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

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  • (PMID = 16444357.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] por
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Brazil
  • [Number-of-references] 36
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2. Szajerka A, Dziegiel P, Szajerka T, Zabel M, Winowski J, Grzebieniak Z: Immunohistochemical evaluation of metallothionein, Mcm-2 and Ki-67 antigen expression in tumors of the adrenal cortex. Anticancer Res; 2008 Sep-Oct;28(5B):2959-65

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

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  • (PMID = 19031940.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / Ki-67 Antigen; 0 / Nuclear Proteins; 9038-94-2 / Metallothionein; EC 3.6.4.12 / MCM2 protein, human; EC 3.6.4.12 / Minichromosome Maintenance Complex Component 2
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3. Komorowski J, Jurczynska J, Stepien T, Kolomecki K, Kuzdak K, Stepien H: Serum concentrations of TNF α and its soluble receptors in patients with adrenal tumors treated by surgery. Int J Mol Sci; 2010;11(6):2281-90
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  • [Title] Serum concentrations of TNF α and its soluble receptors in patients with adrenal tumors treated by surgery.
  • The peripheral blood levels of TNF alpha and its soluble receptors were studied in 39 patients with malignant and benign adrenal tumors treated by adrenalectomy.
  • The concentrations of TNF alpha were significantly elevated in patients with malignant tumors of the adrenal cortex and in patients with Conn's syndrome compared to control.
  • After adrenalectomy, the levels of TNF alpha were decreased in patients with malignant tumors and in patients with Conn's syndrome, nonfunctioniong adenomas and pheochromocytomas compared to the concentration before surgery.
  • However, to confirm practicality of the evaluation of TNF alpha and its soluble receptors in differential diagnosis in patients with adrenal tumors, a larger study group is needed.
  • [MeSH-major] Adrenal Gland Neoplasms / blood. Adrenal Gland Neoplasms / surgery. Receptors, Tumor Necrosis Factor / blood. Tumor Necrosis Factor-alpha / blood
  • [MeSH-minor] Adrenalectomy. Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Receptors, Tumor Necrosis Factor, Type I / blood. Receptors, Tumor Necrosis Factor, Type II / blood

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  • (PMID = 20640152.001).
  • [ISSN] 1422-0067
  • [Journal-full-title] International journal of molecular sciences
  • [ISO-abbreviation] Int J Mol Sci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Receptors, Tumor Necrosis Factor; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Receptors, Tumor Necrosis Factor, Type II; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC2904916
  • [Keywords] NOTNLM ; TNF α / TNF α R1 / TNF α R2 / adrenal tumors / adrenalectomy
  • [General-notes] NLM/ Original DateCompleted: 20110714
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4. Jain M, Kapoor S, Mishra A, Gupta S, Agarwal A: Weiss criteria in large adrenocortical tumors: a validation study. Indian J Pathol Microbiol; 2010 Apr-Jun;53(2):222-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Weiss criteria in large adrenocortical tumors: a validation study.
  • BACKGROUND: Several systems including pathologic criteria alone or in combination with clinical features have been proposed to differentiate between benign and malignant adrenocortical tumors and assess their prognosis.
  • Since we see large adrenocortical carcinoma (ACC), we attempt to evaluate the diagnostic power of Weiss system in large ACC.
  • MATERIALS AND METHODS: In this study clinicopathological characteristics of 42 adrenocortical neoplasms are studied and classified into adrenocortical adenoma (ACA) and ACC based on Weiss score of less than or equal to three or greater than three.
  • RESULTS: The histological criteria of Weiss appeared to predict tumor prognosis accurately.
  • CONCLUSION: Weiss score was found to be a good prognostic factor for tumors of the adrenal cortex.
  • [MeSH-major] Adrenocortical Adenoma / diagnosis. Adrenocortical Adenoma / pathology. Adrenocortical Carcinoma / diagnosis. Adrenocortical Carcinoma / pathology. Histocytochemistry / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Diagnosis, Differential. Female. Humans. Infant. Male. Middle Aged. Prognosis. Young Adult

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  • (PMID = 20551521.001).
  • [ISSN] 0974-5130
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] India
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5. Horvath A, Stratakis CA: Unraveling the molecular basis of micronodular adrenal hyperplasia. Curr Opin Endocrinol Diabetes Obes; 2008 Jun;15(3):227-33

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Unraveling the molecular basis of micronodular adrenal hyperplasia.
  • PURPOSE OF REVIEW: The present review discusses the molecular basis of micronodular adrenal hyperplasia.
  • It focuses on the role of genetic defects in cyclic-AMP (cAMP) signaling-related molecules, namely PRKAR1A, GNAS, PDE11A, and PDE8B in the predisposition to tumor formation.
  • This review also discusses the involvement of cAMP signaling and related pathways and their impact on the adrenocortical tumor formation.
  • RECENT FINDINGS: Molecular abnormalities in the phosphodiesterases family are the most recently discovered genetic abnormalities that predispose individuals to various adrenocortical tumors.
  • SUMMARY: Recent findings indicate the importance of cAMP signaling for normal adrenocortical functioning and the sensitivity of the adrenal gland to subtle alterations in cAMP levels.
  • The identification of low-penetrance mutations in more than one phosphodiesterase in patients with adrenocortical hyperplasia is suggestive for a complementary role of the different phosphodiesterases in adrenal gland abnormalities and possible involvement of other members of this pathway in adrenocortical tumor defects.

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  • (PMID = 18438169.001).
  • [ISSN] 1752-2978
  • [Journal-full-title] Current opinion in endocrinology, diabetes, and obesity
  • [ISO-abbreviation] Curr Opin Endocrinol Diabetes Obes
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / Z01 HD000642; United States / Intramural NIH HHS / / Z99 HD999999
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] England
  • [Number-of-references] 53
  • [Other-IDs] NLM/ NIHMS101741; NLM/ PMC2671149
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6. Puech-Bret N, Bret J, Bennet A, Huyghe E, Mazerolles C, Zabraniecki L, Fournie B: Maffucci syndrome and adrenal cortex tumor. Joint Bone Spine; 2009 Oct;76(5):556-8
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  • [Title] Maffucci syndrome and adrenal cortex tumor.
  • We report the second known case of Maffucci syndrome associated with an adrenal cortex tumor.
  • Endocrine tumors have been reported in patients with multiple enchondromas, although the underlying mechanism of this combination is unknown.
  • Therefore, routine evaluation for involvement of the adrenal cortex may be warranted to improve our knowledge of this syndrome and of its pathophysiology.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Enchondromatosis / complications
  • [MeSH-minor] Abdomen / pathology. Adrenocorticotropic Hormone / blood. Adult. Amputation. Bone Neoplasms / pathology. Bone Neoplasms / radiography. Female. Femoral Neoplasms / pathology. Femoral Neoplasms / radiography. Fingers / surgery. Hemangioma / complications. Hemangioma / pathology. Humans. Hydrocortisone / blood. Leg / pathology. Magnetic Resonance Imaging. Sarcoma / pathology. Sarcoma / surgery. Uterine Neoplasms / pathology

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  • (PMID = 19782627.001).
  • [ISSN] 1778-7254
  • [Journal-full-title] Joint, bone, spine : revue du rhumatisme
  • [ISO-abbreviation] Joint Bone Spine
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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7. Opocher G, Schiavi F, Cicala MV, Patalano A, Mariniello B, Boaretto F, Zovato S, Pignataro V, Macino B, Negro I, Mantero F: Genetics of adrenal tumors. Minerva Endocrinol; 2009 Jun;34(2):107-21
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  • [Title] Genetics of adrenal tumors.
  • Endocrinology pioneered the development of molecular medicine, but also the study of adrenal tumors had a great impact in this field.
  • Particularly important was the detection of genetics of tumors derived from the adrenal medulla, as well as that of those derived from the sympathetic and parasympathetic paraganglia.
  • Less well understood is the genetics of adrenal cortex tumors, in particular adrenocortical carcinoma, a rare and particularly aggressive disease.
  • There are only a few examples of hereditary transmission of adrenocortical carcinoma, but the analysis of low penetrance genes by genome wide association study may enable us to discover new genetic mechanisms responsible for adrenocortical-derived tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Biomarkers, Tumor / genetics. Mutation. Pheochromocytoma / genetics
  • [MeSH-minor] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Genetic Predisposition to Disease. Genomics. Humans. Neoplasm Proteins / genetics. Paraganglioma / genetics

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  • (PMID = 19471236.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
  • [Number-of-references] 81
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8. Rossbach HC, Baschinsky D, Wynn T, Obzut D, Sutcliffe M, Tebbi C: Composite adrenal anaplastic neuroblastoma and virilizing adrenocortical tumor with germline TP53 R248W mutation. Pediatr Blood Cancer; 2008 Mar;50(3):681-3
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  • [Title] Composite adrenal anaplastic neuroblastoma and virilizing adrenocortical tumor with germline TP53 R248W mutation.
  • Composite tumors are extremely rare.
  • Such tumors in adrenal glands are usually of neuroendocrine-neural type and occur mostly in adults.
  • We report a patient with composite neuroblastoma (NB), adrenocortical tumor (ACT), and Li-Fraumeni syndrome (LFS) with germline TP53 R248W mutation.
  • LFS predisposes to the development of leukemia, sarcomas, adrenocortical and breast carcinomas, brain tumors and, questionably, NB.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenal Gland Neoplasms / pathology. Adrenocortical Adenoma / pathology. Genes, p53. Germ-Line Mutation. Li-Fraumeni Syndrome / genetics. Mutation, Missense. Neoplasms, Multiple Primary / pathology. Neuroblastoma / pathology. Point Mutation. Virilism / etiology
  • [MeSH-minor] Amino Acid Substitution. Aneuploidy. Brain Neoplasms / genetics. Breast Neoplasms / genetics. Carcinoma / genetics. Choroid Plexus Neoplasms / genetics. Female. Glioblastoma / genetics. Humans. Infant. Loss of Heterozygosity. Male. Pedigree

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17427234.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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9. Al-Zaid T, Alroy J, Pfannl R, Strissel KJ, Powers JF, Layer A, Carpinito G, Tischler AS: Oncocytic adrenal cortical tumor with cytoplasmic inclusions and hyaline globules. Virchows Arch; 2008 Sep;453(3):301-6
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  • [Title] Oncocytic adrenal cortical tumor with cytoplasmic inclusions and hyaline globules.
  • Adrenal cortical tumors, particularly oncocytic tumors, have been reported to contain a variety of intracytoplasmic and intramitochondrial inclusions.
  • Oncocytic cortical tumors can also morphologically mimic pheochromocytomas.
  • We report an unusual, partially oncocytic cortical neoplasm with nesting architecture, intranuclear inclusions, and hyaline globules reminiscent of pheochromocytoma, together with numerous, small, brightly eosinophilic, periodic acid-Schiff-positive cytoplasmic inclusions and typical cytoplasmic lipid droplets.
  • Immunohistochemistry and immunoblots were utilized to further characterize the tumor.
  • Immunohistochemistry demonstrated immunoreactivity of both the eosinophilic inclusions and the hyaline globules for adipose differentiation-related protein (ADRP), which is one of a group of proteins associated with storage of neutral lipids in many cell types.
  • Immunoblots confirmed the presence of ADRP and demonstrated an imbalance between ADRP and perilipin, another neutral lipid-associated protein, in tumor tissue compared to normal adrenal cortex.
  • The findings suggest that mitochondrial dysfunction in oncocytic cortical tumors may lead to abnormal processing of proteins related to the lipid-storing functions of the adrenal cortex, resulting in unusual cytoplasmic inclusions and extracellular globules resembling the globules in pheochromocytomas.
  • The finding of ADRP as a constituent of inclusions in adrenal cortical tumors has not been previously reported.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Inclusion Bodies / pathology. Oxyphil Cells / pathology
  • [MeSH-minor] Adrenal Cortex / pathology. Humans. Hyalin / metabolism. Male. Membrane Proteins / metabolism. Microscopy, Electron. Middle Aged. Pheochromocytoma / pathology

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  • (PMID = 18688642.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Membrane Proteins; 0 / perilipin 2
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10. Alsultan A, Lovell MA, Hayes KL, Allshouse MJ, Garrington TP: Simultaneous occurrence of right adrenocortical tumor and left adrenal neuroblastoma in an infant with Beckwith-Wiedemann syndrome. Pediatr Blood Cancer; 2008 Nov;51(5):695-8
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  • [Title] Simultaneous occurrence of right adrenocortical tumor and left adrenal neuroblastoma in an infant with Beckwith-Wiedemann syndrome.
  • Children with Beckwith-Wiedemann syndrome (BWS) have increased risk for development of embryonal tumors.
  • We present the case of an infant with BWS who has hypomethylation of LIT1 gene in the 11p15.5 chromosomal region and at 6 months of age presented with simultaneous occurrence of neuroblastoma arising from the left adrenal gland and a right adrenocortical tumor.
  • She underwent surgical resection of both tumors and remains tumor free 18 months after surgery.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenal Gland Neoplasms / complications. Beckwith-Wiedemann Syndrome / complications. Neoplasms, Multiple Primary / complications. Neuroblastoma / complications


11. Karikari IO, Uschold TD, Selznick LA, Carter JH, Cummings TJ, Friedman AH: Primary spinal intramedullary adrenal cortical adenoma associated with spinal dysraphism: case report. Neurosurgery; 2006 Nov;59(5):E1144; discussion E1144
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary spinal intramedullary adrenal cortical adenoma associated with spinal dysraphism: case report.
  • OBJECTIVE: The authors report a primary spinal intramedullary adrenal cortical adenoma in a patient with spinal dysraphism presenting with bilateral leg pain and urinary frequency.
  • METHODS: Magnetic resonance imaging, L2 laminectomy with resection of mass, and pathological and immunohistochemical analysis of resected mass revealed the diagnosis.
  • RESULTS: Microscopic and immunohistochemical findings confirmed the diagnosis as a primary intramedullary tumor of adrenal cortical origin.
  • CONCLUSION: The occurrence of a primary adrenal tumor in the spinal cord is rare and difficult to explain based on our understanding of embryology.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / surgery. Adrenocortical Adenoma / diagnosis. Adrenocortical Adenoma / surgery. Spinal Cord Neoplasms / diagnosis. Spinal Cord Neoplasms / surgery. Spinal Dysraphism / complications

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  • (PMID = 17143207.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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12. Wu W, Kamma H, Fujiwara M, Yano Y, Satoh H, Hara H, Yashiro T, Ueno E, Aiyoshi Y: Altered expression patterns of heterogeneous nuclear ribonucleoproteins A2 and B1 in the adrenal cortex. J Histochem Cytochem; 2005 Apr;53(4):487-95

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Altered expression patterns of heterogeneous nuclear ribonucleoproteins A2 and B1 in the adrenal cortex.
  • Several proteins implicated in hormonogenesis of the adrenal cortex have alternatively spliced isoforms, which respond differently to adrenocorticotropic hormone (ACTH).
  • We examined the expression of A2 and B1 in normal adrenal cortex and tumors.
  • In three kinds of cortical adenomas autonomously producing hormones, B1 was generally overexpressed and there were no significant differences among them.
  • In cortisol-producing tumors, non-tumor parts of the cortex, which were generally atrophic due to low ACTH, had less B1 protein than normal adrenals.
  • In vitro ACTH stimulation induced a biphasic expression of B1 in an H295R cortical carcinoma cell line, and it paralleled hormonogenesis.
  • [MeSH-major] Adrenal Cortex / metabolism. Adrenal Cortex Neoplasms / metabolism. Heterogeneous-Nuclear Ribonucleoprotein Group A-B / biosynthesis
  • [MeSH-minor] Alternative Splicing. Cell Line, Tumor. Electrophoresis, Polyacrylamide Gel. Humans. Immunohistochemistry

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  • (PMID = 15805423.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Heterogeneous-Nuclear Ribonucleoprotein Group A-B
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13. Carden CP, Frentzas S, Langham M, Casamayor I, Stephens AW, Poondru S, Wheaton J, Lippman SM, Kaye SB, Kim ES: Preliminary activity in adrenocortical tumor (ACC) in phase I dose escalation study of intermittent oral dosing of OSI-906, a small-molecule insulin-like growth factor-1 receptor (IGF-1R) tyrosine kinase inhibitor in patients with advanced solid tumors. J Clin Oncol; 2009 May 20;27(15_suppl):3544

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preliminary activity in adrenocortical tumor (ACC) in phase I dose escalation study of intermittent oral dosing of OSI-906, a small-molecule insulin-like growth factor-1 receptor (IGF-1R) tyrosine kinase inhibitor in patients with advanced solid tumors.
  • IGF-1R blockade increases apoptosis and reduces tumor growth in preclinical models.
  • METHODS: Patients (pt) with advanced solid tumours were enrolled to determine safety, tolerability, maximum tolerated dose, pharmacokinetics (PK), pharmacodynamics (PD) and preliminary anti-tumor activity.

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  • (PMID = 27961354.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Palazzo FF, Sebag F, Sierra M, Ippolito G, Souteyrand P, Henry JF: Long-term outcome following laparoscopic adrenalectomy for large solid adrenal cortex tumors. World J Surg; 2006 May;30(5):893-8

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

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  • (PMID = 16680605.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Woods AM, McIlmoil CJ, Rankin EN, Packer AA, Stevens JC, Macievic JA, Brown AB, Porter JP, Judd AM: Leukemia inhibitory factor protein and receptors are expressed in the bovine adrenal cortex and increase cortisol and decrease adrenal androgen release. Domest Anim Endocrinol; 2008 Aug;35(2):217-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leukemia inhibitory factor protein and receptors are expressed in the bovine adrenal cortex and increase cortisol and decrease adrenal androgen release.
  • The release of adrenal steroids during acute stress is primarily regulated by adrenocorticotropic hormone (ACTH).
  • In contrast, during chronic inflammatory stress additional factors are involved in regulating adrenal function.
  • In addition, LIF and LIF receptors (LIFR) are expressed in the human adrenal cortex and the human adrenocortical tumor cell line H295R.
  • However, the expression of LIF and LIFR in non-human adrenal glands and the effects of LIF on the release of cortisol from adrenal cells of non-human species have not been determined.
  • Furthermore, the effects of LIF on adrenal androgen release from all species are unknown.
  • In this study, immunohistochemistry, Western blots, RT-PCR, and nucleotide sequencing was utilized to demonstrate that LIF and its receptor are expressed throughout the bovine adrenal cortex.
  • Although LIF did not modify basal cortisol release from dispersed cells isolated from the bovine adrenal zona fasciculate, this cytokine increased ACTH-stimulated release of cortisol from these cells in a manner dependent on the LIF concentration and exposure interval.
  • In contrast, LIF in a concentration-dependent and time-dependent manner decreased basal and ACTH-stimulated adrenal androgen release from dispersed cells isolated from the bovine adrenal zona reticularis.
  • Because LIF release increases during inflammatory stress and this cytokine stimulates adrenal cortisol release and inhibits adrenal androgen release, this cytokine may play an important role in regulating the release of adrenal steroids during inflammatory stress.
  • [MeSH-major] Adrenal Cortex / metabolism. Androgens / metabolism. Cattle / metabolism. Hydrocortisone / metabolism. Leukemia Inhibitory Factor / metabolism. Receptors, OSM-LIF / metabolism

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  • (PMID = 18638665.001).
  • [ISSN] 0739-7240
  • [Journal-full-title] Domestic animal endocrinology
  • [ISO-abbreviation] Domest. Anim. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Leukemia Inhibitory Factor; 0 / RNA, Messenger; 0 / Receptors, OSM-LIF; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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16. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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).
  • Fifteen normal adrenals and 43 tumors were studied. mRNA expression was examined by real time RT-PCR.
  • 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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17. Mann MW, Ellis SS, Mallory SB: Infantile acne as the initial sign of an adrenocortical tumor. J Am Acad Dermatol; 2007 Feb;56(2 Suppl):S15-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Infantile acne as the initial sign of an adrenocortical tumor.
  • Ultrasound and abdominal computed tomographic scan revealed a large adrenal mass consistent with an adrenocortical tumor.
  • The patient underwent surgical excision of the well-encapsulated tumor with normalization of his hormones and no subsequent recurrence.
  • Although rare, childhood adrenocortical tumors have a poor prognosis, with the majority of tumors having regional and metastatic disease.
  • Because early diagnosis and complete surgical excision improve prognosis, children with refractory infantile acne should be evaluated for signs of virilization and accelerated growth.
  • Elevated levels of DHEA and DHEA-S should prompt an aggressive diagnostic evaluation for an adrenocortical tumor.
  • [MeSH-major] Acne Vulgaris / etiology. Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications

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  • (PMID = 17097383.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 3XMK78S47O / Testosterone; 459AG36T1B / Dehydroepiandrosterone
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18. McNicol AM: Lesions of the adrenal cortex. Arch Pathol Lab Med; 2008 Aug;132(8):1263-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lesions of the adrenal cortex.
  • CONTEXT: In surgical pathology practice adrenal cortical tumors are rare.
  • However, in autopsy series adrenal cortical nodules are found frequently.
  • These are now being identified more commonly in life when the abdomen is scanned for other disease.
  • It is important to differentiate between benign and malignant lesions as adrenal cortical carcinoma is an aggressive tumor.
  • Molecular genetic investigations are providing new information on both pathogenesis of adrenal tumors and basic adrenal development and physiology.
  • OBJECTIVE: To provide an overview of current knowledge on adrenal cortical development and structure that informs our understanding of genetic diseases of the adrenal cortex and adrenal cortical tumors.
  • CONCLUSIONS: The understanding of basic developmental and physiologic processes permits a better understanding of diseases of the adrenal cortex.
  • The information coming from investigation of the molecular pathology of adrenal cortical tumors is beginning to provide additional tests for the assessment of malignant potential in diagnosis but the mainstay remains traditional histologic analysis.
  • [MeSH-major] Adrenal Cortex. Adrenal Gland Diseases
  • [MeSH-minor] Adrenal Cortex Neoplasms / metabolism. Adrenal Cortex Neoplasms / pathology. Growth. Humans. Immunohistochemistry. Prognosis

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  • (PMID = 18684025.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 126
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19. Ranganathan S, Lynshue K, Hunt JL, Kane T, Jaffe R: Unusual adrenal cortical tumor of unknown biologic potential: a nodule in a nodule in a nodule. Pediatr Dev Pathol; 2005 Jul-Aug;8(4):483-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Unusual adrenal cortical tumor of unknown biologic potential: a nodule in a nodule in a nodule.
  • Adrenocortical tumors are uncommon neoplasms in childhood.
  • Most pediatric adrenal tumors are virilizing and carcinomas are more common than adenomas.
  • Recent molecular data suggest an adenoma-to-carcinoma progression sequence in adrenal cortical neoplasms.
  • We report a case of a 5-year-old boy who presented with virilizing symptoms secondary to an adrenal tumor that was resected laparoscopically.
  • The bulk of the tumor was a large, yellow mass with typical features of an adrenal cortical adenoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / pathology
  • [MeSH-minor] Adrenalectomy. Child, Preschool. Cushing Syndrome / etiology. Cushing Syndrome / pathology. DNA, Neoplasm / analysis. Hirsutism / etiology. Hirsutism / pathology. Humans. Loss of Heterozygosity. Male. Neoplasms, Multiple Primary / complications. Neoplasms, Multiple Primary / genetics. Neoplasms, Multiple Primary / pathology. Polymerase Chain Reaction. Treatment Outcome

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  • (PMID = 16010500.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm
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20. Pianovski MA, Maluf EM, de Carvalho DS, Ribeiro RC, Rodriguez-Galindo C, Boffetta P, Zancanella P, Figueiredo BC: Mortality rate of adrenocortical tumors in children under 15 years of age in Curitiba, Brazil. Pediatr Blood Cancer; 2006 Jul;47(1):56-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mortality rate of adrenocortical tumors in children under 15 years of age in Curitiba, Brazil.
  • BACKGROUND: Several reports refer to an increased frequency of adrenal cortex tumors (ACT) among children in Southern Brazil, yet all data have been derived from hospital-based registries.
  • PROCEDURE: We reviewed all death certificates that mentioned ACT or adrenal neuroblastoma (NB) and which were reported to the Paraná State Department of Health between 1998 and 2003, for individuals younger than 15 years who resided in the Curitiba metropolitan region.
  • The ratio of the adrenal NB and ACT age-adjusted mortality rates was 1.43.
  • CONCLUSIONS: Our investigation of population-based mortality confirms the evidence from hospital-based registries of a clustering of ACT in Southern Brazil.
  • [MeSH-major] Adrenal Cortex Neoplasms / mortality

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16200634.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Hishiki T, Kazukawa I, Saito T, Terui K, Mitsunaga T, Nakata M, Matsuura G, Minagawa M, Kohno Y, Yoshida H: Diagnosis of adrenocortical tumor in a neonate by detection of elevated blood 17-hydroxyprogesterone measured as a routine neonatal screening for congenital adrenal hyperplasia: a case report. J Pediatr Surg; 2008 Oct;43(10):e19-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnosis of adrenocortical tumor in a neonate by detection of elevated blood 17-hydroxyprogesterone measured as a routine neonatal screening for congenital adrenal hyperplasia: a case report.
  • We report herein a case of prenatally detected neonatal adrenocortical tumor (ACT).
  • Computed tomography and ultrasonography after birth revealed a round solid tumor 40 mm in diameter in the right suprarenal area.
  • The precise diagnosis of ACT was unexpectedly obtained based on results from the Japanese neonatal mass screening program.
  • Blood 17-hydroxyprogesterone is routinely measured as a part of this program for early detection of congenital adrenal hyperplasia in Japan.
  • Abnormally elevated level of 17-hydroxyprogesterone was reported in the patient and, thus, led to the diagnosis of ACT.
  • Adrenocortical tumors are extremely rare in childhood, particularly in the neonatal period.
  • Some of these tumors secrete abnormally high levels of cortisol, suppressing function of the contralateral adrenal gland and, thus, leading to life-threatening postoperative adrenal insufficiency.
  • Adrenocortical tumor should always be considered among the differential diagnoses for neonatal suprarenal mass because precise diagnosis will enable the physician to develop appropriate treatment strategies.
  • [MeSH-major] 17-alpha-Hydroxyprogesterone / blood. Adrenal Cortex Neoplasms / diagnosis. Adrenal Hyperplasia, Congenital / diagnosis. Carcinoma / diagnosis. Fetal Blood / chemistry. Neonatal Screening
  • [MeSH-minor] Adrenal Insufficiency / prevention & control. Adrenalectomy. Aldosterone / blood. Dehydroepiandrosterone Sulfate / blood. Early Diagnosis. Female. Humans. Hydrocortisone / administration & dosage. Hydrocortisone / therapeutic use. Infant, Newborn. Postoperative Complications / prevention & control. Premedication. Testosterone / blood. Tomography, X-Ray Computed. Ultrasonography, Prenatal


22. Gross MD, Gauger PG, Djekidel M, Rubello D: The role of PET in the surgical approach to adrenal disease. Eur J Surg Oncol; 2009 Nov;35(11):1137-45
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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 PET in the surgical approach to adrenal disease.
  • BACKGROUND: Appropriate surgical approach to diseases of the adrenal requires a diagnosis sufficient to determine the biochemical status of adrenal dysfunction and anatomic evaluation sufficient to differentiate unilateral from bilateral disease, intra-adrenal from extra-adrenal neoplasm, adrenal tumor recurrence or adrenal metastases.
  • High resolution computed tomography (CT) and magnetic resonance have been the primary imaging modalities for the evaluation of anatomy, while scintigraphic studies have played a secondary role in diagnosis.
  • The recent availability of functional imaging provided by positron emission tomography (PET) with radiopharmaceuticals designed to depict substrate precursor uptake, cellular metabolism or receptor binding in neoplasms and CT as a single modality, hybrid PET/CT, to directly correlate function and anatomy has had a significant impact upon the diagnostic and therapeutic approach to many cancers and has been applied to adrenal disease with some early success that we describe in this review.
  • METHODS: In addition to the authors' experience, a search of Medline and PubMed databases was performed using search terms: 'adrenal scintigraphy', 'positron tomography', 'computed tomography', 'adrenal surgery', 'adrenal mass', '(18)F-fluorodeoxyglucose', 'adrenal carcinoma', 'adrenal medulla' and 'pheochromocytoma'.
  • CONCLUSIONS: Present PET radiopharmaceuticals and their use in hybrid PET/CT have demonstrated efficacy in the preoperative and follow-up evaluation of neoplasms of the adrenal cortex and medulla that hopefully will continue to improve with the development of newer tracers that continue to exploit unusual characteristics of the adrenals.
  • [MeSH-major] Adrenal Gland Neoplasms / radionuclide imaging. Adrenal Gland Neoplasms / surgery. Radiopharmaceuticals. Tomography, Emission-Computed
  • [MeSH-minor] Diagnosis, Differential. Humans. Tomography, X-Ray Computed

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  • (PMID = 19243910.001).
  • [ISSN] 1532-2157
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Radiopharmaceuticals
  • [Number-of-references] 75
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23. Lau SK, Weiss LM: The Weiss system for evaluating adrenocortical neoplasms: 25 years later. Hum Pathol; 2009 Jun;40(6):757-68

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The Weiss system for evaluating adrenocortical neoplasms: 25 years later.
  • The evaluation and categorization of adrenocortical neoplasms remain among the most challenging areas in adrenal pathology.
  • The Weiss system, first introduced 25 years ago, provides specific guidelines for differentiating adrenocortical adenoma from adrenocortical carcinoma and is considered the standard for determining malignancy in tumors of the adrenal cortex.
  • Considerable advances in the understanding of the pathology of adrenocortical neoplasia have occurred since delineation of the Weiss system, offering alternative approaches to the contemporary assessment of adrenocortical tumors.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology
  • [MeSH-minor] Adrenal Cortex / pathology. Adrenocortical Adenoma / pathology. Adrenocortical Carcinoma / pathology. Adult. Biopsy, Fine-Needle. Cell Nucleus / pathology. Child. Genes, Neoplasm. Humans. Immunohistochemistry. Mitosis. Necrosis. Neoplasm Invasiveness / pathology. Prognosis

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  • (PMID = 19442788.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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24. Chevalier N, Carrier P, Piche M, Chevallier A, Wagner K, Tardy V, Benchimol D, Fénichel P: Adrenocortical incidentaloma with uncertain prognosis associated with an inadequately treated congenital adrenal hyperplasia. Ann Endocrinol (Paris); 2010 Feb;71(1):56-9
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  • [Title] Adrenocortical incidentaloma with uncertain prognosis associated with an inadequately treated congenital adrenal hyperplasia.
  • Large adrenal tumors are rarely associated with adrenal enzymatic deficiency, except in 11-ss-hydroxylase insufficiency.
  • These tumors are exceptionally malignant.
  • We report here the case of a patient with a congenital 21-hydroxylase deficiency (compound heterozygote for two severe mutations in the CYP21A2 gene) untreated for 20 years.
  • His evaluation at 36 years of age showed a four-centimeter mass in the left adrenal gland, with most characteristics suggestive of malignancy (CT and positron emission tomography [PET] scan).
  • We performed a surgical resection that established the diagnosis of adrenocortical tumor of uncertain prognosis (Weiss's score: 3).
  • Even though malignant tumors are unusual in adrenal deficiency, our observation shows the need for a replacement therapy during adulthood, with a regular CT scan follow up in order to diagnose early isolated adrenal adenoma and remove it in case of malignancy suspicion.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenal Hyperplasia, Congenital / complications
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Adrenal Glands / pathology. Adrenal Glands / radionuclide imaging. Adrenalectomy. Adult. Cushing Syndrome / etiology. Heterozygote. Humans. Male. Positron-Emission Tomography. Prognosis. Steroid 21-Hydroxylase / genetics. Tomography, X-Ray Computed

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  • [Copyright] Copyright (c) 2009 Elsevier Masson SAS. All rights reserved.
  • (PMID = 19942208.001).
  • [ISSN] 0003-4266
  • [Journal-full-title] Annales d'endocrinologie
  • [ISO-abbreviation] Ann. Endocrinol. (Paris)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; EC 1.14.99.10 / CYP21A2 protein, human; EC 1.14.99.10 / Steroid 21-Hydroxylase
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25. 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].
  • 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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26. Betz MJ, Shapiro I, Fassnacht M, Hahner S, Reincke M, Beuschlein F, German and Austrian Adrenal Network: Peroxisome proliferator-activated receptor-gamma agonists suppress adrenocortical tumor cell proliferation and induce differentiation. J Clin Endocrinol Metab; 2005 Jul;90(7):3886-96
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  • [Title] Peroxisome proliferator-activated receptor-gamma agonists suppress adrenocortical tumor cell proliferation and induce differentiation.
  • Moreover, recent evidence has suggested that TZDs might have favorable effects in the treatment of a variety of tumors as differentiation-inducing agents.
  • Adrenocortical carcinoma (ACC) is a rare tumor entity with poor prognosis due to its highly malignant phenotype and lack of effective treatment options.
  • OBJECTIVE: The purpose of this study was to investigate effects of TZDs on adrenocortical cancer cells.
  • RESULTS: PPARgamma mRNA expression was detectable in all adrenocortical tumors including ACCs at similar levels.
  • Furthermore, incubation of the adrenocortical tumor cell line NCI h295 with the PPARgamma agonist rosiglitazone led to a decrease in cell viability, a decrease of cellular proliferation, and an increase in apoptosis as well as steroidogenesis.
  • On the molecular level, NCI h295 cells expressed higher levels of ACTH receptor (melanocortin receptor-2) mRNA upon treatment, whereas cyclin E mRNA was reduced, thus reflecting a shift toward an expression pattern found in less aggressive adrenocortical tumors in vivo.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. PPAR gamma / agonists. Thiazolidinediones / pharmacology
  • [MeSH-minor] Adult. Aged. Anilides / pharmacology. Apoptosis / drug effects. Cell Differentiation. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin E / genetics. Dose-Response Relationship, Drug. Female. Humans. Insulin-Like Growth Factor II / genetics. Male. Middle Aged. Promoter Regions, Genetic. RNA, Messenger / analysis. Receptor, Melanocortin, Type 2 / genetics

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  • (PMID = 15886257.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-chloro-5-nitrobenzanilide; 0 / Anilides; 0 / Cyclin E; 0 / PPAR gamma; 0 / RNA, Messenger; 0 / Receptor, Melanocortin, Type 2; 0 / Thiazolidinediones; 05V02F2KDG / rosiglitazone; 67763-97-7 / Insulin-Like Growth Factor II
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27. Kumar S, Mandal AK, Acharya N, Thingnam SK, Bhalla V, Singh SK: Superior mesenteric artery injury during en bloc excision of a massive left adrenal tumor. Urol Int; 2007;78(2):182-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Superior mesenteric artery injury during en bloc excision of a massive left adrenal tumor.
  • We report the first case of inadvertent injury of the superior mesenteric artery during surgery of a large malignant adrenocortical tumor with inferior vena cava thrombus.
  • The cause of inadvertent injury was anatomical distortion of the great vessels due to the massive nature of the tumor.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenalectomy. Adrenocortical Carcinoma / surgery. Intraoperative Complications / etiology. Mesenteric Artery, Superior / injuries

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  • [Copyright] 2007 S. Karger AG, Basel
  • (PMID = 17293663.001).
  • [ISSN] 0042-1138
  • [Journal-full-title] Urologia internationalis
  • [ISO-abbreviation] Urol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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28. Mannelli M, Cantini G, Poli G, Mangoni M, Nesi G, Canu L, Rapizzi E, Borgogni E, Ercolino T, Piccini V, Luconi M: Role of the PPAR-γ system in normal and tumoral pituitary corticotropic cells and adrenal cells. Neuroendocrinology; 2010;92 Suppl 1:23-7
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  • [Title] Role of the PPAR-γ system in normal and tumoral pituitary corticotropic cells and adrenal cells.
  • In this minireview, we summarize the current knowledge on PPAR-γ in normal and tumoral corticotropic pituitary and adrenal cells.
  • The receptor expression has been shown in ACTH-secreting cells in both normal and adenomal pituitary as well as in normal and tumor adrenal cortex.
  • Preclinical studies conducted both in vitro on tumor cells and in vivo on xenograft tumor models obtained by subcutaneous injection of cancer cells have evidenced the anticancer properties of TZD, in particular rosiglitazone (RGZ) and pioglitazone (PIO).
  • In both pituitary and adrenocortical cancer, RGZ treatment results in inhibition of cell proliferation, through G0/G1 cell-cycle arrest and induction of cell apoptosis, leading to significant inhibition of tumor growth in the xenograft tumor models.
  • In addition, since RGZ can reduce ACTH and corticosterone secretion in mouse corticotropic pituitary tumors, both RGZ and PIO have been used in the treatment of Cushing's disease with variable but generally unsatisfactory results.
  • [MeSH-major] Adrenal Cortex / metabolism. Corticotrophs / metabolism. PPAR gamma / metabolism. Pituitary ACTH Hypersecretion / metabolism. Pituitary Gland / metabolism
  • [MeSH-minor] Adrenal Cortex Neoplasms / drug therapy. Adrenal Cortex Neoplasms / metabolism. Humans. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / metabolism. Thiazolidinediones / therapeutic use

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  • [Copyright] Copyright © 2010 S. Karger AG, Basel.
  • (PMID = 20829614.001).
  • [ISSN] 1423-0194
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / PPAR gamma; 0 / Thiazolidinediones; X4OV71U42S / pioglitazone
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29. Miyoshi Y, Oue T, Oowari M, Soh H, Tachibana M, Kimura S, Kiyohara Y, Yamada H, Bessyo K, Mushiake S, Homma K, Hasegawa T, Sasano H, Ozono K: A case of pediatric virilizing adrenocortical tumor resulting in hypothalamic-pituitary activation and central precocious puberty following surgical removal. Endocr J; 2009;56(8):975-82
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  • [Title] A case of pediatric virilizing adrenocortical tumor resulting in hypothalamic-pituitary activation and central precocious puberty following surgical removal.
  • We present a 6-year-old boy with a virilizing adrenocortical tumor who initially presented with peripheral precocious puberty.
  • Both serum and urinary levels of adrenal androgens were elevated.
  • The histological diagnosis was adrenocortical carcinoma according to the criteria of Weiss.
  • Following surgical removal of the androgen-producing tumor, the patient subsequently developed hypothalamic-pituitary activation and demonstrated central precocious puberty.
  • Clinical follow-up of potential secondary effects of excess hormone secretion after removal is important in some pediatric patients with virilizing adrenocortical tumor.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenal Cortex Neoplasms / surgery. Adrenocortical Carcinoma / complications. Adrenocortical Carcinoma / surgery. Hypothalamo-Hypophyseal System / physiopathology. Puberty, Precocious / etiology

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  • (PMID = 19671995.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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30. Gonzalez RJ, Shapiro S, Sarlis N, Vassilopoulou-Sellin R, Perrier ND, Evans DB, Lee JE: Laparoscopic resection of adrenal cortical carcinoma: a cautionary note. Surgery; 2005 Dec;138(6):1078-85; discussion 1085-6
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  • [Title] Laparoscopic resection of adrenal cortical carcinoma: a cautionary note.
  • BACKGROUND: While laparoscopic removal of small, benign, functioning adrenal tumors is accepted, laparoscopic resection of adrenal tumors that may be adrenal cortical carcinoma (ACC) remains controversial.
  • Open adrenalectomy remains the standard of care for patients presenting with an adrenal cortical tumor for which ACC is in the differential diagnosis.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenalectomy. Carcinoma / surgery. Laparoscopy. Neoplasm Recurrence, Local / epidemiology

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  • (PMID = 16360394.001).
  • [ISSN] 0039-6060
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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31. Delhanty PJ, van Koetsveld PM, Gauna C, van de Zande B, Vitale G, Hofland LJ, van der Lely AJ: Ghrelin and its unacylated isoform stimulate the growth of adrenocortical tumor cells via an anti-apoptotic pathway. Am J Physiol Endocrinol Metab; 2007 Jul;293(1):E302-9
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  • [Title] Ghrelin and its unacylated isoform stimulate the growth of adrenocortical tumor cells via an anti-apoptotic pathway.
  • Ghrelin is expressed in normal human adrenocortical cells and induces their proliferation through growth hormone secretagogue receptor 1a (GHS-R1a).
  • Consequently, it was of interest to us to determine whether acylated ghrelin and its predominant serum isoform, unacylated ghrelin, also act as factors for adrenocortical carcinoma cell growth.
  • To examine a potential ghrelin-regulated system in adrenocortical tumors, we measured proliferative effects of acylated and unacylated ghrelin in the adrenocortical carcinoma cell lines SW-13 and NCI-H295R.
  • Acylated and unacylated ghrelin in the nanomolar range dose-dependently induced adrenocortical cell growth up to 200% of untreated controls, as measured by thymidine uptake and WST1 assay.
  • Acylated and unacylated ghrelin are potential auto/paracrine factors acting through an antiapoptotic pathway to stimulate adrenocortical tumor cell growth.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Apoptosis / drug effects. Cell Proliferation / drug effects. Peptide Hormones / pharmacology
  • [MeSH-minor] Acetylation. Cell Cycle / drug effects. Ghrelin. Humans. Protein Isoforms / pharmacology. Receptors, Corticotropin-Releasing Hormone / antagonists & inhibitors. Receptors, Corticotropin-Releasing Hormone / genetics. Receptors, Corticotropin-Releasing Hormone / metabolism. Receptors, G-Protein-Coupled / antagonists & inhibitors. Receptors, G-Protein-Coupled / genetics. Receptors, G-Protein-Coupled / metabolism. Receptors, Ghrelin. Signal Transduction / drug effects. Tumor Cells, Cultured

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  • (PMID = 17405826.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CRF receptor type 2; 0 / Ghrelin; 0 / Peptide Hormones; 0 / Protein Isoforms; 0 / Receptors, Corticotropin-Releasing Hormone; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Ghrelin
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32. Mazzuco TL, Chabre O, Sturm N, Feige JJ, Thomas M: Ectopic expression of the gastric inhibitory polypeptide receptor gene is a sufficient genetic event to induce benign adrenocortical tumor in a xenotransplantation model. Endocrinology; 2006 Feb;147(2):782-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ectopic expression of the gastric inhibitory polypeptide receptor gene is a sufficient genetic event to induce benign adrenocortical tumor in a xenotransplantation model.
  • Aberrant expression of ectopic G protein-coupled receptors (GPCRs) in adrenal cortex tissue has been observed in several cases of ACTH-independent macronodular adrenal hyperplasias and adenomas associated with Cushing's syndrome.
  • Although there is clear clinical evidence for the implication of these ectopic receptors in abnormal regulation of cortisol production, whether this aberrant GPCR expression is the cause or the consequence of the development of an adrenal hyperplasia is still an open question.
  • To answer it, we genetically engineered primary bovine adrenocortical cells to have them express the gastric inhibitory polypeptide receptor.
  • We observed the formation of an enlarged and hyperproliferative adenomatous adrenocortical tissue that secreted cortisol in a gastric inhibitory polypeptide-dependent manner and induced a mild Cushing's syndrome with hyperglycemia.
  • Moreover, we show that tumor development was ACTH independent.
  • Thus, a single genetic event, inappropriate expression of a nonmutated GPCR gene, is sufficient to initiate the complete phenotypic alterations that ultimately lead to the formation of a benign adrenocortical tumor.
  • [MeSH-major] Adenoma / genetics. Adrenal Cortex / metabolism. Adrenal Gland Neoplasms / genetics. Cell Transformation, Neoplastic / metabolism. Gene Expression Regulation, Neoplastic. Receptors, Gastrointestinal Hormone / metabolism

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  • (PMID = 16254030.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Gastrointestinal Hormone; 0 / gastric inhibitory polypeptide receptor; 128559-51-3 / RAG-1 protein; WI4X0X7BPJ / Hydrocortisone
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33. Castellano JJ, Warren MW, Arroyo MR, Cendan JC: Laparoscopic resection of a virilizing adrenocortical tumor. JSLS; 2008 Jul-Sep;12(3):343-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Laparoscopic resection of a virilizing adrenocortical tumor.
  • Virilizing adrenocortical tumors are rare.
  • Herein, we describe a case of laparoscopic resection of a testosterone-producing adrenal tumor in a sixteen-year-old female.

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  • [Cites] Ann Surg. 2000 Dec;232(6):796-803 [11088074.001]
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  • (PMID = 18765068.001).
  • [ISSN] 1086-8089
  • [Journal-full-title] JSLS : Journal of the Society of Laparoendoscopic Surgeons
  • [ISO-abbreviation] JSLS
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3015862
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34. Trimeche Ajmi S, Chadli Chaieb M, Mokni M, Braham R, Ach K, Maaroufi A, Chaieb L: Corticomedullary mixed tumor of the adrenal gland. Ann Endocrinol (Paris); 2009 Dec;70(6):473-6
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  • [Title] Corticomedullary mixed tumor of the adrenal gland.
  • Abdominal magnetic resonance imaging showed a right heterogeneous adrenal mass measuring 4 x 6 cm with mixed component of fat and adrenal tissue suggesting corticosurrenaloma.
  • In the postoperative course, the patient presented adrenal insufficiency treated with hydrocortisone hemisuccinate.
  • Histological examination showed a single tumor mass composed of an admixed population of adrenal cortical and medullary cells.
  • [MeSH-major] Adrenal Cortex / pathology. Adrenal Gland Neoplasms / diagnosis. Adrenal Medulla / pathology
  • [MeSH-minor] Adipocytes / pathology. Adrenal Insufficiency / drug therapy. Adrenal Insufficiency / etiology. Adrenalectomy / adverse effects. Adult. Amenorrhea. Androgens / blood. Chromogranin A / analysis. Cushing Syndrome. Diagnosis, Differential. Female. Hirsutism. Humans. Hydrocortisone / blood. Hypertension. Hypokalemia. Immunohistochemistry. Magnetic Resonance Imaging. Obesity. Weight Gain

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  • (PMID = 19878923.001).
  • [ISSN] 0003-4266
  • [Journal-full-title] Annales d'endocrinologie
  • [ISO-abbreviation] Ann. Endocrinol. (Paris)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Androgens; 0 / Chromogranin A; WI4X0X7BPJ / Hydrocortisone
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35. Sandrini F, Villani DP, Tucci S, Moreira AC, de Castro M, Elias LL: Inheritance of R337H p53 gene mutation in children with sporadic adrenocortical tumor. Horm Metab Res; 2005 Apr;37(4):231-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inheritance of R337H p53 gene mutation in children with sporadic adrenocortical tumor.
  • Adrenocortical tumors (ACTs) are frequent in Brazil.
  • The mechanisms of adrenal tumorigenesis remain poorly established; the R337H germline mutation in the p53 gene has previously been associated with ACTs in Brazilian children.
  • DNA was extracted from peripheral blood cells and/or tumor tissue for sequencing exon 10 of the p53 gene.
  • Two members of the adult group showed asymptomatic adrenal incidentalomas, two showed virilization, and one presented with Cushing's syndrome.
  • The R337H mutation was found in fifteen samples of the nineteen tumor specimens available (78.9%).
  • None of the parents showed ACTs or any other neoplasia at the time of the study.
  • There was no association between the presence of germline or tissue R337H p53 mutation and malignancy at diagnosis.
  • The R337H p53 mutation was inherited from one of the parents of the patients, and there was no association between the presence of this mutation and tumor malignancy in children.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Genes, p53 / genetics. Mutation / genetics

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  • (PMID = 15952083.001).
  • [ISSN] 0018-5043
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Codon; 9007-49-2 / DNA
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36. Komissarenko IV, Rybakov SI, Kvacheniuk AN, Lazar' SI, Fedorova TI, Kovalenko AE, Mel'nik ND, Negrienko KV: [The role of computer tomography in differential diagnosis of benign and malignant tumors of the adrenals cortex]. Klin Khir; 2005 Jul;(7):42-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [The role of computer tomography in differential diagnosis of benign and malignant tumors of the adrenals cortex].
  • Possibilities of computer tomography (CT) application for differential diagnosis of tumors of the adrenal cortex (TAC) were studied.
  • While the trustworthy signs of malignancy are absent, it is necessary to conduct morphological verification of the adrenal tumors nature using puncture biopsy and/or intraoperative express-cytological investigation.

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  • (PMID = 16255222.001).
  • [ISSN] 0023-2130
  • [Journal-full-title] Klinichna khirurhiia
  • [ISO-abbreviation] Klin Khir
  • [Language] RUS
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Ukraine
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37. Hu ZJ, Tian HY, Wang LT, Tian HY: [Changes in adrenal cortex function and protective effect of dexamethasone in septic rats during early phases]. Zhongguo Wei Zhong Bing Ji Jiu Yi Xue; 2009 Jan;21(1):40-3
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  • [Title] [Changes in adrenal cortex function and protective effect of dexamethasone in septic rats during early phases].
  • OBJECTIVE: To affirm the presence of relative adrenal insufficiency (RAI) in the early phases of sepsis and its probable mechanisms, and to study the optimal time for glucocorticoid replacement therapy.
  • Adrenocorticotrophic hormone (ACTH) test was conducted at 8 hours and 12 hours, and before and after 30 minutes of ACTH administration, the cortisol content in serum was determined with radioimmunoassay (RIA) and the expressions of Toll-like receptor 4 (TLR4), tumor necrosis factor-alpha (TNF-alpha) mRNA in adrenal glands were detected with semiquantitative reverse transcription-polymerase chain reaction (RT-PCR).
  • Ultrastructure of adrenal cortex was observed with transmission electron microscope.
  • But there was no marked change in the levels of cortisol between pre-and post-ACTH in rats with sepsis in the early phases. (2)The expressions of TLR4, TNF-alpha mRNA in adrenal both were significantly increased in CLP group, and they were higher than those in sham operation group (P<0.05 or P<0.01).
  • The expressions of TLR4, TNF-alpha mRNA in dexamethasone prevention group and treatment group were significantly lower than those in CLP group, and those in the dexamethasone prevention group were lower than those in sham operation group. (3)In the groups of CLP, dexamethasone prevention and treatment, ultrastructure changes were observed in the adrenal, especially in CLP group. (4)The survival rate of the dexamethasone prevention and treatment groups at 12 hours were higher than that of CLP group (76.92%, 40.00% vs. 33.33%, P<0.01 and P<0.05).
  • CONCLUSION: (1)RAI occurs during the early stage of sepsis. (2)The expressions of TLR4, TNF-alpha mRNA in adrenal and changes in corticoadrenal ultrastructure participates in the pathogenesis of RAI in the early stage of sepsis in rat. (3) Dexamethasone therapy could effectively increase the survival rate and improve outcome through down-regulating the expression changes in TLR4, TNF-alpha mRNA and alleviating changes in ultrastructure of adrenal glands.
  • [MeSH-major] Adrenal Cortex / physiopathology. Dexamethasone / therapeutic use. Glucocorticoids / therapeutic use. Sepsis / physiopathology
  • [MeSH-minor] Animals. Disease Models, Animal. Male. RNA, Messenger / genetics. Random Allocation. Rats. Rats, Wistar. Toll-Like Receptor 4 / genetics. Toll-Like Receptor 4 / metabolism. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 19141191.001).
  • [ISSN] 1003-0603
  • [Journal-full-title] Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue
  • [ISO-abbreviation] Zhongguo Wei Zhong Bing Ji Jiu Yi Xue
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / RNA, Messenger; 0 / Tlr4 protein, rat; 0 / Toll-Like Receptor 4; 0 / Tumor Necrosis Factor-alpha; 7S5I7G3JQL / Dexamethasone
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38. Szekeres M, Turu G, Orient A, Szalai B, Süpeki K, Cserzo M, Várnai P, Hunyady L: Mechanisms of angiotensin II-mediated regulation of aldosterone synthase expression in H295R human adrenocortical and rat adrenal glomerulosa cells. Mol Cell Endocrinol; 2009 Apr 29;302(2):244-53

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mechanisms of angiotensin II-mediated regulation of aldosterone synthase expression in H295R human adrenocortical and rat adrenal glomerulosa cells.
  • In adrenal zona glomerulosa cells angiotensin II (Ang II) is a key regulator of steroidogenesis.
  • Our purpose was to compare the mechanisms of Ang II-induced changes in the expression level of early transcription factors NR4A1 (NGFIB) and NR4A2 (Nurr1) genes, and the CYP11B2 gene encoding aldosterone synthase in H295R human adrenocortical tumor cells and in primary rat adrenal glomerulosa cells.
  • Real-time PCR studies have demonstrated that Ang II increased the expression levels of NR4A1 and NR4A2 in H295R cells within 1 h after stimulation, which persisted up to 6 h; whereas in rat adrenal glomerulosa cells the kinetics of the expression of these genes were more rapid and transient.
  • Studies using MEK inhibitor (PD98059, 20 microM), protein kinase C inhibitor (BIM1, 3 microM) and calmodulin kinase (CAMK) inhibitor (KN93, 10 microM) revealed that in rat adrenal glomerulosa cells CAMK-mediated mechanisms play a predominant role in the regulation of CYP11B2.
  • These data suggest that the previously reported CAMK-mediated stimulation of early transcription factors NGFIB and Nurr1 has a predominant role in Ang II-induced CYP11B2 activation in rat adrenal glomerulosa cells, whereas in H295R cells ERK activation and G protein-independent mechanisms also contribute to this process.
  • [MeSH-major] Adrenal Cortex / cytology. Angiotensin II / pharmacology. Cytochrome P-450 CYP11B2 / genetics. Gene Expression Regulation / drug effects. Zona Glomerulosa / cytology

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  • (PMID = 19418629.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Transcription Factors; 11128-99-7 / Angiotensin II; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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39. Behrend EN, Weigand CM, Whitley EM, Refsal KR, Young DW, Kemppainen RJ: Corticosterone- and aldosterone-secreting adrenocortical tumor in a dog. J Am Vet Med Assoc; 2005 May 15;226(10):1662-6, 1659
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  • [Title] Corticosterone- and aldosterone-secreting adrenocortical tumor in a dog.
  • An adrenal gland tumor was visualized via ultrasonography and computed tomography.
  • Histologic examination confirmed that the mass was an adrenocortical carcinoma.
  • Excess adrenal secretion of corticosterone was hypothesized to be the cause of the signs of glucocorticoid excess.
  • Treatment with mitotane was instituted and successful for a period of 4-months until the dog was euthanatized for neurologic problems that were most likely unrelated to endocrine disease.
  • [MeSH-major] Adrenal Cortex Neoplasms / veterinary. Aldosterone / secretion. Antineoplastic Agents, Hormonal / therapeutic use. Corticosterone / secretion. Dog Diseases / diagnosis. Mitotane / therapeutic use

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  • (PMID = 15906564.001).
  • [ISSN] 0003-1488
  • [Journal-full-title] Journal of the American Veterinary Medical Association
  • [ISO-abbreviation] J. Am. Vet. Med. Assoc.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 4964P6T9RB / Aldosterone; 78E4J5IB5J / Mitotane; W980KJ009P / Corticosterone
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40. Kelly SN, McKenna TJ, Young LS: Coregulatory protein-orphan nuclear receptor interactions in the human adrenal cortex. J Endocrinol; 2005 Jul;186(1):33-42
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  • [Title] Coregulatory protein-orphan nuclear receptor interactions in the human adrenal cortex.
  • The capacity of the adrenal to produce steroids is controlled in part through the transcriptional regulation of steroid enzymes.
  • We hypothesised that, in the presence of secretagogues, SF-1 and nur77 may differentially interact with coregulatory proteins in the human adrenal cortex.
  • Both coregulatory proteins, steroid receptor coactivator (SRC-1) and silencing mediator for retinoid and thyroid hormones (SMRT), were found to be expressed in the zona fasciculata and reticularis in the human adrenal cortex, but were largely absent from the zona glomerulosa.
  • In the H295R adrenal tumour cell line, SF-1 and nur77 transcripts were increased in cells in the presence of forskolin, whereas nur77 mRNA was also induced with angiotensin II (AII).
  • Orphan nuclear receptor-coregulatory protein interactions may have consequences for the regulation of key steroidogenic enzymes in the human adrenal cortex.
  • [MeSH-major] Adrenal Cortex / chemistry. DNA-Binding Proteins / analysis. Receptors, Cytoplasmic and Nuclear / analysis. Receptors, Steroid / analysis. Repressor Proteins / analysis. Transcription Factors / analysis
  • [MeSH-minor] Angiotensin II / pharmacology. Cell Line, Tumor. Cells, Cultured. Colforsin / pharmacology. Gene Expression / drug effects. Histone Acetyltransferases. Homeodomain Proteins. Humans. Nuclear Receptor Co-Repressor 2. Nuclear Receptor Coactivator 1. Nuclear Receptor Subfamily 4, Group A, Member 1. Protein Interaction Mapping / methods. RNA, Messenger / analysis. Steroidogenic Factor 1. Stimulation, Chemical. Zona Fasciculata / chemistry. Zona Reticularis / chemistry

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  • (PMID = 16002533.001).
  • [ISSN] 0022-0795
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / NCOR2 protein, human; 0 / NR4A1 protein, human; 0 / NR5A1 protein, human; 0 / Nuclear Receptor Co-Repressor 2; 0 / Nuclear Receptor Subfamily 4, Group A, Member 1; 0 / RNA, Messenger; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Steroid; 0 / Repressor Proteins; 0 / Steroidogenic Factor 1; 0 / Transcription Factors; 11128-99-7 / Angiotensin II; 1F7A44V6OU / Colforsin; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / NCOA1 protein, human; EC 2.3.1.48 / Nuclear Receptor Coactivator 1
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41. Takehara K, Sakai H, Shono T, Irie J, Kanetake H: Proliferative activity and genetic changes in adrenal cortical tumors examined by flow cytometry, fluorescence in situ hybridization and immunohistochemistry. Int J Urol; 2005 Feb;12(2):121-7
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  • [Title] Proliferative activity and genetic changes in adrenal cortical tumors examined by flow cytometry, fluorescence in situ hybridization and immunohistochemistry.
  • BACKGROUND: To determine differences in biological features among different adrenal tumors, we investigated the DNA ploidy, numerical chromosomal aberration and proliferative activity in human adrenal cortical neoplasms.
  • METHODS: Our study included six adrenal cortical adenomas with Cushing syndrome, 12 adenomas with hyperaldosteronism, three non-functioning adenomas and three adrenal cortical carcinomas.
  • RESULTS: The mean Ki-67 labeling index (LI) of adrenal cortical carcinomas was markedly higher than that of adrenal cortical adenomas (209.4 vs 8.7).
  • In functional adrenal cortical adenomas, the LI was significantly lower in adenomas with hyperaldosteronism than in those with Cushing syndrome (P = 0.004), although FCM results indicated that tetraploid patterns were more frequently observed in the former type.
  • Tumor size was significantly smaller in adenomas with hyperaldosteronism than in those with Cushing syndrome (P = 0.004).
  • Chromosome 17 showed disomy in all adrenal cortical adenomas, whereas chromosome 17 abnormalities were found in two of three adrenal cortical carcinomas.
  • CONCLUSIONS: Our study characterized various biological features of benign and malignant adrenal cortical tumors.
  • The use of a combination of markers might provide additional information to assist our understanding of the clinical behavior of an individual adrenal cortical tumor.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / metabolism. Flow Cytometry. Immunohistochemistry. In Situ Hybridization, Fluorescence
  • [MeSH-minor] Adenoma / genetics. Adenoma / metabolism. Adenoma / pathology. Adult. Aged. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Carcinoma / genetics. Carcinoma / metabolism. Carcinoma / pathology. Cell Proliferation. Chromosomes, Human, Pair 17. Cushing Syndrome / genetics. Cushing Syndrome / metabolism. Cushing Syndrome / pathology. DNA, Neoplasm / genetics. Female. Humans. Hyperaldosteronism / genetics. Hyperaldosteronism / metabolism. Hyperaldosteronism / pathology. Ki-67 Antigen / metabolism. Male. Middle Aged. Ploidies. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 15733104.001).
  • [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] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
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42. Hantel C, Beuschlein F: Mouse models of adrenal tumorigenesis. Best Pract Res Clin Endocrinol Metab; 2010 Dec;24(6):865-75
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  • [Title] Mouse models of adrenal tumorigenesis.
  • Adrenocortical carcinomas (ACCs) are heterogeneous tumors with a poor prognosis.
  • The rarity of this disorder causes a lack of treatment experience and material availability which is necessary to optimize existing treatments and to develop novel therapeutic strategies.
  • Although surgery is still the treatment of choice, adjuvant therapies are urgently needed as the rate of recurrence for these tumors is high.
  • In recent years molecular characterization of surgical tumor specimen has aided in the understanding of disease mechanisms and definition of therapeutic targets also in adrenocortical carcinoma.
  • Here we give an overview on rodent models that have been described to either have adrenocortical tumors as part of their phenotype or have been utilized for therapeutic screens as adrenocortical tumor models.
  • [MeSH-major] Adrenal Cortex Neoplasms / therapy. Adrenal Gland Neoplasms / physiopathology. Adrenal Gland Neoplasms / therapy. Disease Models, Animal
  • [MeSH-minor] Animals. Animals, Genetically Modified. Mice. Neoplasm Transplantation

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  • [Copyright] 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 21115155.001).
  • [ISSN] 1878-1594
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
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43. Wright CB, Brennan L, Brophy P, Kirsh G, Shapiro M, Potter B, Giss S, Lindeman KE, Obial R, Fannin E: Adrenocortical tumor with left renal vein, vena cava and intrahepatic venous extension. J Cardiovasc Surg (Torino); 2008 Feb;49(1):79-81
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  • [Title] Adrenocortical tumor with left renal vein, vena cava and intrahepatic venous extension.
  • She proved, however, to have an adrenal cortical carcinoma which displaced the kidney, exhibiting vascular invasion within the gland and non-adherent extension into the vena cava, atrium, common hepatic vein and left renal vein, where some adherence was present.
  • This unusual tumor required extensive surgery for removal, including use of cardiopulmonary bypass, with good results.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Carcinoma, Renal Cell / diagnosis. Hepatic Veins / pathology. Kidney Neoplasms / diagnosis. Renal Veins / pathology. Vena Cava, Inferior / pathology
  • [MeSH-minor] Adrenalectomy. Adult. Cardiopulmonary Bypass. Diagnosis, Differential. Female. Heart Atria / pathology. Humans. Neoplasm Invasiveness. Nephrectomy. Treatment Outcome. Vascular Surgical Procedures

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  • (PMID = 18212691.001).
  • [ISSN] 0021-9509
  • [Journal-full-title] The Journal of cardiovascular surgery
  • [ISO-abbreviation] J Cardiovasc Surg (Torino)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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44. Markou A, Tsigou K, Papadogias D, Kossyvakis K, Vamvakidis K, Kounadi T, Piaditis G: A unique case of a benign adrenocortical tumor with triple secretion of cortisol, androgens, and aldosterone: development of multiple sclerosis after surgical removal of the tumor. Hormones (Athens); 2005 Oct-Dec;4(4):226-30
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  • [Title] A unique case of a benign adrenocortical tumor with triple secretion of cortisol, androgens, and aldosterone: development of multiple sclerosis after surgical removal of the tumor.
  • We present a 39-year old female with a benign adrenal tumor characterized by autonomous secretion of cortisol, androgens, and aldosterone.
  • CT of the adrenals revealed a 2.5 x 3.0 cm tumor with characteristics of an adenoma on the left adrenal gland.
  • Further investigations revealed suppressed basal ACTH levels, loss of diurnal rhythm of cortisol, and failure to suppress on low dose dexamethasone suppression test, suggesting autonomous cortisol secretion by the tumor.
  • Complete clinical and biochemical remission of the disease was observed after left adrenalectomy.
  • Histology confirmed the presence of an adrenocortical adenoma.
  • The flare-up of an autoimmune disease (multiple sclerosis) postoperatively could be coincidental or possibly related to the high normalization of the high cortisol levels acting as a precipitating factor.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenal Cortex Neoplasms / surgery. Adrenalectomy / adverse effects. Adrenocortical Adenoma / pathology. Adrenocortical Adenoma / surgery. Multiple Sclerosis / etiology
  • [MeSH-minor] Adult. Aldosterone / secretion. Androgens / secretion. Biopsy, Needle. Female. Follow-Up Studies. Humans. Hydrocortisone / secretion. Immunohistochemistry. Neoplasm Staging. Risk Assessment

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  • (PMID = 16613821.001).
  • [ISSN] 1109-3099
  • [Journal-full-title] Hormones (Athens, Greece)
  • [ISO-abbreviation] Hormones (Athens)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Androgens; 4964P6T9RB / Aldosterone; WI4X0X7BPJ / Hydrocortisone
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45. Coulter CL: Fetal adrenal development: insight gained from adrenal tumors. Trends Endocrinol Metab; 2005 Jul;16(5):235-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fetal adrenal development: insight gained from adrenal tumors.
  • Conversely, tumor progression and the development of cancer probably occur through a process of dysregulation and dedifferentiation.
  • Similarities exist between normal human fetal adrenal cortex and adrenal cancers, such as high expression of growth factors, including insulin-like growth factor II.
  • Therefore, we might gain insight into factors involved in adrenocortical development through better understanding the development and progression of adrenocortical tumors.
  • This review is prompted by recent gene profiling studies that have identified genes differentially expressed between normal and abnormal adrenal glands.
  • Several of these genes are specific growth factors or key cell cycle regulators, in addition to genes not previously associated with adrenal growth or function.
  • [MeSH-major] Adrenal Gland Neoplasms / pathology. Adrenal Glands / embryology

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  • (PMID = 15949953.001).
  • [ISSN] 1043-2760
  • [Journal-full-title] Trends in endocrinology and metabolism: TEM
  • [ISO-abbreviation] Trends Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Somatomedins
  • [Number-of-references] 62
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46. Raparia K, Ayala AG, Sienko A, Zhai QJ, Ro JY: Myxoid adrenal cortical neoplasms. Ann Diagn Pathol; 2008 Oct;12(5):344-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myxoid adrenal cortical neoplasms.
  • Myxoid adrenal cortical neoplasms are rare, and to our knowledge, only about 23 cases have been reported in the literature, including 13 carcinomas and 10 adenomas.
  • We recently experienced 4 cases of myxoid adrenal cortical neoplasms (3 benign and 1 borderline malignancy) and studied the clinical, histopathological, and immunohistochemical features of these neoplasms.
  • The tumors weighed from 24.1 to 94 g (size, 4.1-9.8 cm).
  • Histologically, the tumor cells were arranged in delicate arborizing cords or trabecula with myxoid areas varying from 30% to 70%.
  • Three tumors were benign and 1 was of borderline morphology with mitoses of 3/10 high-power fields and mild to moderate nuclear pleomorphism.
  • The tumor cells were positive for vimentin, synaptophysin, and inhibin but negative for cytokeratin.
  • All patients are alive with no recurrence of their tumors or evidence of metastasis (follow-up of 14-20 months).
  • Myxoid changes in adrenal cortical neoplasms are rare but can be seen in both an adenoma and a tumor of uncertain malignant potential.
  • Because of prominent myxoid changes, other myxoid tumors occurring in the retroperitoneum should be excluded.
  • The usual clinical and histological features can be applied to classify the lesions as benign, borderline tumor, or malignant.
  • In our series, there was no case with frank malignant tumor.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / pathology. Adrenocortical Carcinoma / pathology. Mucins / metabolism
  • [MeSH-minor] Adult. Biomarkers, Tumor / metabolism. Female. Humans. Immunoenzyme Techniques. Inhibins / metabolism. Male. Middle Aged. Synaptophysin / metabolism. Vimentin / metabolism

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  • (PMID = 18774497.001).
  • [ISSN] 1532-8198
  • [Journal-full-title] Annals of diagnostic pathology
  • [ISO-abbreviation] Ann Diagn Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Mucins; 0 / Synaptophysin; 0 / Vimentin; 57285-09-3 / Inhibins
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47. Collins BR: Endocrine diseases of rodents. Vet Clin North Am Exot Anim Pract; 2008 Jan;11(1):153-62, vii-viii
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  • The clinical diagnosis of endocrine diseases almost never occurs in free-ranging animals in their native habitat.
  • Feral animals that have clinical endocrine disease, such as neoplasia, adrenal cortical hyperplasia, or diabetes, would exhibit clinical signs of altered behavior that would result in their removal by predators.
  • The diagnosis of endocrine disease thus takes place in the relatively protective environment of captivity.
  • [MeSH-major] Animals, Domestic. Endocrine System Diseases / veterinary. Rodent Diseases / diagnosis
  • [MeSH-minor] Animals. Cricetinae. Diagnosis, Differential. Female. Gerbillinae. Guinea Pigs. Male. Mice. Rats. Rodentia. Species Specificity

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  • (PMID = 18165143.001).
  • [ISSN] 1094-9194
  • [Journal-full-title] The veterinary clinics of North America. Exotic animal practice
  • [ISO-abbreviation] Vet Clin North Am Exot Anim Pract
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 39
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48. Cotesta D, Petramala L, Serra V, Giustini S, Divona L, Calvieri S, De Toma G, Ciardi A, Corsi A, Massa R, Reale MG, Letizia C: Pheochromocytoma associated with adrenocortical tumor in the same gland. Two case reports and literature review. Minerva Endocrinol; 2006 Jun;31(2):183-9
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  • [Title] Pheochromocytoma associated with adrenocortical tumor in the same gland. Two case reports and literature review.
  • Pheochromocytomas are catecholamine-producing neuroendocrine tumours arising from chromaffin cells of the adrenal medulla or extra-adrenal paraganglionic system that show 2 distinctive features, rarity and clinical variability.
  • Pheochromocytoma occasionally is associated with pathological lesions of the adrenal cortex.
  • We present 2 cases of patients referred to our hospital with a finding of clinical suspected pheochromocytoma.
  • The diagnosis of pheochromocytoma was confirmed in both cases with laboratory analysis and the lesion was achieved by employing 3 imaging techniques: computed tomography (CT), magnetic resonance imaging (MRI) and scintigraphy with (123)I-metaiodobenzilguanidine (MIBG).
  • The patients underwent adrenalectomy and in the same adrenal gland we found a pheochromocytoma associated with a nonfunctioning cortical adenoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenal Gland Neoplasms / diagnosis. Adrenocortical Adenoma / diagnosis. Neoplasms, Multiple Primary / diagnosis. Pheochromocytoma / diagnosis
  • [MeSH-minor] 3-Iodobenzylguanidine. Adrenalectomy. Adult. Humans. Male. Middle Aged. Neurofibromatosis 1 / diagnosis. Radiopharmaceuticals. Treatment Outcome

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  • (PMID = 16682942.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 35MRW7B4AD / 3-Iodobenzylguanidine
  • [Number-of-references] 41
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49. Millard RP, Pickens EH, Wells KL: Excessive production of sex hormones in a cat with an adrenocortical tumor. J Am Vet Med Assoc; 2009 Feb 15;234(4):505-8
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  • [Title] Excessive production of sex hormones in a cat with an adrenocortical tumor.
  • Abdominal ultrasonography revealed a mass in the region of the right adrenal gland.
  • Results of adrenal hormonal analyses revealed considerable increases in serum concentrations of androstenedione and testosterone.
  • TREATMENT AND OUTCOME: A mass associated with the right adrenal gland was found during exploratory laparotomy.
  • Adrenalectomy of the right adrenal gland was performed, and histologic evaluation of the mass revealed an adrenocortical adenoma.
  • CLINICAL RELEVANCE: Adrenal gland tumors can produce a variety of hormones other than cortisol.
  • An adrenal gland tumor should be considered in neutered cats with newly developed physical and behavioral changes of a sexual nature.
  • In the absence of debilitating conditions that are often associated with hyperadrenocorticism, cats undergoing adrenalectomy for an adrenal gland tumor that is producing sex hormones may have resolution of clinical signs and a good prognosis.
  • [MeSH-major] Adenocarcinoma / veterinary. Adrenal Cortex Neoplasms / veterinary. Adrenalectomy / veterinary. Androstenedione / blood. Cat Diseases / blood. Testosterone / blood

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  • (PMID = 19222361.001).
  • [ISSN] 0003-1488
  • [Journal-full-title] Journal of the American Veterinary Medical Association
  • [ISO-abbreviation] J. Am. Vet. Med. Assoc.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 3XMK78S47O / Testosterone; 409J2J96VR / Androstenedione
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50. Galac S, Kars VJ, Klarenbeek S, Teerds KJ, Mol JA, Kooistra HS: Expression of receptors for luteinizing hormone, gastric-inhibitory polypeptide, and vasopressin in normal adrenal glands and cortisol-secreting adrenocortical tumors in dogs. Domest Anim Endocrinol; 2010 Jul;39(1):63-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of receptors for luteinizing hormone, gastric-inhibitory polypeptide, and vasopressin in normal adrenal glands and cortisol-secreting adrenocortical tumors in dogs.
  • Hypercortisolism caused by an adrenocortical tumor (AT) results from adrenocorticotropic hormone (ACTH)-independent hypersecretion of glucocorticoids.
  • Normal adrenal glands served as control tissues.
  • In both normal adrenal glands and ATs, mRNA encoding for all receptors was present, although the expression abundance of the V(1b) receptor was very low.
  • The mRNA expression abundance for GIP and V(2) receptors in ATs were significantly lower (0.03 and 0.01, respectively) than in normal adrenal glands.
  • The zona fasciculata of normal adrenal glands stained immunonegative for the GIP receptor.
  • The zona fasciculata of both normal adrenal glands and AT tissue were immunopositive for LH receptor; in ATs in a homogenous or heterogenous pattern.
  • In normal adrenal glands, no immunolabeling for V(1b)R and V(2) receptor was present, but in ATs, V(2) receptor-immunopositive cells were detected.
  • [MeSH-major] Adrenal Cortex Neoplasms / veterinary. Dog Diseases / metabolism. Hydrocortisone / secretion. Receptors, Gastrointestinal Hormone / genetics. Receptors, LH / genetics. Receptors, Vasopressin / genetics
  • [MeSH-minor] Adrenal Glands / chemistry. Adrenalectomy. Animals. Dogs. Gene Expression. Immunohistochemistry. Polymerase Chain Reaction. RNA, Messenger / analysis. Zona Fasciculata / chemistry

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  • (PMID = 20399066.001).
  • [ISSN] 1879-0054
  • [Journal-full-title] Domestic animal endocrinology
  • [ISO-abbreviation] Domest. Anim. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptors, Gastrointestinal Hormone; 0 / Receptors, LH; 0 / Receptors, Vasopressin; 0 / gastric inhibitory polypeptide receptor; WI4X0X7BPJ / Hydrocortisone
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51. Jarral OA, Todd C, Willson PD: Hemorrhagic shock secondary to spontaneous rupture of a non-secretory adrenal cortical tumour: A case report. Can Urol Assoc J; 2010 Dec;4(6):E161-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hemorrhagic shock secondary to spontaneous rupture of a non-secretory adrenal cortical tumour: A case report.
  • After emergency laparotomy, angiography, embolisation and histological investigation, a diagnosis of spontaneous rupture of a benign non-secretory adrenal cortical tumour was made.
  • To our knowledge, this is the only reported case of this diagnosis.

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  • [Cites] Am J Surg. 2007 Jul;194(1):77-8 [17560914.001]
  • [Cites] J Surg Oncol. 2005 Apr 1;90(1):31-5 [15786413.001]
  • [Cites] Radiat Med. 2003 Sep-Oct;21(5):214-9 [14632297.001]
  • [Cites] Endocr J. 2001 Dec;48(6):691-6 [11873868.001]
  • [Cites] J Urol. 1992 Feb;147(2):311-8 [1346277.001]
  • (PMID = 21749812.001).
  • [ISSN] 1920-1214
  • [Journal-full-title] Canadian Urological Association journal = Journal de l'Association des urologues du Canada
  • [ISO-abbreviation] Can Urol Assoc J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Canada
  • [Other-IDs] NLM/ PMC3038376
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52. Pushkarev VM, Tronko ND, Kostyuchenko NN, Mikosha AS: Effect of o,p'-DDD and Li+ on apoptotic DNA fragmentation in conventionally normal and tumour tissues of human adrenal cortex. Ukr Biokhim Zh (1999); 2007 Mar-Apr;79(2):44-9
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  • [Title] Effect of o,p'-DDD and Li+ on apoptotic DNA fragmentation in conventionally normal and tumour tissues of human adrenal cortex.
  • The actions of 1-(o-chlorophenyl)-1-(p-chlorophenyl)-2,2-dichloroethane (o,p'-DDD), potassium and lithium ions upon apoptotic processes in conventionally normal and tumour tissues of human adrenal cortex were studied.
  • There was no effect of K+ on the apoptosis in tumour tissue. o,p'-DDD--the specific drug for conservative therapy of adrenocortical cancer--enhanced the apoptotic DNA fragmentation in all tested tissues.
  • The conclusion was made that apoptosis may be involved in curative effect of o,p'-DDD in adrenal cortex.
  • Lithium ions, which are used in clinic as antidepressant, inhibited the apoptosis in conventionally normal tissue and in most tumours.
  • On the other hand, lithium enhanced the DNA fragmentation in the postoperative tissue of patients with Cushing disease.
  • The possible mechanisms mediating lithium effects on the adrenal cortex are discussed.
  • [MeSH-major] Adrenal Cortex / drug effects. Adrenal Cortex Neoplasms / pathology. Antineoplastic Agents, Hormonal / pharmacology. Apoptosis / drug effects. DNA Fragmentation / drug effects. Lithium Chloride / pharmacology. Mitotane / pharmacology
  • [MeSH-minor] Humans. Potassium Chloride / pharmacology. Tumor Cells, Cultured

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  • (PMID = 18030749.001).
  • [Journal-full-title] Ukraïnsʹkyĭ biokhimichnyĭ z︠h︡urnal (1999 )
  • [ISO-abbreviation] Ukr Biokhim Zh (1999)
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 660YQ98I10 / Potassium Chloride; 78E4J5IB5J / Mitotane; G4962QA067 / Lithium Chloride
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53. Stephenson TJ: Prognostic and predictive factors in endocrine tumours. Histopathology; 2006 May;48(6):629-43
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  • [Title] Prognostic and predictive factors in endocrine tumours.
  • This review encompasses the diagnostic features of malignancy, the routinely observable prognostic features and the prognostic and predictive features emerging from research techniques in the principal endocrine neoplasms: pancreatic and extrapancreatic endocrine cell tumours, thyroid and parathyroid neoplasia, adrenal cortical neoplasms and adrenal and extra-adrenal paragangliomas.
  • While each endocrine tissue has its own set of diagnostic features for malignancy, and prognostic features once a diagnosis of malignancy has been established, there are a few common themes.
  • For several endocrine neoplasms, definite recognition of malignancy can be difficult and may depend upon frank invasive or metastatic growth at presentation.
  • The accurate documentation of routinely observable histological features interpreted in the light of current literature has not been superseded by special techniques in the statement of diagnosis or prognosis in the vast majority of endocrine neoplasms.
  • [MeSH-major] Endocrine Gland Neoplasms / pathology. Peptide Hormones / analysis
  • [MeSH-minor] Diagnosis, Differential. Glucagon / analysis. Humans. Insulin / analysis. Predictive Value of Tests. Prognosis

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  • (PMID = 16681678.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Insulin; 0 / Peptide Hormones; 9007-92-5 / Glucagon
  • [Number-of-references] 123
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54. Yener S, Ertilav S, Secil M, Akinci B, Demir T, Comlekci A, Yesil S: Natural course of benign adrenal incidentalomas in subjects with extra-adrenal malignancy. Endocrine; 2009 Aug;36(1):135-40
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  • [Title] Natural course of benign adrenal incidentalomas in subjects with extra-adrenal malignancy.
  • Patients with extra-adrenal malignancies are diagnosed increasingly with benign adrenal tumors, as well as non-oncology subjects.
  • We aimed to demonstrate the natural course of adrenal adenomas in terms of mass size and hormonal status in oncology and non-oncology subjects.
  • We also compared the characteristics and behavior of adrenal adenomas with adrenal malignancies.
  • In our registry of adrenal tumors (n = 335), we prospectively evaluated 29 oncology subjects (EAM+) and age, gender, and follow-up duration matched 110 non-oncology subjects (EAM-) with adrenal adenomas.
  • We also included 16 subjects with adrenal malignancies (primary; 3 and metastasis; 13).
  • Tumor size was followed-up with CT or MRI at 6th and 12th months and annually in subsequent visits.
  • Initial tumor size, mean increase in tumor size, and number of subjects who showed mass enlargement or developed subclinical Cushing Syndrome were comparable (P > 0.05) between EAM+ and EAM- groups.
  • Subjects with malignant adrenal tumors were older (P = 0.06), had larger tumors at presentation (P < 0.001), and showed mass enlargement during a shorter follow-up duration (P < 0.001).
  • Oncology subjects with adrenal adenomas featured similar baseline and follow-up parameters in terms of mass enlargement and development of subclinical Cushing Syndrome when compared with non-oncology subjects.
  • Malignant adrenal tumors were characterized with large, rapidly growing tumors of older ages.
  • Conservative approach can be suggested to oncology subjects for adrenal adenomas unless clinical and radiological suspicion of adrenal malignancy is present.
  • [MeSH-major] Adenoma / epidemiology. Adrenal Cortex Neoplasms / epidemiology. Cushing Syndrome / epidemiology. Neoplasms / epidemiology. Pheochromocytoma / epidemiology
  • [MeSH-minor] Adult. Aged. Carcinoma, Non-Small-Cell Lung / epidemiology. Carcinoma, Renal Cell / epidemiology. Disease Progression. Female. Follow-Up Studies. Humans. Incidental Findings. Kidney Neoplasms / epidemiology. Lung Neoplasms / epidemiology. Lymphoma, Non-Hodgkin / epidemiology. Male. Middle Aged. Pancreatic Neoplasms / epidemiology. Prevalence. Registries

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  • (PMID = 19381885.001).
  • [ISSN] 1355-008X
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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55. Johnsen IK, Kappler R, Auernhammer CJ, Beuschlein F: Bone morphogenetic proteins 2 and 5 are down-regulated in adrenocortical carcinoma and modulate adrenal cell proliferation and steroidogenesis. Cancer Res; 2009 Jul 15;69(14):5784-92
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  • [Title] Bone morphogenetic proteins 2 and 5 are down-regulated in adrenocortical carcinoma and modulate adrenal cell proliferation and steroidogenesis.
  • Bone morphogenetic proteins (BMP) have been shown to affect tumorigenesis in a variety of tumors.
  • Quantitative PCR analysis revealed down-regulation of BMP2 and BMP5 in tissue samples from adrenocortical carcinoma and adrenocortical tumor cell lines compared with normal adrenal glands.
  • Taken together, we show that loss of expression of members of the BMP family of ligands is a common finding in adrenocortical tumors and we provide evidence that BMP-dependent pathways are likely to be involved in the modulation of the malignant and functional phenotype of adrenocortical cancer cells.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Bone Morphogenetic Protein 2 / genetics. Bone Morphogenetic Protein 5 / genetics
  • [MeSH-minor] Aldosterone / metabolism. Blotting, Western. Bone Morphogenetic Protein Receptors / genetics. Bone Morphogenetic Protein Receptors / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Colforsin / pharmacology. Dose-Response Relationship, Drug. Down-Regulation / drug effects. GATA6 Transcription Factor / genetics. GATA6 Transcription Factor / metabolism. Humans. Hydrocortisone / metabolism. Insulin-Like Growth Factor I / genetics. Insulin-Like Growth Factor I / pharmacology. Phosphorylation / drug effects. Proto-Oncogene Proteins c-akt / metabolism. Recombinant Proteins / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Steroid 17-alpha-Hydroxylase / genetics. Steroid 17-alpha-Hydroxylase / metabolism. Time Factors. Tretinoin / pharmacology. Tumor Cells, Cultured

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  • (PMID = 19584291.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bone Morphogenetic Protein 2; 0 / Bone Morphogenetic Protein 5; 0 / GATA6 Transcription Factor; 0 / GATA6 protein, human; 0 / Recombinant Proteins; 1F7A44V6OU / Colforsin; 4964P6T9RB / Aldosterone; 5688UTC01R / Tretinoin; 67763-96-6 / Insulin-Like Growth Factor I; EC 1.14.99.9 / Steroid 17-alpha-Hydroxylase; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.30 / Bone Morphogenetic Protein Receptors; WI4X0X7BPJ / Hydrocortisone
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56. Misić M, Vidas Z, Skegro D, Kocman B, Jelić-Puskarić B, Kardum-Skelin I: Fine needle aspiration cytology of adrenocortical carcinoma--case report. Coll Antropol; 2010 Jun;34(2):665-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fine needle aspiration cytology of adrenocortical carcinoma--case report.
  • Ultrasonography (US) revealed a solitary tumor mass, eight cm in size, of the right adrenal gland.
  • Laboratory tests showed it to be a hormonally active, androgen secreting tumor (elevated testosterone level), which was consistent with the clinical picture of the disease.
  • After histopathological analysis tumor was signed out as adrenocortical carcinoma, a low risk carcinoma according to Weiss' classification.
  • The finding was verified by computerized tomography and the patient was reoperated on.
  • Cytologic opinion was recidive of primary malignant disease.
  • ACC is a rare malignant epithelial tumor of adrenal cortical cells, with high malignant potential.
  • Morphologically (histopathology and cytology), differential diagnosis includes adenoma on the one hand, and renal cell carcinoma (RCC) and hepatocellular carcinoma (HCC) on the other hand.
  • A combined evaluation of clinical features, size or weight, microscopic appearance, immunohistochemical and molecular genetic data is necessary to ensure a correct diagnosis.
  • The purpose of this case report is to present clinical and cytomorphologic features of our case of adrenocortical carcinoma which is very rare in cytology practice.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Carcinoma / pathology

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  • (PMID = 20698150.001).
  • [ISSN] 0350-6134
  • [Journal-full-title] Collegium antropologicum
  • [ISO-abbreviation] Coll Antropol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Croatia
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57. Gross MD, Djekidel M, Hay RV, Rubello D: Scintigraphic localization of adrenal tumors. Minerva Endocrinol; 2009 Jun;34(2):171-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Scintigraphic localization of adrenal tumors.
  • Scintigraphy has historically added much to the evaluation of adrenal dysfunction and tumor localization.
  • The early development of radiopharmaceuticals for adrenocortical imaging provided vital clinical information well before the widespread availability of computed tomography (CT), but beginning in the early 1980's nuclear imaging became supplanted in large part by high resolution CT and more recently by magnetic resonance imaging.
  • The parallel emergence of radiopharmaceuticals for adrenomedullary imaging also provided important functional insight in evaluating these neoplasms, but despite the clinical value of such nuclear probes they too, were relegated to a less prominent role in tumor characterization because of advances in anatomic imaging.
  • However, with the recent introduction of dual-modality imaging platforms that directly combine CT with scintigraphy, either as single photon emission tomography (SPECT)/CT or positron emission tomography (PET)/CT, nuclear medicine studies once again play an integral role in adrenal tumor evaluation.
  • [MeSH-major] Adrenal Gland Neoplasms / radionuclide imaging. Positron-Emission Tomography. Radiopharmaceuticals. Tomography, Emission-Computed, Single-Photon
  • [MeSH-minor] Adrenal Cortex Neoplasms / radionuclide imaging. Adrenal Gland Diseases / radionuclide imaging. Adrenocortical Carcinoma / radionuclide imaging. Cushing Syndrome / radionuclide imaging. Diagnosis, Differential. Humans. Incidental Findings. Pheochromocytoma / radionuclide imaging. Reproducibility of Results. Sensitivity and Specificity. Tomography, X-Ray Computed

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  • (PMID = 19333218.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Radiopharmaceuticals
  • [Number-of-references] 93
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58. 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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59. Bovio S, Reimondo G, Daffara F, Allasino B, Angeli A, Terzolo M: [Subclinical Cushing's syndrome in adrenal incidentalomas]. Recenti Prog Med; 2006 Jan;97(1):6-15
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  • [Title] [Subclinical Cushing's syndrome in adrenal incidentalomas].
  • [Transliterated title] La sindrome di Cushing subclinica nei pazienti con incidentaloma surrenalico.
  • In the heyday of high-tech medicine, the incidental discovery of an adrenal mass is a frequent event owing to the routine use of sophisticated radiological techniques.
  • The potential harm to health associated with incidentally discovered cortical adenoma, the most frequent tumor among adrenal incidentalomas, is unclear at present.
  • Incidentally discovered adrenal adenoma may secrete cortisol autonomously, in a way that is no longer under close control by pituitary feedback, in 5 to 20% of cases.
  • At present, data are insufficient to indicate the superiority of a surgical or nonsurgical approach to manage patients with subclinical hyperfunctioning adrenal cortical adenoma.
  • It is of the utmost importance to establish collaborative prospective studies with clearly defined entry criteria and standardized evaluation protocols and treatment modalities to appraise the natural history and long-term morbidity of clinically inapparent adrenal adenoma and subclinical Cushing's syndrome.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications. Cushing Syndrome

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  • (PMID = 16535924.001).
  • [ISSN] 0034-1193
  • [Journal-full-title] Recenti progressi in medicina
  • [ISO-abbreviation] Recenti Prog Med
  • [Language] ita
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] WI4X0X7BPJ / Hydrocortisone
  • [Number-of-references] 87
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60. Wang W, Wang L, Endoh A, Hummelke G, Hawks CL, Hornsby PJ: Identification of alpha-enolase as a nuclear DNA-binding protein in the zona fasciculata but not the zona reticularis of the human adrenal cortex. J Endocrinol; 2005 Jan;184(1):85-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of alpha-enolase as a nuclear DNA-binding protein in the zona fasciculata but not the zona reticularis of the human adrenal cortex.
  • In order to establish whether there are differences in DNA-binding proteins between zona fasciculata (ZF) and zona reticularis (ZR) cells of the human adrenal cortex, we prepared nuclear extracts from separated ZF and ZR cells.
  • We performed immunohistochemistry on sections of adult human adrenal cortex and found alpha-enolase to be located in nuclei of ZF cells but to be predominantly cytoplasmic in ZR cells.
  • Transfection of an alpha-enolase expression vector into NCI-H295R human adrenocortical cells increased HSD3B2 promoter activity, suggesting a possible functional role for this protein in regulation of HSD3B2 expression.
  • [MeSH-major] Cell Nucleus / enzymology. DNA-Binding Proteins / analysis. Phosphopyruvate Hydratase / analysis. Tumor Suppressor Proteins / analysis. Zona Fasciculata / enzymology
  • [MeSH-minor] 3-Hydroxysteroid Dehydrogenases / metabolism. Analysis of Variance. Animals. Biomarkers, Tumor. Cattle. Cell Line. Chromatography, Affinity. Electrophoretic Mobility Shift Assay. Genes, Reporter. Humans. Immunohistochemistry / methods. Isoenzymes / metabolism. Protein Binding. RNA, Messenger / analysis. Transcription, Genetic. Zona Reticularis / enzymology

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  • (PMID = 15642786.001).
  • [ISSN] 0022-0795
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / AG 12287
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Isoenzymes; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins; EC 1.1.- / 3-Hydroxysteroid Dehydrogenases; EC 4.2.1.11 / ENO1 protein, human; EC 4.2.1.11 / Phosphopyruvate Hydratase
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61. Fernandez-Ranvier GG, Weng J, Yeh RF, Shibru D, Khafnashar E, Chung KW, Hwang J, Duh QY, Clark OH, Kebebew E: Candidate diagnostic markers and tumor suppressor genes for adrenocortical carcinoma by expression profile of genes on chromosome 11q13. World J Surg; 2008 May;32(5):873-81
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  • [Title] Candidate diagnostic markers and tumor suppressor genes for adrenocortical carcinoma by expression profile of genes on chromosome 11q13.
  • BACKGROUND: The most common genetic change observed in adrenocortical carcinoma is loss of heterozygozity on chromosome 11q13.
  • As genes on this chromosome may be important in the pathogenesis of adrenocortical carcinoma, we compared their expression profile between benign and malignant adrenocortical tissue.
  • METHODS: We used the Affymetrix GeneChip (U133 plus 2.0) array in 54 adrenocortical tumors (11 carcinoma and 43 benign).
  • The area under the receiver operating characteristic (ROC) curve (AUC) was used to determined the diagnostic accuracy of the differently expressed genes for distinguishing benign from malignant tumors.
  • RESULTS: We found 25 of the 314 genes on chromosome 11q13 to be differentially expressed between adrenocortical carcinoma and benign adrenocortical tumor.
  • All 25 were downregulated in adrenocortical carcinoma by 2-fold to 4.8-fold; 21 were validated to be differentially expressed by RT-PCR (Pearson's coefficient>0.5).
  • Six genes (SERPING1, MRPL48, TM7SF2, DDB1, NDUSF8, PRDX5) validated by RT-PCR were significantly differentially expressed between benign and malignant adrenocortical tumors (p<0.05) with an overall accuracy of 89% for SERPING1, 91% for MRPL48, 87% for TM7SF2, 88% for DDB1, 91% for NDUFS8, and 89% for PRDX5.
  • CONCLUSIONS: We have identified 25 genes located on chromosome 11q13 that are downregulated in adrenocortical carcinoma and may be candidate tumor suppressor genes.
  • Six of these genes were good diagnostic markers for distinguishing adrenocortical carcinoma from adenoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Chromosomes, Human, Pair 11 / genetics. Genes, Tumor Suppressor / physiology. Loss of Heterozygosity / genetics

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  • (PMID = 18324346.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers
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62. Groussin L, Cazabat L, René-Corail F, Jullian E, Bertherat J: Adrenal pathophysiology: lessons from the Carney complex. Horm Res; 2005;64(3):132-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenal pathophysiology: lessons from the Carney complex.
  • Adrenocorticotropic hormone independent Cushing's syndrome due to primary pigmented nodular adrenocortical disease (PPNAD) is a main characteristic of CNC.
  • PPNAD is a very rare cause of Cushing's syndrome due to a primary bilateral adrenal defect that can be also observed in some patients without other CNC manifestations nor familial history.
  • PRKAR1A is a key component of the cyclic AMP signaling pathway that has been implicated in endocrine tumorigenesis and could, at least partly, function as a tumor suppressor gene.
  • Interestingly, patients with isolated PPNAD and no familial history of CNC can also present a germline de novo mutation of PRKAR1A.
  • Somatic mutations of PRKAR1A have been found in PPNAD as a mechanism of inactivation of the wild-type allele, in a patient already presenting a germline mutation, and in a subset of sporadic secreting adrenocortical adenomas with clinical, hormonal, and pathological features quite similar to PPNAD.
  • This review will summarize the recent findings on CNC from the perspective of the pathophysiology of adrenal Cushing's syndrome and PPNAD.
  • [MeSH-major] Adrenal Cortex Diseases / physiopathology. Adrenal Glands / physiopathology. Multiple Endocrine Neoplasia / physiopathology

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  • [Copyright] Copyright (c) 2005 S. Karger AG, Basel.
  • (PMID = 16192737.001).
  • [ISSN] 0301-0163
  • [Journal-full-title] Hormone research
  • [ISO-abbreviation] Horm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [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
  • [Number-of-references] 31
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63. Matsumoto K, Egawa S, Satoh T, Okuno N, Kaseda S, Baba S: Thoracoscopic transdiaphragmatic adrenalectomy for isolated locally recurrent adrenal carcinoma. Int J Urol; 2005 Dec;12(12):1055-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Thoracoscopic transdiaphragmatic adrenalectomy for isolated locally recurrent adrenal carcinoma.
  • A 58-year-old man who had undergone left adrenalectomy 2 years previously for adrenocortical carcinoma was diagnosed to have a left suprarenal solid mass.
  • Thoracoscopic transdiaphragmatic excision of the tumor was conducted under the diagnosis of isolated local recurrence of adrenal carcinoma.
  • There have been no signs of tumor recurrence during 3 years follow up after surgery.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenalectomy / methods. Adrenocortical Carcinoma / surgery. Neoplasm Recurrence, Local / surgery. Thoracoscopy

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  • (PMID = 16409610.001).
  • [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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64. Sturgeon C, Shen WT, Clark OH, Duh QY, Kebebew E: Risk assessment in 457 adrenal cortical carcinomas: how much does tumor size predict the likelihood of malignancy? J Am Coll Surg; 2006 Mar;202(3):423-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Risk assessment in 457 adrenal cortical carcinomas: how much does tumor size predict the likelihood of malignancy?
  • BACKGROUND: Laparoscopic adrenalectomy for tumors > 6 cm is controversial because of the risk of malignancy, but data to support this position are mostly from small series.
  • STUDY DESIGN: Adrenocortical carcinomas (ACC) recorded in the Surveillance, Epidemiology, and End Results (SEER) database (1988 to 2000) were compared with benign functional or nonfunctional adrenal cortical adenomas (excluding aldosteronomas) operated on at our institution between January 1, 1993, and July 1, 2003.
  • RESULTS: We identified 457 patients with ACC and 47 patients with adrenal cortical adenomas; 376 and 44 neoplasms, respectively, had tumor size data available.
  • Tumor size was larger in ACC (12.0 +/- 5.6 versus 4.2 +/- 1.9 cm, mean +/- SD, p < 0.05).
  • For ACC presenting with local disease, the sensitivity, specificity, and likelihood ratios of tumor size to predict malignancy were 96%, 52%, and 2.0, respectively, for tumors > or = 4 cm; 90%, 80%, and 4.4 for tumors > or = 6 cm; 77%, 95%, and 16.9 for tumors > or = 8 cm; and 55%, 98%, and 24.4 for tumors > or = 10 cm.
  • Assuming a pretest probability of malignancy of 5%, the likelihood ratios derived from this study yield a posttest probability of 10%, 19%, and 47% for cancer in adrenal cortical tumors > or = 4 cm, > or = 6 cm, and > or = 8 cm, respectively.
  • CONCLUSIONS: These data suggest that size is useful for predicting malignancy, and that at a size threshold of > or = 4 cm, the likelihood of malignancy doubles (to 10%) and it is more than ninefold higher for tumors > or = 8 cm (47%).
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Diagnosis, Differential. Female. Humans. Infant. Infant, Newborn. Male. Middle Aged. Neoplasm Staging. Prevalence. Probability. Prognosis. Retrospective Studies. Risk Assessment. SEER Program / statistics & numerical data. Severity of Illness Index

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  • (PMID = 16500246.001).
  • [ISSN] 1072-7515
  • [Journal-full-title] Journal of the American College of Surgeons
  • [ISO-abbreviation] J. Am. Coll. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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65. Lu HS, Gan MF, Chen HS, Huang SQ: Adrenal myelolipoma within myxoid cortical adenoma associated with Conn's syndrome. J Zhejiang Univ Sci B; 2008 Jun;9(6):500-5
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  • [Title] Adrenal myelolipoma within myxoid cortical adenoma associated with Conn's syndrome.
  • The coexistence of myelolipoma within adrenal cortical adenoma is extremely rare, for both tumors present usually as separate entities.
  • To the best of our knowledge, the case we reported here is the first one of myxoid adrenal cortical adenoma associated with myelolipoma reported.
  • Clinical history and laboratory results suggest a metabolic disorder as Conn's syndrome.
  • The patient underwent a left adrenalectomy, and a histopathological study confirmed the mass to be a myxoid adrenal cortical adenoma containing myelolipoma.
  • In the present case report, we also discuss the etiology of simultaneous myelolipoma and adrenal adenoma associated with Conn's syndrome, and the methods of the diagnosis and differential diagnosis.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications. Hyperaldosteronism / complications. Myelolipoma / complications. Neoplasms, Multiple Primary / complications
  • [MeSH-minor] Adult. Biomarkers, Tumor / metabolism. Female. Humans. Inhibins / metabolism. Synaptophysin / metabolism. Tomography, X-Ray Computed. Vimentin / metabolism

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  • (PMID = 18543405.001).
  • [ISSN] 1673-1581
  • [Journal-full-title] Journal of Zhejiang University. Science. B
  • [ISO-abbreviation] J Zhejiang Univ Sci B
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Synaptophysin; 0 / Vimentin; 0 / inhibin-alpha subunit; 57285-09-3 / Inhibins
  • [Number-of-references] 21
  • [Other-IDs] NLM/ PMC2408705
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66. Treska V, Wirthová M, Hadravská S, Mukensnábl P, Kuntscher V, Kreuzberg B, Lisá L, Kozák K: [Giant bilateral adrenal myelolipoma associated with congenital adrenal hyperplasia]. Zentralbl Chir; 2006 Feb;131(1):80-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Giant bilateral adrenal myelolipoma associated with congenital adrenal hyperplasia].
  • BACKGROUND: Myelolipoma is a rare benign tumor formed by mature fat tissue with strata of haematopoiesis.
  • It is usually localized in the region of the adrenal gland.
  • Myelolipomas are mostly clinically inert, only a small number of them are associated with Cushing's type of endocrine disorders, Conn's syndrome, Addison's disease, etc.
  • PATIENT AND METHODS: The authors present a rare case of a giant bilateral myelolipoma emerging out of the adrenal gland cortex in a congenital adrenal hyperplasia, with steroid 21-hydroxylase deficiency, in a woman with pronounced virilism.
  • CONCLUSIONS: The coincidence of myelolipoma and congenital disorder with subsequent overproduction of the adrenocorticotropin hormone and androgens, might be explained by the incipient of myelolipoma through chronic hormonal stimulation of the adrenal gland cortex.
  • [MeSH-major] Adrenal Gland Neoplasms / complications. Adrenal Gland Neoplasms / surgery. Adrenal Hyperplasia, Congenital / complications. Adrenal Hyperplasia, Congenital / surgery. Myelolipoma / complications. Myelolipoma / surgery. Neoplasms, Multiple Primary / complications. Neoplasms, Multiple Primary / surgery
  • [MeSH-minor] Adrenal Glands / pathology. Adrenalectomy. Female. Humans. Middle Aged. Steroid 21-Hydroxylase / blood. Tomography, X-Ray Computed


67. Woods AM, Judd AM: Interleukin-4 increases cortisol release and decreases adrenal androgen release from bovine adrenal cells. Domest Anim Endocrinol; 2008 May;34(4):372-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interleukin-4 increases cortisol release and decreases adrenal androgen release from bovine adrenal cells.
  • ACTH is the primary regulator of adrenal function during acute stress.
  • However, during chronic inflammatory stress additional factors play a major role in the regulation of adrenal secretion.
  • Many cytokines circulate in the blood and are synthesized and released from adrenal tissue.
  • Furthermore, these peptides modify adrenal function.
  • Recently, interleukin-4 (IL-4) was demonstrated to be released from a human adrenal tumor cell line.
  • Therefore, we hypothesized that normal bovine adrenocortical cells could express IL-4 and that this cytokine may modify adrenal function.
  • We determined that IL-4 and IL-4 receptors (IL-4R) are expressed in the bovine adrenal cortex whereas the expression of IL-4 and IL-4R in the adrenal medulla was not apparent.
  • Exposure of dispersed bovine adrenocortical cells isolated from the zona fasciculate to IL-4 did not modify basal release of cortisol.
  • However, the ACTH-stimulated release of cortisol from the bovine adrenal cells was augmented by IL-4.
  • IL-4 exposure had no affect on adrenal androgen release from bovine zona reticularis cells, but IL-4 inhibited the ACTH-stimulated release of adrenal androgens from these cells.
  • The effects of IL-4 on ACTH-stimulated cortisol and adrenal androgen release were dependent upon the IL-4 incubation interval and the IL-4 concentration.
  • Because communication between the immune and endocrine systems is important in inflammatory conditions, IL-4 may play a role in coordinating the adrenal response to inflammatory stress.
  • [MeSH-major] Adrenal Glands / drug effects. Adrenal Glands / metabolism. Androgens / secretion. Cattle / metabolism. Hydrocortisone / secretion. Interleukin-4 / pharmacology

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  • (PMID = 18055157.001).
  • [ISSN] 0739-7240
  • [Journal-full-title] Domestic animal endocrinology
  • [ISO-abbreviation] Domest. Anim. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Receptors, Interleukin-4; 207137-56-2 / Interleukin-4; WI4X0X7BPJ / Hydrocortisone
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68. Horvath A, Giatzakis C, Tsang K, Greene E, Osorio P, Boikos S, Libè R, Patronas Y, Robinson-White A, Remmers E, Bertherat J, Nesterova M, Stratakis CA: A cAMP-specific phosphodiesterase (PDE8B) that is mutated in adrenal hyperplasia is expressed widely in human and mouse tissues: a novel PDE8B isoform in human adrenal cortex. Eur J Hum Genet; 2008 Oct;16(10):1245-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A cAMP-specific phosphodiesterase (PDE8B) that is mutated in adrenal hyperplasia is expressed widely in human and mouse tissues: a novel PDE8B isoform in human adrenal cortex.
  • Bilateral adrenocortical hyperplasia (BAH) is the second most common cause of corticotropin-independent Cushing syndrome (CS).
  • Genetic forms of BAH have been associated with complex syndromes such as Carney Complex and McCune-Albright syndrome or may present as isolated micronodular adrenocortical disease (iMAD) usually in children and young adults with CS.
  • In this study we further characterize this mutation; we also found a novel PDE8B isoform that is highly expressed in the adrenal gland.
  • Tumor tissues from patients with iMAD and no mutations in the coding PDE8B sequence or any other related genes (PRKAR1A, PDE11A) showed downregulated PDE8B expression (compared to normal adrenal cortex).
  • Pde8b is detectable in the adrenal gland of newborn mice and is widely expressed in other mouse tissues.
  • We conclude that PDE8B is another PDE gene linked to iMAD; it is a candidate causative gene for other adrenocortical lesions linked to the cAMP signaling pathway and possibly for tumors in other tissues.

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  • (PMID = 18431404.001).
  • [ISSN] 1018-4813
  • [Journal-full-title] European journal of human genetics : EJHG
  • [ISO-abbreviation] Eur. J. Hum. Genet.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / Z01 HD000642; United States / Intramural NIH HHS / / Z99 HD999999; United States / NICHD NIH HHS / HD / Z01-HD-000642-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Isoenzymes; 4QD397987E / Histidine; 9DLQ4CIU6V / Proline; EC 3.1.4.17 / 3',5'-Cyclic-AMP Phosphodiesterases; EC 3.1.4.17 / PDE8B protein, human
  • [Other-IDs] NLM/ NIHMS101720; NLM/ PMC2671148
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69. Harvey PW, Everett DJ, Springall CJ: Adrenal toxicology: a strategy for assessment of functional toxicity to the adrenal cortex and steroidogenesis. J Appl Toxicol; 2007 Mar-Apr;27(2):103-15
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenal toxicology: a strategy for assessment of functional toxicity to the adrenal cortex and steroidogenesis.
  • The adrenal is the most common toxicological target organ in the endocrine system in vivo and yet it is neglected in regulatory endocrine disruption screening and testing.
  • There has been a recent marked increase in interest in adrenal toxicity, but there are no standardised approaches for assessment.
  • Consequently, a strategy is proposed to evaluate adrenocortical toxicity.
  • Human adrenal conditions are reviewed and adrenocortical suppression, known to have been iatrogenically induced leading to Addisonian crisis and death, is identified as the toxicological hazard of most concern.
  • The consequences of inhibition of key steroidogenic enzymes and the possible toxicological modulation of other adrenal conditions are also highlighted.
  • The proposed strategy involves an in vivo rodent adrenal competency test based on ACTH challenge to specifically examine adrenocortical suppression.
  • The H295R human adrenocortical carcinoma cell line is also proposed to identify molecular targets, and is useful for measuring steroids, enzymes or gene expression.
  • Hypothalamo-pituitary-adrenal endocrinology relevant to rodent and human toxicology is reviewed (with an emphasis on multi-endocrine axis effects on the adrenal and also how the adrenal affects a variety of other hormones) and the endocrinology of the H295R cell line is also described.
  • Chemicals known to induce adrenocortical toxicity are reviewed and over 60 examples of compounds and their confirmed steroidogenic targets are presented, with much of this work published very recently using H295R cell systems.
  • In proposing a strategy for adrenocortical toxicity assessment, the outlined techniques will provide hazard assessment data but it will be regulatory agencies that must consider the significance of such data in risk extrapolation models.
  • The cases of etomindate and aminoglutethimide induced adrenal suppression are clearly documented examples of iatrogenic adrenal toxicity in humans.
  • Environmentally, sentinel species, such as fish, have also shown evidence of adrenal endocrine disruption attributed to exposure to chemicals.
  • The extent of human sub-clinical adrenal effects from environmental chemical exposures is unknown, and the extent to which environmental chemicals may act as a contributory factor to human adrenal conditions following chronic low-level exposures will remain unknown unless purposefully studied.
  • [MeSH-major] Adrenal Cortex / drug effects. Adrenal Cortex Hormones / metabolism. Hormone Antagonists / toxicity. Toxicity Tests / methods. Xenobiotics / toxicity
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Hypothalamo-Hypophyseal System / physiology. Pituitary-Adrenal System / physiology. Rats

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  • (PMID = 17265431.001).
  • [ISSN] 0260-437X
  • [Journal-full-title] Journal of applied toxicology : JAT
  • [ISO-abbreviation] J Appl Toxicol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Hormone Antagonists; 0 / Xenobiotics
  • [Number-of-references] 121
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70. De Padua M, Rajagopal V: Myxoid adrenal adenoma with focal pseudoglandular pattern. Indian J Med Sci; 2008 May;62(5):199-203

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myxoid adrenal adenoma with focal pseudoglandular pattern.
  • Adrenal cortical tumors with myxoid change are rare tumors.
  • A pseudoglandular pattern has been described in 9 of these tumors.
  • We report a case of a myxoid adenoma of the left adrenal gland in a 67-year-old woman, with a focal pseudoglandular pattern involving about 20% of the studied tumor.
  • Rest of the tumor was composed of anastomosing cords of tumor cells.
  • Immunophenotype was consistent with an adrenal tumor, i.e., positive for vimentin, inhibin, and melan A.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / pathology

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  • (PMID = 18579979.001).
  • [ISSN] 0019-5359
  • [Journal-full-title] Indian journal of medical sciences
  • [ISO-abbreviation] Indian J Med Sci
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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71. Jurczyńska J, Stepień T, Lawnicka H, Stepień H, Krupiński R, Kołomecki K, Kuzdak K, Komorowski J: Peripheral blood concentrations of vascular endothelial growth factor and its soluble receptors (R1 and R2) in patients with adrenal cortex tumours treated by surgery. Endokrynol Pol; 2009 Jan-Feb;60(1):9-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Peripheral blood concentrations of vascular endothelial growth factor and its soluble receptors (R1 and R2) in patients with adrenal cortex tumours treated by surgery.
  • INTRODUCTION: Neoangiogenesis appears to be an important event in tumour invasion and in the formation of metastases in many endocrine-related human cancers.
  • The aim of the study was to evaluate the plasma blood concentrations of VEGF, sVEGFR1, and sVEGFR2 in patients with benign and malignant adrenal tumours treated by surgery.
  • MATERIAL AND METHODS: We studied the blood before surgery of 41 patients with adrenal cortex tumours and 10 normal subjects without hormonal or CT/USG pathology of the adrenal glands (controls).
  • We studied the blood after adrenalectomy of 16 patients with tumours of the adrenal cortex.
  • VEGF blood concentrations before surgery did not differ in the patients with the cortical tumours as compared to the controls.
  • After surgery VEGF concentrations decreased among the patients, taken in total, with adrenal cortex tumours and cortical adenomas.
  • After surgery, sVEGFR1 concentrations decreased significantly in the group with cortical adenomas only.
  • CONCLUSIONS: Peripheral blood concentrations of VEGF and its receptors cannot be clinically valuable markers that discriminate between benign and malignant adrenocortical tumours before and after adrenalectomy.
  • [MeSH-major] Adrenal Gland Neoplasms / blood. Adrenal Gland Neoplasms / diagnosis. Biomarkers, Tumor / blood. Vascular Endothelial Growth Factor A / blood. Vascular Endothelial Growth Factor Receptor-1 / blood. Vascular Endothelial Growth Factor Receptor-2 / blood
  • [MeSH-minor] Adrenal Gland Diseases / blood. Adrenal Gland Diseases / diagnosis. Adrenalectomy. Adult. Aged. Diagnosis, Differential. Female. Humans. Male. Middle Aged

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  • (PMID = 19224499.001).
  • [ISSN] 0423-104X
  • [Journal-full-title] Endokrynologia Polska
  • [ISO-abbreviation] Endokrynol Pol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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72. Giordano TJ: Classification of adrenal cortical tumors: promise of the 'molecular' approach. Best Pract Res Clin Endocrinol Metab; 2010 Dec;24(6):887-92

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Classification of adrenal cortical tumors: promise of the 'molecular' approach.
  • Surgical pathologists, using routine histological techniques and tumor morphology, have established the overall taxonomy of adrenal cortical tumors that dictates care of patients with these tumors.
  • However, a novel molecular classification of these tumors would provide numerous benefits to clinicians and patients, including a more accurate classification of diagnostically intermediate tumors, separation of carcinomas into prognostically-relevant subgroups, and optimal selection of therapy.
  • Recent advances towards a molecular classification of adrenal cortical tumors are presented and discussed.
  • [MeSH-major] Adrenal Cortex Neoplasms / classification. Adrenal Cortex Neoplasms / diagnosis
  • [MeSH-minor] Animals. Biomarkers, Tumor / metabolism. Humans. Molecular Diagnostic Techniques

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  • [Copyright] 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 21115157.001).
  • [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
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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73. Fenichel P, Bstandig B, Roger C, Chevallier D, Michels JF, Sadoul JL, Hieronimus S, Brucker-Davis F: Unilateral testicular tumour associated to congenital adrenal hyperplasia: Failure of specific tumoral molecular markers to discriminate between adrenal rest and leydigioma. Ann Endocrinol (Paris); 2008 Nov;69(5):453-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Unilateral testicular tumour associated to congenital adrenal hyperplasia: Failure of specific tumoral molecular markers to discriminate between adrenal rest and leydigioma.
  • Testicular adrenal rest tumours are frequently associated with congenital adrenal hyperplasia (CAH).
  • These ACTH-dependent tumours cannot be easily distinguished histologically from Leydig-cell tumours.
  • We report the case of a 30-year-old man who was explored for infertility, azoospermia and unilateral testicular tumour.
  • High levels of 17-OH progesterone and ACTH, low cortisol and undetectable gonadotropins levels, associated to bilateral adrenal hyperplasia, led to the diagnosis of CAH by 21-OH deficiency with a composite heterozygoty.
  • The testicular tumour was first considered as adrenal rest.
  • However, histological analysis of this unilateral painful tumour showed a steroid-hormone-secreting cell proliferation with atypical and frequent mitosis.
  • To discriminate between a benign adrenal rest tumour and a possible malignant leydigioma, tumoral expression of specific gene products was analyzed by RT-PCR.
  • No 11-beta-hydroxylase nor ACTH receptor mRNAs could be found in the tumour, which did not behave like usual adrenal rest cells.
  • For this unilateral testicular tumour, the lack of adrenal-specific markers associated with a high rate of mitosis and pleiomorphism supported a leydigian origin with malignant potential.
  • However, lack of tumoral LH-R mRNA expression and a tumour-free 3-year follow-up led us to retain the diagnosis of adrenal rest tumour with loss of adrenal gene expression and progressive autonomous behaviour.
  • [MeSH-major] Adrenal Hyperplasia, Congenital / complications. Adrenal Hyperplasia, Congenital / diagnosis. Adrenal Rest Tumor / diagnosis. Leydig Cell Tumor / diagnosis. Testicular Neoplasms / complications. Testicular Neoplasms / diagnosis
  • [MeSH-minor] Adrenal Cortex Hormones / blood. Adrenal Cortex Hormones / genetics. Adult. Anti-Inflammatory Agents / therapeutic use. Azoospermia / etiology. Biomarkers, Tumor. Dexamethasone / therapeutic use. Diagnosis, Differential. Gonadal Steroid Hormones / blood. Gonadal Steroid Hormones / genetics. Gonadotropins / blood. Humans. Infertility, Male / etiology. Male. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Testis / pathology


74. O'Neill CJ, Spence A, Logan B, Suliburk JW, Soon PS, Learoyd DL, Sidhu SB, Sywak MS: Adrenal incidentalomas: risk of adrenocortical carcinoma and clinical outcomes. J Surg Oncol; 2010 Oct 1;102(5):450-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenal incidentalomas: risk of adrenocortical carcinoma and clinical outcomes.
  • INTRODUCTION: The number of incidentally discovered adrenal lesions is increasing due to the widespread use of abdominal imaging.
  • The aim of this study is to determine the risk of malignancy in patients undergoing surgery for adrenal incidentaloma; and to compare clinical outcomes in those with adrenocortical carcinoma (ACC) based on the mode of presentation.
  • Data were retrieved from a prospectively maintained adrenal tumor database.
  • Those with adrenal incidentaloma were selected and histopathology reviewed.
  • Benign, non-functioning adrenocortical adenoma was the most common histopathological finding (46 patients, 63%).
  • CONCLUSIONS: Adrenal incidentalomas have a small but important risk of malignancy.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Incidental Findings

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  • [Copyright] J. Surg. Oncol. 2010;102:450-453. © 2010 Wiley-Liss, Inc.
  • (PMID = 20734420.001).
  • [ISSN] 1096-9098
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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75. Ozimek A, Diebold J, Linke R, Heyn J, Hallfeldt K, Mussack T: Bilateral primary adrenal non-Hodgkin's lymphoma and primary adrenocortical carcinoma--review of the literature preoperative differentiation of adrenal tumors. Endocr J; 2008 Aug;55(4):625-38
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bilateral primary adrenal non-Hodgkin's lymphoma and primary adrenocortical carcinoma--review of the literature preoperative differentiation of adrenal tumors.
  • Most of the adrenal tumors that are incidentally detected are benign adenomas.
  • The incidence of malignant adrenal tumors including adrenocortical carcinoma (ACC) and primary adrenal lymphoma (PAL) is rather low.
  • As many patients with ACC and PAL are diagnosed at an advanced stage of disease, the overall survival time of both entities remains poor.
  • Unfortunately hitherto preoperative diagnosis of potentially malignant adrenal masses is still a main problem in the treatment of adrenal tumors.
  • We present the case of a 57-year-old male patient with ACC and the case of an 87-year-old male patient with PAL and provide a systematic comparison of the clinical and pathological features of both entities.
  • In both cases clinical and radiological features resulted in an initially false diagnosis.
  • The patient with ACC showed tumor progression with local and systemic recurrence despite adjuvant therapy with mitotane and additional surgical therapy.
  • We propose some guidelines for diagnosis and surgical management of adrenal tumors.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenal Gland Neoplasms / diagnosis. Adrenocortical Carcinoma / diagnosis. Lymphoma, Non-Hodgkin / diagnosis

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  • (PMID = 18490838.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 78E4J5IB5J / Mitotane
  • [Number-of-references] 55
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76. Morimoto R, Satoh F, Murakami O, Totsune K, Arai Y, Suzuki T, Sasano H, Ito S, Takahashi K: Immunolocalization of urotensin II and its receptor in human adrenal tumors and attached non-neoplastic adrenal tissues. Peptides; 2008 May;29(5):873-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunolocalization of urotensin II and its receptor in human adrenal tumors and attached non-neoplastic adrenal tissues.
  • In addition to its vascular actions, UII has been shown to have mitogenic effects on tumor growth and some regulatory effects on adrenal steroidogenesis.
  • In the present study, we examined expression of UII and UT-R in human adrenal tumors and attached non-neoplastic adrenal tissues by immunohistochemistry.
  • Both UII and UT-R were immunolocalized in tumor cells of all adrenal tumors examined: 8 cases of cortisol-producing adenomas, 8 cases of aldosterone-producing adenomas, 2 cases of non-functioning adenomas, 17 cases of adrenocortical carcinomas, and 8 cases of pheochromocytomas.
  • In attached adrenals, immunoreactivity for UII was detected in medulla, but much weaker in the cortex than in cortical tumors, suggesting that expression of UII was up-regulated in neoplastic adrenocortical tissues.
  • No significant differences were found in the degree of immunoreactivity for UT-R between the tumors and the attached adrenal tissues.
  • The present study showed that both UII and UT-R were expressed in the adrenal tumors and attached non-neoplastic adrenal tissues, and suggests possible roles of UII and UT-R in tumor growth and/or secretory activities of these tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / metabolism. Adrenal Glands / metabolism. Receptors, G-Protein-Coupled / metabolism. Urotensins / metabolism

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  • (PMID = 17686550.001).
  • [ISSN] 0196-9781
  • [Journal-full-title] Peptides
  • [ISO-abbreviation] Peptides
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, G-Protein-Coupled; 0 / UTS2R protein, human; 0 / Urotensins; 9047-55-6 / urotensin II
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77. Mokos I, Bernat MM, Mareković Z, Pasini J: Virilizing adrenal cancer and bail-out nephrectomy. Coll Antropol; 2005 Dec;29(2):753-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Virilizing adrenal cancer and bail-out nephrectomy.
  • We report a rare case of virilizing adrenal cancer with tumorous invasion of the left renal vein in which a retroperitoneal adrenalectomy with bail-out nephrectomy was performed.
  • A tumor thrombus infiltrated the wall of the left adrenal vein and extended into the left renal vein.
  • To the authors' awareness, this is the first report of a virilizing adrenal cancer with a tumor thrombus infiltration of the renal vein and surgical tendency for kidney preservation.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenal Cortex Neoplasms / surgery. Adrenalectomy. Neoplastic Cells, Circulating / pathology. Nephrectomy. Renal Veins / pathology. Virilism / etiology

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  • (PMID = 16417195.001).
  • [ISSN] 0350-6134
  • [Journal-full-title] Collegium antropologicum
  • [ISO-abbreviation] Coll Antropol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Croatia
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78. Gruschwitz T, Breza J, Wunderlich H, Junker K: Improvement of histopathological classification of adrenal gland tumors by genetic differentiation. World J Urol; 2010 Jun;28(3):329-34

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Improvement of histopathological classification of adrenal gland tumors by genetic differentiation.
  • PURPOSE: There are often problems in differentiating between benign and malignant adrenal gland tumors by imaging and histopathology.
  • On account of considerable differences in the therapy and aftercare of benign and malignant adrenal tumors, correct classification of tumor type is of greatest importance.
  • METHODS: DNA was isolated from tumor areas in paraffin sections and amplified by a modified protocol for DOP-PCR.
  • After labeling of tumor-DNA and normal DNA with biotin-dUTP and digoxigenin-dUTP, respectively, comparative genomic hybridization (CGH) was carried out according to standard protocols.
  • Retrospectively, 26 (16 adenomas and 10 carcinomas) tumors of the adrenal cortex were analyzed.
  • RESULTS: Genetic alterations were found in 5/16 adenomas (31.25%) and in all adrenocortical carcinomas.
  • The mean number of genetic changes per tumor was 8.7 (range 6-12) in carcinomas.
  • The benign cortical tumors present 1.6 changes (range 0-3) per tumor.
  • Only a moderate correlation between number of alterations and size of tumor was seen.
  • CONCLUSIONS: Genetic evaluation facilitates differentiation between adrenal gland tumors.
  • Genetic tests should be used in routine diagnostics of adrenal specimens.
  • Potentially, fine-needle biopsy can be established as standard diagnostics of adrenal tumors with unknown genesis.
  • [MeSH-major] Adenoma / classification. Adenoma / genetics. Adrenal Cortex Neoplasms / classification. Adrenal Cortex Neoplasms / genetics. Carcinoma / genetics
  • [MeSH-minor] Adrenalectomy / methods. Adult. Aged. Biomarkers, Tumor / analysis. Biopsy, Fine-Needle. Chromosome Aberrations. Chromosome Mapping. Cohort Studies. DNA, Neoplasm / analysis. Female. Humans. Immunohistochemistry. Male. Middle Aged. Polymerase Chain Reaction. Retrospective Studies. Sensitivity and Specificity. Statistics, Nonparametric. Young Adult

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  • (PMID = 20364258.001).
  • [ISSN] 1433-8726
  • [Journal-full-title] World journal of urology
  • [ISO-abbreviation] World J Urol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm
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79. Takahashi K, Totsune K, Saruta M, Fukuda T, Suzuki T, Hirose T, Imai Y, Sasano H, Murakami O: Expression of urocortin 3/stresscopin in human adrenal glands and adrenal tumors. Peptides; 2006 Jan;27(1):178-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of urocortin 3/stresscopin in human adrenal glands and adrenal tumors.
  • In the present study, we studied expression of Ucn3/SCP in the normal adrenal and adrenal tumors by radioimmunoassay and reverse transcriptase-polymerase chain reaction (RT-PCR).
  • High concentrations of immunoreactive (IR)-Ucn3 were present in the normal portions of adrenal glands (4.2+/-0.51 pmol/g wet weight, mean+/-S.E.M., n = 14), and the levels were higher than those in the brain.
  • IR-Ucn3 was also detected in the tumor tissues of aldosterone-secreting adenomas (6.2+/-0.6 pmol/g wet weight, n = 10), cortisol-secreting adenomas (5.0+/-1.2 pmol/g wet weight, n = 4), and pheochromocytomas (1.9+/-0.4 pmol/g wet weight, n = 7).
  • Reverse phase high performance liquid chromatography showed that IR-Ucn3 in normal portions of adrenal glands and aldosterone-secreting adenomas was eluted mainly in the positions of Ucn3 and SCP with several minor peaks eluting earlier.
  • The RT-PCR showed expression of Ucn3 mRNA in normal portions of adrenal gland (positive ratio; 4/4), aldosterone-secreting adenomas (3/4), cortisol-secreting adenomas (1/3) and pheochromocytomas (6/7).
  • These findings indicate that Ucn3 is produced in normal adrenal and adrenal tumors (both adrenocortical tumors and pheochromocytomas), and suggest that Ucn3 acts as an autocrine or paracrine regulator in normal adrenal and adrenal tumors.
  • [MeSH-major] Adenoma / metabolism. Adrenal Cortex / metabolism. Adrenal Gland Neoplasms / metabolism. Adrenal Medulla / metabolism. Corticotropin-Releasing Hormone / biosynthesis. Pheochromocytoma / metabolism. Urocortins / biosynthesis

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  • (PMID = 16095756.001).
  • [ISSN] 0196-9781
  • [Journal-full-title] Peptides
  • [ISO-abbreviation] Peptides
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / UCN3 protein, human; 0 / Urocortins; 9015-71-8 / Corticotropin-Releasing Hormone
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80. Grogan RH, Mitmaker E, Vriens MR, Harari A, Gosnell JE, Shen WT, Clark OH, Duh QY: Adrenal incidentaloma: does an adequate workup rule out surprises? Surgery; 2010 Aug;148(2):392-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenal incidentaloma: does an adequate workup rule out surprises?
  • BACKGROUND: Adrenal incidentaloma remains a diagnostic challenge.
  • We sought to determine how accurately these guidelines identify functioning incidentalomas and how often these guidelines result in adrenalectomy for benign tumors.
  • METHODS: We catalogued adrenal incidentalomas from a retrospective review of 500 consecutive adrenalectomies at a single institution.
  • The outcome measures studied were patient demographics, preoperative biochemical analysis, imaging characteristics, tumor size, type of operation performed, and postoperative histologic diagnosis.
  • Size was the only significant characteristic that distinguished cortical cancers from benign adenomas.
  • Only 1 out of 26 functioning tumors was incorrectly identified on preoperative workup.
  • We also found that 25% of cortisol-secreting incidentalomas were cystic, and that benign adenomas accounted for 42% of all tumors resected.
  • CONCLUSION: Current guidelines accurately predict the functional status of adrenal incidentalomas.
  • However, even with the most up-to-date diagnostic tools available, most adrenal incidentalomas resected are benign tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis. Adrenal Gland Neoplasms / surgery. Adrenalectomy. Incidental Findings
  • [MeSH-minor] Adenoma / diagnosis. Adenoma / pathology. Adenoma / physiopathology. Adenoma / surgery. Adrenal Cortex Hormones / secretion. Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / pathology. Adrenal Cortex Neoplasms / physiopathology. Adrenal Cortex Neoplasms / surgery. Adult. Aged. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Practice Guidelines as Topic. Retrospective Studies

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  • [Copyright] Copyright 2010 Mosby, Inc. All rights reserved.
  • (PMID = 20576282.001).
  • [ISSN] 1532-7361
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
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81. Zografos GN, Vasiliadis G, Farfaras AN, Aggeli C, Digalakis M: Laparoscopic surgery for malignant adrenal tumors. JSLS; 2009 Apr-Jun;13(2):196-202
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  • [Title] Laparoscopic surgery for malignant adrenal tumors.
  • Advances in imaging have improved early detection of primary and metastatic adrenal tumors.
  • The laparoscopic approach, the gold standard for benign adrenal diseases, is controversial for malignant adrenal tumors.
  • A prospective randomized study of the role of laparoscopic surgery in adrenal cancer is not feasible because of the rarity of the disease.
  • A review of the literature demonstrates the safety and efficacy of laparoscopic adrenalectomy for solitary adrenal tumors.
  • In primary adrenal malignancies, the laparoscopic approach should be considered cautiously, only when it can achieve complete tumor resection with an intact adrenal capsule.
  • Conversion to an open procedure should be an early decision, prior to tumor morcellation or fracture of the tumor capsule.
  • Patients who have local invasion, tumors that are too large, or require organ resection require an open procedure.

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  • (PMID = 19660215.001).
  • [ISSN] 1086-8089
  • [Journal-full-title] JSLS : Journal of the Society of Laparoendoscopic Surgeons
  • [ISO-abbreviation] JSLS
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 63
  • [Other-IDs] NLM/ PMC3015945
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82. Bertagna X, Groussin L, Libe R, Bertherat J: [Adrenal cortical carcinoma: advances in the pathophysiology and management of this malignancy]. Bull Acad Natl Med; 2008 Jan;192(1):87-102; discussion 102-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Adrenal cortical carcinoma: advances in the pathophysiology and management of this malignancy].
  • [Transliterated title] Le corticosurrénalome: progrès dans la physiopathologie et la prise en charge d'un cancer rare.
  • Adrenal cortical carcinoma is a rare malignancy, with only one or two new cases being diagnosed per million subjects per year.
  • The best chances of cure are obtained when a "localized" tumor can undergo "complete" surgical removal.
  • Most often, however, the diagnosis is made when the tumor is already invasive and non secretory Clinical, hormonal and imaging features, including 18-fluorodeoxyglucose PET scan, can provide strong evidence of malignancy and indicate open surgical excision in expert hands.
  • Recent advances in the genetics of adrenal cortical carcinomas have identified molecular factors that can be used as diagnostic and prognostic markers.
  • A better understanding of the pathophysiology of these tumors is required in order to develop targeted therapies.
  • [MeSH-major] Adrenal Cortex Neoplasms / therapy. Carcinoma / therapy
  • [MeSH-minor] Humans. Neoplasm Staging. Prognosis

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  • (PMID = 18663984.001).
  • [ISSN] 0001-4079
  • [Journal-full-title] Bulletin de l'Académie nationale de médecine
  • [ISO-abbreviation] Bull. Acad. Natl. Med.
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 30
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83. Paton BL, Novitsky YW, Zerey M, Harrell AG, Norton HJ, Asbun H, Kercher KW, Heniford BT: Outcomes of adrenal cortical carcinoma in the United States. Surgery; 2006 Dec;140(6):914-20; discussion 919-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outcomes of adrenal cortical carcinoma in the United States.
  • BACKGROUND: Improvements in the sensitivity of radiographic imaging have lead to an increase in the number of adrenal masses diagnosed.
  • The purpose of this study is to determine if technologic advancements have resulted in the diagnosis of earlier-staged adrenal cortical cancer (ACC) and to determine if the survival of patients with ACC has improved over the past 15 years.
  • RESULTS: We identified 602 patients with a mean age of 53 years and an average tumor size of 11.8 cm.
  • Two hundred thirty-eight (39.5%) patients presented with localized disease (stages I and II), and 311 (52%) patients presented with advanced disease (stages III and IV).
  • Patients with masses less than 5 cm were statistically more likely to have localized disease (P <. 001).
  • Age (P = .10), tumor size (P = .85), tumor stage (P = .45), and 5-year survival (P = .5) did not change over the 15-year study.
  • CONCLUSIONS: Over the 15-year study, patients with ACC were not diagnosed at an earlier stage or with tumors smaller, and survival did not improve.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / pathology. Neoplasm Staging. SEER Program / statistics & numerical data
  • [MeSH-minor] Adrenal Glands / pathology. Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Prognosis. Survival Rate. United States / epidemiology

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  • (PMID = 17188138.001).
  • [ISSN] 0039-6060
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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84. Miyoshi T, Otsuka F, Suzuki J, Inagaki K, Kano Y, Ogura T, Kiura K, Saika T, Makino H: Abrupt enlargement of adrenal incidentaloma: a case of isolated adrenal metastasis. Endocr J; 2005 Dec;52(6):785-8
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  • [Title] Abrupt enlargement of adrenal incidentaloma: a case of isolated adrenal metastasis.
  • A 56-year-old Japanese man was referred for examination of right adrenal tumor (3 cm).
  • He had no apparent preexisting cancer by radiological workup and accordingly, the patient was considered as a nonfunctioning adrenocortical adenoma and scheduled for periodic CT scans every 6 months.
  • However, five months after the initial diagnosis the patient complained of severe right back pain with remarkable enlargement of both adrenals (~20-fold volume).
  • Although the origin of adrenal tumor was uncertain by pathological workup, positron emission tomography (PET) scan with (18)F-2-fluoro-D-deoxyglucose (FDG) eventually revealed a hot spot on left upper lung, which was consistent with a lesion of thickened bulla wall observed by chest CT.
  • The present case is a very rare example of abrupt enlargement of bilateral adrenals due to clinically isolated adrenal metastasis, suggesting the requirement of frequent observation with greatest care regarding morphologic changes of adrenal incidentalomas.
  • [MeSH-major] Adenocarcinoma / secondary. Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / secondary. Adrenocortical Adenoma / diagnosis. Lung Neoplasms / pathology
  • [MeSH-minor] Adrenal Glands / pathology. Adrenal Glands / radiography. Adrenal Glands / ultrasonography. Humans. Hydrocortisone / blood. Incidental Findings. Male. Middle Aged. Positron-Emission Tomography

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  • [CommentIn] Endocr J. 2007 Dec;54(5):829 [17878608.001]
  • (PMID = 16410674.001).
  • [ISSN] 0918-8959
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] WI4X0X7BPJ / Hydrocortisone
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85. Haase M, Willenberg HS: Adrenal cortical tumors and multiple endocrine neoplasia-related syndromes. Minerva Endocrinol; 2009 Jun;34(2):123-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenal cortical tumors and multiple endocrine neoplasia-related syndromes.
  • Relatively frequent, adrenal masses include a multitude of different tumor types: uni- or bilateral hyperplasias, adenomas, and the rare entity of adrenocortical carcinomas.
  • With significant progress in our appreciation of their underlying molecular pathomechanisms and from analysis of affected individuals and their families, a number of inherited diseases and tumor syndromes have been linked to adrenocortical tumorigenesis.
  • These syndromes and diseases include the Carney complex, the McCune-Albright syndrome, multiple endocrine neoplasia type 1, familial adenomatosis coli, congenital adrenal hyperplasia, familial forms of primary aldosteronism, the Beckwith-Wiedemann syndrome, and the Li-Fraumeni syndrome.
  • The key to successful management of these syndromes is identification of patients harboring adrenal tumors within the context of hereditary diseases, since diagnostic procedures, therapy and follow-up may significantly differ from the management of sporadic, isolated adrenal tumors.
  • This review explores the underlying genetic defects, diagnosis and therapy of the major heritable tumor syndromes associated with adrenocortical tumorigenesis.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Multiple Endocrine Neoplasia / genetics. Mutation
  • [MeSH-minor] Adenomatous Polyposis Coli / genetics. Adrenal Hyperplasia, Congenital / genetics. Beckwith-Wiedemann Syndrome / genetics. Fibrous Dysplasia, Polyostotic / genetics. Heart Neoplasms / genetics. Humans. Hyperaldosteronism / genetics. Li-Fraumeni Syndrome / genetics. Multiple Endocrine Neoplasia Type 1 / genetics. Myxoma / genetics. Pigmentation Disorders / genetics

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  • (PMID = 19471237.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Number-of-references] 100
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86. McNicol AM: Assessment of malignancy in adrenal cortical tumors. Endocr Pathol; 2006;17(2):131-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Assessment of malignancy in adrenal cortical tumors.
  • The roles of the pathologist in assessing adrenal cortical tumors are, first, to differentiate adenoma from carcinoma, and, second, to assess prognosis when the diagnosis of malignancy is made.
  • [MeSH-major] Adenoma / pathology. Adrenal Cortex Neoplasms / pathology. Carcinoma / pathology. Neoplasm Invasiveness / diagnosis
  • [MeSH-minor] Biomarkers, Tumor / analysis. Humans. Immunohistochemistry. Molecular Biology. Prognosis

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  • (PMID = 17159245.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 36
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87. Gutenberg A, Lange B, Gunawan B, Larsen J, Brück W, Rohde V, Verheggen R: Spontaneous adrenal hemorrhage: a little-known complication of intracranial tumor surgery. Case report. J Neurosurg; 2007 Jun;106(6):1086-8
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  • [Title] Spontaneous adrenal hemorrhage: a little-known complication of intracranial tumor surgery. Case report.
  • Nontraumatic adrenal hemorrhage in adults is uncommon and unexpected in the context of intracranial surgery.
  • In this brief report they seek to draw attention to this rare but life-threatening complication, because rapid diagnosis can be life-saving.
  • [MeSH-major] Adrenal Gland Diseases / etiology. Adrenalectomy. Hemorrhage / etiology. Intraoperative Complications / etiology. Meningioma / surgery. Neurosurgical Procedures / adverse effects
  • [MeSH-minor] Adrenal Cortex Function Tests. Adrenal Cortex Hormones / therapeutic use. Aged. Humans. Male. Seizures / drug therapy. Seizures / etiology

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  • (PMID = 17564184.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
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88. Baba Y, Beppu T, Imai K, Masuda T, Iyama K, Sasano H, Baba H: A case of adrenal rest tumor of the liver: Radiological imaging and immunohistochemical study of steroidogenic enzymes. Hepatol Res; 2008;38(11):1154-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of adrenal rest tumor of the liver: Radiological imaging and immunohistochemical study of steroidogenic enzymes.
  • A case of adrenal rest tumor in the liver of a 67-year-old female was reported.
  • The tumor appeared on diagnostic imaging as a hypervascular and fat-containing mass at the periphery of right hepatic lobe and required differential diagnosis from hepatocellular carcinoma (HCC).
  • Pathological diagnosis of the intraoperative frozen section taken under laparoscopic liver biopsy could not exclude fat-containing HCC.
  • Histologically, the mass presented features similar to those of the adrenal cortex and was composed of pale cells.
  • Immunohistochemically, the mass expressed the adrenal 4-binding protein and several enzymes involved in the synthesis of adrenocortical steroids.
  • Based on these findings, the hepatic mass was finally diagnosed as an adrenal rest tumor of the liver.

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  • (PMID = 18564144.001).
  • [ISSN] 1386-6346
  • [Journal-full-title] Hepatology research : the official journal of the Japan Society of Hepatology
  • [ISO-abbreviation] Hepatol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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89. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • Tumor size ranged from 0.2 to 5.0 cm (mean 1.5+/-0.8 cm).
  • Final histology described a solitary adenoma in 127 patients and adrenal hyperplasia in 56 patients.
  • The mean operating time was 58+/-32 minutes (range 20-230 minutes) and was associated with sex (p<0.001) but not with the extent of resection (partial vs. total, p=0.51) or with tumor size (<or=1.5 vs. >1.5 cm; p=0.43) or tumor site (p=0.77).
  • 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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90. Qin ZK, Zhou FJ, Dai YP, Chen W, Hou JH, Han H, Liu ZW, Yu SL, Zhang DZ, Yang JA: [Expression and clinical significance of survivin and PTEN in adrenal tumors]. Ai Zheng; 2007 Oct;26(10):1143-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression and clinical significance of survivin and PTEN in adrenal tumors].
  • BACKGROUND & OBJECTIVE: Since the histomorphology of adrenal tumor is very special, it is difficult to assess the malignancy of the tumors.
  • This study was to explore the expression and clinical significance of Survivin and PTEN proteins in adrenal tumors.
  • METHODS: The expression of Survivin and PTEN in 116 specimens of adrenal tumors, including 39 cases of cortex adenoma, 22 cases of cortex adenocarcinoma, 35 cases of pheochromocytoma, and 20 cases of malignant pheochromocytoma, were detected by LSAB immunohistochemistry.
  • The expression intensity of Survivin was correlated to that of PTEN in adrenal tumors (r=-0.486, P<0.05).
  • The expression intensity of Survivin and PTEN in adrenal tumors were not related to patient's age, sex, tumor position, and so on (P>0.05).
  • The expression intensity of Survivin was significantly lower in adrenal cortex adenoma than in adrenal cortex adenocarcinoma (P<0.05), and was significantly lower in pheochromocytoma than in malignant pheochromocytoma (P<0.05).
  • The expression intensity of PTEN was related to the differentiation of adrenal tumor.
  • The expression intensity of PTEN was significantly higher in adrenal cortex adenoma than in adrenal cortex adenocarcinoma (P<0.05), and was significantly higher in pheochromocytoma than in malignant pheochromocytoma (P<0.05).
  • The expression of Survivin protein and PTEN protein was correlated to the prognosis of adrenal cortex adenocarcinoma and malignant pheochromocytoma: the higher the expression intensity of Survivin protein and the lower the expression intensity of PTEN protein, the worse the patient's prognosis (P<0.05).
  • CONCLUSION: The expression of Survivin and PTEN proteins are closely related to the prognosis of adrenal tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / metabolism. Adrenocortical Adenoma / metabolism. Adrenocortical Carcinoma / metabolism. Microtubule-Associated Proteins / metabolism. PTEN Phosphohydrolase / metabolism. Pheochromocytoma / metabolism

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  • (PMID = 17927889.001).
  • [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
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
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91. Giordano TJ: Molecular pathology of adrenal cortical tumors: separating adenomas from carcinomas. Endocr Pathol; 2006;17(4):355-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular pathology of adrenal cortical tumors: separating adenomas from carcinomas.
  • Adrenal cortical carcinoma is a rare but interesting endocrine tumor.
  • Its diagnosis is usually straightforward using morphologic assessment and supplemental immunohistochemistry.
  • Here, the relevant molecular pathology of adrenal cortical tumors is reviewed with special reference to those methods (e.g., DNA microarrays) that hold promise for improved diagnosis and prognosis, and prediction of therapeutic response.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / pathology. Adrenocortical Carcinoma / pathology
  • [MeSH-minor] Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. DNA, Neoplasm / analysis. Diagnosis, Differential. Humans. Immunohistochemistry. Oligonucleotide Array Sequence Analysis. Principal Component Analysis

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  • (PMID = 17525484.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm
  • [Number-of-references] 59
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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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Black adrenal adenoma causing preclinical Cushing's syndrome.
  • Functioning black adrenal adenoma (BAA) rarely causes preclinical Cushing's syndrome (CS).
  • Abdominal computed tomography showed that she had a 15-mm in diameter, round, left adrenal adenoma.
  • The left adrenal adenoma was laparoscopically removed.
  • Examination of the surgical specimen revealed unilateral double adrenal adenomas of the left adrenal gland, one of which was a BAA.
  • There were also foci of myelolipomatous degenerative changes in the tumor.
  • The compact cell zones remained in the adrenal cortex adjacent to the BAA showed atrophic change.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications. Cushing Syndrome / etiology

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  • (PMID = 21319027.001).
  • [ISSN] 2185-2243
  • [Journal-full-title] The Tokai journal of experimental and clinical medicine
  • [ISO-abbreviation] Tokai J. Exp. Clin. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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93. Ait-Ali D, Stroth N, Sen JM, Eiden LE: PACAP-cytokine interactions govern adrenal neuropeptide biosynthesis after systemic administration of LPS. Neuropharmacology; 2010 Jan;58(1):208-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PACAP-cytokine interactions govern adrenal neuropeptide biosynthesis after systemic administration of LPS.
  • We have examined induction of neuropeptide expression in adrenal medulla after treatment of mice with lipopolysaccharide (LPS), a model for septic shock, which activates both immune and stress responses in vivo.
  • Messenger RNAs encoding vasoactive intestinal polypeptide (VIP) and galanin, both modulators of steroidogenesis in neighboring adrenal cortex, are up-regulated at 24 h (eight-fold for VIP and two-fold for galanin) after LPS injection, and remain elevated for the following 24 h.
  • Up-regulation of VIP and galanin by LPS is abrogated in pituitary adenylate cyclase-activating polypeptide (PACAP)-deficient mice, suggesting an interaction between LPS, or LPS-induced cytokines, and PACAP released in adrenal medulla from the splanchnic nerve.
  • Treatment of cultured chromaffin cells with 100 nM PACAP and 10 nM tumor necrosis factor-alpha (TNF-alpha), a cytokine whose production is elevated by LPS, results in long-term synergistic up-regulation of VIP and galanin mRNA.

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  • [ErratumIn] Neuropharmacology. 2010 Jun;58(7):1187
  • (PMID = 19647754.001).
  • [ISSN] 1873-7064
  • [Journal-full-title] Neuropharmacology
  • [ISO-abbreviation] Neuropharmacology
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / / Z01 AG000768-04; United States / Intramural NIH HHS / / Z01 AG000772-01; United States / NIMH NIH HHS / MH / Z01 MH002386; United States / Intramural NIH HHS / / Z01 MH002386-21
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Lipopolysaccharides; 0 / Neuropeptides; 0 / Pituitary Adenylate Cyclase-Activating Polypeptide; 0 / Tumor Necrosis Factor-alpha; 37221-79-7 / Vasoactive Intestinal Peptide; 88813-36-9 / Galanin
  • [Other-IDs] NLM/ NIHMS141772; NLM/ PMC2783598
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94. Iwase K, Nagasaka A, Kato K, Itoh A, Jimbo S, Hibi Y, Kobayashi N, Yamamoto H, Seko T, Miura K: Cu/Zn- and Mn-superoxide dismutase distribution and concentration in adrenal tumors. J Surg Res; 2006 Sep;135(1):150-5
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  • [Title] Cu/Zn- and Mn-superoxide dismutase distribution and concentration in adrenal tumors.
  • The tissue distribution of Cu/Zn- and Mn-superoxide dismutases (SOD) in adrenal tumors was studied by an immunohistochemical technique, and the concentrations of both SODs were measured by a sensitive sandwich enzyme immunoassay technique.
  • In the normal adrenal gland, both Cu/Zn- and Mn-SODs were localized predominantly in the reticular zone of the cortex.
  • Cu/Zn-SOD was stained clearly in the inner fascicular zone of the cortex, but not in the medulla, whereas Mn-SOD was stained weakly in the medulla.
  • In different adrenal tumors, the localization of both stained SODs reflected the origin of the tumor cell.
  • Thus, in one section of a pheochromocytoma only Mn-SOD was stained clearly.
  • The concentrations of both SODs in the tissues of medullary tumors were lower than those in the normal adrenal gland and adrenocortical adenomas.
  • The concentration of Cu/Zn-SOD in the tumor tissue of Cushing's syndrome adenoma was higher, and that of Mn-SOD was lower than the concentrations in the normal adrenal gland.
  • The ratio of the tissue concentrations of Mn-SOD to Cu/Zn-SOD was lower in adrenal medullary tumors and Cushing's syndrome adenomas than in the normal adrenal gland and primary aldosteronism adenomas, indicating the predominance of Cu/Zn-SOD in the former, and Mn-SOD in the latter.
  • These data suggest that the localization of Cu/Zn- and Mn-SODs in adrenal tissues reflects the specificity of the adrenal cells that produce the tissue-specific hormones.
  • An investigation of changes in these enzymes in adrenal tumors may also provide useful information on adrenal tumor cell differentiation.
  • [MeSH-major] Adrenal Cortex / enzymology. Adrenal Cortex Neoplasms / metabolism. Adrenocortical Adenoma / metabolism. Superoxide Dismutase / metabolism

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  • (PMID = 16780879.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.15.1.1 / Superoxide Dismutase
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95. Wang FF, Chang YH, Pan CC, Tu DG, Won JG: Unusual visualization of an adrenal carcinoma on NP-59 scintiscan. J Formos Med Assoc; 2006 Apr;105(4):340-5
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  • [Title] Unusual visualization of an adrenal carcinoma on NP-59 scintiscan.
  • [Iodine-131]6-beta-iodomethylnorcholesterol (NP-59) visualization of adrenocortical carcinoma is unusual.
  • Magnetic resonance imaging disclosed a 9-cm right adrenal mass.
  • NP-59 adrenal scanning displayed unilateral uptake of tracer and no visualization of the contralateral adrenal gland.
  • Exploratory laparotomy revealed adrenocortical carcinoma.
  • Subsequent immunohistochemical studies confirmed that the tumor was capable of producing a mixture of steroids, including testosterone, DHEAS and aldosterone.
  • Visualization of an adrenal tumor on NP-59 scintiscan is an unusual finding, which cannot exclude the possibility of malignancy.

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  • (PMID = 16618615.001).
  • [ISSN] 0929-6646
  • [Journal-full-title] Journal of the Formosan Medical Association = Taiwan yi zhi
  • [ISO-abbreviation] J. Formos. Med. Assoc.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Singapore
  • [Chemical-registry-number] 3XMK78S47O / Testosterone; 4964P6T9RB / Aldosterone; 55623-03-5 / Adosterol; 57B09Q7FJR / Dehydroepiandrosterone Sulfate
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96. 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.
  • MATERIAL AND METHODS: Our series consisted of 74 tumour samples from 164 patients operated for incidentalomas.
  • 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.
  • [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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97. Mattos GE, Lotfi CF: Differences between the growth regulatory pathways in primary rat adrenal cells and mouse tumor cell line. Mol Cell Endocrinol; 2005 Dec 21;245(1-2):31-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differences between the growth regulatory pathways in primary rat adrenal cells and mouse tumor cell line.
  • In this study, DNA synthesis, phosphorylation of ERK1/2 and CREB proteins, as well as induction of c-Fos protein, were examined in rat adrenocortical, glomerulosa and fasciculata/reticularis cells, as well as in the Y1 cell line.
  • We found that FGF2 was mitogenic only in glomerulosa cells and although ACTH did not activate ERK1/2, it did activate CREB protein, indicating efficient transduction of signals initiated in the ACTH receptors of rat adrenocortical cells.
  • The FGF2 activated ERK1/2 in rat adrenal cells by a mechanism that might be modulated by upstream PKA pathway phosphorylation of MEK and despite the nonmitogenic effect of ACTH on rat adrenal cells it effectively induces c-Fos protein.
  • The results presented herein describe distinct differences between the ACTH and FGF2 signal transduction mechanisms seen in adrenocortical cells and those observed in the Y1 cell line, indicating that, in vitro, ACTH blockage of the mitogenic effect occurs in normal adrenal cells after induction of c-Fos protein.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Cell Proliferation. Zona Fasciculata / cytology. Zona Glomerulosa / cytology. Zona Reticularis / cytology
  • [MeSH-minor] Adrenocorticotropic Hormone / pharmacology. Animals. Cell Cycle / physiology. Cell Line, Tumor. Cell Survival. Cells, Cultured. Cyclic AMP Response Element-Binding Protein / metabolism. Cyclic AMP-Dependent Protein Kinases / physiology. Cytochrome P-450 CYP11B2 / genetics. Cytochrome P-450 CYP11B2 / metabolism. Enzyme Activation. Extracellular Signal-Regulated MAP Kinases / metabolism. Fibroblast Growth Factor 2 / pharmacology. Gene Expression Regulation. Male. Mice. Phosphorylation. Proto-Oncogene Proteins c-fos / metabolism. Rats. Rats, Wistar. Signal Transduction

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  • (PMID = 16289304.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Cyclic AMP Response Element-Binding Protein; 0 / Proto-Oncogene Proteins c-fos; 103107-01-3 / Fibroblast Growth Factor 2; 9002-60-2 / Adrenocorticotropic Hormone; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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98. Cardoso CC, Bornstein SR, Hornsby PJ: Optimizing orthotopic cell transplantation in the mouse adrenal gland. Cell Transplant; 2010;19(5):565-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Optimizing orthotopic cell transplantation in the mouse adrenal gland.
  • Orthotopic cell transplantation models are important for a complete understanding of cell-cell interactions as well as tumor biology.
  • In published studies of orthotopic transplantation in the mouse adrenal gland, human neuroblastoma cells have been shown to invade and occupy the adrenal, but in these investigations a true orthotopic model was not established.
  • Here we show an orthotopic model in which transplanted cells are retained within the adrenal gland by formation of a fibrin clot.
  • To establish an appropriate technique, we used brightly fluorescent 10 microm polystyrene microspheres injected into the mouse adrenal gland.
  • When the microspheres were injected in a fibrinogen/thrombin mixture, fluorescence was confined to the adrenal gland.
  • As a model neoplastic cell originating from the cortex of the gland, we used a tumorigenic bovine adrenocortical cell line.
  • When 3 x 10(5) cells were implanted orthotopically, by 16 days the cell mass had expanded and had invaded the cortex, whereas when 1 x 10(5) cells were used, tumor masses were much smaller.
  • When mice were sacrificed at different time points, we found that tumor growth resulting was progressive and that by 26 days cells there was extensive invasion into the cortex or almost complete replacement of the cortex with tumor cells.
  • In summary, the present orthotopic model for intra-adrenal cell transplantation is valuable for investigation of growth of neoplastic cells of both cortical and medullary origin and should be useful for future studies of cortex-medulla interactions.

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  • (PMID = 20525431.001).
  • [ISSN] 1555-3892
  • [Journal-full-title] Cell transplantation
  • [ISO-abbreviation] Cell Transplant
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / AG012287-14; United States / NIA NIH HHS / AG / P01 AG020752-020006; United States / NIA NIH HHS / AG / AG020752-020006; United States / NIA NIH HHS / AG / P01 AG020752; United States / NIA NIH HHS / AG / R37 AG012287-14; United States / NIA NIH HHS / AG / R37 AG012287
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 9001-31-4 / Fibrin; 9001-32-5 / Fibrinogen; EC 3.4.21.5 / Thrombin
  • [Other-IDs] NLM/ NIHMS246503; NLM/ PMC3735364
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99. Vilar L, Freitas Mda C, Canadas V, Albuquerque JL, Botelho CA, Egito CS, Arruda MJ, Moura e Silva L, Coelho CE, Casulari LA, Naves LA: Adrenal incidentalomas: diagnostic evaluation and long-term follow-up. Endocr Pract; 2008 Apr;14(3):269-78
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenal incidentalomas: diagnostic evaluation and long-term follow-up.
  • OBJECTIVE: To evaluate the cause and the clinical and laboratory features of adrenal incidentalomas (AI) in 52 patients and to assess the evolution of nonsurgically treated lesions during long-term follow-up.
  • RESULTS: In our study group, nonfunctioning adenomas were the most frequent cause of AI (42%), followed by cortisol-secreting adenomas (15%), metastatic disease (10%), pheochromocytomas (8%), myelolipomas (6%), cysts (6%), carcinomas (4%), lymphomas (4%), tuberculosis (4%), and aldosteronoma (2%).
  • Carcinomas were the largest adrenal masses (mean diameter, 11.7 +/- 1.3 cm).
  • During follow-up of 21 patients with nonsurgically treated AI for 6 to 36 months (mean, 24.8 +/- 8.9), no patient had tumor reduction or disappearance.
  • After 12 months of follow-up, however, a 45-year-old woman had adrenal mass enlargement from 3.2 cm to 4.4 cm; the excised lesion proved to be an adenoma.
  • Moreover, evidence of cortisol hypersecretion developed after 24 months of follow-up in a 30-year-old man with a 3.5-cm adenoma in the left adrenal gland.
  • CONCLUSION: Our findings demonstrate that most AI are nonfunctioning benign lesions and emphasize the need for long-term follow-up of patients with conservatively managed lesions, in light of the potential for evolution to hormonal hypersecretion or tumor growth.
  • [MeSH-major] Adenoma / diagnosis. Adrenal Gland Neoplasms / diagnosis. Incidental Findings
  • [MeSH-minor] Adrenal Cortex Neoplasms / blood. Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / surgery. Adrenocortical Adenoma / blood. Adrenocortical Adenoma / diagnosis. Adrenocortical Adenoma / surgery. Adult. Brazil. Female. Follow-Up Studies. Humans. Hydrocortisone / blood. Longitudinal Studies. Male. Middle Aged. Prognosis. Retrospective Studies

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  • [CommentIn] Endocr Pract. 2008 Apr;14(3):267-8 [18463031.001]
  • (PMID = 18463032.001).
  • [ISSN] 1934-2403
  • [Journal-full-title] Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
  • [ISO-abbreviation] Endocr Pract
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] WI4X0X7BPJ / Hydrocortisone
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100. Gaisa NT, Klöppel G, Brehmer B, Neulen J, Stephan P, Knüchel R, Donner A: [Virilizing adrenal ganglioneuroma : A rare differential diagnosis in testosterone secreting adrenal tumours]. Pathologe; 2009 Sep;30(5):407-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Virilizing adrenal ganglioneuroma : A rare differential diagnosis in testosterone secreting adrenal tumours].
  • Testosterone secreting tumours of the adrenal glands are usually adrenal carcinomas or adenomas.
  • Here we report the rare case of an adrenal ganglioneuroma with ectopic Leydig cells, a so-called virilizing adrenal ganglioneuroma.
  • Clinically it is characterized by symptoms of virilization, histologically by the occurrence of a population of eosinophilic cells.
  • [MeSH-major] Adrenal Gland Neoplasms / pathology. Adrenal Gland Neoplasms / secretion. Ganglioneuroma / pathology. Ganglioneuroma / secretion. Testosterone / secretion. Virilism / pathology
  • [MeSH-minor] Adrenal Cortex / pathology. Adrenal Gland Diseases / pathology. Adrenal Gland Diseases / surgery. Adrenalectomy. Aged. Biomarkers, Tumor / analysis. Calbindin 2. Choristoma / pathology. Choristoma / surgery. Diagnosis, Differential. Female. Humans. Inhibins / analysis. Laparoscopy. Leydig Cells. Male. S100 Calcium Binding Protein G / analysis. Tomography, X-Ray Computed

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  • (PMID = 19396442.001).
  • [ISSN] 1432-1963
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CALB2 protein, human; 0 / Calbindin 2; 0 / S100 Calcium Binding Protein G; 3XMK78S47O / Testosterone; 57285-09-3 / Inhibins
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