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1. Katsumata N: [Virilizing adrenocortical tumor]. Nihon Rinsho; 2006 May 28;Suppl 1:705-7
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  • [Title] [Virilizing adrenocortical tumor].
  • [MeSH-major] Adrenal Cortex Neoplasms. Virilism
  • [MeSH-minor] Adrenalectomy. Androgens / biosynthesis. Androgens / secretion. Combined Modality Therapy. Diagnosis, Differential. Female. Humans. Mitotane / therapeutic use. Prognosis

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  • (PMID = 16776254.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Androgens; 78E4J5IB5J / Mitotane
  • [Number-of-references] 5
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2. 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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  • [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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3. Beuschlein F, Reincke M: Adrenocortical tumorigenesis. Ann N Y Acad Sci; 2006 Nov;1088:319-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenocortical tumorigenesis.
  • Through the widespread use of imaging techniques with great sensitivity adrenal tumors are often diagnosed as an incidental finding.
  • Although the majority of these adrenal lesions are benign and without evidence of endocrine activity or malignancy, hormone hypersecretion needs to be ruled out by specific tests.
  • In addition to the classical forms of overt adrenocortical hypersecretion, it has become evident over the recent years that modest adrenocortical steroid autonomy as present in normokalemic primary aldosteronism and subclinical Cushing's syndrome is also associated with a significant morbidity.
  • However, detection and differential diagnosis of these subtle changes in adrenal steroidogenesis can pose a diagnostic challenge to the clinician and is dependent on tests with reliable sensitivity and specificity.
  • Regulation of adrenocortical development and growth, which results in clinical symptoms if disrupted, is dependent upon the distinct spatiotemporal expression of a variety of transcription factors as well as stimulation by extra-adrenal peptide hormones.
  • Contributions to the elucidation of growth regulation of the adrenal cortex come from rare familiar syndromes associated with adrenocortical tumors, expression studies of adrenal tumor samples, in vitro studies on adrenocortical tumor cell lines, and mouse models displaying adrenal growth defects.
  • In this review, we will summarize the important molecular aspects of adrenal tumorigenesis and highlight some prospects for clinical applications.
  • [MeSH-major] Adrenal Cortex / pathology. Adrenal Cortex Neoplasms / pathology. Adrenal Cortex Neoplasms / physiopathology
  • [MeSH-minor] Animals. Genes, Tumor Suppressor. Humans. Hyperaldosteronism / genetics. Hyperaldosteronism / pathology. Hyperaldosteronism / physiopathology

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  • (PMID = 17192577.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 112
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4. Schteingart DE, Doherty GM, Gauger PG, Giordano TJ, Hammer GD, Korobkin M, Worden FP: Management of patients with adrenal cancer: recommendations of an international consensus conference. Endocr Relat Cancer; 2005 Sep;12(3):667-80
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  • [Title] Management of patients with adrenal cancer: recommendations of an international consensus conference.
  • Adrenocortical carcinomas are rare, highly malignant tumors that account for only 0.2% of deaths due to cancer.
  • Given the limited number of patients seen in most medical centers with this diagnosis, series usually reported are small and clinical trials not randomized or blinded.
  • In an attempt to answer important questions concerning the management of patients with adrenal cancer, a consensus conference was organized and held at the University of Michigan in Ann Arbor, MI, 11-13 September 2003, with the participation of an international group of physicians who had reported on the largest series of patients with this disease and who had recognized basic and clinical research expertise in adrenal cortical cancer.
  • In addition to setting up guidelines in specific areas of the diagnosis and treatment of adrenal cancer, the conference recommended and initiated the planning of an international prospective trial for treatment of patients with adrenal cancer in stages III and IV.
  • In terms of new therapies, first trials of dendritic cell therapy in human subjects with adrenal cancer have been started, but it is too early to comment on efficacy.
  • There are no clinical gene therapy trials for human adrenal cortical cancer.
  • In addition, there is evidence that histone deacetylase inhibitors can further enhance the rate of adenoviral infectivity in human adrenal cancer cells.
  • The use of these and other agents in the treatment of adrenal cancer should be hypothesis-driven and based on a thorough analysis of tumor biology.
  • [MeSH-major] Adrenal Gland Neoplasms / therapy
  • [MeSH-minor] Humans. Neoplasm Staging

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  • (PMID = 16172199.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / M 01-RR000 42
  • [Publication-type] Consensus Development Conference; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] England
  • [Number-of-references] 75
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5. 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
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  • [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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6. 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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  • [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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7. 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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8. Perrier ND, Kennamer DL, Bao R, Jimenez C, Grubbs EG, Lee JE, Evans DB: Posterior retroperitoneoscopic adrenalectomy: preferred technique for removal of benign tumors and isolated metastases. Ann Surg; 2008 Oct;248(4):666-74
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  • [Title] Posterior retroperitoneoscopic adrenalectomy: preferred technique for removal of benign tumors and isolated metastases.
  • OBJECTIVE: Posterior retroperitoneoscopic adrenalectomy (PRA) is a minimally invasive approach to removal of the adrenal gland.
  • This anatomically direct approach, popularized by Walz, minimizes dissection and affords early access to the adrenal vein.
  • Indications for adrenalectomy were functional tumors in 43 patients (20 pheochromocytomas, 13 Cushing disease or syndrome, and 10 others), nonfunctional cortical adenomas in 4, and isolated adrenal metastases in 15.
  • Mean tumor size was 3.4 cm.
  • PRA may be the preferred technique for removing benign adrenal tumors and isolated metastases.
  • [MeSH-major] Adrenal Gland Neoplasms / surgery. Adrenalectomy / methods. Laparoscopy / methods. Retroperitoneal Space / surgery
  • [MeSH-minor] Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Metastasis. Prospective Studies. Treatment Outcome


9. Moreno S, Guillermo M, Decoulx M, Dewailly D, Bresson R, Proye Ch: Feminizing adreno-cortical carcinomas in male adults. A dire prognosis. Three cases in a series of 801 adrenalectomies and review of the literature. Ann Endocrinol (Paris); 2006 Mar;67(1):32-8
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  • [Title] Feminizing adreno-cortical carcinomas in male adults. A dire prognosis. Three cases in a series of 801 adrenalectomies and review of the literature.
  • We describe the clinical presentation, biochemical features, diagnostic criteria, clinical course and differential diagnosis in three cases of feminizing adreno-cortical carcinoma (FACC) with a review of the literature.
  • Imaging studies suggested malignancy in 3/3 patients by the presence of necrosis, heterogeneity, calcifications, size of the tumor and compression of adjacent organs.
  • Size and weight of the tumors were 30, 20, 15cm and 3750, 480 and 275g respectively.
  • All 3 patients received mitotane and cortisone post-operatively and at follow up (7, 3 and 2 years) all 3 died of the disease.
  • CONCLUSIONS: Feminizing adreno-cortical carcinomas in adults are exceedingly rare (1-2% of adreno-cortical carcinomas).
  • Tumors are huge and even after surgery for cure their prognosis is worse than for other varieties of adreno-cortical carcinomas either secreting or non secreting.
  • Early diagnosis and treatment may improve overall prognosis.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenalectomy. Feminization / etiology

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  • (PMID = 16596055.001).
  • [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 / Estrogens; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone
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10. Bielinska M, Kiiveri S, Parviainen H, Mannisto S, Heikinheimo M, Wilson DB: Gonadectomy-induced adrenocortical neoplasia in the domestic ferret (Mustela putorius furo) and laboratory mouse. Vet Pathol; 2006 Mar;43(2):97-117
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  • [Title] Gonadectomy-induced adrenocortical neoplasia in the domestic ferret (Mustela putorius furo) and laboratory mouse.
  • Sex steroid-producing adrenocortical adenomas and carcinomas occur frequently in neutered ferrets, but the molecular events underlying tumor development are not well understood.
  • Prepubertal gonadectomy elicits similar tumors in certain inbred or genetically engineered strains of mice, and these mouse models shed light on tumorigenesis in ferrets.
  • In mice and ferrets, the neoplastic adrenocortical cells, which functionally resemble gonadal steroidogenic cells, arise from progenitors in the subcapsular or juxtamedullary region.
  • Tumorigenesis in mice is influenced by the inherent susceptibility of adrenal tissue to gonadectomy-induced hormonal changes.
  • Gonadectomy alters the plasma or local concentrations of steroid hormones and other factors that affect adrenocortical tumor development, including inhibins, activins, and Müllerian inhibiting substance.
  • Cases of human adrenocortical neoplasia have been linked to precocious expression of hormone receptors and to mutations that alter the activity of G-proteins or downstream effectors.
  • Whether such genetic changes contribute to tissue susceptibility to neoplasia in neutered ferrets and mice awaits further study.
  • [MeSH-major] Adrenal Cortex Neoplasms / veterinary. Castration / veterinary. Ferrets

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  • (PMID = 16537928.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK52574; United States / NHLBI NIH HHS / HL / HL61006
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 135
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11. 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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12. Doghman M, Cazareth J, Lalli E: The T cell factor/beta-catenin antagonist PKF115-584 inhibits proliferation of adrenocortical carcinoma cells. J Clin Endocrinol Metab; 2008 Aug;93(8):3222-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The T cell factor/beta-catenin antagonist PKF115-584 inhibits proliferation of adrenocortical carcinoma cells.
  • CONTEXT: Mutations of the beta-catenin (CTNNB1) gene are frequently found in adrenocortical tumors.
  • OBJECTIVE: The objective of the study was to investigate the effect of the small-molecule inhibitor of the T cell factor (Tcf)/beta-catenin complex PKF115-584 on beta-catenin-dependent transcription and proliferation of H295R adrenocortical tumor cells, which harbor mutations in CTNNB1 as well as the TP53 tumor suppressor gene.
  • CONCLUSIONS: Inhibitors of the Tcf/beta-catenin complex may prove useful in the treatment of adrenocortical tumors in which multiple genetic alterations have accumulated.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. TCF Transcription Factors / antagonists & inhibitors. beta Catenin / antagonists & inhibitors
  • [MeSH-minor] Cell Proliferation / drug effects. Genes, p53. Humans. Mutation. Tumor Cells, Cultured

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  • (PMID = 18544621.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / TCF Transcription Factors; 0 / beta Catenin
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13. Jeon JH, Kim KY, Kim JH, Baek A, Cho H, Lee YH, Kim JW, Kim D, Han SH, Lim JS, Kim KI, Yoon DY, Kim SH, Oh GT, Kim E, Yang Y: A novel adipokine CTRP1 stimulates aldosterone production. FASEB J; 2008 May;22(5):1502-11
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  • In the present study, we investigated stimulation of aldosterone production by CTRP1, since it was observed that CTRP1 was specifically expressed in the zona glomerulosa of the adrenal cortex, where aldosterone is produced.
  • Increased aldosterone production by CTRP1 in cells of the human adrenal cortical cell line H295R was dose-dependent.
  • [MeSH-minor] Angiotensin II / pharmacology. Animals. Calcium / metabolism. Cytochrome P-450 CYP11B2 / genetics. DNA-Binding Proteins / biosynthesis. Humans. Hypertension / blood. Losartan / pharmacology. Male. Nuclear Receptor Subfamily 4, Group A, Member 1. Nuclear Receptor Subfamily 4, Group A, Member 2. RNA, Messenger / metabolism. Rats. Rats, Sprague-Dawley. Receptors, Cytoplasmic and Nuclear / biosynthesis. Receptors, Steroid / biosynthesis. Transcription Factors / biosynthesis. Tumor Cells, Cultured

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  • (PMID = 18171693.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adipokines; 0 / CTRP1 protein, rat; 0 / DNA-Binding Proteins; 0 / NR4A1 protein, human; 0 / NR4A2 protein, human; 0 / Nr4a1 protein, rat; 0 / Nr4a2 protein, rat; 0 / Nuclear Receptor Subfamily 4, Group A, Member 1; 0 / Nuclear Receptor Subfamily 4, Group A, Member 2; 0 / Proteins; 0 / RNA, Messenger; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Steroid; 0 / Transcription Factors; 11128-99-7 / Angiotensin II; 4964P6T9RB / Aldosterone; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; JMS50MPO89 / Losartan; SY7Q814VUP / Calcium
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14. Walz MK, Alesina PF, Wenger FA, Koch JA, Neumann HP, Petersenn S, Schmid KW, Mann K: Laparoscopic and retroperitoneoscopic treatment of pheochromocytomas and retroperitoneal paragangliomas: results of 161 tumors in 126 patients. World J Surg; 2006 May;30(5):899-908
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  • [Title] Laparoscopic and retroperitoneoscopic treatment of pheochromocytomas and retroperitoneal paragangliomas: results of 161 tumors in 126 patients.
  • MATERIALS: In a prospective clinical study 161 chromaffine neoplasias (134 pheochromocytomas, 27 paragangliomas) were removed endoscopically in 126 patients (67 males, 59 females, age 41.7 +/- 16.4 years; 130 operations).
  • Six patients showed multiple (2-5) tumors.
  • Tumor size ranged from 0.5 to 12 cm (mean 3.5 +/- 1.9 cm).
  • Twenty-four patients had bilateral adrenal diseases; in 14 patients pheochromocytomas were removed on both sides synchroneously.
  • Ten neoplasias were local or loco-regional recurrences (7 pheochromocytomas, 3 paragangliomas).
  • Partial adrenalectomies were performed in 57 operations (in all but one of the patients with bilateral disease).
  • Operating time for unilateral retroperitoneoscopically removed primary pheochromocytomas (n = 113) was 82 +/- 49 minutes (range: 20-300 minutes) and depended on tumor size (< 3 cm vs. > or = 3 cm; P < 0.05) and gender (P < 0.001), but not on extent of resection (partial vs. total, P = 0.266).
  • In 22 of 24 patients with bilateral disease, complete preservation of cortical function was achieved.
  • [MeSH-major] Adrenal Gland Neoplasms / surgery. Adrenalectomy. Laparoscopy. Paraganglioma, Extra-Adrenal / surgery. Pheochromocytoma / surgery. Retroperitoneal Neoplasms / surgery

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  • (PMID = 16617419.001).
  • [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. Pascual Piédrola JI, Cuesta Alcalá JA, Grasa Lanau V, Labairu Huerta L, Napal Lecumberri S, Ipiens Aznar AP: [Laparoscopic adrenalectomy. Reflections after 24 procedures]. Actas Urol Esp; 2007 Feb;31(2):98-105
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  • [Transliterated title] Adrenalectomía laparoscópica. Consideraciones a propósito de 24 procedimientos.
  • Currently it is the technique of choice for the surgical treatment of the adrenal gland.
  • Surgery was bilateral in two cases (one was MEN II, the other bilateral cortical hyperplasia).
  • Clinical diagnosis was: Pheochromocytoma (n = 10), Cushing (n = 6), Conn (n = 4), metastases from lung carcinoma (n = 2) and non-functioning tumor (n = 2).
  • Tumour diameter was between 1.3 and 6 cm (mean 3.08 +/- 1.25 cm) and tumour weight was between 8 and 92g (mean 30.13 +/- 21 g).
  • Cases by histologic type were: nine cortical adenomas, nine pheochromocytomas, three nodular hyperplasias, two metastases from lung carcinoma, and one adrenal pseudocyst.
  • CONCLUSIONS: The adrenal laparoscopic approach is currently the technique of choice for removing adrenal tumours although with malign tumours or over 7 cm in diameter there are some contraindications and disadvantages relative to open surgery.
  • [MeSH-major] Adrenal Gland Diseases / surgery. Adrenalectomy / methods. Laparoscopy

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  • (PMID = 17645088.001).
  • [ISSN] 0210-4806
  • [Journal-full-title] Actas urologicas españolas
  • [ISO-abbreviation] Actas Urol Esp
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
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16. Zeugswetter F, Hoyer MT, Pagitz M, Benesch T, Hittmair KM, Thalhammer JG: The desmopressin stimulation test in dogs with Cushing's syndrome. Domest Anim Endocrinol; 2008 Apr;34(3):254-60
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  • The V3-receptor is overexpressed in pituitary corticotrope tumors and the injection of desmopressin induces a marked ACTH and cortisol release in human patients with pituitary- (PDH), but not adrenal tumor (AT) dependent hyperadrenocorticism.
  • According to standard tests the dogs were divided into 3 groups (group 1=other disease, n=27; group 2=PDH, n=46; group 3=AT, n=7).
  • The results of this study suggest that the desmopressin test could be a useful tool in differentiating pituitary from adrenal dependent Cushing's syndromes.
  • Additional dogs with adrenocortical tumor must be tested in order to recommend its use in clinical practice.
  • [MeSH-major] Cushing Syndrome / diagnosis. Deamino Arginine Vasopressin. Dog Diseases / diagnosis
  • [MeSH-minor] Adrenal Gland Neoplasms / veterinary. Animals. Diagnosis, Differential. Dogs. Hydrocortisone / blood. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / veterinary. Prospective Studies. ROC Curve

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  • (PMID = 17851017.001).
  • [ISSN] 0739-7240
  • [Journal-full-title] Domestic animal endocrinology
  • [ISO-abbreviation] Domest. Anim. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] ENR1LLB0FP / Deamino Arginine Vasopressin; WI4X0X7BPJ / Hydrocortisone
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17. Lapinski JE, Chen L, Zhou M: Distinguishing clear cell renal cell carcinoma, retroperitoneal paraganglioma, and adrenal cortical lesions on limited biopsy material: utility of immunohistochemical markers. Appl Immunohistochem Mol Morphol; 2010 Oct;18(5):414-21
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  • [Title] Distinguishing clear cell renal cell carcinoma, retroperitoneal paraganglioma, and adrenal cortical lesions on limited biopsy material: utility of immunohistochemical markers.
  • This study explores the diagnostic utility of a panel of immunohistochemical markers and emphasizes potential pitfalls in dealing with this differential diagnosis.
  • A tissue microarray with 1 mm tissue cores was constructed to include 21 CCRCC, 19 adrenocortical lesions, and 15 retroperitoneal or mediastinal paragangliomas.
  • The tissue microarray was then immunostained with epithelial, RCC, adrenocortical, and neuroendocrine markers.
  • AE1/3 and epithelial membrane antigen were negative in all adrenocortical lesions and paraganglioma cases, whereas CAM5.2 was positive in 78.9% of adrenocortical lesions and 6.7% of paragangliomas.
  • RCC markers, including RCC Ag, CA9, and CD10, were positive in 76.2%, 85.7%, and 100% of CCRCC cases and were negative in all adrenocortical lesions and paragangliomas.
  • Calretinin and Melan-A were positive in 100% and 94.7% of adrenal, 0% and 14.3% of CCRCC, and 26.7% and 26.7% of paragangliomas.
  • Epithelial markers may be entirely negative in CCRCC, whereas pancytokeratin CAM5.2 is often positive in adrenocortical lesions.
  • Furthermore, neuroendocrine markers are frequently positive in adrenocortical lesions.
  • Therefore, a panel of, rather than single, epithelial, "CCRCC-specific," adrenocortical and neuroendocrine markers should be applied in the differential diagnosis of CCRCC, adrenocortical lesions, and paragangliomas.


18. Zhou J, Ye D, Wu M, Zheng F, Wu F, Wang Z, Li H: Bilateral adrenal tumor: causes and clinical features in eighteen cases. Int Urol Nephrol; 2009;41(3):547-51
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  • [Title] Bilateral adrenal tumor: causes and clinical features in eighteen cases.
  • Bilateral adrenal neoplasms are very rare.
  • Studies have shown that most are metastatic tumors, and clinical presentation varies with tumor type.
  • We retrospectively reviewed medical records of 18 cases of bilateral adrenal tumor in our hospital between 2002 and 2007.
  • The etiology was pheochromocytoma in six, primary lymphoma in four, nonfunctioning cortical adenoma in four, metastatic tumors in two, primary aldosteronism in one, and Cushing syndrome in one.
  • Patients with lymphoma had largest average tumor size.
  • Our findings suggest that pheochromocytoma, primary lymphoma, and nonfunctioning cortical adenoma are common causes of bilateral adrenal tumor.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis

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  • (PMID = 18850298.001).
  • [ISSN] 1573-2584
  • [Journal-full-title] International urology and nephrology
  • [ISO-abbreviation] Int Urol Nephrol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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19. Wagner AS, Fleitz JM, Kleinschmidt-Demasters BK: Pediatric adrenal cortical carcinoma: brain metastases and relationship to NF-1, case reports and review of the literature. J Neurooncol; 2005 Nov;75(2):127-33
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  • [Title] Pediatric adrenal cortical carcinoma: brain metastases and relationship to NF-1, case reports and review of the literature.
  • Adrenal cortical carcinoma (ACC) is a rare childhood neoplasm that seldom manifests brain metastases; hence few papers in the literature focus on neurological manifestations associated with ACC.
  • Although ACC is known to be a signature tumor type in several inherited cancer predisposition syndromes, particularly Li Fraumeni, ACC has not been previously associated with neurofibromatosis, type 1 (NF-1), an inherited disorder with frequent CNS lesions that might prompt concern for metastatic disease by neuroimaging studies.
  • The first child developed metastasis to the brain 4 years after resection of his adrenal primary and 2 and 1 years, respectively, after metastases to the liver and lungs.
  • Disseminated disease prompted concern that her complex intracranial lesions identified by neuroimaging studies might represent brain metastases, but this proved to be NF1-related hamartomatous lesions.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / diagnosis. Adrenocortical Carcinoma / pathology. Brain Neoplasms / secondary. Neurofibromatosis 1
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Chromosome Aberrations. Chylothorax / complications. Chylothorax / surgery. Diagnosis, Differential. Fatal Outcome. Female. Follow-Up Studies. Hamartoma / diagnosis. Humans. Liver Neoplasms / secondary. Lung Neoplasms / secondary. Magnetic Resonance Imaging. Male. Neoplasm Metastasis. Receptor, Epidermal Growth Factor / metabolism. Time Factors. Treatment Outcome

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  • (PMID = 16132517.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Number-of-references] 28
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20. Assié G, Guillaud-Bataille M, Ragazzon B, Bertagna X, Bertherat J, Clauser E: The pathophysiology, diagnosis and prognosis of adrenocortical tumors revisited by transcriptome analyses. Trends Endocrinol Metab; 2010 May;21(5):325-34
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  • [Title] The pathophysiology, diagnosis and prognosis of adrenocortical tumors revisited by transcriptome analyses.
  • Accumulating data on adrenal cortex and adrenocortical tumor transcriptomes have already identified striking transcriptome differences not only between adenoma and carcinoma but also between two sets of carcinoma, which have very different prognoses.
  • These transcriptome data observing adrenocortical tumor phenotype in great but complex detail, combined with genomic and proteomic information, will function for future research investigating the pathophysiology of their tumorigenesis and hormonal secretion.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / physiopathology. Gene Expression Profiling
  • [MeSH-minor] Adenoma / genetics. Adenoma / pathology. Adenoma / physiopathology. Adrenal Cortex / metabolism. Animals. Carcinoma / genetics. Carcinoma / pathology. Carcinoma / physiopathology. Humans. Hyperaldosteronism / physiopathology. Oligonucleotide Array Sequence Analysis. Prognosis

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  • [Copyright] 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20097573.001).
  • [ISSN] 1879-3061
  • [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
  • [Number-of-references] 39
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21. Ikoma A, Saito T, Murata M, Toyoshima H, Nakamura Y, Kawakami M, Sasano H, Ishikawa SE: Bilateral aldosteronoma associated with secondary aldosteronism in a chronic hemodialysis subject. Intern Med; 2010;49(11):1017-21
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  • Abdominal computed tomography revealed bilateral adrenocortical tumors, measuring 34 and 40 mm in diameter in right and left tumors, respectively. (131)I-Adosterol scintigram showed bilateral accumulation.
  • The tumor was encapsulated and well-circumscribed.
  • The majority of the tumor was composed of a dark-brown portion admixed with sporadic foci of golden-yellow portions.
  • The tumor was composed of clear cortical cells in viable portions.
  • Tumor cells demonstrated immunoreactivity for the cholesterol side-chain cleavage enzyme, 3beta-hydroxysteroid dehydrogenase (3beta-HSD II) and 21-hydroxylase, but not 17 alpha-hydroxylase.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis. Adrenocortical Adenoma / diagnosis. Hyperaldosteronism / diagnosis. Kidney Failure, Chronic / therapy. Renal Dialysis / adverse effects

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  • (PMID = 20519819.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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22. Kastelan D, Ravic KG, Cacic M, Stern-Padovanr R, Coric M, Jelcic J, Perkovic Z, Giljevic Z, Aganovic I, Korsic M: Severe postoperative hypoglycemia in a patient with pheochromocytoma and preclinical Cushing's syndrome. Med Sci Monit; 2007 Mar;13(3):CS34-7
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  • BACKGROUND: Postoperative hypoglycemia is not a common complication following the removal of a pheochromocytoma.
  • CASE REPORT: We report a 43-year-old woman with a very rare association of pheochromocytoma and preclinical Cushing's syndrome (PCS) in the same adrenal gland who developed severe postoperative hypoglycemia.
  • In the early postoperative period after surgical removal of right adrenal gland, the patient lapsed into a stuporous state.
  • Pathology revealed medullary pheochromocytoma and a cortical tumor of right adrenal gland.
  • CONCLUSIONS: This report indicates the importance of close monitoring of blood glucose level in a patient with pheochromocytoma after removal of an adrenal gland.
  • [MeSH-major] Adrenal Gland Neoplasms / complications. Cushing Syndrome / complications. Hypoglycemia / complications. Pheochromocytoma / complications. Postoperative Complications


23. Saeger W, Fassnacht M: [Effects of drugs on the adrenal cortex and its tumors]. Pathologe; 2006 Feb;27(1):61-4
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  • [Title] [Effects of drugs on the adrenal cortex and its tumors].
  • [Transliterated title] Wirkungen von Medikamenten auf die Nebennierenrinde und ihre Tumoren.
  • The structure of the normal adrenal cortex is changed by stimulating hormones (ACTH) and inhibiting hormonal drugs (especially glucocorticoids).
  • In the therapy of patients with adrenocortical cancer, mitotane can cause an increase in of necrosis and fibrosis, but also in intracellular lipid.
  • [MeSH-major] Adrenal Cortex / pathology. Adrenal Cortex Neoplasms / drug therapy. Antineoplastic Agents / therapeutic use

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  • (PMID = 16320017.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Hormonal; 0O54ZQ14I9 / Aminoglutethimide; 9002-60-2 / Adrenocorticotropic Hormone
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24. 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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  • [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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25. Rodriguez FJ, Scheithauer BW, Erickson LA, Jenkins RB, Giannini C: Ectopic low-grade adrenocortical carcinoma in the spinal region: immunohistochemical and molecular cytogenetic study of a pediatric case. Am J Surg Pathol; 2009 Jan;33(1):142-8
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  • [Title] Ectopic low-grade adrenocortical carcinoma in the spinal region: immunohistochemical and molecular cytogenetic study of a pediatric case.
  • Ectopic adrenocortical neoplasms arising in the nervous system are very rare.
  • We encountered an intradural, extramedullary case of an adrenocortical neoplasm of indeterminate malignant potential affecting a spinal nerve root in the distal lumbar region of a 5-month-old girl.
  • The tumor in both resections had increased mitotic activity (5/10 high power fields) and MIB-1 labeling indices of 23% and 33% at initial resection and recurrence, respectively.
  • Both tumors demonstrated gains of chromosomes 5 and 12 by interphase cytogenetics, whereas insulin growth factor 2 was identified in the recurrent tumor by immunohistochemistry.
  • This report demonstrates that ectopic adrenocortical tumors in the nervous system may exhibit clinicopathologic and cytogenetic features suggestive of adrenocortical carcinoma.

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  • (PMID = 18941403.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / T32 NS007494; United States / NINDS NIH HHS / NS / T32 NS07494-04
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS396174; NLM/ PMC3427599
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26. Solís-López DR, Rodríguez-Hernández Z, Solís-López DH: Incidental adreno-cortical adenoma, why surgery? a case report. P R Health Sci J; 2010 Jun;29(2):130-2
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  • [Title] Incidental adreno-cortical adenoma, why surgery? a case report.
  • INTRODUCTION: Incidental adrenal tumors are commonly benign, but reports demonstrate that if the characteristics of the tumor are not clear, on images surgery is the procedure of choice.
  • Our objective through this case is to show that laparoscopic adrenalectomy is a safe approach for adrenal incidental tumor regardless of radiological findings.
  • She went for check up and a left adrenal mass on MRI described as myelolipoma was found incidentally.
  • The pathological report was adrenal cortical adenoma with central hemorrhage and not a myelolipoma as described in images on magnetic resonance imaging (MRI).
  • CONCLUSION: The use of imaging for diagnosis, clinical management and decision making is very controversial.
  • Laparoscopic surgery for adrenal masses is a safe procedure for tumors of 6 cm regardless of the radiological description.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenocortical Adenoma / surgery

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  • (PMID = 20496530.001).
  • [ISSN] 0738-0658
  • [Journal-full-title] Puerto Rico health sciences journal
  • [ISO-abbreviation] P R Health Sci J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Puerto Rico
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27. Patel AA, Gupta D, Seligson D, Hattab EM, Balis UJ, Ulbright TM, Kohane IS, Berman JJ, Gilbertson JR, Dry S, Schirripa O, Yu H, Becich MJ, Parwani AV, Shared Pathology Informatics Network: Availability and quality of paraffin blocks identified in pathology archives: a multi-institutional study by the Shared Pathology Informatics Network (SPIN). BMC Cancer; 2007 Feb 28;7:37
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  • METHODS: Four centers evaluated pathology reports (1990-2005) for common and rare tumors to determine the percentage of cases where suitable tissue blocks with tumor were available.
  • Each site generated a list of 100 common tumor cases (25 cases each of breast adenocarcinoma, colonic adenocarcinoma, lung squamous carcinoma, and prostate adenocarcinoma) and 100 rare tumor cases (25 cases each of adrenal cortical carcinoma, gastro-intestinal stromal tumor [GIST], adenoid cystic carcinoma, and mycosis fungoides) using a combination of Tumor Registry, laboratory information system (LIS) and/or SPIN-related tools.
  • Pathologists identified the slides/blocks with tumor and noted first 3 slides with largest tumor and availability of the corresponding block.
  • RESULTS: Common tumors cases (n = 400), the institutional retrieval rates (all blocks) were 83% (A), 95% (B), 80% (C), and 98% (D).
  • Retrieval rate (tumor blocks) from all centers for common tumors was 73% with mean largest tumor size of 1.49 cm; retrieval (tumor blocks) was highest-lung (84%) and lowest-prostate (54%).
  • Rare tumors cases (n = 400), each institution's retrieval rates (all blocks) were 78% (A), 73% (B), 67% (C), and 84% (D).
  • Retrieval rate (tumor blocks) from all centers for rare tumors was 66% with mean largest tumor size of 1.56 cm; retrieval (tumor blocks) was highest for GIST (72%) and lowest for adenoid cystic carcinoma (58%).
  • This study serves to compliment the data from which uniform use of the SPIN query tools by all four centers will be measured to assure and highlight the usefulness of archival material for obtaining tumor tissues for research.

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  • (PMID = 17386082.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01CA091343; United States / NCI NIH HHS / CA / U01 CA091429; United States / NCI NIH HHS / CA / U01CA091429; United States / NCI NIH HHS / CA / P30 CA016042; United States / NCI NIH HHS / CA / U01 CA091343; United States / NCI NIH HHS / CA / UO1CA91338-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1810540
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28. Bhargav PR, Mishra A, Agarwal G, Agarwal A, Verma AK, Mishra SK: Adrenal incidentalomas: experience in a developing country. World J Surg; 2008 Aug;32(8):1802-8
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  • [Title] Adrenal incidentalomas: experience in a developing country.
  • BACKGROUND: The incidence of adrenal incidentalomas is rising worldwide.
  • The aim of this study was to analyze the clinical presentation, functional status, and final diagnosis of adrenal incidentalomas and, in particular, to look into the incidence of adrenal cortical carcinoma (ACC) in large adrenal incidentalomas managed at a tertiary referral hospital in northern India.
  • METHODS: This is a retrospective study (January 1991-December 2005) of 59 patients with adrenal incidentaloma managed at our department.
  • The mean tumor diameter was 7.8 +/- 4.0 cm.
  • Six patients in which the mass was ultimately found to arise from extra-adrenal tissue were excluded from final analysis RESULTS: Mean age of the patients was 46 +/- 12 years (M:F = 1:1.1).
  • The incidence of functioning tumors was 41.5% (hypercatecholinism 37.7 % and hypercortisolism 1.9%).
  • The important final pathology included ACC (7.5%), pheochromocytoma (PCC) (43%), adrenal cysts (13.2%), myelolipoma (11.3%), and inflammatory lesions (9.4%).
  • CONCLUSION: In our experience, the incidence of PCC was high among large adrenal incidentalomas while that of ACC was lower than expected.
  • [MeSH-major] Adenoma / epidemiology. Adrenal Gland Neoplasms / epidemiology
  • [MeSH-minor] Adolescent. Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / epidemiology. Adrenal Cortex Neoplasms / surgery. Adult. Aged. Aged, 80 and over. Developing Countries. Diagnostic Imaging. Female. Humans. Incidence. Incidental Findings. India / epidemiology. Male. Middle Aged. Retrospective Studies. Treatment Outcome

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  • (PMID = 18425548.001).
  • [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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29. Pinto EM, Billerbeck AE, Fragoso MC, Mendonca BB, Latronico AC: Deletion mapping of chromosome 17 in benign and malignant adrenocortical tumors associated with the Arg337His mutation of the p53 tumor suppressor protein. J Clin Endocrinol Metab; 2005 May;90(5):2976-81
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  • [Title] Deletion mapping of chromosome 17 in benign and malignant adrenocortical tumors associated with the Arg337His mutation of the p53 tumor suppressor protein.
  • The human p53 tumor suppressor gene is located at the short arm of chromosome 17.
  • A germinative mutation (Arg337His) in the tetramerization domain of p53 has been frequently identified in Brazilian children with sporadic adrenocortical tumors.
  • In the present study, we performed deletion mapping of chromosome 17 in 30 adrenocortical tumors from 29 Brazilian patients (15 children and 14 adults).
  • One boy had bilateral adrenocortical tumor.
  • Loss of heterozygosity analysis using six polymorphic microsatellite markers disclosed loss of the entire chromosome 17 in 18 tumors (10 adenomas and eight carcinomas) from 17 patients.
  • The concomitant loss of chromosomes 2, 9, 11, and 17 was evidenced exclusively in malignant tumors.
  • Therefore, chromosomal instability involving three or more chromosomes may contribute to define the malignant adrenocortical lesions.
  • In addition, the isolated loss of the entire chromosome 17 did not correlate with aggressive tumor behavior in these patients with adrenocortical tumors.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Chromosome Mapping. Chromosomes, Human, Pair 17. Genes, p53. Mutation


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

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  • (PMID = 19270420.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] EC 1.1.1.145 / 3 beta-hydroxysteroid dehydrogenase type II; EC 1.1.1.145 / Progesterone Reductase; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase
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31. Kimura M, Irie A, Minei S, Ishii J, Okawa A, Takashima R, Kadowaki K, Morinaga S, Baba S: [A case of adrenocortical adenoma coexisting with gastrointestinal stromal tumor]. Hinyokika Kiyo; 2007 Aug;53(8):551-5
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  • [Title] [A case of adrenocortical adenoma coexisting with gastrointestinal stromal tumor].
  • A 48-year-old man was referred to our institute for the evaluation of a concomitant gastric submucosal tumor and right adrenal tumor, incidentally found by ultrasound examination.
  • Computed tomography showed a mass with a diameter of 6 cm adjacent to the stomach and the right adrenal tumor with a diameter of 3 cm.
  • These tumors had similar characteristics in both plain and enhanced imagings.
  • By magnetic resonance imaging, the intensity of the right adrenal tumor was equivalent to the liver in both T1 and T2 weighted images.
  • On the other hand, the gastric submucosal tumor showed low intensity in T1 weighted images and high intensity in T2 weighted images.
  • An adosterol scintigram showed slight accumulation at the region of adrenal tumor.
  • Pathological diagnosis of the adrenal tumor was a cortical adenoma, and that of the gastric submucosal tumor was gastrointestinal stromal tumor (GIST).
  • The gastric tumor was immunohistochemically stained positive with the C-kit and CD34 and negative for s-100 protein and desmin.
  • Histopathological diagnosis was coincident with gastric GIST and right adrenocortical adenoma, and the GIST was diagnosed as a high risk tumor because its diameter was over 5 cm.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenocortical Adenoma / surgery. Gastrointestinal Stromal Tumors / surgery. Laparoscopy. Stomach Neoplasms / surgery

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  • (PMID = 17874546.001).
  • [ISSN] 0018-1994
  • [Journal-full-title] Hinyokika kiyo. Acta urologica Japonica
  • [ISO-abbreviation] Hinyokika Kiyo
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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32. Polamaung W, Wisedopas N, Vasinanukorn P, Pak-art P, Snabboon T: Asymptomatic bilateral giant adrenal myelolipomas: case report and review of literature. Endocr Pract; 2007 Oct;13(6):667-71
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  • [Title] Asymptomatic bilateral giant adrenal myelolipomas: case report and review of literature.
  • OBJECTIVE: To describe an unusual case of bilateral giant adrenal masses caused by a primary adrenal myelolipoma.
  • METHODS: We present the clinical, laboratory, and pathologic findings in a 32-year-old man with bilateral adrenal masses.
  • A computed tomographic scan of the abdomen disclosed bilateral adrenal masses; the one on the left was approximately 27 by 24 by 12 cm, and the one on the right side was 9 by 5 by 5 cm.
  • An endocrinologic evaluation revealed no evidence of adrenal cortical or medullary functional abnormalities.
  • CONCLUSION: Myelolipoma is a relatively rare benign tumor of the adrenal glands composed of adipose cells and mature hematopoietic elements.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis. Myelolipoma / diagnosis

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  • (PMID = 17954426.001).
  • [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] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 31
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33. Ziegler CG, Brown JW, Schally AV, Erler A, Gebauer L, Treszl A, Young L, Fishman LM, Engel JB, Willenberg HS, Petersenn S, Eisenhofer G, Ehrhart-Bornstein M, Bornstein SR: Expression of neuropeptide hormone receptors in human adrenal tumors and cell lines: antiproliferative effects of peptide analogues. Proc Natl Acad Sci U S A; 2009 Sep 15;106(37):15879-84
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  • [Title] Expression of neuropeptide hormone receptors in human adrenal tumors and cell lines: antiproliferative effects of peptide analogues.
  • A hallmark of adrenocortical tumor formation is the aberrant expression of peptide receptors relating to uncontrolled cell proliferation and hormone overproduction.
  • Our microarray results have also demonstrated a differential expression of neuropeptide hormone receptors in tumor subtypes of human pheochromocytoma.
  • In light of these findings, we performed a comprehensive analysis of relevant receptors in both human adrenomedullary and adrenocortical tumors and tested the antiproliferative effects of peptide analogues targeting these receptors.
  • Specifically, we examined the receptor expression of somatostatin-type-2 receptor, growth hormone-releasing hormone (GHRH) receptor or GHRH receptor splice variant-1 (SV-1) and luteinizing hormone-releasing hormone (LHRH) receptor at the mRNA and protein levels in normal human adrenal tissues, adrenocortical and adrenomedullary tumors, and cell lines.
  • Cytotoxic derivatives of somatostatin AN-238 and, to a lesser extent, AN-162, reduced cell numbers of uninduced and NGF-induced adrenomedullary pheochromocytoma cells and adrenocortical cancer cells.
  • Both the splice variant of GHRH receptor SV-1 and the LHRH receptor were also expressed in adrenocortical cancer cell lines but not in the pheochromocytoma cell line.
  • The GHRH receptor antagonist MZ-4-71 and LHRH antagonist Cetrorelix both significantly reduced cell growth in the adrenocortical cancer cell line.
  • In conclusion, the expression of receptors for somatostatin, GHRH, and LHRH in the normal human adrenal and in adrenal tumors, combined with the growth-inhibitory effects of the antitumor peptide analogues, may make possible improved treatment approaches to adrenal tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / drug therapy. Adrenal Gland Neoplasms / metabolism. Neuropeptides / pharmacology. Receptors, Neuropeptide / metabolism
  • [MeSH-minor] 2-Hydroxyphenethylamine / analogs & derivatives. 2-Hydroxyphenethylamine / pharmacology. Adrenal Glands / metabolism. Aniline Compounds / pharmacology. Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Cytostatic Agents / pharmacology. Doxorubicin / analogs & derivatives. Doxorubicin / pharmacology. Gene Expression. Humans. Oligonucleotide Array Sequence Analysis. PC12 Cells. Pyrroles / pharmacology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Receptors, LHRH / genetics. Receptors, LHRH / metabolism. Receptors, Somatostatin / genetics. Receptors, Somatostatin / metabolism. Somatostatin / analogs & derivatives. Somatostatin / pharmacology

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  • (PMID = 19717419.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AN 238; 0 / Aniline Compounds; 0 / Cytostatic Agents; 0 / Neuropeptides; 0 / Pyrroles; 0 / RNA, Messenger; 0 / Receptors, LHRH; 0 / Receptors, Neuropeptide; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 2PK59M9GFF / vapreotide; 33189-65-0 / N-(2-diethylaminoethyl)-N-(2-hydroxy-2-phenylethyl)-2,5-dichloroaniline; 51110-01-1 / Somatostatin; 7568-93-6 / 2-Hydroxyphenethylamine; 80168379AG / Doxorubicin
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34. Liao CH, Chueh SC, Lai MK, Hsiao PJ, Chen J: Laparoscopic adrenalectomy for potentially malignant adrenal tumors greater than 5 centimeters. J Clin Endocrinol Metab; 2006 Aug;91(8):3080-3
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  • [Title] Laparoscopic adrenalectomy for potentially malignant adrenal tumors greater than 5 centimeters.
  • PURPOSE: Laparoscopic adrenalectomy (LA) is controversial for large, potentially malignant tumors.
  • We report a series of LA or hand-assisted LA for large (>5 cm) adrenal tumors.
  • PATIENTS AND METHODS: Among 210 LAs performed in 6 yr, 39 patients had potentially malignant tumors greater than 5 cm in diameter.
  • The mean tumor size was 6.2 cm (range, 5-12 cm), operative time 207 min (115-315 min), and blood loss 75 ml (minimal-1400 ml).
  • Preoperatively there were 27 nonfunctioning tumors, seven pheochromocytomas, three cortisol-secreting tumors, and two virilizing tumors.
  • Final pathology revealed eight malignant (four adrenocortical carcinomas and four metastatic carcinomas) and 31 benign tumors (14 cortical adenomas, eight pheochromocytomas, six myelolipomas, and three ganglioneuromas).
  • Four patients (two adrenocortical carcinomas, one metastatic hepatoma, and one lymphoma) died 24, 10, 9, and 3 months after surgery, respectively.
  • Only the tumor size was larger and length of postoperative hospital stay longer for those in the hand-assisted group.
  • CONCLUSIONS: LA is a reasonable option for selected large adrenal tumors when complete resection is technically feasible and there is no evidence of local invasion.
  • Hand-assisted LA is a good alternative to open conversion if a difficult dissection is encountered intraoperatively.
  • [MeSH-major] Adrenal Gland Neoplasms / pathology. Adrenal Gland Neoplasms / surgery. Adrenalectomy / methods. Laparoscopy
  • [MeSH-minor] Adenoma / pathology. Adenoma / surgery. Adolescent. Adult. Aged. Child. Child, Preschool. Ganglioneuroma / pathology. Ganglioneuroma / surgery. Humans. Middle Aged. Myelolipoma / pathology. Myelolipoma / surgery. Neoplasm Metastasis. Pheochromocytoma / pathology. Pheochromocytoma / surgery. Prognosis. Survival Rate

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  • [CommentIn] Nat Clin Pract Endocrinol Metab. 2007 Mar;3(3):210-1 [17262068.001]
  • (PMID = 16720665.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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35. Mahe E, El-Shinnawy I: A "tumour trifecta:" myelolipomata arising within an adrenocortical adenoma ipsilateral to a synchronous clear cell renal cell carcinoma. Malays J Pathol; 2010 Dec;32(2):123-8
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  • [Title] A "tumour trifecta:" myelolipomata arising within an adrenocortical adenoma ipsilateral to a synchronous clear cell renal cell carcinoma.
  • We present an intriguing case of adrenal myelolipomata occurring within an adrenocortical adenoma in concert with an ipsilateral clear cell renal cell carcinoma.
  • Computed tomography indicated a 2.5 cm right renal mass as well as a 5 cm right adrenal mass.
  • The adrenal mass was a cortical adenoma with solid and nested patterns, with discrete zones consisting of erythroid, myeloid and megakaryocytic cells intermixed with mature adipocytes.
  • The solid tumour component was strongly positive for vimentin, inhibin and CD56, focally positive for low-molecular-weight cytokeratin (Cam 5.2), calretinin and CD10 (chiefly in the myelolipomatous zones), and negative for chromogranin, S100, HMB-45, melan-A (A103), Mart-1, synaptophysin, SMA, CK7, CK20, ER, PR, TTF-1, CD99 and GCDFP (BRST-2).
  • Ki67 (MIB1) staining indicated a low tumour proliferation index.
  • We also present a relevant review of the literature pertaining to adrenal lesions.
  • In particular, we emphasize the epidemiological, histological and immunohistochemical features that are helpful in determining the origin and malignant potential of adrenal lesions.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / pathology. Carcinoma, Renal Cell / pathology. Kidney Neoplasms / pathology. Myelolipoma / pathology. Neoplasms, Multiple Primary / pathology
  • [MeSH-minor] Biomarkers, Tumor / analysis. Female. Humans. Immunohistochemistry. Middle Aged


36. Taniguchi Y, Horio H, Suzuki Y, Nakamura H: Bronchoplastic lobectomy with wide wedge resection for lung cancer with long-term steroid medication. Ann Thorac Cardiovasc Surg; 2007 Dec;13(6):403-6
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  • A bronchoscopy revealed a tumor nearly obstructing the right upper lobe bronchus.
  • Bronchoplastic lobectomy with wide wedge resection is a useful procedure in cases with risk factors of anastomotic dehiscence, such as after induction therapy or during long-term administration of adrenal cortical steroids.
  • [MeSH-major] Dermatitis, Exfoliative / drug therapy. Lung Neoplasms / surgery. Pneumonectomy / methods

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  • (PMID = 18292724.001).
  • [ISSN] 1341-1098
  • [Journal-full-title] Annals of thoracic and cardiovascular surgery : official journal of the Association of Thoracic and Cardiovascular Surgeons of Asia
  • [ISO-abbreviation] Ann Thorac Cardiovasc Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Glucocorticoids; 9PHQ9Y1OLM / Prednisolone
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37. Puwanant S, Click RL, Kalra M, Farley DR, Chandrasekaran K: Incidental detection of inferior vena caval dissection by intraoperative high frequency vascular duplex ultrasonography. Echocardiography; 2007 Mar;24(3):269-71
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  • We first report a case of IVC dissection detected by high frequency surface ultrasonography following tumor thrombectomy of adrenal cortical carcinoma.
  • [MeSH-minor] Adrenal Gland Neoplasms / complications. Adrenal Gland Neoplasms / surgery. Aged. Humans. Incidental Findings. Intraoperative Care. Male. Thrombectomy

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  • (PMID = 17313640.001).
  • [ISSN] 0742-2822
  • [Journal-full-title] Echocardiography (Mount Kisco, N.Y.)
  • [ISO-abbreviation] Echocardiography
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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38. Soon PS, Libe R, Benn DE, Gill A, Shaw J, Sywak MS, Groussin L, Bertagna X, Gicquel C, Bertherat J, McDonald KL, Sidhu SB, Robinson BG: Loss of heterozygosity of 17p13, with possible involvement of ACADVL and ALOX15B, in the pathogenesis of adrenocortical tumors. Ann Surg; 2008 Jan;247(1):157-64
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  • [Title] Loss of heterozygosity of 17p13, with possible involvement of ACADVL and ALOX15B, in the pathogenesis of adrenocortical tumors.
  • OBJECTIVE: To determine the minimal common region of loss on 17p13 in a cohort of adrenocortical carcinomas (ACCs) (defined by a Weiss score > or =3) and adrenocortical adenomas (ACAs) (defined by a Weiss score <3) and subsequently to assess 3 genes in this region that could be involved in adrenocortical tumorigenesis.
  • METHODS: Using 12 microsatellite markers across 17p13, LOH analysis was performed on 37 paired blood and adrenocortical tumor samples (23 ACC and 14 ACA samples) to determine the minimal common region of loss for ACCs and ACAs.
  • [MeSH-major] Acyl-CoA Dehydrogenases / genetics. Adrenal Cortex Neoplasms / genetics. Arachidonate 12-Lipoxygenase / genetics. Chromosomes, Human, Pair 17. Genes, Tumor Suppressor. Loss of Heterozygosity

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  • (PMID = 18156936.001).
  • [ISSN] 0003-4932
  • [Journal-full-title] Annals of surgery
  • [ISO-abbreviation] Ann. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers; EC 1.13.11.31 / Arachidonate 12-Lipoxygenase; EC 1.3.- / Acyl-CoA Dehydrogenases
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39. 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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40. Koga Y, Ohe K, Gondo S, Watanabe T, Sakamoto R, Nomura M, Okabe T, Kawazoe N, Sasano K, Yanase T: [MEN type I presenting hypokalemia and hypertension, complicated with acromegaly, adrenal cortical tumor and rectal carcinoid tumor]. Nihon Naika Gakkai Zasshi; 2006 Nov 10;95(11):2298-301
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  • [Title] [MEN type I presenting hypokalemia and hypertension, complicated with acromegaly, adrenal cortical tumor and rectal carcinoid tumor].
  • [MeSH-major] Acromegaly / etiology. Adrenocortical Adenoma / complications. Carcinoid Tumor / complications. Growth Hormone-Secreting Pituitary Adenoma / complications. Hypertension / etiology. Hypokalemia / etiology. Multiple Endocrine Neoplasia Type 1 / complications. Rectal Neoplasms / complications


41. Nogueira EF, Vargas CA, Otis M, Gallo-Payet N, Bollag WB, Rainey WE: Angiotensin-II acute regulation of rapid response genes in human, bovine, and rat adrenocortical cells. J Mol Endocrinol; 2007 Dec;39(6):365-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Angiotensin-II acute regulation of rapid response genes in human, bovine, and rat adrenocortical cells.
  • Angiotensin-II (Ang-II) regulates adrenal steroid production and gene transcription through several signaling pathways.
  • Microarray analyses were performed using samples from control and Ang-II (10 nM)-treated (1 h) cells from human adrenocortical tumor cell line H295R, and primary adrenal glomerulosa cells from bovine and rat, applied respectively to human, bovine, and rat chips. qPCR was performed to confirm up-regulation of selected genes using mRNA.
  • The Ang-II gene targets have been defined in three different adrenocortical model systems.
  • Several of the listed genes have previously been described as being key regulators of adrenocortical function.
  • The presence of adrenal cell common genes in such distinct cell models strengthens the hypothesis that these genes are regulators of aldosterone production.
  • [MeSH-major] Adrenal Cortex / cytology. Adrenal Cortex / drug effects. Angiotensin II / pharmacology. Gene Expression Regulation / drug effects
  • [MeSH-minor] Animals. Cattle. Cell Line, Tumor. Female. Humans. Male. Microarray Analysis. Rats. Species Specificity. Zona Glomerulosa / cytology. Zona Glomerulosa / drug effects. Zona Glomerulosa / metabolism

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  • (PMID = 18055484.001).
  • [ISSN] 1479-6813
  • [Journal-full-title] Journal of molecular endocrinology
  • [ISO-abbreviation] J. Mol. Endocrinol.
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE8442
  • [Grant] United States / NIDDK NIH HHS / DK / DK43140; United States / NHLBI NIH HHS / HL / HL70046
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 11128-99-7 / Angiotensin II
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42. 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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43. Slater EP, Diehl SM, Langer P, Samans B, Ramaswamy A, Zielke A, Bartsch DK: Analysis by cDNA microarrays of gene expression patterns of human adrenocortical tumors. Eur J Endocrinol; 2006 Apr;154(4):587-98
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  • [Title] Analysis by cDNA microarrays of gene expression patterns of human adrenocortical tumors.
  • OBJECTIVES: Adrenocortical carcinoma (ACC) is a rare malignant neoplasm with extremely poor prognosis.
  • The molecular mechanisms of adrenocortical tumorigenesis are still not well understood.
  • The comparative analysis by cDNA microarrays of gene-expression patterns of benign and malignant adrenocortical tumors allows us to identify new tumor-suppressor genes and proto-oncogenes underlying adrenocortical tumorigenesis.
  • DESIGN AND METHODS: Total RNA from fresh-frozen tissue of 10 ACC and 10 benign adrenocortical adenomas was isolated after histologic confirmation of neoplastic cellularity of at least 85%.
  • The reference consisted of pooled RNA of 10 normal adrenal cortex samples.
  • Amplified RNA of tumor and reference was used to synthesize Cy3- and Cy5-fluorescently labeled cDNA in a flip-color technique.
  • RESULTS: The comparative analysis of gene expression revealed many genes with more than fourfold expression difference between ACC and normal tissue (42 genes), cortical adenoma and normal tissue (11 genes), and ACC and cortical adenoma (21 genes) respectively.
  • As confirmed by real-time PCR, the IGF2 gene was significantly upregulated in ACCs versus cortical adenomas and normal cortical tissue.
  • Genes that were downregulated in adrenocortical tumors included chromogranin B and early growth response factor 1.
  • CONCLUSIONS: Comprehensive expression profiling of adrenocortical tumors by the cDNA microarray technique is a very powerful tool to elucidate the molecular steps associated with the tumorigenesis of these ill-defined neoplasms.

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  • (PMID = 16556722.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 4964P6T9RB / Aldosterone; WI4X0X7BPJ / Hydrocortisone
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44. Bouasker I, Zoghlami A, Farah Klibi F, Smaali I, El Ouaer MA, Zermani R, Dziri C: Adreno-cortical oncocytoma: a case report. Tunis Med; 2010 May;88(5):353-6
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  • [Title] Adreno-cortical oncocytoma: a case report.
  • BACKGROUND: Adrenal oncocytoma is a very rare lesion, non functioning and benignin most cases.
  • AIM: This study aimed to report a new case of adrenal oncocytic tumor with uncertain malignant potential.
  • Ultrasonography and omputed tomography scan revealed a large mass in the right adrenal gland with extension to the right kidney.
  • The diagnosis of adrenal oncocytoma with malignant potential was confirmed by pathology.
  • He was followed up for 8 months, no tumor recurrence detected.
  • CONCLUSION: Adreno cortical oncocytoma is a rare tumor.
  • [MeSH-major] Adenoma, Oxyphilic / pathology. Adrenal Gland Neoplasms / pathology. Kidney Cortex / pathology. Kidney Neoplasms / pathology

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  • (PMID = 20517834.001).
  • [ISSN] 0041-4131
  • [Journal-full-title] La Tunisie médicale
  • [ISO-abbreviation] Tunis Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Tunisia
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45. 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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46. Sutter JA, Grimberg A: Adrenocortical tumors and hyperplasias in childhood--etiology, genetics, clinical presentation and therapy. Pediatr Endocrinol Rev; 2006 Sep;4(1):32-9
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  • [Title] Adrenocortical tumors and hyperplasias in childhood--etiology, genetics, clinical presentation and therapy.
  • Adrenocortical tumors are rare in children and are associated with a poor prognosis when malignant.
  • Evaluation of genetic disorders associated with the development of adrenocortical disorders has allowed researchers to identify a number of mutations that may be involved in tumorigenesis, including alterations in the GNAS1, PRKAR1A, TP53 and IGF2 genes.
  • Most children have localized disease at presentation which may be associated with a better prognosis when compared to adults.
  • Broader participation in multi-center research, such as the International Pediatric Adrenocortical Tumor Registry, is needed to collect sufficient data to better guide our clinical management.

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  • (PMID = 17021581.001).
  • [ISSN] 1565-4753
  • [Journal-full-title] Pediatric endocrinology reviews : PER
  • [ISO-abbreviation] Pediatr Endocrinol Rev
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / K08 DK064352; United States / NIDDK NIH HHS / DK / 5K08 DK64352
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Israel
  • [Number-of-references] 73
  • [Other-IDs] NLM/ NIHMS22957; NLM/ PMC1907361
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47. Capone G, Della Pepa GM, Sabatino G, Bartoccioni E, Albanese A, Mannino S, Maira G: A rare bone-leptomeningeal metastasis from an adrenal cortical carcinoma. J Clin Neurosci; 2009 Jul;16(7):977-80
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  • [Title] A rare bone-leptomeningeal metastasis from an adrenal cortical carcinoma.
  • We report a rare bone-leptomeningeal metastasis from an adrenal cortical carcinoma (ACC).
  • The CT scans and MRI showed a large tumor with bone and leptomeningeal involvement.
  • Thus, the patient underwent excision of the mass; histopathological diagnosis confirmed that it was an ACC metastasis.
  • At post-operative follow-up, the patient was in a good neurological condition with no radiological evidence of a cranial recurrence; however, there was a voluminous abdominal regrowth of the primary tumor.
  • This patient report confirms the effectiveness of aggressive surgery for management of large intracranial metastases, particularly those that arise from primary tumors that are resistant to radiotherapy and chemotherapy.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Bone Neoplasms / secondary. Meningeal Carcinomatosis / secondary

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  • (PMID = 19375918.001).
  • [ISSN] 0967-5868
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Scotland
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48. McNicol AM: Assessment of malignancy in adrenal cortical tumors. Endocr Pathol; 2006;17(2):131-6
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  • [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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49. Ragazzon B, Lefrançois-Martinez AM, Val P, Sahut-Barnola I, Tournaire C, Chambon C, Gachancard-Bouya JL, Begue RJ, Veyssière G, Martinez A: Adrenocorticotropin-dependent changes in SF-1/DAX-1 ratio influence steroidogenic genes expression in a novel model of glucocorticoid-producing adrenocortical cell lines derived from targeted tumorigenesis. Endocrinology; 2006 Apr;147(4):1805-18
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  • [Title] Adrenocorticotropin-dependent changes in SF-1/DAX-1 ratio influence steroidogenic genes expression in a novel model of glucocorticoid-producing adrenocortical cell lines derived from targeted tumorigenesis.
  • We established the first adrenocortical tumor cell lines with complete zona fasciculata (ZF) cell phenotype from tumors induced in transgenic mice by large T-antigen of simian virus 40 under the control of the aldose reductase-like akr1b7 gene promoter.
  • Adrenocortical tumor cell lines produced high amounts of corticosterone and were responsive to ACTH.
  • Taking advantage of these cells, we have examined the effect of ACTH on DAX-1 (dosage-sensitive sex reversal-adrenal hypoplasia congenita critical region on X-chromosome, gene 1) and SF-1 (steroidogenic factor 1), two transcription factors known to respectively repress and activate adrenocortical steroidogenesis by acting on common target genes.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenocorticotropic Hormone / pharmacology. Corticosterone / biosynthesis. DNA-Binding Proteins / analysis. Homeodomain Proteins / analysis. Receptors, Cytoplasmic and Nuclear / analysis. Transcription Factors / analysis. Zona Fasciculata / metabolism
  • [MeSH-minor] Adrenal Cortex. Aldehyde Reductase / genetics. Animals. Cell Line, Tumor. DAX-1 Orphan Nuclear Receptor. Gene Expression Regulation. Humans. Male. Mice. Mice, Transgenic. Promoter Regions, Genetic. RNA, Messenger / analysis. Steroidogenic Factor 1

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  • (PMID = 16439455.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DAX-1 Orphan Nuclear Receptor; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / NR0B1 protein, human; 0 / NR5A1 protein, human; 0 / Nr0b1 protein, mouse; 0 / RNA, Messenger; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Steroidogenic Factor 1; 0 / Transcription Factors; 0 / steroidogenic factor 1, mouse; 9002-60-2 / Adrenocorticotropic Hormone; EC 1.1.1.21 / Akr1b7 protein, mouse; EC 1.1.1.21 / Aldehyde Reductase; W980KJ009P / Corticosterone
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50. Makino K, Kojima R, Nakamura H, Morioka M, Iyama K, Shigematsu K, Kuratsu J: Ectopic adrenal cortical adenoma in the spinal region: case report and review of the literature. Brain Tumor Pathol; 2010 Oct;27(2):121-5
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  • [Title] Ectopic adrenal cortical adenoma in the spinal region: case report and review of the literature.
  • Ectopic adrenal cortical neoplasms are extremely rare; few involve the central nervous system (CNS).
  • We report a 17-month-old girl with spinal adrenal cortical neoplasms.
  • Immunohistochemically, the tumor cells were strongly positive for inhibin-alpha, positive for synaptophysin and vimentin, and negative for GFAP, EMA, S-100, NSA, and chromogranin A.
  • In addition, the nuclei stained positive for steroidogenic factor 1 (Ad4BP/SF-1), which is involved in adrenal steroidogenesis.
  • This case confirms the occurrence of adrenocortical adenoma in the CNS.
  • We suggest that this tumor should be considered in the differential diagnosis of CNS tumors.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / pathology. Spinal Cord Neoplasms / pathology
  • [MeSH-minor] Adrenal Cortex Diseases. Choristoma. Dura Mater / pathology. Female. Humans. Immunohistochemistry. Infant. Inhibins / metabolism. Magnetic Resonance Imaging. Spinal Cord. Steroidogenic Factor 1 / metabolism. Tissue Fixation

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  • (PMID = 21046315.001).
  • [ISSN] 1861-387X
  • [Journal-full-title] Brain tumor pathology
  • [ISO-abbreviation] Brain Tumor Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Steroidogenic Factor 1; 0 / inhibin-alpha subunit; 57285-09-3 / Inhibins
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51. Trezzi R, Poli F, Fellegara G: "Dedifferentiated" adrenal cortical neoplasm. Int J Surg Pathol; 2009 Aug;17(4):343-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] "Dedifferentiated" adrenal cortical neoplasm.
  • [MeSH-major] Adenoma / pathology. Adrenal Cortex Neoplasms / pathology. Cell Dedifferentiation. Cell Transformation, Neoplastic
  • [MeSH-minor] Aged. Antigens, CD56 / analysis. Antigens, Neoplasm / analysis. Biomarkers, Tumor / analysis. Female. Humans. MART-1 Antigen. Neoplasm Proteins / analysis. Synaptophysin / analysis

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  • (PMID = 19443867.001).
  • [ISSN] 1066-8969
  • [Journal-full-title] International journal of surgical pathology
  • [ISO-abbreviation] Int. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / MART-1 Antigen; 0 / MLANA protein, human; 0 / Neoplasm Proteins; 0 / Synaptophysin
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52. Oller AR, Kirkpatrick DT, Radovsky A, Bates HK: Inhalation carcinogenicity study with nickel metal powder in Wistar rats. Toxicol Appl Pharmacol; 2008 Dec 1;233(2):262-75
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  • No increased incidence of neoplasm of the respiratory tract was observed.
  • Adrenal gland pheochromocytomas (benign and malignant) in males and combined cortical adenomas/carcinomas in females were induced in a dose-dependent manner by the nickel metal exposure.
  • Pheochromocytomas appear to be secondary to the lung toxicity associated with the exposure rather than being related to a direct nickel effect on the adrenal glands.
  • The incidence of cortical tumors among 0.4 mg Ni/m(3) females, although statistically higher compared to the concurrent controls, falls within the historical control range; therefore, in the present study, this tumor is of uncertain relationship to nickel metal exposure.
  • The lack of respiratory tumors in the present animal study is consistent with the findings of the epidemiological studies.
  • [MeSH-minor] Adrenal Cortex Neoplasms / chemically induced. Adrenal Gland Neoplasms / chemically induced. Adrenocortical Adenoma / chemically induced. Adrenocortical Carcinoma / chemically induced. Animals. Dose-Response Relationship, Drug. Female. Male. Models, Animal. Occupational Exposure / adverse effects. Pheochromocytoma / chemically induced. Powders. Rats. Rats, Wistar. Respiratory Tract Neoplasms / epidemiology. Respiratory Tract Neoplasms / etiology. Sex Factors

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  • (PMID = 18822311.001).
  • [ISSN] 1096-0333
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Powders; 7OV03QG267 / Nickel
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53. 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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  • [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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54. Chien HP, Chang YS, Hsu PS, Lin JD, Wu YC, Chang HL, Chuang CK, Tsuei KH, Hsueh C: Adrenal cystic lesions: a clinicopathological analysis of 25 cases with proposed histogenesis and review of the literature. Endocr Pathol; 2008;19(4):274-81
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  • [Title] Adrenal cystic lesions: a clinicopathological analysis of 25 cases with proposed histogenesis and review of the literature.
  • Adrenal cystic lesions are uncommon and we analyzed clinical and pathologic features of 25 such cases from a single institute over 23 years.
  • The proposed mesothelial origin of adrenal epithelial cyst cannot be confirmed in our example.
  • Seven adrenal pseudocysts were associated with tumor, including two pheochromocytomas, one neuroblastoma, one adrenal cortical carcinoma, one adrenal cortical adenoma, one myelolipoma, and one schwannoma.
  • The distinction of true cystic lesion from cystic neoplasm is important and requires thorough sampling of the specimens.
  • [MeSH-major] Adrenal Gland Diseases / pathology. Adrenal Glands / pathology. Cysts / pathology

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  • (PMID = 18972224.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
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55. 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
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  • [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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56. Fudge EB, von Allmen D, Volmar KE, Calikoglu AS: Cushing Syndrome in a 6-Month-Old Infant due to Adrenocortical Tumor. Int J Pediatr Endocrinol; 2009;2009:168749
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  • [Title] Cushing Syndrome in a 6-Month-Old Infant due to Adrenocortical Tumor.
  • Cushing syndrome is rare in infancy and usually due to an adrenocortical tumor (ACT).
  • We report an infant with Cushing syndrome due to adrenocortical carcinoma.
  • Abdominal MRI revealed a heterogeneous right adrenal mass extending into the inferior vena cava.
  • The tumor was removed surgically en bloc.
  • In conclusion, adrenocortical neoplasms in children are rare, but should be considered in the differential diagnosis of Cushing syndrome.

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  • (PMID = 20049152.001).
  • [ISSN] 1687-9856
  • [Journal-full-title] International journal of pediatric endocrinology
  • [ISO-abbreviation] Int J Pediatr Endocrinol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2798106
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57. Gruschwitz T, Breza J, Wunderlich H, Junker K: Improvement of histopathological classification of adrenal gland tumors by genetic differentiation. World J Urol; 2010 Jun;28(3):329-34
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  • [Title] Improvement of histopathological classification of adrenal gland tumors by genetic differentiation.
  • PURPOSE: There are often problems in differentiating between benign and malignant adrenal gland tumors by imaging and histopathology.
  • On account of considerable differences in the therapy and aftercare of benign and malignant adrenal tumors, correct classification of tumor type is of greatest importance.
  • 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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58. 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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  • [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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59. Chang HW, Wu VC, Huang CY, Huang HY, Chen YM, Chu TS, Wu KD, Hsieh BS: D4 dopamine receptor enhances angiotensin II-stimulated aldosterone secretion through PKC-epsilon and calcium signaling. Am J Physiol Endocrinol Metab; 2008 Mar;294(3):E622-9
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  • Experiments were done with primary human adrenal cortical cells and human adrenocarcinoma (NCI-H295R) cells.
  • [MeSH-minor] Adrenal Cortex / chemistry. Adrenal Cortex / drug effects. Adrenal Cortex / physiology. Adrenal Cortex Neoplasms. Cell Line, Tumor. Cells, Cultured. Cytochrome P-450 CYP11B2 / genetics. Humans. Inositol 1,4,5-Trisphosphate / analysis. Phosphorylation. RNA, Messenger / analysis

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  • (PMID = 18171914.001).
  • [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 / RNA, Messenger; 11128-99-7 / Angiotensin II; 137750-34-6 / Receptors, Dopamine D4; 4964P6T9RB / Aldosterone; 85166-31-0 / Inositol 1,4,5-Trisphosphate; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 2.7.11.13 / Protein Kinase C-epsilon; SY7Q814VUP / Calcium
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60. Kim J, Yamamoto F, Gondo S, Yanase T, Mukai T, Maeda M: 6-Deoxy-6-[131I]iodo-L-ascorbic acid for the in vivo study of ascorbate: autoradiography, biodistribution in normal and hypolipidemic rats, and in tumor-bearing nude mice. Biol Pharm Bull; 2009 Nov;32(11):1906-11
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  • [Title] 6-Deoxy-6-[131I]iodo-L-ascorbic acid for the in vivo study of ascorbate: autoradiography, biodistribution in normal and hypolipidemic rats, and in tumor-bearing nude mice.
  • Normal female rat distribution studies showed high and specific uptake of 6-deoxy-6-[(131)I]iodo-L-ascorbic acid (6-(131)IAsA) into the adrenal glands, known to highly express the ascorbate sodium-dependent vitamin C transporter-2 (SVCT-2), and the adrenal gland was clearly visualized by whole-body autoradiography.
  • Preinjection of sulfinpyrazone, a known blocker of ascorbate transport, with 6-(131)IAsA resulted in decreased uptake of radioactivity in rat adrenal glands compared to the control group, seemingly illustrating the participation of the SVCT transporter (probably the SVCT-2 subtype) in the uptake process in vivo.
  • 4-Aminopyrazolo[3,4-d]pyrimidine-induced hypolipidemic rats showed a 1.7-fold increase in adrenal uptake of radioactivity at 30 min postinjection of 6-(131)IAsA, compared to the control, with increased adrenal-to-liver and adrenal-to-kidney ratios.
  • To further characterize 6-(131)IAsA for its tumor uptake properties, biodistribution studies were also performed using male nude mice implanted with either Y-1 adrenocortical tumor cells or adrenal medulla-derived PC12 cells.
  • None of these tumors exhibited relevant uptake of 6-(131)IAsA while normal adrenal glands showed high uptake of radioactivity, suggesting that these tumors in this model have only a poor transport capacity for this agent.
  • The present study demonstrates that the use of radioiodinated 6-IAsA may help to obtain information about functional alterations in diseased adrenal glands, but it does not exhibit desirable properties as a tumor-seeking agent for ascorbic acid bioactivity.
  • [MeSH-major] Adrenal Gland Neoplasms / metabolism. Iodine Radioisotopes / pharmacokinetics. Lipids / blood. Neoplasms, Experimental / metabolism

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  • (PMID = 19881306.001).
  • [ISSN] 1347-5215
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / 6-deoxy-6-iodoascorbic acid; 0 / Iodine Radioisotopes; 0 / Lipids; PQ6CK8PD0R / Ascorbic Acid
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61. Ferraz-de-Souza B, Martin F, Mallet D, Hudson-Davies RE, Cogram P, Lin L, Gerrelli D, Beuschlein F, Morel Y, Huebner A, Achermann JC: CBP/p300-interacting transactivator, with Glu/Asp-rich C-terminal domain, 2, and pre-B-cell leukemia transcription factor 1 in human adrenal development and disease. J Clin Endocrinol Metab; 2009 Feb;94(2):678-83
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  • [Title] CBP/p300-interacting transactivator, with Glu/Asp-rich C-terminal domain, 2, and pre-B-cell leukemia transcription factor 1 in human adrenal development and disease.
  • CONTEXT: Disorders of adrenal development result in significant morbidity and mortality.
  • However, the molecular basis of human adrenal development, and many forms of disease, is still poorly understood.
  • OBJECTIVES: We evaluated the role of two new candidate genes, CBP/p300-interacting transactivator, with Glu/Asp-rich C-terminal domain, 2 (CITED2), and pre-B-cell leukemia transcription factor 1 (PBX1), in human adrenal development and disease.
  • DESIGN: CITED2 and PBX1 expression in early human fetal adrenal development was assessed using RT-PCR and in situ hybridization.
  • The regulation of CITED2 and PBX1 by steroidogenic factor-1 (SF-1) and dosage-sensitive sex reversal, adrenal hypoplasia congenital, critical region on the X chromosome, gene-1 (DAX1) was evaluated in NCI-H295R human adrenocortical tumor cells by studying promoter regulation.
  • Finally, mutational analysis of CITED2 and PBX1 was performed in patients with primary adrenal disorders.
  • RESULTS: CITED2 and PBX1 are expressed in the human fetal adrenal gland during early development.
  • Mutational analysis failed to reveal significant coding sequence changes in individuals with primary adrenal disorders.
  • CONCLUSIONS: CITED2 and PBX1 are likely to be important mediators of adrenal development and function in humans, but mutations in these genes are not common causes of adrenal failure in patients in whom a molecular diagnosis remains unknown.
  • [MeSH-major] Adrenal Gland Diseases / genetics. Adrenal Glands / embryology. DNA-Binding Proteins / physiology. Proto-Oncogene Proteins / physiology. Repressor Proteins / physiology. Trans-Activators / physiology

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  • (PMID = 18984668.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / / ; United Kingdom / Wellcome Trust / / 079666; United Kingdom / Medical Research Council / / G0700089; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CITED2 protein, human; 0 / DAX-1 Orphan Nuclear Receptor; 0 / DNA-Binding Proteins; 0 / NR0B1 protein, human; 0 / NR5A1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Receptors, Retinoic Acid; 0 / Repressor Proteins; 0 / Steroidogenic Factor 1; 0 / Trans-Activators; 0 / pbx1 protein, human
  • [Other-IDs] NLM/ PMC2814552
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62. 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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63. Karim RZ, Wills EJ, McCarthy SW, Scolyer RA: Myxoid variant of adrenocortical carcinoma: report of a unique case. Pathol Int; 2006 Feb;56(2):89-94
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  • [Title] Myxoid variant of adrenocortical carcinoma: report of a unique case.
  • Myxoid variant of adrenocortical carcinomas (ACC) are rare, there being only 11 cases in the literature to date.
  • Reported herein are the findings of a case, which in contrast to all previously reported myxoid ACC, was devoid of typical non-myxoid areas.
  • The patient was a 61-year-old man in whom a left adrenal mass was detected during investigation of Cushing's syndrome.
  • The adrenal was replaced by malignant cells and expanses of myxoid material.
  • The ultrastructural features of the cells were typical of adrenal cortical differentiation.
  • The differential diagnosis of myxoid ACC includes extraskeletal myxoid chondrosarcoma, chordoma, myxoid adenocarcinoma, myxoma, lipomatous tumors, nerve sheath tumors, smooth muscle tumors, gastrointestinal stromal tumor and other sarcomas.
  • The presence of myxoid material in a retroperitoneal lesion raises a broad differential diagnosis in which myxoid adrenocortical neoplasms should be included.
  • Clinicoradiological correlation may be helpful, but special stains, immunohistochemistry and ultrastructural examination may be necessary to establish the diagnosis.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenocortical Carcinoma / diagnosis
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Antigens, Neoplasm. Chordoma / diagnosis. Chordoma / pathology. Diagnosis, Differential. Humans. Immunohistochemistry. MART-1 Antigen. Male. Microscopy, Electron. Middle Aged. Myxoma / diagnosis. Myxoma / pathology. Neoplasm Proteins / analysis. Nerve Sheath Neoplasms / diagnosis. Nerve Sheath Neoplasms / pathology. Retroperitoneal Neoplasms / diagnosis. Retroperitoneal Neoplasms / pathology. Synaptophysin / analysis. Vimentin / analysis

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  • (PMID = 16445821.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / MART-1 Antigen; 0 / MLANA protein, human; 0 / Neoplasm Proteins; 0 / Synaptophysin; 0 / Vimentin
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64. Li Q, Zhang XQ, Nie L, Chen GS, Li H, Zhang F, Zhang LY, Hong L, Wang SF, Wang H: Expression of interferon-gamma in human adrenal gland and kidney tumours. Br J Cancer; 2007 Aug 6;97(3):420-5
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  • [Title] Expression of interferon-gamma in human adrenal gland and kidney tumours.
  • Our previous studies have shown that IFN-gamma-like immunoreactivity also appears in human adrenal cortical tumour and phaeochromocytoma.
  • To investigate whether human tumour cells can produce IFN-gamma, we examined 429 biopsy specimens of 30 kinds of tumour and tumour-surrounding tissues in adrenal glands and in kidneys by using immunohistochemistry and in situ hybridisation.
  • IFN-gamma immunoactivity was shown in 34.3% of the adrenal cortical adenomas, 50% of the adrenal cortical carcinomas, 26.7% of the phaeochromocytomas, 26.7% of the clear cell renal cell carcinomas (RCCs), 22% of the adrenal cortexes and 40% of medullas adjacent to tumours.
  • Western blot analysis has further confirmed the immunohistochemistry results by showing a distinct IFN-gamma band corresponding to 17.4 kDa in tissue extracts from adrenal cortical adenoma, phaeochromocytoma and clear cell RCCs.
  • These results indicate that IFN-gamma is produced by some types of tumour cells, suggesting it may play a dual role in the development of these tumours.
  • [MeSH-major] Adrenal Gland Neoplasms / metabolism. Interferon-gamma / metabolism. Kidney Neoplasms / metabolism

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  • (PMID = 17622250.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC2360327
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65. Aubert S: [Adrenal cortex tumors: a lesion continuum?]. Ann Pathol; 2008 Nov;28 Spec No 1(1):S39-41
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  • [Title] [Adrenal cortex tumors: a lesion continuum?].
  • [Transliterated title] Les tumeurs corticosurrénaliennes : un continuum lésionnel ?
  • [MeSH-major] Adenocarcinoma / pathology. Adenoma / pathology. Adrenal Cortex / pathology. Adrenal Cortex Neoplasms / pathology
  • [MeSH-minor] Biomarkers, Tumor. Diagnosis, Differential. Gene Expression Profiling. Humans. Hyperplasia. Neoplasm Proteins / analysis. Neoplasm Proteins / genetics. Organ Size. Prevalence. Tumor Burden

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  • (PMID = 18984295.001).
  • [ISSN] 0242-6498
  • [Journal-full-title] Annales de pathologie
  • [ISO-abbreviation] Ann Pathol
  • [Language] fre
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
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66. 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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67. 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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  • [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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68. West AN, Ribeiro RC, Jenkins J, Rodriguez-Galindo C, Figueiredo BC, Kriwacki R, Zambetti GP: Identification of a novel germ line variant hotspot mutant p53-R175L in pediatric adrenal cortical carcinoma. Cancer Res; 2006 May 15;66(10):5056-62
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  • [Title] Identification of a novel germ line variant hotspot mutant p53-R175L in pediatric adrenal cortical carcinoma.
  • Hotspot mutations in the p53 tumor suppressor gene result in the disruption of DNA contact points or alter the overall structure of the protein to prevent DNA binding.
  • We have identified a novel germ line variant of the 175 mutant (Arg to Leu; R175L) in a pediatric patient who developed adrenal cortical carcinoma.
  • Surprisingly, the family is not tumor prone or associated with LFS.
  • In vitro, the R175L mutant displayed an attenuated tumor suppressor activity in the regulation of transcription, colony formation, and apoptosis when compared with wild-type p53 and the R175H mutant.
  • These findings suggest that p53-R175L retains sufficient activity to suppress LFS, but not adrenal cortical carcinoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Genes, p53 / genetics. Germ-Line Mutation

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  • (PMID = 16707427.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA104568; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / CA63230; United States / NCI NIH HHS / CA / CA71907
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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69. Cohen MM Jr: Beckwith-Wiedemann syndrome: historical, clinicopathological, and etiopathogenetic perspectives. Pediatr Dev Pathol; 2005 May-Jun;8(3):287-304
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  • Complications include neonatal hypoglycemia and an increased risk for Wilms tumor, adrenal cortical carcinoma, hepatoblastoma, rhabdomyosarcoma, and neuroblastoma, among others.
  • [MeSH-minor] Diagnosis, Differential. Female. Humans. Infant, Newborn. Male

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  • (PMID = 16010495.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 140
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70. Forti FL, Dias MH, Armelin HA: ACTH receptor: ectopic expression, activity and signaling. Mol Cell Biochem; 2006 Dec;293(1-2):147-60
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  • Failure in obtaining expression of functional adrenocorticotropic hormone receptor (ACTHR, or melanocortin 2 receptor, MC2R) in non-adrenal cells has hindered molecular analysis of ACTH signaling pathways.
  • Natural constitutive expression of the MC2R accessory protein (MRAP) in Balb3T3 and other mouse 3T3 fibroblasts (NIH, Swiss and 3T3-L1) renders these fibroblastic lines suitable for ectopic expression of ACTHR in its active form properly inserted into the plasma membrane at levels similar to those found in mouse Y1 adrenocortical tumor cells.
  • The Y1 cell line is a cultured cell system well known for stably displaying normal adrenal specific metabolic pathways, ACTHR expression and ACTH functional responses.
  • Fourteen 3T3-AR and four 3T3-0 clones were screened for response to ACTH(39) in comparison with Y1 adrenocortical cells.
  • Eight 3T3-AR clones responded to ACTH(39) with activation of adenylate cyclase and induction of c-Fos protein, but the levels of, respectively, activation and induction were not strictly correlated.
  • In Y1 cells, specific inhibitors (H89/PKA; PD98059/MEK; Go6983/PKC and SP600125/JNK) show that signals initiated in the ACTH/ACTHR-system activate 4 pathways to induce the c-fos gene, namely: (a) cAMP/PKA/CREB;.
  • On the other hand, SP600125 caused 85% inhibition of c-Fos induction by ACTH(39) and, in addition, ACTH(39) promotes JNK1/2 phosphorylation, suggesting that JNK is a major signaling pathway mediating c-Fos induction by ACTH(39) in these cells.
  • However, activation of cAMP/PKA/CREB and JNK pathways and induction of fos and jun genes are not yet sufficient to enable ACTH for interference in morphology, migration and proliferation of Balb3T3 fibroblasts as it does in Y1 adrenocortical cells.
  • [MeSH-minor] 3T3 Cells. Adenylyl Cyclases / metabolism. Adrenal Cortex / metabolism. Adrenocorticotropic Hormone / metabolism. Animals. Cell Line, Tumor. Enzyme Activation. Fluorescent Antibody Technique. Gene Expression. Genes, fos. Genes, jun. Mice. Models, Biological. Phosphorylation. Transfection


71. 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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  • [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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72. Sand SL, Oppegård C, Ohara S, Iijima T, Naderi S, Blomhoff HK, Nissen-Meyer J, Sand O: Plantaricin A, a peptide pheromone produced by Lactobacillus plantarum, permeabilizes the cell membrane of both normal and cancerous lymphocytes and neuronal cells. Peptides; 2010 Jul;31(7):1237-44
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  • Ca(2+) imaging based on a combination of fluo-4 and fura-red was used to monitor PlnA-induced membrane permeabilization in normal rat cortical neurons and glial cells, PC12 cells (from a rat adrenal chromaffin tumor), and murine N2A cells (from a spinal cord tumor).

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20416350.001).
  • [ISSN] 1873-5169
  • [Journal-full-title] Peptides
  • [ISO-abbreviation] Peptides
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Bacteriocins; 0 / Pheromones; 131463-18-8 / plantaricin A
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73. Mazzuco TL, Chabre O, Feige JJ, Thomas M: Aberrant GPCR expression is a sufficient genetic event to trigger adrenocortical tumorigenesis. Mol Cell Endocrinol; 2007 Feb;265-266:23-8
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  • [Title] Aberrant GPCR expression is a sufficient genetic event to trigger adrenocortical tumorigenesis.
  • Aberrant expression of G protein-coupled receptors (GPCR) in the adrenal cortex is observed in some cases of ACTH-independent macronodular adrenal hyperplasias and adenomas associated with Cushing syndrome (CS).
  • Although there is clinical evidence for the implication of these receptors in abnormal regulation of cortisol secretion, whether this aberrant expression also directly causes the development of a benign adrenocortical tumor is an open question.
  • Cell transplantation provides a way to study genes that may be important in human tumor development.
  • The system we developed uses genetically modified adrenocortical cells transplanted into adrenalectomized immunodeficient mice, which form a functional tissue structure.
  • We observed that enforcing expression of the gastric inhibitory polypeptide (GIP) receptor or the luteinizing hormone (LH) receptor genes (taken as canonical examples of aberrantly expressed GPCRs) in adrenocortical cells resulted in the formation of hyperplastic tissues and the development of Cushing syndrome features in transplanted mice.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Receptors, G-Protein-Coupled / genetics
  • [MeSH-minor] Adrenal Cortex / cytology. Adrenal Cortex / metabolism. Animals. Cell Transplantation. Cushing Syndrome / genetics. Humans

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  • (PMID = 17250952.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Receptors, G-Protein-Coupled
  • [Number-of-references] 35
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74. Waalkes MP, Liu J, Diwan BA: Transplacental arsenic carcinogenesis in mice. Toxicol Appl Pharmacol; 2007 Aug 1;222(3):271-80
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  • In C3H mice, two separate studies show male offspring exposed to arsenic in utero developed liver carcinoma and adrenal cortical adenoma in a dose-related fashion during adulthood.
  • Prenatally exposed female C3H offspring show dose-related increases in ovarian tumors and lung carcinoma and in proliferative lesions (tumors plus preneoplastic hyperplasia) of the uterus and oviduct.
  • In addition, prenatal arsenic plus postnatal exposure to the tumor promoter, 12-O-tetradecanoyl phorbol-13-acetate (TPA) in C3H mice produces excess lung tumors in both sexes and liver tumors in females.
  • Male CD1 mice treated with arsenic in utero develop tumors of the liver and adrenal and renal hyperplasia while females develop tumors of urogenital system, ovary, uterus and adrenal and hyperplasia of the oviduct.

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  • (PMID = 17306315.001).
  • [ISSN] 0041-008X
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / N01CO12400; United States / Intramural NIH HHS / / Z01 BC005488-21; United States / Intramural NIH HHS / / Z99 ES999999; United States / NCI NIH HHS / CO / N01-CO-12400
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Arsenicals; 0 / Carcinogens; 0 / Estrogens; 094ZI81Y45 / Tamoxifen; 731DCA35BT / Diethylstilbestrol; N712M78A8G / Arsenic; NI40JAQ945 / Tetradecanoylphorbol Acetate
  • [Other-IDs] NLM/ NIHMS28781; NLM/ PMC1995036
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75. Dehner LP, Hill DA: Adrenal cortical neoplasms in children: why so many carcinomas and yet so many survivors? Pediatr Dev Pathol; 2009 Jul-Aug;12(4):284-91
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  • [Title] Adrenal cortical neoplasms in children: why so many carcinomas and yet so many survivors?
  • Adrenal cortical neoplasms in children are represented by a disproportionate number of cases that have been diagnosed pathologically as adrenocortical carcinomas (ACCs)-as many as 90% of all cortical tumors in some pediatric series.
  • Most are sporadically occurring neoplasms, but ACCs are a manifestation of Beckwith-Wiedemann and Li-Fraumeni syndromes.
  • Tumor weight is seemingly a significant determinant in prognosis at a threshold of greater than 400 g.
  • A risk assessment system is proposed that incorporates tumor weight, localization of tumor to the gland without invasion into the surrounding tissues or organs, and absence of metastasis.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology
  • [MeSH-minor] Beckwith-Wiedemann Syndrome / genetics. Beckwith-Wiedemann Syndrome / pathology. Child, Preschool. Humans. Infant. Infant, Newborn. Li-Fraumeni Syndrome / genetics. Li-Fraumeni Syndrome / pathology. Neoplasm Staging. Prognosis. Risk Assessment. Survivors

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  • (PMID = 19326954.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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76. 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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  • [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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77. Mann MW, Ellis SS, Mallory SB: Infantile acne as the initial sign of an adrenocortical tumor. J Am Acad Dermatol; 2007 Feb;56(2 Suppl):S15-8
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  • [Title] Infantile acne as the initial sign of an adrenocortical tumor.
  • Ultrasound and abdominal computed tomographic scan revealed a large adrenal mass consistent with an adrenocortical tumor.
  • The patient underwent surgical excision of the well-encapsulated tumor with normalization of his hormones and no subsequent recurrence.
  • Although rare, childhood adrenocortical tumors have a poor prognosis, with the majority of tumors having regional and metastatic disease.
  • Because early diagnosis and complete surgical excision improve prognosis, children with refractory infantile acne should be evaluated for signs of virilization and accelerated growth.
  • Elevated levels of DHEA and DHEA-S should prompt an aggressive diagnostic evaluation for an adrenocortical tumor.
  • [MeSH-major] Acne Vulgaris / etiology. Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications

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  • (PMID = 17097383.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 3XMK78S47O / Testosterone; 459AG36T1B / Dehydroepiandrosterone
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78. Ahmed AA: Adrenocortical neoplasms in young children: age as a prognostic factor. Ann Clin Lab Sci; 2009;39(3):277-82
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  • [Title] Adrenocortical neoplasms in young children: age as a prognostic factor.
  • Adrenal cortical neoplasms in pediatric patients are rare.
  • The clinical manifestations and biologic behavior of these tumors can be quite distinct from their histologically similar counterparts in the adult population.
  • We report 5 cases of adrenocortical neoplasms in young children and review their clinical presentations, pathology, and follow-up data.
  • Imaging studies revealed neoplasms in the left adrenal gland in 3 cases and the right adrenal gland in 2 cases.
  • No evidence of disease was identified at any other site of the body.
  • The tumors were grossly confined to the adrenal glands and ranged in diameter from 3 to 6 cm (mean 4.3 cm).
  • Microscopically, the tumors had histological and immunophenotypic features characteristic of adrenocortical tumors.
  • After follow-up periods ranging from 5 mo to 9.5 yr, all patients were alive and free of disease.
  • Despite histological and immunophenotypical evidence of malignancy, these localized adrenocortical neoplasms had a benign clinical course with no evidence of metastasis or recurrence.
  • Because of the discrepancy between pathology and clinical outcome, adrenocortical tumors in this age group should be classified as neoplasms of unknown malignant potential.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis
  • [MeSH-minor] Age Factors. Child, Preschool. Dehydroepiandrosterone / blood. Dehydroepiandrosterone / urine. Female. Humans. Infant. Ki-67 Antigen / metabolism. Male. Prognosis. Testosterone / blood. Tumor Suppressor Protein p53 / metabolism. Virilism / diagnosis. Virilism / etiology

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  • (PMID = 19667412.001).
  • [ISSN] 1550-8080
  • [Journal-full-title] Annals of clinical and laboratory science
  • [ISO-abbreviation] Ann. Clin. Lab. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53; 3XMK78S47O / Testosterone; 459AG36T1B / Dehydroepiandrosterone
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79. McNicol AM: Lesions of the adrenal cortex. Arch Pathol Lab Med; 2008 Aug;132(8):1263-71
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  • [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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80. 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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81. Lan MS, Breslin MB: Structure, expression, and biological function of INSM1 transcription factor in neuroendocrine differentiation. FASEB J; 2009 Jul;23(7):2024-33
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  • Further, deletion of INSM1 severely impairs catecholamine biosynthesis and secretion from the adrenal gland that results in early embryonic lethality.
  • Genetically, INSM1 acts as a downstream factor of Mash 1 and Phox2b in the differentiation of the sympatho-adrenal lineage.
  • In the developing neocortex, mouse embryos lacking INSM1 expression contain half the number of basal progenitors and show a reduction in cortical plate radial thickness.
  • INSM1 is highly expressed in tumors of neuroendocrine origin.
  • Hence, its promoter could serve as a tumor-specific promoter that drives a specific targeted cancer gene therapy for the treatment of neuroendocrine tumors.

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  • (PMID = 19246490.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK061436; United States / NIDDK NIH HHS / DK / DK-61436
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Repressor Proteins; 0 / Transcription Factors; 147955-03-1 / INSM1 protein, human
  • [Number-of-references] 55
  • [Other-IDs] NLM/ PMC2704596
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82. Betz MJ, Shapiro I, Fassnacht M, Hahner S, Reincke M, Beuschlein F, German and Austrian Adrenal Network: Peroxisome proliferator-activated receptor-gamma agonists suppress adrenocortical tumor cell proliferation and induce differentiation. J Clin Endocrinol Metab; 2005 Jul;90(7):3886-96
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Peroxisome proliferator-activated receptor-gamma agonists suppress adrenocortical tumor cell proliferation and induce differentiation.
  • 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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83. Ermetici F, Malavazos AE, Corbetta S, Morricone L, Dall'Asta C, Corsi MM, Ambrosi B: Adipokine levels and cardiovascular risk in patients with adrenal incidentaloma. Metabolism; 2007 May;56(5):686-92
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  • [Title] Adipokine levels and cardiovascular risk in patients with adrenal incidentaloma.
  • Adrenal incidentalomas (AIs) have been associated with an increased incidence of several cardiovascular risk factors, similar to overt Cushing syndrome.
  • The aim of the present study was to evaluate plasma interleukin 6 (IL-6), adiponectin, resistin, tumor necrosis factor alpha (TNF-alpha), and monocyte chemoattractant protein 1 (MCP-1) levels in patients with AI.
  • Plasma IL-6, adiponectin, resistin, TNF-alpha, and MCP-1 levels were measured in 20 healthy subjects (6 males; 14 females; age, 58.5 +/- 2.2 years; body mass index, 28.1 +/- 0.9 kg/m(2)) and in 20 patients (5 males; 15 females; age, 57.9 +/- 2.0 years; body mass index, 28.0 +/- 0.8 kg/m(2)) with AI and typical computed tomographic features of cortical adenoma, who were not affected by diabetes mellitus, hypertension, or other relevant diseases.
  • In conclusion, patients with AI may show increased levels of adipokines (apparently not related to the presence of diabetes, hypertension, or obesity), which may be affected by the presence of the adrenal adenoma.
  • For some adipokines, a direct production from the adrenal gland may be hypothesized even if other studies are needed to better investigate the role of adipokines in states of altered cortisol secretion.
  • [MeSH-major] Adrenal Cortex Neoplasms / blood. Adrenocortical Adenoma / blood. Atherosclerosis / blood
  • [MeSH-minor] Adiponectin / blood. Adrenocorticotropic Hormone / blood. Chemokine CCL2 / blood. Dexamethasone / pharmacology. Female. Glucocorticoids / pharmacology. Humans. Hydrocortisone / blood. Hydrocortisone / urine. Interleukin-6 / blood. Male. Middle Aged. Resistin / blood. Risk Factors. Tumor Necrosis Factor-alpha / blood


84. Lau SK, Weiss LM: The Weiss system for evaluating adrenocortical neoplasms: 25 years later. Hum Pathol; 2009 Jun;40(6):757-68
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  • [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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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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  • [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. Fragoso MC, Kohek MB, Martin RM, Latronico AC, Lucon AM, Zerbini MC, Longui CA, Mendonca BB, Domenice S: An inhibin B and estrogen-secreting adrenocortical carcinoma leading to selective FSH suppression. Horm Res; 2007;67(1):7-11
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  • [Title] An inhibin B and estrogen-secreting adrenocortical carcinoma leading to selective FSH suppression.
  • OBJECTIVE: Hormone-secreting adrenocortical tumors are frequently associated with endocrine syndromes.
  • Abdominal magnetic resonance imaging revealed a very large tumor in the right adrenal gland.
  • Cortisol and adrenal androgen levels were normal.
  • The unusual finding of selective FSH suppression suggested secretion of inhibin B by the adrenocortical tumor.
  • Right adrenalectomy and nephrectomy were performed and the tumor was classified as a malignant tumor (Weiss score: 7.0) and unilateral mastectomy disclosed a lipoma.
  • Immunohistochemical analysis with anti-B-inhibin antibody revealed intense staining in the adrenocortical tumor cells.
  • One month after surgery, an abdominal magnetic resonance imaging revealed a local recurrence of the tumor and a second surgery was performed with partial resection of the tumor and the patient died 1 year after the first surgery.
  • CONCLUSION: We herein report the first inhibin B and estradiol-secreting adrenocortical carcinoma.
  • The unusual selective inhibition of FSH secretion should be considered a valuable hormonal finding for the diagnosis of inhibin B-secreting adrenocortical tumors.
  • [MeSH-major] Adrenal Cortex Neoplasms / blood. Carcinoma / blood. Estradiol / blood. Follicle Stimulating Hormone / blood. Inhibins / blood

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  • [Copyright] Copyright (c) 2007 S. Karger AG, Basel.
  • (PMID = 16974107.001).
  • [ISSN] 0301-0163
  • [Journal-full-title] Hormone research
  • [ISO-abbreviation] Horm. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / inhibin B; 4TI98Z838E / Estradiol; 57285-09-3 / Inhibins; 9002-68-0 / Follicle Stimulating Hormone
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87. 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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88. 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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89. Tedoldi S, Paterson JC, Cordell J, Tan SY, Jones M, Manek S, Dei Tos AP, Roberton H, Masir N, Natkunam Y, Pileri SA, Facchetti F, Hansmann ML, Mason DY, Marafioti T: Jaw1/LRMP, a germinal centre-associated marker for the immunohistological study of B-cell lymphomas. J Pathol; 2006 Aug;209(4):454-63
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  • It was absent, or present at only low levels, in mature T-cells, although cortical thymocytes were weakly positive.
  • Among lymphoid neoplasms, Jaw1/LRMP was found in germinal centre-derived lymphomas (follicle centre lymphoma, Burkitt's lymphoma, lymphocyte-predominant Hodgkin's disease) but not in T-cell neoplasms (with the exception of a single T lymphoblastic lymphoma).
  • Classical Hodgkin's disease and myeloma lacked Jaw1/LRMP but many cases of chronic lymphocytic leukaemia (but not mantle zone lymphoma) were Jaw1/LRMP-positive.
  • Finally, the expression of Jaw1/LRMP in other types of lymphoma and in non-lymphoid tissues/tumours may be of interest in differential diagnosis and research.
  • [MeSH-major] Biomarkers, Tumor / analysis. Gene Expression Regulation, Neoplastic. Germinal Center / chemistry. Lymphoma, B-Cell / chemistry. Lymphoma, Large B-Cell, Diffuse / chemistry. Membrane Proteins / analysis
  • [MeSH-minor] Adrenal Glands / chemistry. B-Lymphocytes / chemistry. B-Lymphocytes / ultrastructure. Biomarkers / analysis. Blotting, Western. Cell Line. Cerebral Cortex / chemistry. Epithelial Cells / chemistry. Humans. Immunohistochemistry / methods. Male. Neurons / chemistry. Palatine Tonsil / chemistry. Seminal Vesicles. Stomach

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  • [Copyright] Copyright 2006 Pathological Society of Great Britain and Ireland.
  • (PMID = 16739114.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Biomarkers, Tumor; 0 / LRMP protein, human; 0 / Membrane Proteins
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90. López PJ, Pierro A, Curry JI, Mushtaq I: Retroperitoneoscopic adrenalectomy: an early institutional experience. J Pediatr Urol; 2007 Apr;3(2):96-9
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  • Swift access to the vascular pedicle makes this approach ideal for adrenal surgery where haemodynamic instability is a common feature.
  • Dissection was performed with diathermy and/or Harmonic Scalpeltrade mark and the adrenal vessels were divided between clips.
  • Histopathological diagnosis included adrenal cyst (n=1), cystic phaeochromocytoma (n=1), adrenal cortical tumour (n=2) and central Cushing's disease (n=1).
  • This is our technique of choice as it provides a superior view of the adrenal gland and vessels, with good intraoperative haemodynamic stability.

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  • (PMID = 18947710.001).
  • [ISSN] 1873-4898
  • [Journal-full-title] Journal of pediatric urology
  • [ISO-abbreviation] J Pediatr Urol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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91. Schalin-Jäntti C: [Adrenal incidentaloma--a common dilemma]. Duodecim; 2010;126(9):1037-45
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  • [Title] [Adrenal incidentaloma--a common dilemma].
  • An adrenal incidentaloma is an adrenal tumor larger than 1 cm, incidentally detected in imaging studies carried out for other reasons than adrenal disease.
  • The most frequent explanation is a benign, non-functional adenoma, other frequent diagnoses include cortisol- or aldosterone-secreting adenomas, pheochromocytoma, cortical carcinoma and metastatic lesions.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis
  • [MeSH-minor] Adenoma / diagnosis. Adenoma / surgery. Aldosterone / secretion. Humans. Hydrocortisone / secretion. Incidental Findings. Phenotype. Pheochromocytoma / diagnosis. Pheochromocytoma / surgery. Tomography, X-Ray Computed

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  • (PMID = 20593627.001).
  • [ISSN] 0012-7183
  • [Journal-full-title] Duodecim; lääketieteellinen aikakauskirja
  • [ISO-abbreviation] Duodecim
  • [Language] fin
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Finland
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone; WI4X0X7BPJ / Hydrocortisone
  • [Number-of-references] 21
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92. Cavalier ME, Davis MM, Croop JM: Germline p53 mutation presenting as synchronous tumors. J Pediatr Hematol Oncol; 2005 Aug;27(8):441-3
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  • [Title] Germline p53 mutation presenting as synchronous tumors.
  • Li-Fraumeni syndrome and the LF-like syndrome, rare heritable conditions that predispose to the development of malignancy, are associated with germline mutations of the tumor suppressor gene p53.
  • The authors describe a 14-month-old boy who presented with synchronous rhabdomyosarcoma and adrenal cortical carcinoma and a novel mutation of the p53 gene.
  • Although codon 273 is a known hotspot region for p53 mutation, the patient's mutation, R273H, has not been associated with development of adrenal cortical carcinoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Carcinoma / genetics. Genes, p53. Germ-Line Mutation. Li-Fraumeni Syndrome / complications. Neoplasms, Multiple Primary / genetics. Rhabdomyosarcoma / genetics

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  • (PMID = 16096528.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon
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93. Fujii H, Kamide K, Miyake O, Abe T, Nagai M, Nakahama H, Horio T, Takiuchi S, Okuyama A, Yutani C, Kawano Y: Primary aldosteronism combined with preclinical Cushing's syndrome in an elderly patient. Circ J; 2005 Nov;69(11):1425-7
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  • Pre-clinical Cushing's syndrome (pre-CS) is sometimes seen with adrenal cortical tumors.
  • The tumor consisted of mostly light clear cells and scattered dark compact cells resembling islands.
  • [MeSH-major] Adrenal Cortex Neoplasms. Cushing Syndrome. Hyperaldosteronism. Hypokalemia
  • [MeSH-minor] Adrenal Glands / metabolism. Adrenalectomy / methods. Aged, 80 and over. Aldosterone / metabolism. Cytochrome P-450 CYP11B2 / metabolism. Female. Humans. Hydrocortisone / metabolism

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  • (PMID = 16247222.001).
  • [ISSN] 1346-9843
  • [Journal-full-title] Circulation journal : official journal of the Japanese Circulation Society
  • [ISO-abbreviation] Circ. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; WI4X0X7BPJ / Hydrocortisone
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94. Kalof AN, Cooper K: D2-40 immunohistochemistry--so far! Adv Anat Pathol; 2009 Jan;16(1):62-4
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  • Since its introduction, D2-40 immunoexpression has been described in a variety of lymphovascular neoplasms including lymphangioma, Kaposi sarcoma, and hemangioendothelioma, as well as nonvascular neoplasms such as epithelioid mesothelioma, seminoma, and hemangioblastoma.
  • More recently, D2-40 immunoexpression has been reported in primary adrenal cortical tumors, schwannomas, and adnexal tumors of the skin.
  • [MeSH-major] Antibodies, Monoclonal. Biomarkers, Tumor / analysis
  • [MeSH-minor] Adrenal Cortex Neoplasms / immunology. Adrenal Cortex Neoplasms / pathology. Antibodies, Monoclonal, Murine-Derived. Antigens, CD / analysis. Central Nervous System Neoplasms / immunology. Central Nervous System Neoplasms / pathology. Endothelium, Lymphatic / immunology. Endothelium, Lymphatic / pathology. Hemangioblastoma / immunology. Hemangioblastoma / pathology. Humans. Immunohistochemistry. Lymphangioma / immunology. Lymphangioma / pathology. Mesothelioma / immunology. Mesothelioma / pathology. Sarcoma, Kaposi / immunology. Sarcoma, Kaposi / pathology

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  • (PMID = 19098468.001).
  • [ISSN] 1533-4031
  • [Journal-full-title] Advances in anatomic pathology
  • [ISO-abbreviation] Adv Anat Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD; 0 / Biomarkers, Tumor; 0 / monoclonal antibody D2-40
  • [Number-of-references] 14
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95. Tala HP, Carvajal CA, González AA, Garrido JL, Tobar J, Solar A, Campino C, Arteaga E, Fardella CE: New splicing mutation of MEN1 gene affecting the translocation of menin to the nucleus. J Endocrinol Invest; 2006 Nov;29(10):888-93
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  • Multiple endocrine neoplasia type 1 (MEN1) is a syndrome inherited in an autosomal dominant trait caused by the inactivation of the tumor suppressor gene MEN1.
  • PATIENTS AND METHODS: We studied 5 members of a family with symptomatic hyperparathyroidism (HPT).
  • One of them had also a neuroendocrine pancreatic tumor, and 2 had non-functional multinodular cortical adrenal hyperplasia compatible with the diagnosis of MEN1.
  • RT-PCR from leukocyte's isolated mRNA and western blot from pancreatic tumor tissue were performed.
  • [MeSH-major] Cell Nucleus / metabolism. Germ-Line Mutation / genetics. Multiple Endocrine Neoplasia Type 1 / genetics. Proto-Oncogene Proteins / metabolism

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  • (PMID = 17185897.001).
  • [ISSN] 1720-8386
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins; 9007-49-2 / DNA
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96. 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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  • [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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97. Nomikos IN, Zizi-Serbetzoglou A, Matsakis G, Elemenoglou J, Vamvakopoulos NC: Association of an oversized adrenal cortical adenoma with expression of pheochromocytoma-like neurosecretory features. J BUON; 2008 Jul-Sep;13(3):425-8
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  • [Title] Association of an oversized adrenal cortical adenoma with expression of pheochromocytoma-like neurosecretory features.
  • Abnormal stimulation of adrenal function may be either direct, affecting similarly cortical and medullary secretion, or indirect affecting primarily the medulla.
  • Indirect activation of clinically detectable adrenomedullary function may develop as a physical consequence of a non-functional adrenal tumor exerting pressure on the medulla by its size, location and direction of growth.
  • Our case of an oversized and overweight adrenal tumor associated with expression of late-onset pheochromocytoma-like clinical symptoms may be explained by the physical indirect rather than the biological direct activation of adrenomedullary function like hyperplasia or cancer.
  • [MeSH-major] Adenoma / pathology. Adrenal Cortex Neoplasms / pathology. Adrenal Medulla / pathology. Pheochromocytoma / pathology

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  • (PMID = 18979561.001).
  • [ISSN] 1107-0625
  • [Journal-full-title] Journal of B.U.ON. : official journal of the Balkan Union of Oncology
  • [ISO-abbreviation] J BUON
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 57285-09-3 / Inhibins
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98. 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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  • [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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99. Diner EK, Franks ME, Behari A, Linehan WM, Walther MM: Partial adrenalectomy: the National Cancer Institute experience. Urology; 2005 Jul;66(1):19-23
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  • OBJECTIVES: To report our experience of partial adrenalectomy and demonstrate whether adrenal function can be preserved in patients with hereditary adrenal pheochromocytoma.
  • Total adrenalectomy has largely been used in the treatment of patients with hereditary adrenal pheochromocytomas.
  • Adrenal cortical-sparing surgery is an alternative approach that aims to balance tumor removal with preservation of adrenocortical function.
  • METHODS: From 1995 to 2004, 33 patients with hereditary pheochromocytoma presented with adrenal masses.
  • Partial adrenalectomy (open or laparoscopic) was performed if normal adrenocortical tissue was evident on preoperative imaging or intraoperative ultrasonography.
  • Various operative parameters, as well as postoperative function of the residual adrenal remnants, were determined.
  • Ten patients underwent simultaneous, bilateral partial adrenalectomy and 8 underwent surgery on a solitary adrenal gland, 4 of whom received postoperative steroid replacement (stopped in 3 after 1 to 3 months).
  • All other patients had normal catecholamine levels and remained tumor free by imaging at a mean follow-up of 36 months (range 3 to 102).
  • CONCLUSIONS: Partial adrenalectomy can preserve adrenal function in patients with adrenal masses.
  • The laparoscopic approach is technically safe and associated with less morbidity without compromising tumor removal.
  • With careful surgical planning, especially in patients with tumors in solitary glands, adrenocortical function may be preserved, thereby avoiding the morbidity associated with medical adrenal replacement.
  • [MeSH-major] Adrenal Gland Neoplasms / surgery. Adrenalectomy / methods. Pheochromocytoma / surgery

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  • (PMID = 15961144.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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100. Oki K, Yamane K, Sakashita Y, Kamei N, Watanabe H, Toyota N, Shigeta M, Sasano H, Kohno N: Primary aldosteronism and hypercortisolism due to bilateral functioning adrenocortical adenomas. Clin Exp Nephrol; 2008 Oct;12(5):382-7
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  • [Title] Primary aldosteronism and hypercortisolism due to bilateral functioning adrenocortical adenomas.
  • A 50-year-old male patient with a 15-year history of hypertension was referred to our hospital for evaluation of bilateral adrenal tumors.
  • Computed tomographic scan showed 10-mm masses in each adrenal gland.
  • The results of a subsequent adrenal venous catheterization study were consistent with the presence of a left cortisol-producing tumor and a right aldosterone-producing tumor.
  • This is an extremely rare case of bilateral adrenal tumors, in which the left adrenocortical tumor produced and secreted cortisol or both cortisol and aldosterone and the right one produced and secreted both aldosterone and cortisol, as confirmed by clinical findings and pathological studies using immunohistochemical analysis.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications. Cushing Syndrome / etiology. Hyperaldosteronism / etiology
  • [MeSH-minor] Aldosterone / metabolism. Diagnosis, Differential. Humans. Hydrocortisone / metabolism. Male. Middle Aged

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  • (PMID = 18543063.001).
  • [ISSN] 1342-1751
  • [Journal-full-title] Clinical and experimental nephrology
  • [ISO-abbreviation] Clin. Exp. Nephrol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone; WI4X0X7BPJ / Hydrocortisone
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