (RT-PCR).
  • The expression of AT1R in adenoma, tissues adjacent to tumor, and normal tissues of the adrenal gland showed no significant differences.
  • The expression of AT2R in APA tissue was lower than that in normal adrenal gland tissues (P<0.05).
  • [MeSH-major] Adenoma / metabolism. Adrenal Gland Neoplasms / metabolism. Aldosterone / blood. Receptor, Angiotensin, Type 1 / metabolism. Receptor, Angiotensin, Type 2 / metabolism

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  • (PMID = 20714875.001).
  • [ISSN] 1672-0733
  • [Journal-full-title] Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban
  • [ISO-abbreviation] J. Huazhong Univ. Sci. Technol. Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / AGTR1 protein, human; 0 / RNA, Messenger; 0 / Receptor, Angiotensin, Type 1; 0 / Receptor, Angiotensin, Type 2; 4964P6T9RB / Aldosterone
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24. 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
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  • [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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25. Bertherat J, Bertagna X: Pathogenesis of adrenocortical cancer. Best Pract Res Clin Endocrinol Metab; 2009 Apr;23(2):261-71
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  • [Title] Pathogenesis of adrenocortical cancer.
  • The study of the clonality of adrenocortical tumours (ACTs) has shown that adrenocortical cancers (ACCs) are of monoclonal origin.
  • Numerous chromosomal alterations have been observed in ACCs, and they are much more frequent than in adrenocortical adenomas.
  • This recent progress in the molecular genetics of ACC has led to the development of new molecular markers for the diagnosis of malignancy; these might also help to identify prognostic markers of ACC and may ultimately lead to novel therapeutic approaches.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology

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  • (PMID = 19500768.001).
  • [ISSN] 1878-1594
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 67
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26. 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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27. Bertherat J, Groussin L, Bertagna X: Mechanisms of disease: adrenocortical tumors--molecular advances and clinical perspectives. Nat Clin Pract Endocrinol Metab; 2006 Nov;2(11):632-41
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  • [Title] Mechanisms of disease: adrenocortical tumors--molecular advances and clinical perspectives.
  • Most adrenocortical tumors are benign, unilateral, adrenocortical adenomas that are often discovered incidentally.
  • Adrenocortical cancer is rare.
  • Exceptionally, adrenocortical tumors can be bilateral.
  • Although most adrenocortical tumors occur sporadically, they may also feature in congenital and/or familial disease.
  • The identification of germline genetic defects in familial diseases associated with adrenocortical tumors helped to define the somatic alterations in sporadic disease: for example, overexpression of insulin-like growth factor 2 and alterations at the 11p15 locus (observed in Beckwith-Wiedemann syndrome) are also found in most adrenocortical cancers.
  • Similarly, inactivating mutations of the TP53 gene, located at 17p13 (observed in Li-Fraumeni syndrome), can also be found at the somatic level in sporadic adrenocortical cancers, as can 17p13 allelic losses.
  • Components of the cyclic AMP signaling pathway--for example, adrenocorticotropic hormone receptors and other membrane receptors, Gs proteins and protein kinase A--can be altered to various degrees in adrenocortical tumors.
  • More recently, gene profiling and genetic studies have shown that the Wnt-beta-catenin signaling pathway is frequently activated in adrenocortical tumors.
  • These research findings already have profound implications for clinical management of patients with adrenocortical tumors, for example in unraveling the genetic origin of the disease in some patients, and in the development of molecular markers for diagnosis and prognosis.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics

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  • (PMID = 17082810.001).
  • [ISSN] 1745-8366
  • [Journal-full-title] Nature clinical practice. Endocrinology & metabolism
  • [ISO-abbreviation] Nat Clin Pract Endocrinol Metab
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 54
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28. 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

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  • [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.
  • 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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29. Oki K, Yamane K, Sakashita Y, Kamei N, Watanabe H, Toyota N, Shigeta M, Sasano H, Kohno N: Primary aldosteronism and hypercortisolism due to bilateral functioning adrenocortical adenomas. Clin Exp Nephrol; 2008 Oct;12(5):382-7
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  • [Title] Primary aldosteronism and hypercortisolism due to bilateral functioning adrenocortical adenomas.
  • A 50-year-old male patient with a 15-year history of hypertension was referred to our hospital for evaluation of bilateral adrenal tumors.
  • Computed tomographic scan showed 10-mm masses in each adrenal gland.
  • The results of a subsequent adrenal venous catheterization study were consistent with the presence of a left cortisol-producing tumor and a right aldosterone-producing tumor.
  • Pathological examination of the resected specimens, including immunohistochemical analysis, demonstrated that both adenomas possibly produced cortisol and aldosterone.
  • This is an extremely rare case of bilateral adrenal tumors, in which the left adrenocortical tumor produced and secreted cortisol or both cortisol and aldosterone and the right one produced and secreted both aldosterone and cortisol, as confirmed by clinical findings and pathological studies using immunohistochemical analysis.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications. Cushing Syndrome / etiology. Hyperaldosteronism / etiology
  • [MeSH-minor] Aldosterone / metabolism. Diagnosis, Differential. Humans. Hydrocortisone / metabolism. Male. Middle Aged

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  • (PMID = 18543063.001).
  • [ISSN] 1342-1751
  • [Journal-full-title] Clinical and experimental nephrology
  • [ISO-abbreviation] Clin. Exp. Nephrol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone; WI4X0X7BPJ / Hydrocortisone
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30. Orhan D, Kale G, Cağlar M, Göğüş S, Karaağaoğlu E: Histone mRNA in situ hybridization and Ki 67 immunohistochemistry in pediatric adrenocortical tumors. Virchows Arch; 2006 May;448(5):591-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Histone mRNA in situ hybridization and Ki 67 immunohistochemistry in pediatric adrenocortical tumors.
  • Adrenocortical tumors in the pediatric population are rare.
  • Classification of these tumors as adenomas or carcinomas using histological criteria is often difficult.
  • Immunohistochemical expressions of proliferative markers are currently under investigation for utilization in the differential diagnosis and prediction of clinical outcomes.
  • The value of histone proteins as prognostic markers in adrenocortical tumors has not yet been elucidated.
  • We evaluated the histological features, immunohistochemical staining of Ki 67, and in situ hybridization for histone mRNA in 30 pediatric adrenocortical tumors.
  • Using the classification proposed by Weiss, 19 tumors were classified as carcinomas and 11 as adenomas.
  • Ki 67 and histone mRNA labeling indices (LIs, the percentage of Ki 67-positive and histone mRNA-positive tumor cells, respectively) were significantly higher in carcinomas than in adenomas (Ki 67 LI was 14.62+/-5.79 in adenomas and 20.35+/-6.23 in carcinomas, p=0.02.
  • Histone mRNA LI was 1.73+/-1.71 in adenomas and 6.62+/-2.28 in carcinomas, p=0.00).
  • The cut off point for the diagnosis of malignancy was found to be 14.55 for Ki 67 LI and 5.75 for histone mRNA LI.
  • We concluded that the proliferative activity of the tumor assessed by Ki 67 and histone mRNA may assist in differentiating adrenocortical adenomas and carcinomas.
  • In addition, our results suggest that the most reliable parameter to predict prognosis in pediatric adrenocortical tumors is the histone mRNA LI.
  • [MeSH-major] Adrenocortical Adenoma / diagnosis. Adrenocortical Carcinoma / diagnosis. Biomarkers, Tumor / analysis. Histones / metabolism. Ki-67 Antigen / metabolism. RNA, Messenger / analysis
  • [MeSH-minor] Child. Diagnosis, Differential. Humans. Immunohistochemistry. In Situ Hybridization. Prognosis. ROC Curve

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  • (PMID = 16489441.001).
  • [ISSN] 0945-6317
  • [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 / Biomarkers, Tumor; 0 / Histones; 0 / Ki-67 Antigen; 0 / RNA, Messenger
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31. 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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32. Willenberg HS, Haase M, Papewalis C, Schott M, Scherbaum WA, Bornstein SR: Corticotropin-releasing hormone receptor expression on normal and tumorous human adrenocortical cells. Neuroendocrinology; 2005;82(5-6):274-81
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  • [Title] Corticotropin-releasing hormone receptor expression on normal and tumorous human adrenocortical cells.
  • Corticotropin-releasing hormone (CRH) is not only the principal regulator of the central hypothalamic-pituitary-adrenal (HPA) axis but also exerts direct actions on peripheral tissues.
  • We analyzed the expression of CRH receptors in microdissected preparations of normal human adrenal glands and in adrenocortical and adrenomedullary tumors, employing immunohistochemistry, quantitative RT-PCR of microdissected adrenal tissues, and in situ hybridization.
  • The effect of CRH on adrenal steroidogenesis was tested in adrenal cells.
  • In addition, we found a higher expression of CRH type-1 and 2 receptors mRNAs in preparations of adrenal cortices as compared to pheochromocytomas, a 6-fold increase in preparations of clinically unapparent adrenocortical adenomas, and a 10- to 60-fold increase in cortisol-producing adrenal adenomas.
  • Stimulation of the adrenal tumor cell line NCI-H295R with CRH elicited a 1.4-fold increase in DHEA secretion.
  • This result could be reproduced in a culture of primary human adrenocortical cells.
  • We conclude that adrenocortical cells exhibit a higher expression of functional CRH receptors than chromaffin cells and that CRH acts on adrenal DHEA production.
  • The data support the assertion of a direct action of CRH on human adrenocortical cells in addition to an intra-adrenal CRH receptor/adrenocorticotropin system.
  • Enhanced CRH1R expression may be involved in adrenocortical tumorigenesis.
  • [MeSH-major] Adrenal Cortex / chemistry. Adrenal Cortex Neoplasms / chemistry. Adrenocortical Adenoma / chemistry. Adrenocortical Carcinoma / chemistry. Pheochromocytoma / chemistry. Receptors, Corticotropin-Releasing Hormone / genetics

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  • (PMID = 16721033.001).
  • [ISSN] 0028-3835
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / CRF receptor type 1; 0 / CRF receptor type 2; 0 / RNA, Messenger; 0 / Receptors, Corticotropin-Releasing Hormone; 9015-71-8 / Corticotropin-Releasing Hormone
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33. Onoda N, Ishikawa T, Nishio K, Tahara H, Inaba M, Wakasa K, Sumi T, Yamazaki T, Shigematsu K, Hirakawa K: Cushing's syndrome by left adrenocortical adenoma synchronously associated with primary aldosteronism by right adrenocortical adenoma: report of a case. Endocr J; 2009;56(3):495-502
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  • [Title] Cushing's syndrome by left adrenocortical adenoma synchronously associated with primary aldosteronism by right adrenocortical adenoma: report of a case.
  • Synchronous associations of Cushing's syndrome (CS) and primary aldosteronism (PA) with multiple adrenocortical adenomas secreting each hormone independently have rarely been reported.
  • Bilateral adrenal masses with clinical symptoms of CS and PA were found in a 43-year-old woman.
  • The right adrenal tumor (3 cm) was yellow in color with abundant lipofuscin granules, and was composed of both eosinophilic compact cells and clear cells.
  • Left adrenal tumor (2.4 cm) was golden-yellow in color, and composed of clear cells only.
  • Furthermore, minute nodules were found at the surface of normal-appearing cortex on both sides of the adrenal glands, and the expression of HSD3B2 and CYP11B mRNAs was clearly demonstrated within the nodules, indicating aldosterone synthesis.
  • We diagnosed that the present case had 1) cortisol-producing right adrenocortical adenoma, 2) aldosterone producing left adrenocortical adenoma, and 3) cortical minute nodules with aldosterone production in both adrenal glands compatible with idiopathic adrenal hyperplasia.
  • We reviewed the cases reported, and discussed the significance of the minute nodules in the adrenal cortex, often found in association with the adrenocortical adenoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications. Cushing Syndrome / etiology. Hyperaldosteronism / etiology

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  • (PMID = 19270420.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] EC 1.1.1.145 / 3 beta-hydroxysteroid dehydrogenase type II; EC 1.1.1.145 / Progesterone Reductase; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase
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34. Barzon L, Masi G, Pacenti M, Trevisan M, Fallo F, Remo A, Martignoni G, Montanaro D, Pezzi V, Palù G: Expression of aromatase and estrogen receptors in human adrenocortical tumors. Virchows Arch; 2008 Feb;452(2):181-91
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  • [Title] Expression of aromatase and estrogen receptors in human adrenocortical tumors.
  • We recently demonstrated that adrenocortical carcinoma cells express aromatase and estrogen receptors (ERs) and that 17beta-estradiol enhances adrenocortical cell proliferation.
  • To provide a clue to the role of estrogens in adrenal tumorigenesis, we investigated the expression profile of genes involved in sex steroid hormone production and activity in a large series of normal and neoplastic human adrenocortical tissues.
  • Quantitative reverse transcriptase-polymerase chain reaction, Western blotting, and immunohistochemistry showed that ERalpha and ERbeta, androgen receptor (AR), and aromatase were expressed in the adrenal cortex and in adrenocortical tumors.
  • ERbeta was the predominant ER subtype and was mainly expressed in the zona glomerulosa and fasciculata.
  • Western blot analysis revealed the presence of a truncated form of AR in adrenocortical tissues.
  • With respect to the normal adrenal cortex and adrenocortical adenomas, carcinomas were characterized by significantly lower ERbeta levels, ERalpha upregulation, and aromatase overexpression.
  • In agreement with our in vitro findings, the results of this study suggest that estrogens, locally produced by aromatase, could enhance adrenocortical cell proliferation though autocrine/paracrine mechanisms.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenocortical Adenoma / metabolism. Adrenocortical Carcinoma / metabolism. Aromatase / metabolism. Receptors, Estrogen / metabolism
  • [MeSH-minor] Adrenal Cortex / embryology. Adrenal Cortex / metabolism. Adult. Aged. Biomarkers, Tumor / metabolism. Blotting, Western. Female. Gene Expression. Humans. Male. Middle Aged. RNA, Messenger / metabolism. RNA, Neoplasm / analysis

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  • [CommentIn] Virchows Arch. 2008 Aug;453(2):221-2 [18553103.001]
  • (PMID = 18157729.001).
  • [ISSN] 0945-6317
  • [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 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Estrogen; EC 1.14.14.1 / Aromatase
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35. Razifar P, Hennings J, Monazzam A, Hellman P, Långström B, Sundin A: Masked volume wise Principal Component Analysis of small adrenocortical tumours in dynamic [11C]-metomidate Positron Emission Tomography. BMC Med Imaging; 2009;9:6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Masked volume wise Principal Component Analysis of small adrenocortical tumours in dynamic [11C]-metomidate Positron Emission Tomography.
  • METHODS: In this study, MVW-PCA was applied to 14 dynamic 11C-metomidate-PET (MTO-PET) examinations of 7 patients with small adrenocortical tumours.
  • Time activity curves derived from "50% cut-off" ROIs based on an isocontour function whereby the pixels with SUVs between 50 to 100% of the highest radioactivity concentration were delineated, showed a significant decrease of the SUVs in normal adrenal glands and in adrenocortical adenomas after cortisone treatment.
  • [MeSH-major] Adrenal Cortex Neoplasms / radionuclide imaging. Algorithms. Etomidate / analogs & derivatives. Image Interpretation, Computer-Assisted / methods. Imaging, Three-Dimensional / methods. Pattern Recognition, Automated / methods. Positron-Emission Tomography / methods

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  • (PMID = 19386097.001).
  • [ISSN] 1471-2342
  • [Journal-full-title] BMC medical imaging
  • [ISO-abbreviation] BMC Med Imaging
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 5377-20-8 / metomidate; Z22628B598 / Etomidate
  • [Other-IDs] NLM/ PMC2680831
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36. Barzon L, Pacenti M, Masi G, Stefani AL, Fincati K, Palù G: Loss of growth hormone secretagogue receptor 1a and overexpression of type 1b receptor transcripts in human adrenocortical tumors. Oncology; 2005;68(4-6):414-21
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  • [Title] Loss of growth hormone secretagogue receptor 1a and overexpression of type 1b receptor transcripts in human adrenocortical tumors.
  • OBJECTIVE AND METHODS: Quantitative analysis of mRNA expression of ghrelin and its receptors GHS-R1a and -R1b in a large series of normal and neoplastic human adrenocortical tissues.
  • Evaluation of the effects of ghrelin on GHS-R expression and proliferation of human adrenocortical carcinoma (ACC) cell lines.
  • RESULTS: Ghrelin and GHS-R transcripts are expressed in normal adrenal cortex, with GHS-R1b mRNA levels being 5- to 10-fold higher than GHS-R1amRNA.
  • A significant increase in ghrelin expression was observed in adrenocortical adenomas, but not in carcinomas.
  • GHS-R1a was undetectable in about 60% of both benign and malignant tumor samples, except for cortisol-producing adenomas, which showed increased receptor expression.
  • At variance, GHS-R1b was overexpressed in both benign and malignant adrenocortical tumors.
  • In vitro studies in human ACC cell lines demonstrated that GHS-R1a is downregulated and GHS-R1bmRNA expression is upregulated by ghrelin, while inhibiting cell proliferation.
  • CONCLUSION: Downregulation ofGHS-R1a in adrenal tumors and the presence of high levels of GHS-R1b transcripts in adrenocortical tissue suggest a role for these receptors in adrenal function and growth.
  • In this regard, ghrelin inhibits cell proliferation and modulates GHS-R expression in ACC cells in vitro.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenocortical Adenoma / metabolism. Adrenocortical Carcinoma / metabolism. Gene Expression Regulation, Neoplastic. Receptors, G-Protein-Coupled / metabolism
  • [MeSH-minor] Adrenal Cortex / metabolism. Cell Proliferation. Ghrelin. Growth Hormone / pharmacology. Humans. Peptide Hormones / pharmacology. Peptides / genetics. Peptides / metabolism. RNA, Messenger. Receptors, Ghrelin. Tumor Cells, Cultured

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  • [Copyright] (c) 2005 S. Karger AG, Basel
  • (PMID = 16020971.001).
  • [ISSN] 0030-2414
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Ghrelin; 0 / Peptide Hormones; 0 / Peptides; 0 / RNA, Messenger; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Ghrelin; 9002-72-6 / Growth Hormone
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37. 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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  • [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 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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38. 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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39. 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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40. Farkas A, Horányi J, Gláz E, Kulka J: [Oncocytic tumor of the adrenal gland]. Orv Hetil; 2005 Jul 3;146(27):1453-8
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  • [Title] [Oncocytic tumor of the adrenal gland].
  • [Transliterated title] Oncocytás mellékvese-adenoma.
  • Oncocytic tumor of the adrenal gland.
  • The authors describe a case of a rare tumor arising in the adrenal gland.
  • The tumor 6 cm in diameter, connected to the right adrenal gland, was found incidentally in a healthy young man of 34 years of age, who suffered an accident and had a rib fracture.
  • The right adrenal gland with the tumor was removed by laparoscopic surgery.
  • Histopathological examination revealed an oncocytic adenoma of the adrenal cortex.
  • The authors describe the morphology and the differential diagnosis of this rare tumor of the adrenal gland.
  • [MeSH-major] Adenoma, Oxyphilic / diagnosis. Adrenal Gland Neoplasms / diagnosis
  • [MeSH-minor] Adult. Diagnosis, Differential. Humans. Incidental Findings. Male

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  • (PMID = 16089107.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Number-of-references] 12
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41. Slater EP, Diehl SM, Langer P, Samans B, Ramaswamy A, Zielke A, Bartsch DK: Analysis by cDNA microarrays of gene expression patterns of human adrenocortical tumors. Eur J Endocrinol; 2006 Apr;154(4):587-98
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  • [Title] Analysis by cDNA microarrays of gene expression patterns of human adrenocortical tumors.
  • OBJECTIVES: Adrenocortical carcinoma (ACC) is a rare malignant neoplasm with extremely poor prognosis.
  • The molecular mechanisms of adrenocortical tumorigenesis are still not well understood.
  • The comparative analysis by cDNA microarrays of gene-expression patterns of benign and malignant adrenocortical tumors allows us to identify new tumor-suppressor genes and proto-oncogenes underlying adrenocortical tumorigenesis.
  • DESIGN AND METHODS: Total RNA from fresh-frozen tissue of 10 ACC and 10 benign adrenocortical adenomas was isolated after histologic confirmation of neoplastic cellularity of at least 85%.
  • The reference consisted of pooled RNA of 10 normal adrenal cortex samples.
  • RESULTS: The comparative analysis of gene expression revealed many genes with more than fourfold expression difference between ACC and normal tissue (42 genes), cortical adenoma and normal tissue (11 genes), and ACC and cortical adenoma (21 genes) respectively.
  • As confirmed by real-time PCR, the IGF2 gene was significantly upregulated in ACCs versus cortical adenomas and normal cortical tissue.
  • Genes that were downregulated in adrenocortical tumors included chromogranin B and early growth response factor 1.
  • CONCLUSIONS: Comprehensive expression profiling of adrenocortical tumors by the cDNA microarray technique is a very powerful tool to elucidate the molecular steps associated with the tumorigenesis of these ill-defined neoplasms.

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  • (PMID = 16556722.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 4964P6T9RB / Aldosterone; WI4X0X7BPJ / Hydrocortisone
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42. Papotti M, Volante M, Duregon E, Delsedime L, Terzolo M, Berruti A, Rosai J: Adrenocortical tumors with myxoid features: a distinct morphologic and phenotypical variant exhibiting malignant behavior. Am J Surg Pathol; 2010 Jul;34(7):973-83
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  • [Title] Adrenocortical tumors with myxoid features: a distinct morphologic and phenotypical variant exhibiting malignant behavior.
  • Myxoid changes have been rarely reported both in adrenocortical adenomas and carcinomas.
  • The recent observation by our group of an adrenal myxoid tumor with morphologically borderline features, but aggressive clinical behavior prompted us to review a series of 196 adrenocortical lesions, comprising 122 carcinomas and 74 adenomas, to define the morphologic, phenotypical and clinical characteristics of adrenocortical tumors with myxoid features.
  • Fourteen cases, including 12 carcinomas and 2 borderline tumors, formed the basis of this report, and were characterized by a variably abundant myxoid component (from 5% to 90% of tumor) and 2 distinct cellular growth patterns: the first (10 cases), mostly associated with a predominant myxoid stromal component, was made of small cells with mild atypia arranged in cords and microcysts; the second (4 cases) was characterized by focal myxoid changes in tumors otherwise similar to conventional adrenocortical carcinoma, with large atypical cells having an eosinophilic cytoplasm and a diffuse or nodular architecture.
  • The above mentioned patterns were absent in all adenomas reviewed.
  • 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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43. 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).
  • 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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44. 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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45. 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.
  • The pAKT/AKT ratio was significantly increased in pheochromocytomas (338 +/- 49% vs. 100 +/- 11%) but not in ACC, aldosterone-producing adenomas, and cortisol-producing adenomas.
  • 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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46. Nishimoto K, Nakagawa K, Li D, Kosaka T, Oya M, Mikami S, Shibata H, Itoh H, Mitani F, Yamazaki T, Ogishima T, Suematsu M, Mukai K: Adrenocortical zonation in humans under normal and pathological conditions. J Clin Endocrinol Metab; 2010 May;95(5):2296-305
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  • [Title] Adrenocortical zonation in humans under normal and pathological conditions.
  • CONTEXT: Aldosterone synthase (CYP11B2) and steroid 11 beta-hydroxylase (CYP11B1) catalyze the terminal steps for aldosterone and cortisol syntheses, respectively, thereby determining the functional differentiation of human adrenocortical cells.
  • OBJECTIVE: The objective of the study was to determine the localization of CYP11B2 and -B1 in human adrenal specimens by using developed antibodies capable of distinguishing the two enzymes from each other.
  • Adrenocortical cells lacking both enzymes were observed in the outer cortical regions.
  • In addition to conventional zonation, we found a variegated zonation consisting of a subcapsular cell cluster expressing CYP11B2, which we termed aldosterone-producing cell cluster, and a CYP11B1-expressing area.
  • Aldosterone-producing adenomas differed in cell populations expressing CYP11B2 from one another, whereas CYP11B1-expressing and double-negative cells were also intermingled.
  • Adenomas from patients with Cushing's syndrome expressed CYP11B1 entirely but not CYP11B2, resulting in atrophic nontumor glands.
  • The nontumor portions of both types of adenomas bore frequently one or more aldosterone-producing cell clusters, which sustained CYP11B2 expression markedly under the conditions of the suppressed renin-angiotensin system.
  • CONCLUSION: Immunohistochemistry of the human normal adrenal cortex for CYP11B2 and CYP11B1 revealed a variegated zonation with cell clusters constitutively expressing CYP11B2.
  • This technique may provide a pathological confirmatory diagnosis of adrenocortical adenomas.
  • [MeSH-major] Adrenal Cortex / pathology. Adrenal Cortex / physiology
  • [MeSH-minor] Aldosterone / metabolism. Amino Acid Sequence. Animals. Antibodies. Carcinoma, Renal Cell / enzymology. Corticosterone / metabolism. Cushing Syndrome / enzymology. Cytochrome P-450 CYP11B2 / deficiency. Cytochrome P-450 CYP11B2 / metabolism. Humans. Kidney Neoplasms / enzymology. Mammals. Peptide Fragments / chemistry. Rabbits. Reference Values. Rodentia. Steroid 11-beta-Hydroxylase / metabolism. Zona Fasciculata / enzymology. Zona Glomerulosa / enzymology

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  • (PMID = 20200334.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Peptide Fragments; 4964P6T9RB / Aldosterone; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase; W980KJ009P / Corticosterone
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47. Bielinska M, Kiiveri S, Parviainen H, Mannisto S, Heikinheimo M, Wilson DB: Gonadectomy-induced adrenocortical neoplasia in the domestic ferret (Mustela putorius furo) and laboratory mouse. Vet Pathol; 2006 Mar;43(2):97-117
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  • [Title] Gonadectomy-induced adrenocortical neoplasia in the domestic ferret (Mustela putorius furo) and laboratory mouse.
  • Sex steroid-producing adrenocortical adenomas and carcinomas occur frequently in neutered ferrets, but the molecular events underlying tumor development are not well understood.
  • In mice and ferrets, the neoplastic adrenocortical cells, which functionally resemble gonadal steroidogenic cells, arise from progenitors in the subcapsular or juxtamedullary region.
  • Tumorigenesis in mice is influenced by the inherent susceptibility of adrenal tissue to gonadectomy-induced hormonal changes.
  • Gonadectomy alters the plasma or local concentrations of steroid hormones and other factors that affect adrenocortical tumor development, including inhibins, activins, and Müllerian inhibiting substance.
  • Cases of human adrenocortical neoplasia have been linked to precocious expression of hormone receptors and to mutations that alter the activity of G-proteins or downstream effectors.
  • [MeSH-major] Adrenal Cortex Neoplasms / veterinary. Castration / veterinary. Ferrets

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  • (PMID = 16537928.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK52574; United States / NHLBI NIH HHS / HL / HL61006
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 135
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48. Schittenhelm J, Jacob SN, Rutczynska J, Tsiflikas I, Meyermann R, Beschorner R: Extra-adrenal paravertebral myelolipoma mimicking a thoracic schwannoma. BMJ Case Rep; 2009;2009

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  • [Title] Extra-adrenal paravertebral myelolipoma mimicking a thoracic schwannoma.
  • Myelolipoma of the adrenal gland is composed of both adipose tissue and normal haematopoietic elements.
  • Extra-adrenal myelolipomas are rare.
  • We present the case of a 63-year-old female patient with adenoma of the adrenal gland and an additional paravertebral lesion in the thoracic spine.
  • Post-mortem histopathology showed the incidental finding of a paravertebral myelolipoma.

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  • [Cites] Radiographics. 2005 Jan-Feb;25(1):69-85 [15653588.001]
  • [Cites] Am J Surg Pathol. 1982 Jun;6(4):363-74 [7051876.001]
  • [Cites] Arch Pathol Lab Med. 1994 Sep;118(9):895-6 [8080359.001]
  • [Cites] Radiographics. 1997 Nov-Dec;17(6):1373-85 [9397452.001]
  • (PMID = 21686745.001).
  • [ISSN] 1757-790X
  • [Journal-full-title] BMJ case reports
  • [ISO-abbreviation] BMJ Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC3027965
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49. Araki A, Shinohara M, Yamakawa J, Tanaka M, Natsui S, Izumi Y: Gastric diverticulum preoperatively diagnosed as one of two left adrenal adenomas. Int J Urol; 2006 Jan;13(1):64-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gastric diverticulum preoperatively diagnosed as one of two left adrenal adenomas.
  • A 47-year-old man was diagnosed with primary aldosteronism due to two left adrenal adenomas, suggested on computed tomography (CT) to be located at the upper and lower adrenal portion.
  • However, adosterol scintigraphy revealed negligible uptake at the upper portion of the left adrenal.
  • Laparoscopic left adrenalectomy was performed, but macroscopic examination of the specimen revealed only one adrenal tumor.
  • Postoperatively, aldosteronism resolved and repeat CT revealed staining of the adrenal pseudotumor when oral contrast was administered.
  • Since organs located near the adrenals can simulate adrenal tumors, caution must be exercised in interpreting suprarenal masses on CT.
  • To our knowledge, this is the first reported case of concurrent pseudotumor and true tumor of the ipsilateral adrenal.
  • [MeSH-major] Adrenocortical Adenoma / diagnosis. Diverticulum, Stomach / diagnosis. Preoperative Care
  • [MeSH-minor] Adrenalectomy / methods. Diagnosis, Differential. Humans. Hyperaldosteronism / diagnosis. Hyperaldosteronism / etiology. Laparoscopy. Male. Middle Aged. Tomography, X-Ray Computed

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  • (PMID = 16448434.001).
  • [ISSN] 0919-8172
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
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50. Park BK, Kim B, Ko K, Jeong SY, Kwon GY: Adrenal masses falsely diagnosed as adenomas on unenhanced and delayed contrast-enhanced computed tomography: pathological correlation. Eur Radiol; 2006 Mar;16(3):642-7
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  • [Title] Adrenal masses falsely diagnosed as adenomas on unenhanced and delayed contrast-enhanced computed tomography: pathological correlation.
  • OBJECTIVES: To assess the accuracy of CT for the diagnosis of histologically confirmed adrenal adenoma and nonadenoma using CT numbers.
  • MATERIALS AND METHODS: Our study included 91 adrenal masses in 83 patients; histopathological diagnoses were 45 adenomas, 31 pheochromocytomas, 6 hyperplasias, 4 metastasis, and 5 miscellaneous lesions.
  • RESULTS: Sensitivity, specificity, and accuracy for adenoma were 40% (18/45), 91% (42/46), and 66% (60/91) with unenhanced CT, and 96% (24/25), 61% (11/18), and 81% (35/43) with DCE CT.
  • Adrenal masses falsely diagnosed as adenoma on unenhanced CT included three hyperplasias and one endothelial cyst, and those falsely diagnosed as adenoma on DCE CT were five pheochromocytomas, one oncocytic cortical tumor, and one primary pigmented nodular adrenocortical dysplasia.
  • Twenty-five lipid-poor adenomas were falsely diagnosed as nonadenomas on unenhanced CT and one degenerated adenoma both on unenhanced CT and on DCE CT.
  • CONCLUSION: Diagnosing adenoma merely on CT numbers can lead to misdiagnosis.
  • [MeSH-major] Adenoma / radiography. Adrenal Gland Neoplasms / radiography. Tomography, X-Ray Computed / methods
  • [MeSH-minor] Adult. Analysis of Variance. Contrast Media. Diagnosis, Differential. Diagnostic Errors. Female. Humans. Hyperplasia. Male. Middle Aged. Neoplasm Metastasis. Pheochromocytoma / pathology. Pheochromocytoma / radiography. Sensitivity and Specificity

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  • [ErratumIn] Eur Radiol. 2006 Mar;16(3):768
  • (PMID = 16215735.001).
  • [ISSN] 0938-7994
  • [Journal-full-title] European radiology
  • [ISO-abbreviation] Eur Radiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Contrast Media
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51. Mete O, Asa SL: Aldosterone-producing adrenal cortical adenoma with oncocytic change and cytoplasmic eosinophilic globular inclusions. Endocr Pathol; 2009;20(3):182-5
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  • [Title] Aldosterone-producing adrenal cortical adenoma with oncocytic change and cytoplasmic eosinophilic globular inclusions.
  • We report an interesting morphological alteration in the adrenal of a 72-year-old woman suffering from severe hypertension due to primary hyperaldosteronism.
  • The laparoscopic left adrenalectomy specimen revealed an adrenal cortical adenoma composed of varying proportions of oncocytic and clear cells, predominantly showing central oncocytic change.
  • Oncocytes also exhibited numerous eosinophilic intracytoplasmic globular inclusions, which are not commonly observed in aldosterone-producing adrenal cortical adenomas.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / pathology. Aldosterone / secretion. Inclusion Bodies / pathology

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  • (PMID = 19462261.001).
  • [ISSN] 1559-0097
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antihypertensive Agents; 4964P6T9RB / Aldosterone
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52. Szabó PM, Wiener Z, Tömböl Z, Kovács A, Pócza P, Horányi J, Kulka J, Riesz P, Tóth M, Patócs A, Gaillard RC, Falus A, Rácz K, Igaz P: Differences in the expression of histamine-related genes and proteins in normal human adrenal cortex and adrenocortical tumors. Virchows Arch; 2009 Aug;455(2):133-42
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  • [Title] Differences in the expression of histamine-related genes and proteins in normal human adrenal cortex and adrenocortical tumors.
  • Histamine is involved in the pathogenesis of several tumors; however, there are no data on its possible involvement in human adrenocortical tumorigenesis.
  • The expression of genes and proteins involved in the biosynthesis (histidine decarboxylase, HDC), action (histamine receptors: HRH1-HRH4), and metabolism of histamine is largely unknown both in the normal human adrenal cortex and in adrenocortical tumors.
  • In this study, we examined the expression of histamine-related genes and proteins and histamine content in normal adrenal cortex, benign adrenocortical adenomas, and malignant adrenocortical cancer (ACC).
  • We found that all proteins involved in histamine biosynthesis and action are present both in the normal adrenal cortex and in the tumors studied.
  • HDC expression and histamine content was highest in the normal tissues and lower in benign tumors, whereas it was significantly less in ACCs.
  • Adrenocortical tumorigenesis might, thus, be characterized by reduced histamine biosynthesis; furthermore, different adrenocortical tumor subtypes may show unique histamine receptor expression profiles.
  • [MeSH-major] Adrenal Cortex / metabolism. Adrenal Cortex Neoplasms / metabolism. Adrenocortical Adenoma / metabolism. Histamine / metabolism. Histidine Decarboxylase / metabolism. Receptors, Histamine / metabolism

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  • (PMID = 19568768.001).
  • [ISSN] 1432-2307
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / HRH4 protein, human; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Histamine; 0 / Receptors, Histamine H1; 0 / Receptors, Histamine H2; 0 / Receptors, Histamine H3; 820484N8I3 / Histamine; EC 4.1.1.22 / Histidine Decarboxylase
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53. Walz MK, Gwosdz R, Levin SL, Alesina PF, Suttorp AC, Metz KA, Wenger FA, Petersenn S, Mann K, Schmid KW: Retroperitoneoscopic adrenalectomy in Conn's syndrome caused by adrenal adenomas or nodular hyperplasia. World J Surg; 2008 May;32(5):847-53
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  • [Title] Retroperitoneoscopic adrenalectomy in Conn's syndrome caused by adrenal adenomas or nodular hyperplasia.
  • BACKGROUND: In patients with primary hyperaldosteronism, solitary adrenal adenomas are an indication for surgical intervention.
  • In contrast, adrenal hyperplasia is almost exclusively treated by drugs.
  • PATIENTS AND METHODS: In a prospective clinical study 183 patients (81 men, 102 women; age 49.6+/-12.8 years) with Conn's syndrome were operated on using the posterior retroperitoneoscopic approach.
  • Final histology described a solitary adenoma in 127 patients and adrenal hyperplasia in 56 patients.
  • CONCLUSIONS: Retroperitoneoscopic removal of adrenal glands in patients with Conn's syndrome is a safe, rapidly performed surgical procedure and can thus be considered as first choice option for treatment of both solitary adrenal adenomas and hyperplasia presenting with a clinically predominating nodule.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenal Glands / pathology. Adrenalectomy / methods. Adrenocortical Adenoma / surgery. Endoscopy. Hyperaldosteronism / surgery

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  • [CommentIn] World J Surg. 2008 May;32(5):854-5 [18246389.001]
  • (PMID = 18343972.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
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54. Pena FJ, Quirce R, Allende RH, Banzo I, Carril JM: Bilateral adrenocortical uptake of Ga-67 SPECT during septicemia in a heart transplant patient. Clin Nucl Med; 2005 May;30(5):349-50
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  • [Title] Bilateral adrenocortical uptake of Ga-67 SPECT during septicemia in a heart transplant patient.
  • Ga-67 SPECT showed bilateral abnormal adrenal gland uptake that disappeared after intensive antibiotic therapy as assessed by a new Ga-67 scintigraphy obtained 3 months later.
  • Unilateral and bilateral adrenal uptake of gallium has been reported in several clinical settings, ranging from adrenocortical adenomas to malignant disease such as lymphoma or adrenal metastases.
  • Only one similar case, septicemia with transient adrenal uptake of gallium, has been previously reported.
  • [MeSH-major] Adrenal Cortex / radionuclide imaging. Bacteremia / radionuclide imaging. Citrates. Gallium. Heart Transplantation / adverse effects. Heart Transplantation / radionuclide imaging. Staphylococcal Infections / radionuclide imaging. Tomography, Emission-Computed, Single-Photon / methods
  • [MeSH-minor] Fever of Unknown Origin / diagnosis. Fever of Unknown Origin / etiology. Humans. Male. Middle Aged. Radiopharmaceuticals / pharmacokinetics. Sepsis. Staphylococcus haemolyticus

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  • (PMID = 15827412.001).
  • [ISSN] 0363-9762
  • [Journal-full-title] Clinical nuclear medicine
  • [ISO-abbreviation] Clin Nucl Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Citrates; 0 / Radiopharmaceuticals; 27905-02-8 / gallium citrate; CH46OC8YV4 / Gallium
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55. Lubikowski J, Umiński M, Andrysiak-Mamos E, Pynka S, Fuchs H, Wójcicki M, Szajko M, Moleda P, Post M, Zochowska E, Kiedrowicz B, Safranow K, Syrenicz A: From open to laparoscopic adrenalectomy: thirty years' experience of one medical centre. Endokrynol Pol; 2010 Jan-Feb;61(1):94-101
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  • INTRODUCTION: Laparoscopic adrenalectomy (LA) has become the standardized treatment of benign adrenal lesions over the last two decades, making the indications to open adrenalectomy (OA) limited.
  • The purpose of this study was to show the thirty years of experience in open (OA) and laparoscopic adrenalectomy (LA) gained in one medical centre as well as to compare the results of OA and LA performed for benign adrenal lesions.
  • Analyzed factors included patients demographic data, ASA score, indication for surgery, tumour size and side, characteristics of the removed tumours, intraoperative and postoperative outcome of LA and OA, postoperative pain sensation, intraoperative and postoperative complications, and conversion rate from LA to OA.
  • The mean operative time was longer in the LA group (137 v. 82 min., p < 0.0001) and the blood loss was lower in LA group (110 v. 254 mL, p < 0.0001).
  • The mean time until resumption of normal diet was shorter after LA (22 v. 44 h), as was the mean time until ambulation (17 v. 36 h), mean length of the hospital stay (4.6 v. 6.8 days), and mean time until return to normal activities (14 v. 23 days, p < 0.0001 for each difference).
  • The analgesic requirement on the first and the second day postoperatively was lower in the LA group (p < 0.0001).
  • The rate of the conversion from LA to OA was 16%.
  • The histopathological diagnosis was adenoma of the adrenal gland in the majority of cases.
  • CONCLUSIONS: This study shows that LA is a safe, effective, and well-tolerated procedure.
  • It may be recommended as a "gold standard" surgery in a case of benign functioning or non-functioning adrenal tumours with diameter less than 8 cm. (Pol J Endocrinol 2010; 61 (1): 94-101).
  • [MeSH-major] Adrenal Gland Diseases / surgery. Adrenalectomy / methods. Laparoscopy / methods
  • [MeSH-minor] Adolescent. Adrenal Gland Neoplasms / surgery. Adult. Aged. Aged, 80 and over. Female. Humans. Length of Stay / statistics & numerical data. Male. Middle Aged. Poland. Treatment Outcome. Young Adult

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  • (PMID = 20205111.001).
  • [ISSN] 0423-104X
  • [Journal-full-title] Endokrynologia Polska
  • [ISO-abbreviation] Endokrynol Pol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
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56. Saner-Amigh K, Mayhew BA, Mantero F, Schiavi F, White PC, Rao CV, Rainey WE: Elevated expression of luteinizing hormone receptor in aldosterone-producing adenomas. J Clin Endocrinol Metab; 2006 Mar;91(3):1136-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Elevated expression of luteinizing hormone receptor in aldosterone-producing adenomas.
  • CONTEXT: The mechanisms driving steroid production in aldosterone-producing adenomas (APAs) are poorly defined.
  • However, previous studies have shown that steroid production in some cortisol-producing adenomas is regulated by aberrant expression of G protein-coupled receptors.
  • Aberrant adrenal expression of LH receptors has been shown to cause Cushing's syndrome, but the role of LH receptors in Conn's disease (hyperaldosteronism) has not been studied.
  • OBJECTIVE: The objective of the study was to determine whether APAs express elevated LH receptor, compared with normal adrenal (NA).
  • Aldosterone synthase transcription was studied in H295R adrenocortical cells transfected with an LH receptor expression construct and reporter constructs prepared from CYP11B2 5'-flanking DNA.
  • PATIENTS: The patient population consisted of 20 normal control adrenals and 18 adenomas from patients with APAs.
  • MAIN OUTCOME MEASURE: Regulation of CYP11B2 gene expression by aberrant LH receptor expression in aldosterone-producing adrenal adenoma was measured.
  • CONCLUSION: LH receptor expression is elevated in many APAs, which makes LH a potential cause of the excessive production of aldosterone in a subset of these adrenal tumors.
  • [MeSH-major] Adenoma / genetics. Adrenal Cortex Neoplasms / genetics. Aldosterone / metabolism. Receptors, LH / genetics
  • [MeSH-minor] Adrenal Glands / embryology. Adrenal Glands / physiology. Corpus Luteum / physiology. DNA Primers. Female. Gene Expression Regulation, Neoplastic. Humans. Oligonucleotide Array Sequence Analysis. Ovarian Follicle / physiology. Plasmids. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transfection. Tumor Cells, Cultured

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  • (PMID = 16332935.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK43140
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / RNA, Messenger; 0 / Receptors, LH; 4964P6T9RB / Aldosterone
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57. Adam P, Hahner S, Hartmann M, Heinrich B, Quinkler M, Willenberg HS, Saeger W, Sbiera S, Schmull S, Voelker HU, Ströbel P, Allolio B, Fassnacht M: Epidermal growth factor receptor in adrenocortical tumors: analysis of gene sequence, protein expression and correlation with clinical outcome. Mod Pathol; 2010 Dec;23(12):1596-604
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  • [Title] Epidermal growth factor receptor in adrenocortical tumors: analysis of gene sequence, protein expression and correlation with clinical outcome.
  • Adrenocortical carcinoma is a rare but highly malignant neoplasm with still limited treatment options.
  • Epidermal growth factor receptor (EGFR) has been shown to be overexpressed in many solid tumors, but its expression in adrenocortical carcinoma has been studied only in a limited number of cases.
  • Therefore, we analyzed the expression of EGFR in 169 adrenocortical carcinoma samples and compared it with 31 adrenocortical adenomas.
  • Additionally, in 30 cases of adrenocortical carcinoma, exons 18-21 of the EGFR gene were cloned and sequenced.
  • EGFR expression was found in 128 of 169 adrenocortical carcinoma samples (76%), and in 60 of these samples (=36%) strong membrane staining was detected.
  • In contrast, only 1 out of 31 adrenocortical adenomas weakly expressed the EGFR (3%).
  • In summary, EGFR was overexpressed in more than three-quarters of adrenocortical carcinoma cases of this series.
  • As EGFR is hardly expressed in adrenocortical adenomas, our results suggest that its expression in adrenocortical tumors indicates a malignant phenotype, which may be used in the differential diagnosis between adrenocortical adenomas and carcinomas.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / metabolism. Adrenocortical Adenoma / pathology. Receptor, Epidermal Growth Factor / biosynthesis

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  • (PMID = 20693985.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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58. 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.
  • 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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59. Kamiyama T, Fukukura Y, Yoneyama T, Takumi K, Nakajo M: Distinguishing adrenal adenomas from nonadenomas: combined use of diagnostic parameters of unenhanced and short 5-minute dynamic enhanced CT protocol. Radiology; 2009 Feb;250(2):474-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distinguishing adrenal adenomas from nonadenomas: combined use of diagnostic parameters of unenhanced and short 5-minute dynamic enhanced CT protocol.
  • PURPOSE: To retrospectively examine the diagnostic values of individual parameters obtained from unenhanced and 35-second and 5-minute contrast material-enhanced (enhanced) computed tomography (CT) in distinguishing adenomas, particularly lipid-poor adenomas, from nonadenomas and to determine the best diagnostic method by using these parameters.
  • The study population consisted of 61 patients (20 men and 41 women; mean age, 58 years) with 68 adrenal masses (53 adenomas and 15 nonadenomas).
  • Adenomas were classified as 30 lipid-rich (<or=10 HU) and 23 lipid-poor (>10 HU) adenomas by using unenhanced attenuation.
  • The sensitivity, specificity, and accuracy for diagnosing adenomas were calculated by using a threshold level of each parameter determined by the least sum of false-positive and false-negative cases and a combination of the threshold levels with 100% specificity.
  • RESULTS: The best results were obtained by using a combination of the threshold levels with 100% (15 of 15) specificity (presence of at least one of the following criteria for diagnosing adenomas: unenhanced attenuation of <or=19 HU, 5-minute attenuation of <or=50 HU, PEW of >or=45%, and RPEW of >or=31%).
  • Sensitivity was 94% (50 of 53) or 87% (20 of 23) and accuracy was 96% (65 of 68) or 92% (35 of 38) for diagnosing total adrenal adenomas or lipid-poor adenomas, respectively.
  • [MeSH-major] Adrenal Gland Neoplasms / radiography. Adrenocortical Adenoma / radiography. Tomography, X-Ray Computed / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Chi-Square Distribution. Contrast Media. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Radiographic Image Interpretation, Computer-Assisted. Retrospective Studies. Sensitivity and Specificity. Statistics, Nonparametric

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  • (PMID = 19037020.001).
  • [ISSN] 1527-1315
  • [Journal-full-title] Radiology
  • [ISO-abbreviation] Radiology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
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60. Almeida MQ, Soares IC, Ribeiro TC, Fragoso MC, Marins LV, Wakamatsu A, Ressio RA, Nishi MY, Jorge AA, Lerario AM, Alves VA, Mendonca BB, Latronico AC: Steroidogenic factor 1 overexpression and gene amplification are more frequent in adrenocortical tumors from children than from adults. J Clin Endocrinol Metab; 2010 Mar;95(3):1458-62

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  • [Title] Steroidogenic factor 1 overexpression and gene amplification are more frequent in adrenocortical tumors from children than from adults.
  • BACKGROUND: Steroidogenic factor 1 (SF-1) is a key determinant of endocrine development and function of adrenal cortex.
  • SF-1 overexpression and gene amplification were previously demonstrated in a small group of pediatric adrenocortical tumors.
  • OBJECTIVE: Our objective was to determine the frequency of SF-1 protein expression and gene amplification in a large cohort of pediatric and adult adrenocortical tumors.
  • PATIENTS: SF-1 protein expression was assessed in a cohort of 103 adrenocortical tumors from 36 children and 67 adults, whereas gene amplification was studied in 38 adrenocortical tumors (17 from children).
  • RESULTS: A strong nuclear SF-1 expression was detected by tissue microarray in 56% (20 of 36) and 19% (13 of 67) of the pediatric and adult adrenocortical tumors, respectively (P = 0.0004).
  • Increased SF-1 copy number was identified in 47% (eight of 17) and 10% (two of 21) of the pediatric and adult adrenocortical tumors, respectively (P = 0.02).
  • All adrenocortical tumors with SF-1 gene amplification showed a strong SF-1 staining, whereas most of the tumors (61%) without SF-1 amplification displayed a weak or negative staining (P = 0.0008).
  • Interestingly, a strong SF-1 staining was identified in five (29%) pediatric adrenocortical tumors without SF-1 amplification.
  • The frequency of SF-1 overexpression and gene amplification was similar in adrenocortical adenomas and carcinomas.
  • CONCLUSION: We demonstrated a higher frequency of SF-1 overexpression and gene amplification in pediatric than in adult adrenocortical tumors, suggesting an important role of SF-1 in pediatric adrenocortical tumorigenesis.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics. Adrenocortical Carcinoma / genetics. Gene Amplification / genetics. Steroidogenic Factor 1 / genetics

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  • (PMID = 20080844.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Steroidogenic Factor 1
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61. Tömböl Z, Szabó PM, Molnár V, Wiener Z, Tölgyesi G, Horányi J, Riesz P, Reismann P, Patócs A, Likó I, Gaillard RC, Falus A, Rácz K, Igaz P: Integrative molecular bioinformatics study of human adrenocortical tumors: microRNA, tissue-specific target prediction, and pathway analysis. Endocr Relat Cancer; 2009 Sep;16(3):895-906
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  • [Title] Integrative molecular bioinformatics study of human adrenocortical tumors: microRNA, tissue-specific target prediction, and pathway analysis.
  • MicroRNAs (miRs) are involved in the pathogenesis of several neoplasms; however, there are no data on their expression patterns and possible roles in adrenocortical tumors.
  • Our objective was to study adrenocortical tumors by an integrative bioinformatics analysis involving miR and transcriptomics profiling, pathway analysis, and a novel, tissue-specific miR target prediction approach.
  • Thirty-six tissue samples including normal adrenocortical tissues, benign adenomas, and adrenocortical carcinomas (ACC) were studied by simultaneous miR and mRNA profiling.
  • Expression of miR-210 was significantly lower in cortisol-secreting adenomas than in ACCs.
  • By calculating the difference between dCT(miR-511) and dCT(miR-503) (delta cycle threshold), ACCs could be distinguished from benign adenomas with high sensitivity and specificity.
  • 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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62. Saito T, Ikoma A, Saito T, Tamemoto H, Suminaga Y, Yamada S, Kawakami M, Suzuki T, Sasano H, Ishikawa SE: Possibly simultaneous primary aldosteronism and preclinical Cushing's syndrome in a patient with double adenomas of right adrenal gland. Endocr J; 2007 Apr;54(2):287-93
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  • [Title] Possibly simultaneous primary aldosteronism and preclinical Cushing's syndrome in a patient with double adenomas of right adrenal gland.
  • We reported a rare case of simultaneous primary aldosteronism and preclinical Cushing's syndrome due to unilateral double adrenocortical adenomas in a 57 year-old woman who had had hypertension for the last 10 years.
  • Abdominal computed tomography showed double tumors in her right adrenal gland.
  • They were macroscopically composed of a golden-yellow portion admixed with a brown portion, which corresponded to clear cells and compact cells, respectively.
  • Immunohistochemical staining for steroidogenic enzymes demonstrated the presence of all the enzymes involved in corticosteroidogenesis in these two adenomas, indicating that the two adenomas produced both cortisol and mineralocorticoid.
  • Specifically, one adenoma mainly caused excessive production of cortisol as compared to the other one.
  • These findings indicate that overproduction of both cortisol and mineralocorticoid was evident in the two adenomas of the right adrenal gland in immunohistochemical study for steroidogenic enzymes, whereas there was less clinical manifestation of primary aldosteronism and Cushing's syndrome in the present patient.
  • [MeSH-major] Adenoma / complications. Adrenal Gland Neoplasms / complications. Cushing Syndrome / etiology. Hyperaldosteronism / etiology


63. Garduno-García Jde J, Reza-Albarrán A, Márquez MA, Pérez FJ: [Adrenal adenoma as a cause of Cushing's syndrome: twenty years' experience in a referral center in Mexico]. Endocrinol Nutr; 2010 Nov;57(9):421-5
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  • [Title] [Adrenal adenoma as a cause of Cushing's syndrome: twenty years' experience in a referral center in Mexico].
  • [Transliterated title] Adenoma adrenal como etiología de síndrome de Cushing: veinte años de experiencia en un centro mexicano de tercer nivel.
  • Adrenal adenomas are an uncommon cause of adult CS.
  • OBJECTIVE: To describe the characteristics and outcome of patients with CS caused by adrenal adenomas in a referral center.
  • METHODS: We performed a retrospective cross-sectional observational study of patients with a diagnosis of CS caused by adrenal adenomas managed in our center over a 20-year period.
  • Our clinical experience in the diagnosis and treatment of this entity was analyzed.
  • The results of dynamic testing with dexamethasone suggested adrenal adenoma in 100% of the patients.
  • Seventy percent of adenomas were found in the left gland.
  • ACTH measurement in our center was not reliable in identifying adrenal adenoma as a cause of CS.
  • [MeSH-major] Adenoma / complications. Adrenal Gland Neoplasms / complications. Cushing Syndrome / etiology

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  • [Copyright] Copyright © 2010 SEEN. Published by Elsevier Espana. All rights reserved.
  • (PMID = 20863774.001).
  • [ISSN] 1579-2021
  • [Journal-full-title] Endocrinología y nutrición : órgano de la Sociedad Española de Endocrinología y Nutrición
  • [ISO-abbreviation] Endocrinol Nutr
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
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64. Babinska A, Sworczak K, Wisniewski P, Nałecz A, Jaskiewicz K: The role of immunohistochemistry in histopathological diagnostics of clinically "silent" incidentally detected adrenal masses. Exp Clin Endocrinol Diabetes; 2008 Apr;116(4):246-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of immunohistochemistry in histopathological diagnostics of clinically "silent" incidentally detected adrenal masses.
  • BACKGROUND: The detectability of adrenal incidentalomas (incidentally found adrenal tumours) in the whole population is estimated at 0.1%; 0.42% in non-endocrine patients and at 4.3% in oncologically diagnosed ones.
  • Even up to 16% of incidentalomas of adrenal glands can be malignant lesions.
  • The issue of crucial importance is the histopathological differentiation between benign lesions and malignant tumours of the adrenal cortex and medulla.
  • OBJECTIVES: To evaluate whether the immunohistochemical analysis of the expression of p53, p21, PCNA and Ki67 in the tumour's tissue can be useful in the histopathological diagnostics of adrenal incidentalomas and whether it is important for prognosis.
  • There were 43 cortical adenomas, 11 cortical adrenocarcinomas and 20 PHEOs (including 5 malignant lesions).
  • RESULTS: We found a statistically significant correlation between the expression of p53, p21, Ki67 and the differential diagnosis of adrenal cortical adenoma and adrenocortical carcinoma (for proteins: p53 p=0.010, for p21 p=0.010, for Ki67 p<0.001).
  • The statistical significant correlation between PCNA protein and diagnosis of adrenal cortical adenoma and adrenocortical carcinoma was not found.
  • The statistically significant correlation between p21, PCNA proteins and the diagnosis of benign and malignant PHEOs was not estimated.
  • There was no expression of Ki67 or p53 protein above the assumed level in benign and malignant pheochromocytomas.
  • [MeSH-major] Adenoma / pathology. Adrenal Gland Neoplasms / pathology. Pheochromocytoma / pathology
  • [MeSH-minor] Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Ki-67 Antigen / genetics. Proliferating Cell Nuclear Antigen / genetics. Proto-Oncogene Proteins c-bcl-2 / genetics. Tumor Suppressor Protein p53 / genetics. p21-Activated Kinases / genetics

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  • (PMID = 18393131.001).
  • [ISSN] 0947-7349
  • [Journal-full-title] Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
  • [ISO-abbreviation] Exp. Clin. Endocrinol. Diabetes
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Proliferating Cell Nuclear Antigen; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; EC 2.7.11.1 / p21-Activated Kinases
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65. Piaditis GP, Kaltsas GA, Androulakis II, Gouli A, Makras P, Papadogias D, Dimitriou K, Ragkou D, Markou A, Vamvakidis K, Zografos G, Chrousos G: High prevalence of autonomous cortisol and aldosterone secretion from adrenal adenomas. Clin Endocrinol (Oxf); 2009 Dec;71(6):772-8
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  • [Title] High prevalence of autonomous cortisol and aldosterone secretion from adrenal adenomas.
  • OBJECTIVES: Previous studies based on standard endocrine testing have shown a variable incidence of autonomous cortisol secretion (ACS) or autonomous aldosterone secretion (AAS) in patients with single adrenal adenomas (SAA).
  • Patients We investigated 151 patients with SAA and 72 matched controls with normal adrenal computerized tomography.
  • [MeSH-major] Adrenocortical Adenoma / blood. Aldosterone / blood. Hydrocortisone / blood
  • [MeSH-minor] Adrenal Glands / drug effects. Adrenal Glands / metabolism. Adrenocorticotropic Hormone / administration & dosage. Adrenocorticotropic Hormone / pharmacology. Case-Control Studies. Dexamethasone / administration & dosage. Dexamethasone / pharmacology. Female. Humans. Male. Middle Aged. Radioimmunoassay

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  • (PMID = 19226269.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone; 7S5I7G3JQL / Dexamethasone; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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66. Raff H, Bruder ED, St. Luke's Medical Center Adrenal Tumor Study Group: Steroidogenesis in human aldosterone-secreting adenomas and adrenal hyperplasias: effects of hypoxia in vitro. Am J Physiol Endocrinol Metab; 2006 Jan;290(1):E199-E203
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  • [Title] Steroidogenesis in human aldosterone-secreting adenomas and adrenal hyperplasias: effects of hypoxia in vitro.
  • The synthesis of adrenal steroids requires molecular oxygen.
  • Because arterial hypoxemia is a common clinical condition, the purpose of the present study was to examine steroidogenesis in vitro under physiological changes in O(2) tension (Po(2)) in cells from human adrenal glands with aldosterone-secreting adenomas (ASA; n=3) or with bilateral adrenal hyperplasia causing Cushing's syndrome (n=4).
  • Furthermore, cortisol and DHEA production in cells from histologically normal tissue, adjacent to ASA and from bilateral adrenal hyperplasias, was also inhibited under a Po(2) of 40 mmHg.
  • We conclude that physiological decreases in Po(2) to levels typical for adrenal venous Po(2) under mild hypoxia inhibit steroidogenesis.
  • These studies may have implications for oxygen therapy in critically ill patients with functional adrenal insufficiency, as well as for therapeutic options in patients with adrenal neoplasms.
  • [MeSH-major] Adrenal Glands / metabolism. Adrenocortical Adenoma / metabolism. Aldosterone / secretion. Steroids / biosynthesis
  • [MeSH-minor] Adrenocorticotropic Hormone / pharmacology. Cell Hypoxia. Cells, Cultured. Cyclic AMP / pharmacology. Dehydroepiandrosterone / biosynthesis. Humans. Hydrocortisone / biosynthesis. Hyperplasia / metabolism. Hyperplasia / pathology. Oxygen / pharmacology. Partial Pressure. Tumor Cells, Cultured

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  • (PMID = 16105860.001).
  • [ISSN] 0193-1849
  • [Journal-full-title] American journal of physiology. Endocrinology and metabolism
  • [ISO-abbreviation] Am. J. Physiol. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Steroids; 459AG36T1B / Dehydroepiandrosterone; 4964P6T9RB / Aldosterone; 9002-60-2 / Adrenocorticotropic Hormone; E0399OZS9N / Cyclic AMP; S88TT14065 / Oxygen; WI4X0X7BPJ / Hydrocortisone
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67. Gaujoux S, Tissier F, Groussin L, Libé R, Ragazzon B, Launay P, Audebourg A, Dousset B, Bertagna X, Bertherat J: Wnt/beta-catenin and 3',5'-cyclic adenosine 5'-monophosphate/protein kinase A signaling pathways alterations and somatic beta-catenin gene mutations in the progression of adrenocortical tumors. J Clin Endocrinol Metab; 2008 Oct;93(10):4135-40

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Wnt/beta-catenin and 3',5'-cyclic adenosine 5'-monophosphate/protein kinase A signaling pathways alterations and somatic beta-catenin gene mutations in the progression of adrenocortical tumors.
  • BACKGROUND: The Wnt/beta-catenin and cAMP signaling pathways play an important role in adrenal cortex tumorigenesis.
  • Somatic activating mutations of the beta-catenin gene (CTNNB1) are the most frequent genetic defects identified both in adrenocortical adenomas (ACAs) and adrenocortical cancers (ACCs).
  • PRKAR1A mutations leading to cAMP pathway dysregulation are observed in primary pigmented nodular adrenocortical diseases (PPNADs) and some sporadic ACAs.
  • OBJECTIVE: The objective of the investigation was to study Wnt/beta-catenin dysregulation in adrenocortical tumors (ACTs) with cAMP pathway genetic alteration and search for secondary CTNNB1 somatic mutations in heterogeneous tumors.
  • In addition, the occurrence as an additional hit of a CTNNB1 somatic mutation is associated with larger or more aggressive ACTs.
  • This underlines the importance of the Wnt/beta-catenin pathway in adrenal cortex tumorigenesis and the importance of genetic accumulation in the progression of ACTs.
  • [MeSH-major] Adenoma / genetics. Adrenal Cortex Neoplasms / genetics. Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / genetics. Mutation. Signal Transduction / genetics. Wnt Proteins / genetics. beta Catenin / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Cyclic AMP / metabolism. DNA Mutational Analysis. Disease Progression. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Neoplasm Invasiveness. Tumor Burden / genetics

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  • (PMID = 18647815.001).
  • [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 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human; 0 / Wnt Proteins; 0 / beta Catenin; E0399OZS9N / Cyclic AMP
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68. Bagwan IN, Cook G, Mudan S, Wotherspoon A: Unusual presentation of metastatic adenocarcinoma. World J Surg Oncol; 2007;5:116
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  • BACKGROUND: The most common tumours of the adrenal gland are adenoma, pheochromocytoma, adrenocortical carcinoma, and metastases.
  • Although the imaging features of these tumours are established, the imaging characteristics of uncommon adrenal masses are less well known.
  • In patients with extradrenal tumour, incidental discovery of an adrenal mass necessitates excluding the possibility of metastatic malignancy.
  • Sixteen months later on staging CT scan a 2 x 2 cm adrenal mass was detected, which increased in size over a period of time to 3 x 3 cm in size.
  • Adrenalectomy was performed and histological examination revealed metastatic adenocarcinoma within an adrenal adenoma.
  • CONCLUSION: The present case highlights the unusual behaviour of an oesophageal adenocarcinoma causing metastasis to an adrenocortical adenoma.
  • [MeSH-major] Adenocarcinoma / secondary. Adrenal Gland Neoplasms / secondary. Esophageal Neoplasms / pathology

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  • (PMID = 17949483.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2100056
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69. Tian L, Guo Y, Wu YP, Liu LZ: [CT features of adrenal cortical adenoma: a report of 109 cases]. Ai Zheng; 2008 Jan;27(1):66-70

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [CT features of adrenal cortical adenoma: a report of 109 cases].
  • BACKGROUND & OBJECTIVE: Adrenal cortical adenoma (ACA) is a common disease, and can be diagnosed easily with CT examination.
  • However, some atypical adenomas are likely to be misdiagnosed.
  • RESULTS: Of the 109 cases of ACA, 104 showed unilateral single adenoma, 1 showed unilateral 2 adenomas, and 4 showed bilateral adenomas.
  • The maximal diameter of non-functional adenomas was larger than that of Cushing's adenomas, and the latter was larger than that of Conn's adenomas.
  • The probability of degeneration was higher in large adenomas than in small adenomas.
  • [MeSH-major] Adrenal Cortex Neoplasms / radiography. Adrenocortical Adenoma / radiography. Radiographic Image Enhancement / methods. Tomography, Spiral Computed / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Diagnosis, Differential. Female. Humans. Infant. Male. Middle Aged. Neoplasm Recurrence, Local. Tumor Burden. Young Adult

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  • (PMID = 18184467.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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70. Hennings J, Lindhe O, Bergström M, Långström B, Sundin A, Hellman P: [11C]metomidate positron emission tomography of adrenocortical tumors in correlation with histopathological findings. J Clin Endocrinol Metab; 2006 Apr;91(4):1410-4

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

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  • (PMID = 16403816.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Radiopharmaceuticals; 5377-20-8 / metomidate; Z22628B598 / Etomidate
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71. Caoili EM, Korobkin M, Brown RK, Mackie G, Shulkin BL: Differentiating adrenal adenomas from nonadenomas using (18)F-FDG PET/CT: quantitative and qualitative evaluation. Acad Radiol; 2007 Apr;14(4):468-75
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  • [Title] Differentiating adrenal adenomas from nonadenomas using (18)F-FDG PET/CT: quantitative and qualitative evaluation.
  • RATIONALE AND OBJECTIVES: We sought to assess the ability of (18)F-fluoro-2-deoxy-d-glucose (FDG) PET/CT to distinguish adrenal adenomas from nonadenomas in patients with suspected malignancy.
  • METHODS: Fifty-nine adrenal masses were evaluated with coregistered (18)F-FDG PET (PET/CT).
  • Two reviewers independently graded uptake of (18)F-FDG by visual inspection of the adrenal mass in comparison to liver and background.
  • CT attenuation value of the adrenal mass and the standardized uptake value (SUV) of the mass, liver, background, and primary neoplasm (when visible) were measured.
  • Mean SUVs of the adrenal mass, liver, and background and ratios of the SUVs were calculated.
  • RESULTS: Of 47 adenomas, 43 measured <10 HU on unenhanced CT.
  • Using qualitative assessment of FDG activity in the adrenal mass compared with liver, adenomas were less than, equal to, or more active than the liver in 51%, 38%, and 10%, respectively.
  • The mean SUV of adenomas (4.2) was significantly lower (P = .002) than that of their primary malignancies (9.2) but not that of liver (4.3).
  • The mean SUV of adenomas was not significantly different than that of nonadenomas (5.2), but the mean adrenal/liver ratio (1.0) for the adenomas was significantly lower (P = .006) than that of the nonadenomas (2.1).
  • CONCLUSION: Adrenal adenomas were better differentiated from nonadenomas using unenhanced CT measurements in combination with ratios of the SUvs. Adrenal mass activity, which was visibly less than liver, was more specific for adenoma, whereas adrenal mass activity visibly greater than liver was more specific for malignancy.
  • [MeSH-major] Adrenal Gland Neoplasms / radiography. Adrenal Gland Neoplasms / radionuclide imaging. Adrenocortical Adenoma / radiography. Adrenocortical Adenoma / radionuclide imaging. Tomography, Emission-Computed / methods. Tomography, X-Ray Computed / methods
  • [MeSH-minor] Aged. Aged, 80 and over. Diagnosis, Differential. Female. Fluorodeoxyglucose F18. Humans. Male. Middle Aged. Radiopharmaceuticals. Retrospective Studies. Sensitivity and Specificity

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  • (PMID = 17368217.001).
  • [ISSN] 1076-6332
  • [Journal-full-title] Academic radiology
  • [ISO-abbreviation] Acad Radiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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72. Libé R, Mantovani G, Bondioni S, Lania AG, Pedroni C, Beck-Peccoz P, Spada A: Mutational analysis of PRKAR1A and Gs(alpha) in sporadic adrenocortical tumors. Exp Clin Endocrinol Diabetes; 2005 May;113(5):248-51

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  • [Title] Mutational analysis of PRKAR1A and Gs(alpha) in sporadic adrenocortical tumors.
  • Little is known about the pathogenesis of adrenocortical tumors.
  • The cAMP-dependent pathway is physiologically activated by ACTH in adrenocortical cells and different components of this cascade may be altered in some functioning adrenocortical tumors.
  • Recently, mutations of the gene encoding the PKA type 1 A regulatory subunit (R1 A), PRKAR1A, associated with loss of heterozygosity (LOH) at PRKAR1A locus, have been demonstrated in primary pigmented nodular adrenocortical disease (PPNAD), either isolated or associated with Carney complex.
  • Moreover, activating mutations of the Gs(alpha) gene (the gsp oncogene) have also been found in a small number of adrenocortical cortisol-secreting adenomas.
  • Aim of this study was to investigate the presence of such genetic alterations on a series of 10 ACTH-independent Cushing syndrome due to non-PPNAD adrenocortical adenomas.
  • In one single adenoma gsp mutation was detected.
  • PRKAR1A mutations and gsp oncogene, are a rare event in adrenocortical tumors.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. DNA Mutational Analysis. GTP-Binding Protein alpha Subunits, Gs / genetics. Proteins / genetics

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  • (PMID = 15926108.001).
  • [ISSN] 0947-7349
  • [Journal-full-title] Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
  • [ISO-abbreviation] Exp. Clin. Endocrinol. Diabetes
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human; 0 / Proteins; E0399OZS9N / Cyclic AMP; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
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73. Libé R, Bertherat J: Molecular genetics of adrenocortical tumours, from familial to sporadic diseases. Eur J Endocrinol; 2005 Oct;153(4):477-87
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  • [Title] Molecular genetics of adrenocortical tumours, from familial to sporadic diseases.
  • Adrenal masses can be detected in up to 4% of the population, and are mostly of adrenocortical origin.
  • Adrenocortical tumours (ACTs) may be responsible for excess steroid production and, in the case of adrenocortical cancers, for morbidity or mortality due to tumour growth.
  • The familial diseases concerned are Li-Fraumeni syndrome, which may be due to germline mutation of the tumour-suppressor gene TP53 and Beckwith-Wiedemann syndrome, which is caused by dys-regulation of the imprinted IGF-II locus at 11p15.
  • Cushing's syndrome due to primary pigmented nodular adrenocortical disease (PPNAD) has been observed in Carney complex patients presenting inactivating germline PRKAR1A mutations.
  • Interestingly, allelic losses at 17p13 and 11p15 have been demonstrated in sporadic adrenocortical cancer and somatic PRKAR1A mutations have been found in secreting adrenocortical adenomas.
  • The genetics of another group of adrenal diseases that can lead to adrenal nodular hyperplasia -- congenital adrenal hyperplasia (CAH) and glucocorticoid-remediable aldosteronism (GRA) -- have also been studied extensively.
  • This review summarizes recent advances in the genetics of ACTs, highlighting both improvements in our understanding of the pathophysiology and the diagnosis of these tumours.

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  • (PMID = 16189167.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 97
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74. Satoh F, Abe T, Tanemoto M, Nakamura M, Abe M, Uruno A, Morimoto R, Sato A, Takase K, Ishidoya S, Arai Y, Suzuki T, Sasano H, Ishibashi T, Ito S: Localization of aldosterone-producing adrenocortical adenomas: significance of adrenal venous sampling. Hypertens Res; 2007 Nov;30(11):1083-95
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  • [Title] Localization of aldosterone-producing adrenocortical adenomas: significance of adrenal venous sampling.
  • Accurate localization of aldosterone-producing adenoma (APA) is essential for the treatment of primary aldosteronism (PA).
  • In order to confirm the clinical usefulness of adrenal venous sampling (AVS), we retrospectively studied 87 cases of PA in whom AVS was conducted.
  • We collected right and left adrenal venous effluents simultaneously before and after adrenocorticotropic hormone (ACTH) stimulation for measurements of aldosterone concentration (A) and cortisol concentration (C).
  • Of the above 66 subjects, 61 underwent laparoscopic removal of the adrenal gland through a retroperitoneal approach.
  • The receiver operator characteristics (ROC) curve analysis between the operated and no-apparent-laterality groups revealed that the ratio of A/C on the higher side to A/C on the lower side (A/C ratio) after ACTH stimulation is a useful index, with a cutoff value of 2.6, a sensitivity of 0.98 and a specificity of 1.0.
  • The ROC curve analysis between the APA side and contralateral side within the operated patients revealed that the cutoff value of A was 1,340 ng/dL, with a sensitivity of 0.92 and a specificity of 1.00.
  • [MeSH-major] Adenoma / diagnosis. Adrenal Cortex Neoplasms / diagnosis. Aldosterone / blood. Blood Specimen Collection / methods. Hydrocortisone / blood

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  • [CommentIn] Hypertens Res. 2007 Nov;30(11):1009-10 [18250546.001]
  • (PMID = 18250558.001).
  • [ISSN] 0916-9636
  • [Journal-full-title] Hypertension research : official journal of the Japanese Society of Hypertension
  • [ISO-abbreviation] Hypertens. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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75. Waldmann J, Feldmann G, Slater EP, Langer P, Buchholz M, Ramaswamy A, Saeger W, Rothmund M, Fendrich V: Expression of the zinc-finger transcription factor Snail in adrenocortical carcinoma is associated with decreased survival. Br J Cancer; 2008 Dec 2;99(11):1900-7
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  • [Title] Expression of the zinc-finger transcription factor Snail in adrenocortical carcinoma is associated with decreased survival.
  • In this study, we evaluate whether Snail is expressed in adrenocortical cancer (ACC) and if its expression is related to patient outcome.
  • Snail expression was neither detected in normal adrenocortical tissue, nor in benign adrenocortical adenomas.
  • Survival rates were significantly decreased in Snail-positive tumours compared to Snail-negative tumours: 10 out of 16 vs one out of eight patients succumbed to disease after a median follow up of 14.5 and 28.5 months, respectively (P=0.03).
  • Patients with Snail-expressing ACCs presented in advanced disease (11 out of 12 vs 6 out of 14, P=0.01) and tend to develop distant metastases more frequently than patients with negative staining (7 out of 11 vs two out of eight, P=0.19).
  • Furthermore, Snail expression is associated with decreased survival, advanced disease and higher risk of developing distant metastases.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenocortical Carcinoma / metabolism. Biomarkers, Tumor / analysis. Transcription Factors / biosynthesis

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  • (PMID = 19018264.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cadherins; 0 / Ki-67 Antigen; 0 / RNA, Messenger; 0 / Transcription Factors; 0 / snail family transcription factors
  • [Other-IDs] NLM/ PMC2600683
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76. Yip L, Tublin ME, Falcone JA, Nordman CR, Stang MT, Ogilvie JB, Carty SE, Yim JH: The adrenal mass: correlation of histopathology with imaging. Ann Surg Oncol; 2010 Mar;17(3):846-52
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  • [Title] The adrenal mass: correlation of histopathology with imaging.
  • BACKGROUND: Computed tomography (CT) and magnetic resonance (MR) imaging can help diagnose benign adrenal adenomas, but prior studies rely on nonoperative follow-up as proof of a lesion's benign nature.
  • Imaging results were considered to signify benign adrenal adenoma if one or more of the following was present: Hounsfield units <10 on unenhanced CT, contrast-enhanced CT quantifying absolute contrast washout of >60% or relative contrast washout of >40%, or MR with chemical-shift imaging demonstrating loss of signal intensity on out-of-phase images.
  • RESULTS: The sensitivity and specificity of preoperative imaging in predicting benign adrenal adenoma were 57 and 94%, respectively.
  • Histopathology confirmed that all 66 adrenal masses with imaging characteristics suggesting benign adenoma were indeed benign lesions and included 61 benign adrenal adenomas and 5 benign nonadenomatous lesions (3 myelolipomas, 1 composite myelolipoma/adenoma, and 1 ganglioliponeuroma).
  • Malignant adrenal lesions were diagnosed in 17/130 (13%) masses: 8 metastases, 7 adrenal cortical carcinomas, 1 epithelioid angiosarcoma, and 1 ganglioneuroblastoma.
  • CONCLUSION: CT or MR characteristics predicted the presence of benign lesions with 100% specificity.
  • Every adrenal malignancy had CT or MR results that were inconsistent with benign adenoma (100% sensitivity).
  • To exclude malignancy, adrenal masses with non-benign imaging characteristics should be resected.
  • [MeSH-major] Adrenal Gland Neoplasms / pathology. Adrenal Gland Neoplasms / radiography. Adrenocortical Adenoma / pathology. Adrenocortical Adenoma / radiography. Magnetic Resonance Imaging. Tomography, X-Ray Computed

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  • (PMID = 19960266.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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77. Fenske W, Völker HU, Adam P, Hahner S, Johanssen S, Wortmann S, Schmidt M, Morcos M, Müller-Hermelink HK, Allolio B, Fassnacht M: Glucose transporter GLUT1 expression is an stage-independent predictor of clinical outcome in adrenocortical carcinoma. Endocr Relat Cancer; 2009 Sep;16(3):919-28
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  • [Title] Glucose transporter GLUT1 expression is an stage-independent predictor of clinical outcome in adrenocortical carcinoma.
  • Owing to the rarity of adrenocortical carcinoma (ACC) no prognostic markers have been established beyond stage and resection status.
  • Immunohistochemical analysis was performed on tissue microarrays of paraffin-embedded tissue samples from 167 ACCs, 15 adrenal adenomas and 4 normal adrenal glands.
  • GLUT1 and -3 were expressed in 33 and 17% of ACC samples respectively, but in none of the benign tumours or normal adrenals glands.
  • By contrast, TKTL1 and M2-PK were detectable in all benign tissues and the vast majority of ACCs.
  • When analysing patients in their early stages and advanced disease separately, similar results were obtained.
  • HR for survival was 5.31 (1.80-15.62) in patients with metastatic ACC and in patients after radical resection the HR for disease-free survival was 6.10 (2.16-16.94).
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / metabolism. Adrenocortical Carcinoma / diagnosis. Adrenocortical Carcinoma / metabolism. Glucose Transporter Type 1 / metabolism

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  • (PMID = 19465749.001).
  • [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 / Glucose Transporter Type 1; 0 / SLC2A1 protein, human; IY9XDZ35W2 / Glucose
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78. Cazabat L, Ragazzon B, Groussin L, Bertherat J: PRKAR1A mutations in primary pigmented nodular adrenocortical disease. Pituitary; 2006;9(3):211-9
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  • [Title] PRKAR1A mutations in primary pigmented nodular adrenocortical disease.
  • Primary Pigmented Nodular Adrenocortical Disease (PPNAD) is a rare primary bilateral adrenal defect causing corticotropin-independent Cushing's syndrome.
  • Macroscopic appearance of the adrenals is characteristic with small pigmented micronodules observed in the cortex.
  • Somatic inactivating mutations of PRKAR1A have been observed in macronodules of PPNAD and in sporadic cortisol secreting adrenal adenomas.
  • Isolated PPNAD is a genetic heterogenous disease, and recently inactivating mutations of the gene of the phosphodiesterase 11A4 (PDE11A4) located at 2q31-2q35 have been identified in patients without PRKAR1A mutations.
  • [MeSH-major] Adrenal Cortex Diseases / genetics. Cushing Syndrome / genetics. Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / genetics. Mutation. Pigmentation Disorders / genetics
  • [MeSH-minor] Animals. Cyclic AMP / metabolism. Cyclic AMP-Dependent Protein Kinases / metabolism. Gene Expression Regulation, Enzymologic. Genetic Predisposition to Disease. Hormones / metabolism. Humans. Multiple Endocrine Neoplasia / enzymology. Multiple Endocrine Neoplasia / genetics. Signal Transduction / genetics

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  • (PMID = 17036196.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / Hormones; 0 / PRKAR1A protein, human; E0399OZS9N / Cyclic AMP; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
  • [Number-of-references] 49
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79. Bertherat J, Gimenez-Roqueplo AP: New insights in the genetics of adrenocortical tumors, pheochromocytomas and paragangliomas. Horm Metab Res; 2005 Jun;37(6):384-90
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  • [Title] New insights in the genetics of adrenocortical tumors, pheochromocytomas and paragangliomas.
  • Recent advances in the molecular genetic of adrenal tumors give new insights in the pathophysiology of these neoplasms in both hereditary and sporadic cases.
  • The practice of genetic counselling in patients with adrenal tumors have been recently changed by the identification and the understanding of new specific hereditary cancer susceptibility syndromes.
  • In the case of sporadic adrenocortical tumors these progress also offer new prognosis predictors.
  • The genetic predisposition to adrenocortical cancer in children has been well established in the Li-Fraumeni and Beckewith-Wiedeman syndromes due to germline p53 mutation located at 17p13 and dysregulation of the imprinted IGF-2 locus at 11p15, respectively.
  • Adrenocortical tumors are also observed in Multiple Endocrine Neoplasia type I syndrome.
  • Cushing's syndrome due to primary pigmented nodular adrenocortical disease have been observed in patients with germline PRKAR1A inactivating mutations.
  • Interestingly allelic loss at 17p13 and 11p15 have been observed in sporadic adrenocortical cancer and somatic PRKAR1A mutations in secreting adrenocortical adenomas.
  • The potential interest of these finding for the diagnosis of these tumors will be discussed.
  • Up to date, four diagnosis of familal disease (multiple endocrine neoplasia type II, von Hippel Lindau disease, neurofibromatosis type 1 and hereditary paraganglioma) should be discussed and causative mutations in six different phaechomocytoma susceptibility genes (RET, VHL, NF1, SDHB, SDHD, SDHC) could be identified.
  • We will suggest guidelines for the practice of the phaeochomocytoma genetic testing in the patients and their families, and for an early detection of tumors in the patients or in individuals determined to be at-risk of disease by the presymptomatic genetic testing.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Gene Expression Regulation, Neoplastic / genetics. Paraganglioma / genetics. Pheochromocytoma / genetics

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  • (PMID = 16001332.001).
  • [ISSN] 0018-5043
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Number-of-references] 53
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80. 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

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  • [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.
  • Only tetraploid percentage (P = .0496) and 5cER (P = .0352) distinguished polyclonal (3.64 +/- 2.20 and 0.14 +/- 0.15) from monoclonal (7.25 +/- 7.52 and 1.00 +/- 1.74) benign lesions.
  • 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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81. Yoh T, Hosono M, Komeya Y, Im SW, Ashikaga R, Shimono T, Tsuchiya N, Okada M, Hanada K, Yagyu Y, Nishimura Y, Murakami T: Quantitative evaluation of norcholesterol scintigraphy, CT attenuation value, and chemical-shift MR imaging for characterizing adrenal adenomas. Ann Nucl Med; 2008 Jul;22(6):513-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Quantitative evaluation of norcholesterol scintigraphy, CT attenuation value, and chemical-shift MR imaging for characterizing adrenal adenomas.
  • OBJECTIVE: The objective of our study was to evaluate diagnostic ability and features of quantitative indices of three modalities: uptake rate on norcholesterol scintigraphy, computed tomography (CT) attenuation value, and fat suppression on chemical-shift magnetic resonance imaging (MRI) for characterizing adrenal adenomas.
  • METHODS: Image findings of norcholesterol scintigraphy, CT, and MRI were reviewed for 78 patients with functioning (n = 48) or nonfunctioning (n = 30) adrenal masses.
  • The norcholesterol uptake rate, attenuation value on unenhanced CT, and suppression on in-phase to opposed-phase MRI were measured for adrenal masses.
  • RESULTS: The norcholesterol uptake rate, CT attenuation value, and MR suppression index showed the sensitivity of 60%, 82%, and 100%, respectively, for functioning adenomas of <2.0 cm, and 96%, 79%, and 67%, respectively, for those of >or=2.0 cm.
  • Regarding norcholesterol uptake, the adenoma-to-contralateral gland ratio was significantly higher in cortisol releasing than in aldosterone-releasing adenomas.
  • CONCLUSIONS: The norcholesterol uptake rate was reliable for characterization of adenomas among adrenal masses of >or=2.0 cm.
  • [MeSH-major] 19-Iodocholesterol. Adrenal Gland Neoplasms / diagnosis. Adrenocortical Adenoma / diagnosis. Image Interpretation, Computer-Assisted / methods. Magnetic Resonance Imaging / methods. Tomography, X-Ray Computed / methods

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  • (PMID = 18670858.001).
  • [ISSN] 0914-7187
  • [Journal-full-title] Annals of nuclear medicine
  • [ISO-abbreviation] Ann Nucl Med
  • [Language] eng
  • [Publication-type] Controlled Clinical Trial; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 30461-91-7 / 19-Iodocholesterol
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82. Inan N, Arslan A, Akansel G, Anik Y, Balci NC, Demirci A: Dynamic contrast enhanced MRI in the differential diagnosis of adrenal adenomas and malignant adrenal masses. Eur J Radiol; 2008 Jan;65(1):154-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dynamic contrast enhanced MRI in the differential diagnosis of adrenal adenomas and malignant adrenal masses.
  • OBJECTIVE: To evaluate the value of dynamic MR imaging in the differential diagnosis of adrenal adenomas and malignant tumors, especially in cases with atypical adenomas.
  • MATERIALS AND METHODS: Sixty-four masses (48 adenomas, 16 malignant tumors) were included in this prospective study.
  • RESULTS: Chemical shift MR imaging was able to differentiate 44 out of 48 adenomas (91.7%) from non-adenomas.
  • The 4 adenomas (8.3%) which could not be differentiated from non-adenomas by this technique did not exhibit signal loss on out-of-phase images.
  • With a cut-off value of 30, SI indices of adenomas had a sensitivity of 93.8%, specificity of 100% and a positive predictive value of 100%.
  • On visual evaluation of dynamic MR imaging, early phase contrast enhancement patterns were homogeneous in 75% and punctate in 20,83% of the adenomas; while patchy in 56.25% and peripheral in 25% of the malignant tumors.
  • On the late phase images 58.33% of the adenomas showed peripheral ring-shaped enhancement and 10.41% showed heterogeneous enhancement.
  • At the 25th second, the SIs and wash-in rates of the adenomas were significantly higher than those of the malignant masses (p=0.010).
  • Time-to-peak enhancement of the malignant masses was significantly longer than that of the adenomas.
  • CONCLUSION: Chemical shift MR has a high sensitivity and specificity in the differential diagnosis of adenomas and malignant adrenal masses.
  • However, taking into consideration only the atypical adenomas, chemical shift MRI is of no diagnostic value.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis. Adrenocortical Adenoma / diagnosis. Magnetic Resonance Imaging / methods
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Contrast Media. Diagnosis, Differential. Female. Humans. Image Interpretation, Computer-Assisted. Male. Middle Aged. ROC Curve. Sensitivity and Specificity. Statistics, Nonparametric

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  • (PMID = 17466481.001).
  • [ISSN] 0720-048X
  • [Journal-full-title] European journal of radiology
  • [ISO-abbreviation] Eur J Radiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Contrast Media
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83. Monjero-Ares I, Gegundez-Gómez C, Couselo-Villanueva JM, Moreda-Pérez M, Jorge-Iglesias M, Torres-García I, Alvarez-Gutiérrez AE, Arija-Val JF: [Association of pheochromocytoma with contralateral nonfunctioning adrenal adenoma]. Cir Esp; 2006 Feb;79(2):126-8
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  • [Title] [Association of pheochromocytoma with contralateral nonfunctioning adrenal adenoma].
  • [Transliterated title] Asociación de feocromocitoma con adenoma suprarrenal contralateral no funcionante.
  • A 52-year-old woman complaining of abdominal pain, headaches and palpitations was admitted to our hospital for investigation of a bilateral adrenal tumor.
  • The definitive diagnosis was right pheochromocytoma and left adrenocortical adenoma.
  • Only four cases of pheochromocytoma associated with nonfunctioning adrenal adenoma have previously been reported.
  • [MeSH-major] Adenoma. Adrenal Gland Neoplasms. Neoplasms, Multiple Primary. Pheochromocytoma

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  • (PMID = 16539953.001).
  • [ISSN] 0009-739X
  • [Journal-full-title] Cirugía española
  • [ISO-abbreviation] Cir Esp
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
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84. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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85. Jeong BC, Park YH, Han DH, Kim HH: Laparoendoscopic single-site and conventional laparoscopic adrenalectomy: a matched case-control study. J Endourol; 2009 Dec;23(12):1957-60

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: The purpose of this study was to describe our initial clinical experience and assess the feasibility of laparoendoscopic single-site surgery (LESS) in the treatment of benign adrenal adenoma.
  • PATIENTS AND METHODS: Nine patients undergoing LESS adrenalectomy for benign adrenal adenoma were compared with 17 patients undergoing conventional laparoscopic adrenalectomy.
  • CONCLUSIONS: LESS adrenalectomy for benign adrenal adenoma is comparable to the conventional laparoscopic approach with regard to the operative time, blood loss, length of hospital stay, and degree of complication, and has demonstrated more desirable cosmetic outcomes.

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  • (PMID = 19909074.001).
  • [ISSN] 1557-900X
  • [Journal-full-title] Journal of endourology
  • [ISO-abbreviation] J. Endourol.
  • [Language] ENG
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
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86. Hanna AM, Pham TH, Askegard-Giesmann JR, Grams JM, Iqbal CW, Stavlo P, Moir CR: Outcome of adrenocortical tumors in children. J Pediatr Surg; 2008 May;43(5):843-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outcome of adrenocortical tumors in children.
  • PURPOSE: This study reviews adrenocortical tumors in children to determine factors that significantly affect outcome.
  • METHODS: An institutional review board-approved retrospective review from 1976 to 2005 identified 23 patients younger than 19 years old with histologic confirmation of adrenocortical carcinoma (ACC) and adenomas.
  • RESULTS: The mean age of the 23 children was 9.0 +/- 1.6 years; girls predominated (female-to-male ratio = 1.9:1) as did cancers (ACC 16, adenoma 7); tumor hormone production (74%); and advanced stage for disease (66%).
  • Adrenalectomy, including en bloc resection of adjacent structures (35%) achieved grossly negative margins in 70% of patients.
  • There was no perioperative mortality; morbidity was 10% (pneumothorax, acute renal failure, chylous ascites, and thrombocytosis).
  • Surgical cure without adjuvant therapy was achieved for all adenomas and ACC stages I and II.
  • Surgically negative margins with or without en bloc resection improves survival.
  • [MeSH-major] Adenoma / mortality. Adenoma / surgery. Adrenal Cortex Neoplasms / mortality. Adrenal Cortex Neoplasms / surgery. Adrenocortical Carcinoma / mortality. Adrenocortical Carcinoma / surgery

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  • (PMID = 18485950.001).
  • [ISSN] 1531-5037
  • [Journal-full-title] Journal of pediatric surgery
  • [ISO-abbreviation] J. Pediatr. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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87. Giordano TJ, Kuick R, Else T, Gauger PG, Vinco M, Bauersfeld J, Sanders D, Thomas DG, Doherty G, Hammer G: Molecular classification and prognostication of adrenocortical tumors by transcriptome profiling. Clin Cancer Res; 2009 Jan 15;15(2):668-76
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular classification and prognostication of adrenocortical tumors by transcriptome profiling.
  • PURPOSE: Our understanding of adrenocortical carcinoma (ACC) has improved considerably, yet many unanswered questions remain.
  • EXPERIMENTAL DESIGN: We did a whole genome gene expression study of a large cohort of adrenocortical tissues annotated with clinicopathologic data.
  • Using Affymetrix Human Genome U133 Plus 2.0 oligonucleotide arrays, transcriptional profiles were generated for 10 normal adrenal cortices (NC), 22 adrenocortical adenomas (ACA), and 33 ACCs.
  • RESULTS: The overall classification of adrenocortical tumors was recapitulated using principal component analysis of the entire data set.
  • Cluster analysis of the ACCs revealed two subtypes that reflected tumor proliferation, as measured by mitotic counts and cell cycle genes.
  • CONCLUSIONS: This study lays the foundation for the molecular classification and prognostication of adrenocortical tumors and also provides a rich source of potential diagnostic and prognostic markers.

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  • (PMID = 19147773.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA046592-209023; United States / NCI NIH HHS / CA / CA046592-219023; United States / NCI NIH HHS / CA / P30 CA046592; United States / NCI NIH HHS / CA / 5 P30 CA46592; United States / NCI NIH HHS / CA / CA046592-199023; United States / NCI NIH HHS / CA / P30 CA046592-219023; United States / NCI NIH HHS / CA / P30 CA046592-199023; United States / NCI NIH HHS / CA / P30 CA046592-209023
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclin E
  • [Other-IDs] NLM/ NIHMS78831; NLM/ PMC2629378
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88. Ishida M, Yoshida K, Miyamoto K, Iwai M, Miyahira Y, Kushima R, Okabe H: Cytological features of myxoid adrenocortical adenoma with a pseudoglandular component: a case report with differential diagnostic considerations. Diagn Cytopathol; 2008 Aug;36(8):576-80

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytological features of myxoid adrenocortical adenoma with a pseudoglandular component: a case report with differential diagnostic considerations.
  • Myxoid adrenocortical tumors are extremely rare neoplasms with only nine adenomas and eleven carcinomas reported in the literature.
  • They occasionally have a pseudoglandular component resembling metastatic mucinous adenocarcinoma in the adrenal gland.
  • We report here the first cytopathological study of a myxoid adrenocortical adenoma with a pseudoglandular component, contributing especially to the differential diagnosis from metastatic mucinous adenocarcinoma.
  • Two major cytopathological features distinguishing myxoid adrenocortical adenoma from metastatic mucinous adenocarcinoma in the adrenal gland are:.
  • Careful observation of these cytological features and positive immunoreactivity to Melan A, alpha-inhibin and synaptophysin can lead to the correct diagnosis.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / diagnosis. Adrenocortical Adenoma / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Diagnosis, Differential. Female. Humans. Male. Middle Aged

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  • (PMID = 18618725.001).
  • [ISSN] 1097-0339
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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89. 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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90. Else T, Giordano TJ, Hammer GD: Evaluation of telomere length maintenance mechanisms in adrenocortical carcinoma. J Clin Endocrinol Metab; 2008 Apr;93(4):1442-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of telomere length maintenance mechanisms in adrenocortical carcinoma.
  • CONTEXT: Adrenocortical cancer (ACC) is a rare disease with an often fatal outcome.
  • The clinical and pathological diagnosis of a malignant vs. benign adrenocortical tumor is sometimes challenging.
  • Telomere maintenance mechanisms (TMMs) are critical for the persistence of the malignant phenotype, but little is known about these mechanisms or their diagnostic value in adrenocortical lesions.
  • OBJECTIVE: Tissue samples of diagnostically known adrenocortical neoplasms were evaluated for parameters of known TMMs, telomerase activity (TA), and alternative telomere lengthening (ALT).
  • DESIGN: The study analyzed retrospectively collected frozen adrenocortical tissue samples from the University of Michigan Health System.
  • PATIENT SAMPLES: Samples included 24 ACCs, 11 adrenocortical adenomas (ACAs), and three normal adrenal tissues.
  • The TMM classification was: 19 of 24 TA (79%), two of which displayed very long telomeres, one of 24 ALT (4%) and two of 24 (8%) TA and ALT.
  • None of the normal adrenal tissues (none of three) or ACA (none of 11) samples had signs of an active TMM.
  • Determination of telomere maintenance mechanisms in diagnostically challenging adrenocortical tumors might be of additional diagnostic value in the pathological diagnosis of malignant vs. benign lesions.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Telomere

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  • (PMID = 18198226.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.7.49 / Telomerase
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91. Adissu HA, Hayes G, Wood GA, Caswell JL: Cardiac myxosarcoma with adrenal adenoma and pituitary hyperplasia resembling Carney complex in a dog. Vet Pathol; 2010 Mar;47(2):354-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cardiac myxosarcoma with adrenal adenoma and pituitary hyperplasia resembling Carney complex in a dog.
  • The pathological evaluation revealed a left atrial ossifying myxosarcoma, bilateral adrenocortical adenomas, multifocal pituitary hyperplasia with expression of adrenocorticotrophic hormone, and multiple pituitary Rathke's cleft cysts.
  • [MeSH-major] Adrenal Cortex Neoplasms / veterinary. Dog Diseases / pathology. Heart Neoplasms / veterinary. Myxosarcoma / veterinary. Pituitary Neoplasms / veterinary
  • [MeSH-minor] Animals. Diagnosis, Differential. Dogs. Fatal Outcome. Female

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  • (PMID = 20110224.001).
  • [ISSN] 1544-2217
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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92. Inomoto C, Sato H, Kanai G, Hirukawa T, Shoji S, Terachi T, Kajiwara H, Osamura RY: Black adrenal adenoma causing preclinical Cushing's syndrome. Tokai J Exp Clin Med; 2010 Jul;35(2):57-61
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  • [Title] Black adrenal adenoma causing preclinical Cushing's syndrome.
  • Functioning black adrenal adenoma (BAA) rarely causes preclinical Cushing's syndrome (CS).
  • Abdominal computed tomography showed that she had a 15-mm in diameter, round, left adrenal adenoma.
  • The left adrenal adenoma was laparoscopically removed.
  • Examination of the surgical specimen revealed unilateral double adrenal adenomas of the left adrenal gland, one of which was a BAA.
  • The compact cell zones remained in the adrenal cortex adjacent to the BAA showed atrophic change.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications. Cushing Syndrome / etiology

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  • (PMID = 21319027.001).
  • [ISSN] 2185-2243
  • [Journal-full-title] The Tokai journal of experimental and clinical medicine
  • [ISO-abbreviation] Tokai J. Exp. Clin. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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93. Ors F, Lev-Toaff A, O'Kane P, Qazi N, Bergin D: Paraovarian adrenal rest with MRI features characteristic of an adrenal adenoma. Br J Radiol; 2007 Sep;80(957):e205-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Paraovarian adrenal rest with MRI features characteristic of an adrenal adenoma.
  • We report MR and sonographic imaging features of an incidentally detected paraovarian adrenal rest in a 44-year-old woman who was being evaluated for menorrhagia.
  • This is the first report of chemical shift imaging identifying the presence of lipid within an adrenal rest as well as rapid washout of contrast.
  • Both of these MR characteristics are typically seen with an adrenal adenoma.
  • [MeSH-major] Adrenal Rest Tumor / diagnosis. Fallopian Tube Neoplasms / diagnosis
  • [MeSH-minor] Adenoma / diagnosis. Adenoma / ultrasonography. Adrenal Gland Neoplasms / diagnosis. Adrenal Gland Neoplasms / ultrasonography. Adult. Diagnosis, Differential. Female. Humans. Magnetic Resonance Imaging

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  • (PMID = 17928489.001).
  • [ISSN] 1748-880X
  • [Journal-full-title] The British journal of radiology
  • [ISO-abbreviation] Br J Radiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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94. Sereg M, Szappanos A, Toke J, Karlinger K, Feldman K, Kaszper E, Varga I, Gláz E, Rácz K, Tóth M: Atherosclerotic risk factors and complications in patients with non-functioning adrenal adenomas treated with or without adrenalectomy: a long-term follow-up study. Eur J Endocrinol; 2009 Apr;160(4):647-55
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  • [Title] Atherosclerotic risk factors and complications in patients with non-functioning adrenal adenomas treated with or without adrenalectomy: a long-term follow-up study.
  • OBJECTIVE: Despite the increased prevalences of hypertension, type 2 diabetes mellitus (T2DM), hyperlipidemy, and obesity in patients with non-functioning adrenal adenomas (NFAAs), there is a paucity of data on long-term atherosclerotic morbidity as well as the long-term cardiovascular effects of adrenalectomy in these patients.

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  • (PMID = 19174533.001).
  • [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] 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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95. Qiao ZW, Xia CM, Zhu YB, Shi WP, Miao F: First-pass perfusion computed tomography: initial experience in differentiating adrenal adenoma from metastasis. Eur J Radiol; 2010 Mar;73(3):657-63
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  • [Title] First-pass perfusion computed tomography: initial experience in differentiating adrenal adenoma from metastasis.
  • OBJECTIVE: To differentiate adrenal adenoma from metastasis in patients using perfusion computed tomography (PCT) imaging.
  • METHODS: Thirty-two patients with adrenal masses underwent first-pass PCT imaging.
  • Of these patients, twenty-one were diagnosed with adrenal adenoma, and the others with metastases.
  • RESULTS: The perfusion parameters such as BV, BF and PS were statistically significant different between the two groups, with adenomas showing higher mean BV (12.18 versus 3.86), BF (97.51 versus 45.99) and PS (21.73 versus 10.93) compared with metastases (p<0.05).
  • For BV, a cutoff point of 7.30 was found to have a sensitivity of 95.2% and a specificity of 100% to differentiate between adenoma and metastasis.
  • The sensitivity and specificity were 81.0 and 80.0%, respectively, for BF with a cutoff point of 71.96; and 85.7 and 86.7%, respectively, for PS with a cutoff point of 12.70 to differentiate adenoma and metastasis.
  • A comparison of MVD counts from adenomas with those from metastases showed a significant difference (p<0.05).
  • However, no significant differences were observed in the four perfusion parameters and MVD between lipid rich and lipid poor adenomas.
  • CONCLUSION: PCT may be useful for evaluating the neovascularization of adrenal masses and differentiating adenoma from metastasis on the basis of PCT parameters.
  • Adenomas show higher BV, BF and PS compared with metastases.
  • According our data, the optimal threshold BV is 7.30, resulting in a sensitivity of 95.2% and a specificity of 100% for the differentiation of adenoma from metastasis.
  • Adrenal adenomas have similar hemodynamic profiles, which are apparently independent of the lipid content of an adenoma.
  • [MeSH-major] Adrenal Gland Neoplasms / radiography. Adrenocortical Adenoma / radiography. Tomography, X-Ray Computed / methods
  • [MeSH-minor] Adult. Contrast Media. Diagnosis, Differential. Female. Humans. Iohexol / analogs & derivatives. Male. Microcirculation. ROC Curve. Radiographic Image Interpretation, Computer-Assisted

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  • [Copyright] Copyright 2009 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 19200677.001).
  • [ISSN] 1872-7727
  • [Journal-full-title] European journal of radiology
  • [ISO-abbreviation] Eur J Radiol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Contrast Media; 4419T9MX03 / Iohexol; 712BAC33MZ / iopromide
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96. 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.
  • A large number of genes were accordingly found to be differentially expressed comparing carcinomas to adenomas.
  • Regarding adenomas with aldosterone overproduction, OSBP and VEGFB were among the most up-regulated genes compared with the other samples.
  • 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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97. Takeda Y, Usukura M, Yoneda T, Oda N, Ito Y, Mabuchi H: The expression of messenger RNA for ADP-ribosyl cyclase in aldosterone-producing adenomas. Clin Endocrinol (Oxf); 2005 Apr;62(4):504-8
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  • [Title] The expression of messenger RNA for ADP-ribosyl cyclase in aldosterone-producing adenomas.
  • To determine whether the cADPR system plays a signalling role in angiotensin II (Ang II)-induced aldosterone synthesis in the human adrenal gland, we investigated the effects of Ang II on ADP-ribosyl cyclase activity in human adrenal cortical tissue.
  • In addition, the expression of ADP-ribosyl cyclase messenger RNA was evaluated in aldosterone-producing adenomas (APAs) and compared with normal adrenal tissue and nonfunctioning adenomas.
  • DESIGN: ADP-ribosyl cyclase activity was measured in crude membrane fractions of human adrenocortical tissues with Ang II or with Ang II plus the Ang II receptor (AT(1)R) antagonist losartan or plus the AT(2)R antagonist PD123319.
  • The effect of 8-bromo-cADPR on Ang II-induced aldosterone production from adrenal tissue was estimated.
  • The expression of ADP-ribosyl cyclase, CYP11B2 and AT(1)R mRNA was measured in APAs, nonfunctioning adenomas, adjacent adrenal tissue and normal adrenal tissue.
  • The expression of ADP-ribosyl cyclase, CYP11B2 and AT(1)R mRNA was increased in APAs compared with that of nonfunctioning adenomas, adjacent adrenal tissue or normal adrenal tissue.
  • CONCLUSIONS: These results demonstrated the existence of a signalling pathway from the Ang II receptor to ADP-ribosyl cyclase in the human adrenal gland and suggest that the cADP-ribose signalling system might play an important role in the pathogenesis of APAs.
  • [MeSH-major] ADP-ribosyl Cyclase / genetics. Adenoma / secretion. Adrenal Cortex Neoplasms / secretion. Aldosterone / secretion. Angiotensins / pharmacology. Cyclic ADP-Ribose / analogs & derivatives. RNA, Messenger / analysis

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  • (PMID = 15807884.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 8-bromo-cyclic-ADP-ribose; 0 / Angiotensins; 0 / Imidazoles; 0 / Pyridines; 0 / RNA, Messenger; 0 / Receptor, Angiotensin, Type 1; 119340-53-3 / Cyclic ADP-Ribose; 130663-39-7 / PD 123319; 4964P6T9RB / Aldosterone; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 3.2.2.5 / ADP-ribosyl Cyclase; JMS50MPO89 / Losartan
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98. 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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99. Yoon JH, Kim SH, Kim MA, Han JK, Choi BI: MDCT and Gd-EOB-DTPA enhanced MRI findings of adrenal adenoma arising from an ectopic adrenal gland within the liver: radiologic-pathologic correlation. Korean J Radiol; 2010 Jan-Feb;11(1):126-30
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  • [Title] MDCT and Gd-EOB-DTPA enhanced MRI findings of adrenal adenoma arising from an ectopic adrenal gland within the liver: radiologic-pathologic correlation.
  • We report a case of an adenoma arising from an ectopic adrenal gland mimicking a hepatocellular carcinoma in a heavy alcohol abuser.
  • A tumorectomy was performed and adrenal adenoma from an ectopic adrenal gland within the liver was confirmed.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenocortical Adenoma / diagnosis. Choristoma / diagnosis. Contrast Media. Gadolinium DTPA. Liver Neoplasms / diagnosis. Magnetic Resonance Imaging. Tomography, X-Ray Computed
  • [MeSH-minor] Adrenal Glands. Carcinoma, Hepatocellular / diagnosis. Diagnosis, Differential. Humans. Male. Middle Aged

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  • (PMID = 20046505.001).
  • [ISSN] 2005-8330
  • [Journal-full-title] Korean journal of radiology
  • [ISO-abbreviation] Korean J Radiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Contrast Media; 0 / gadolinium ethoxybenzyl DTPA; K2I13DR72L / Gadolinium DTPA
  • [Other-IDs] NLM/ PMC2799643
  • [Keywords] NOTNLM ; Adrenal adenoma / Ectopic adrenal gland / Liver / Magnetic resonance (MR) / Multi-detector computed tomography (MDCT)
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100. Lee R, Storr M, Hershfield NB: A case of Conn's syndrome revealed after oral sodium phosphate (Fleet) preparation for colonoscopy. J Dig Dis; 2010 Apr;11(2):111-4
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  • [Title] A case of Conn's syndrome revealed after oral sodium phosphate (Fleet) preparation for colonoscopy.
  • The patient was subsequently diagnosed with primary aldosteronism secondary to an adenoma of the adrenal gland.
  • Bilateral adrenal venous sampling revealed excessive levels of aldosterone in the left adrenal vein prior to definitive surgery.
  • This case indicates that an oral sodium phosphate bowel preparation, though safe for most patients, can be complicated by a previously not diagnosed endocrine disease like the primary aldosteronism (Conn's syndrome) reported here.
  • This is the first report of a Conn's syndrome diagnosed after bowel cleansing with a sodium phosphate solution.
  • [MeSH-major] Colonoscopy / methods. Hyperaldosteronism / chemically induced. Hyperaldosteronism / diagnosis. Phosphates / adverse effects
  • [MeSH-minor] Adenoma / complications. Adenoma / diagnosis. Administration, Oral. Adrenal Gland Neoplasms / complications. Adrenal Gland Neoplasms / diagnosis. Aldosterone / blood. Female. Humans. Middle Aged. Renin / blood

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  • (PMID = 20402838.001).
  • [ISSN] 1751-2980
  • [Journal-full-title] Journal of digestive diseases
  • [ISO-abbreviation] J Dig Dis
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Phosphates; 4964P6T9RB / Aldosterone; EC 3.4.23.15 / Renin; SE337SVY37 / sodium phosphate
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