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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. Sperone P, Ferrero A, Daffara F, Priola A, Zaggia B, Volante M, Santini D, Vincenzi B, Badalamenti G, Intrivici C, Del Buono S, De Francia S, Kalomirakis E, Ratti R, Angeli A, Dogliotti L, Papotti M, Terzolo M, Berruti A: Gemcitabine plus metronomic 5-fluorouracil or capecitabine as a second-/third-line chemotherapy in advanced adrenocortical carcinoma: a multicenter phase II study. Endocr Relat Cancer; 2010 Jun;17(2):445-53
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  • [Title] Gemcitabine plus metronomic 5-fluorouracil or capecitabine as a second-/third-line chemotherapy in advanced adrenocortical carcinoma: a multicenter phase II study.
  • Adrenocortical carcinoma (ACC) is a rare neoplasm characterized by poor prognosis.
  • First-line systemic treatments in advanced disease include mitotane, either alone or in combination with chemotherapy.
  • They received a combination of i.v. gemcitabine (800 mg/m(2), on days 1 and 8, every 21 days) and i.v.
  • A complete response was observed in 1 patient (3.5%); 1 patient (3.5%) obtained a partial regression, 11 patients (39.3%) obtained a disease stabilization and 15 patients (53.7%) progressed.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Adrenocortical Carcinoma / drug therapy. Deoxycytidine / analogs & derivatives. Fluorouracil / administration & dosage. Fluorouracil / analogs & derivatives
  • [MeSH-minor] Adult. Aged. Antimetabolites, Antineoplastic / administration & dosage. Antimetabolites, Antineoplastic / adverse effects. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Capecitabine. Disease Progression. Drug Administration Schedule. Female. Humans. Leukopenia / chemically induced. Male. Middle Aged. Mucositis / chemically induced. Thrombocytopenia / chemically induced. Treatment Outcome

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  • [CommentIn] Nat Rev Endocrinol. 2010 Jul;6(7):355 [20583342.001]
  • (PMID = 20410174.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; 6804DJ8Z9U / Capecitabine; B76N6SBZ8R / gemcitabine; U3P01618RT / Fluorouracil
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3. Zivadinov R, Reder AT, Filippi M, Minagar A, Stüve O, Lassmann H, Racke MK, Dwyer MG, Frohman EM, Khan O: Mechanisms of action of disease-modifying agents and brain volume changes in multiple sclerosis. Neurology; 2008 Jul 8;71(2):136-44
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  • [Title] Mechanisms of action of disease-modifying agents and brain volume changes in multiple sclerosis.
  • Disease-modifying agents (DMAs), including interferon beta (IFNbeta) and glatiramer acetate (GA), are the mainstays of long-term treatment of multiple sclerosis (MS).
  • Other potent anti-inflammatory agents like natalizumab and different types of chemotherapeutics are increasingly being used for treatment of MS, particularly in patients with breakthrough disease activity.
  • Brain volume (BV) loss occurs early in the disease process, accelerates over time, and may be only partially affected by DMA therapy.
  • [MeSH-minor] Adrenal Cortex Hormones / adverse effects. Antibodies, Monoclonal / adverse effects. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / adverse effects. Atrophy / chemically induced. Cladribine / adverse effects. Glatiramer Acetate. Humans. Immunoglobulins, Intravenous / adverse effects. Interferon-beta / adverse effects. Natalizumab. Organ Size / drug effects. Peptides / adverse effects

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  • (PMID = 18606968.001).
  • [ISSN] 1526-632X
  • [Journal-full-title] Neurology
  • [ISO-abbreviation] Neurology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Anti-Inflammatory Agents; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Immunoglobulins, Intravenous; 0 / Natalizumab; 0 / Peptides; 3A189DH42V / alemtuzumab; 47M74X9YT5 / Cladribine; 5M691HL4BO / Glatiramer Acetate; 77238-31-4 / Interferon-beta
  • [Number-of-references] 60
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4. 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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5. Beuschlein F, Reincke M: Adrenocortical tumorigenesis. Ann N Y Acad Sci; 2006 Nov;1088:319-34
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  • [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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6. 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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7. Evans DG, Lunt P, Clancy T, Eeles R: Childhood predictive genetic testing for Li-Fraumeni syndrome. Fam Cancer; 2010 Mar;9(1):65-9
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  • In certain cancer prone conditions such as Familial Adenomatous Polyposis and Von Hippel Lindau disease there are risks of disease in childhood and benefit to children not inheriting a mutation in being able to forego unpleasant screening tests.
  • Li-Fraumeni syndrome caused by constitutional TP53 mutations there are also implications in childhood with a risk of around 20% of a childhood malignancy.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Adrenal Cortex Neoplasms / genetics. Genetic Predisposition to Disease. Genetic Testing / methods. Li-Fraumeni Syndrome / genetics. Prenatal Diagnosis / methods. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Adult. Age of Onset. Attitude to Health. Child. Databases, Genetic. Female. Forecasting. Genetic Counseling / ethics. Genotype. Humans. Loss of Heterozygosity. Molecular Sequence Data. MutS Homolog 2 Protein / genetics. Mutation. Neoplasm Proteins. Pedigree. Phenotype. Pregnancy. Protein Kinases. von Hippel-Lindau Disease / etiology. von Hippel-Lindau Disease / genetics

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  • (PMID = 19404774.001).
  • [ISSN] 1573-7292
  • [Journal-full-title] Familial cancer
  • [ISO-abbreviation] Fam. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Neoplasm Proteins; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; EC 2.7.- / Protein Kinases; EC 3.6.1.3 / MutS Homolog 2 Protein
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8. Yavascaoglu I, Yilmaz M, Kordan Y: Cardiac and caval invasion of left adrenocortical carcinoma. Urol Int; 2008;81(2):244-6
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  • [Title] Cardiac and caval invasion of left adrenocortical carcinoma.
  • Adrenocortical carcinoma (ACC) is a rare and highly malignant neoplasm.
  • We present the case of a 51-year-old male patient with a left-sided ACC admitted to hospital with ipsilateral flank pain, weight loss, difficulty in breathing, abdominal discomfort and swelling and bilateral leg edema.
  • Thoracoabdominal computed tomography revealed a huge adrenal mass with obvious tumor thrombus involvement of the inferior vena cava and right atrium.
  • This is the first report describing caval and opposite side renal vein invasion of a left-sided ACC treated with grafting of the vessels.
  • Histopathological examination of the tumors confirmed the diagnosis of ACC.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Heart Atria / pathology. Vena Cava, Inferior / pathology
  • [MeSH-minor] Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Invasiveness

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  • [Copyright] (c) 2008 S. Karger AG, Basel.
  • (PMID = 18758230.001).
  • [ISSN] 1423-0399
  • [Journal-full-title] Urologia internationalis
  • [ISO-abbreviation] Urol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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9. 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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10. 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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11. Laigle-Donadey F, Sanson M: [Pattern of care of high-grade gliomas]. Rev Prat; 2006 Oct 31;56(16):1779-86
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  • [Transliterated title] Prise en charge des gliomes de haut grade.
  • High grade gliomas are the most frequent and malignant primary brain tumours in adults.
  • Surgery is necessary for histological diagnosis.
  • This effect was particularly clear for patients with MGMT inactivation in the tumour, confirming here also the impact of molecular biology for future management of gliomas.
  • [MeSH-major] Brain Neoplasms / therapy. Glioma / therapy
  • [MeSH-minor] Adrenal Cortex Hormones / administration & dosage. Adrenal Cortex Hormones / therapeutic use. Adult. Age Factors. Aged. Anticonvulsants / therapeutic use. Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Agents, Alkylating / therapeutic use. Brain / pathology. Combined Modality Therapy. Dacarbazine / administration & dosage. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Epilepsy / prevention & control. Forecasting. Genetic Markers. Glioblastoma / drug therapy. Glioblastoma / radiotherapy. Humans. Magnetic Resonance Imaging. Neoplasm Recurrence, Local / drug therapy. Oligodendroglioma / drug therapy. Prognosis. Quality of Life. Radiotherapy Dosage. Randomized Controlled Trials as Topic. Survival Analysis. Thromboembolism / prevention & control. Time Factors. Tomography, X-Ray Computed

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  • (PMID = 17315503.001).
  • [ISSN] 0035-2640
  • [Journal-full-title] La Revue du praticien
  • [ISO-abbreviation] Rev Prat
  • [Language] fre
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Anticonvulsants; 0 / Antineoplastic Agents, Alkylating; 0 / Genetic Markers; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
  • [Number-of-references] 19
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12. Fassnacht M, Wittekind C, Allolio B: [Current TNM classification systems for adrenocortical carcinoma]. Pathologe; 2010 Sep;31(5):374-8
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  • [Title] [Current TNM classification systems for adrenocortical carcinoma].
  • Adrenocortical carcinoma (ACC) is a rare malignancy and often difficult to diagnose.
  • Therefore, the European Network for the Study of Adrenal Tumours (ENSAT) developed a revised staging system, the superiority of which was recently confirmed in an independent American cohort.
  • In the ENSAT classification, stage I (tumors ≤ 5 cm) and II (tumors < 5 cm) are non-infiltrating tumors without positive lymph nodes and distant metastases.
  • Stage III is defined by the presence of positive lymph nodes, infiltration of surrounding tissue, or venous tumor thrombus.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Neoplasm Staging / methods
  • [MeSH-minor] Adrenal Cortex / pathology. Cohort Studies. Disease Progression. Humans. Lymphatic Metastasis / pathology. Neoplasm Invasiveness / pathology. Neoplastic Cells, Circulating. Prognosis. Registries

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  • (PMID = 20703482.001).
  • [ISSN] 1432-1963
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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13. 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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14. de Reyniès A, Assié G, Rickman DS, Tissier F, Groussin L, René-Corail F, Dousset B, Bertagna X, Clauser E, Bertherat J: Gene expression profiling reveals a new classification of adrenocortical tumors and identifies molecular predictors of malignancy and survival. J Clin Oncol; 2009 Mar 1;27(7):1108-15
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  • [Title] Gene expression profiling reveals a new classification of adrenocortical tumors and identifies molecular predictors of malignancy and survival.
  • PURPOSE: Adrenocortical tumors, especially cancers, remain challenging both for their diagnosis and prognosis assessment.
  • PATIENTS AND METHODS: One hundred fifty-three unilateral adrenocortical tumors were studied by microarray (n = 92) or reverse transcription quantitative polymerase chain reaction (n = 148).
  • A two-gene predictor of malignancy was built using the disease-free survival as the end point in a training cohort (n = 47), then validated in an independent validation cohort (n = 104).
  • Similarly, for malignant tumors, a two-gene predictor of survival was built using the overall survival as the end point in a training cohort (n = 23), then tested in an independent validation cohort (n = 35).
  • RESULTS: Unsupervised clustering analysis discriminated robustly the malignant and benign tumors, and identified two groups of malignant tumors with very different outcome.
  • The combined expression of DLG7 and PINK1 was the best predictor of disease-free survival (log-rank P approximately 10(-12)), could overcome the uncertainties of intermediate pathological Weiss scores, and remained significant after adjustment to the Weiss score (P < 1.3 x 10(-2)).
  • Among the malignant tumors, the combined expression of BUB1B and PINK1 was the best predictor of overall survival (P < 2 x 10(-6)), and remained significant after adjusting for MacFarlane staging (P < .005).
  • CONCLUSION: Gene expression analysis unravels two distinct groups of adrenocortical carcinomas.
  • The molecular predictors of malignancy and of survival are reliable and provide valuable independent information in addition to pathology and tumor staging.
  • These original tools should provide important improvements for adrenal tumors management.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Biomarkers, Tumor / genetics. Neoplasm Proteins / genetics. Protein Kinases / genetics. Protein-Serine-Threonine Kinases / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cluster Analysis. Diagnosis, Differential. Disease-Free Survival. Female. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Proportional Hazards Models. Prospective Studies. Reproducibility of Results. Survival Analysis

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  • (PMID = 19139432.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DLGAP5 protein, human; 0 / Neoplasm Proteins; EC 2.7.- / Protein Kinases; EC 2.7.11.1 / Bub1 spindle checkpoint protein; EC 2.7.11.1 / PTEN-induced putative kinase; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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15. Grubbs EG, Callender GG, Xing Y, Perrier ND, Evans DB, Phan AT, Lee JE: Recurrence of adrenal cortical carcinoma following resection: surgery alone can achieve results equal to surgery plus mitotane. Ann Surg Oncol; 2010 Jan;17(1):263-70
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  • [Title] Recurrence of adrenal cortical carcinoma following resection: surgery alone can achieve results equal to surgery plus mitotane.
  • BACKGROUND: A recent nonrandomized interinstitutional study reported that adjuvant mitotane following surgery for adrenocortical carcinoma (ACC) was associated with decreased recurrence.
  • SI patients had a superior disease-free survival compared with SO patients (median 25 versus 12 months, P = 0.003), and SI patients also had a superior overall survival compared with SO patients (median not reached versus 44 months, P = 0.02).
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenocortical Carcinoma / surgery. Antineoplastic Agents, Hormonal / therapeutic use. Mitotane / therapeutic use. Neoplasm Recurrence, Local / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Chemotherapy, Adjuvant. Child. Child, Preschool. Combined Modality Therapy. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Staging. Retrospective Studies. Survival Rate. Treatment Outcome. Young Adult

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  • (PMID = 19851811.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 78E4J5IB5J / Mitotane
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16. Machens A, Dralle H: Adjuvant mitotane in adrenocortical carcinoma. N Engl J Med; 2007 Sep 20;357(12):1258-9; author reply 1259
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  • [Title] Adjuvant mitotane in adrenocortical carcinoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Adrenocortical Carcinoma / drug therapy. Antineoplastic Agents, Hormonal / administration & dosage. Mitotane / administration & dosage
  • [MeSH-minor] Chemotherapy, Adjuvant. Dose-Response Relationship, Drug. Humans. Multivariate Analysis. Neoplasm Recurrence, Local / prevention & control. Survival Analysis

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  • [CommentOn] N Engl J Med. 2007 Jun 7;356(23):2372-80 [17554118.001]
  • (PMID = 17891837.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 78E4J5IB5J / Mitotane
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17. Borne E, Serafi R, Piette F, Mortier L: Tumour lysis syndrome induced by corticosteroid in metastatic melanoma presenting with initial hyperkalemia. J Eur Acad Dermatol Venereol; 2009 Jul;23(7):855-6
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  • [Title] Tumour lysis syndrome induced by corticosteroid in metastatic melanoma presenting with initial hyperkalemia.
  • [MeSH-major] Adrenal Cortex Hormones / adverse effects. Hyperkalemia / complications. Melanoma / complications. Skin Neoplasms / complications. Tumor Lysis Syndrome / complications
  • [MeSH-minor] Adult. Humans. Male. Neoplasm Metastasis

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  • (PMID = 19646138.001).
  • [ISSN] 1468-3083
  • [Journal-full-title] Journal of the European Academy of Dermatology and Venereology : JEADV
  • [ISO-abbreviation] J Eur Acad Dermatol Venereol
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
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18. 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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  • [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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19. Bernini GP, Moretti A, Mannelli M, Ercolino T, Bardini M, Caramella D, Taurino C, Salvetti A: Unique association of non-functioning pheochromocytoma, ganglioneuroma, adrenal cortical adenoma, hepatic and vertebral hemangiomas in a patient with a new intronic variant in the VHL gene. J Endocrinol Invest; 2005 Dec;28(11):1032-7
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  • [Title] Unique association of non-functioning pheochromocytoma, ganglioneuroma, adrenal cortical adenoma, hepatic and vertebral hemangiomas in a patient with a new intronic variant in the VHL gene.
  • This was characterized by right adrenal pheochromocytoma associated with homolateral ganglioneuroma and controlateral adrenal cortical adenoma.
  • The three tumors, incidentally discovered, proved to be non-functioning (normal secretion of catecholamines and of other neuroendocrine peptides, glucocorticoids, mineralcorticoids and androgens).
  • Accordingly, the patient showed no sign or symptom of endocrine disease.
  • Computed tomography (CT) and magnetic resonance (MR) demonstrated a typical adenomatous lesion on the left adrenal gland with precocious uptake of the radiotracer on radioidine (131I)-norcholesterol adrenal scintigraphy, while the controlateral gland showed hyperdensity on CT, hyperintensity on MR and no uptake at adrenal scintigraphy.
  • The right adrenal gland was surgically removed and, microscopically, pheochromocytoma and ganglioneuroma areas appeared intermixed without a predominant component.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Adrenocortical Adenoma / genetics. Ganglioneuroma / genetics. Hemangioma / genetics. Liver Neoplasms / genetics. Neoplasms, Multiple Primary. Pheochromocytoma / genetics. Spinal Neoplasms / genetics. Von Hippel-Lindau Tumor Suppressor Protein / genetics
  • [MeSH-minor] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / pathology. Aged. DNA, Neoplasm / analysis. Female. Genetic Variation. Humans. Introns / genetics. Magnetic Resonance Imaging. Radionuclide Imaging. Tomography, X-Ray Computed

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  • (PMID = 16483185.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 2.3.2.27 / Von Hippel-Lindau Tumor Suppressor Protein; EC 6.3.2.- / VHL protein, human
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20. Kirwan C, Carney D, O'Keefe M: Merkel cell carcinoma metastasis to the iris in a 23 year old female. Ir Med J; 2009 Feb;102(2):53-4
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  • Histological diagnosis can be difficult and electron microscopy or immunohistochemistry are frequently required in addition to light microscopy.
  • Early diagnosis and complete surgical excision is associated with a favourable prognosis.
  • However, aggressive tumours with regional recurrence or distant metastases result in a median survival of 9 months.
  • [MeSH-major] Carcinoma, Merkel Cell / secondary. Iris / pathology. Iris Neoplasms / secondary. Skin Neoplasms / pathology
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Adult. Fatal Outcome. Female. Humans. Mydriatics. Neoplasm Recurrence, Local / radiotherapy. Scalp

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  • (PMID = 19405321.001).
  • [ISSN] 0332-3102
  • [Journal-full-title] Irish medical journal
  • [ISO-abbreviation] Ir Med J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Mydriatics
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21. 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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22. Menéndez Calderón MJ, Casal F, Prieto J, Cacho L, Tusón C: [Adrenocortical carcinoma. A retrospective analysis of five cases]. An Med Interna; 2006 Nov;23(11):533-6
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  • [Title] [Adrenocortical carcinoma. A retrospective analysis of five cases].
  • [Transliterated title] Carcinoma suprarrenal. Análisis retrospectivo de cinco casos.
  • We present five cases of adrenal cortical carcinoma, diagnosed in our hospital and we describe the clinical presentation, diagnostic methods and treatment.
  • It is a rare tumor, highly aggressive and prognosis is poor.
  • The diagnosis is based on the biochemical characterization of the hormonal profile and on imaging techniques, especially computed tomography and magnetic resonance.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology
  • [MeSH-minor] Adrenalectomy. Aged. Female. Humans. Male. Middle Aged. Neoplasm Staging. Retrospective Studies. Treatment Outcome

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  • (PMID = 17222069.001).
  • [ISSN] 0212-7199
  • [Journal-full-title] Anales de medicina interna (Madrid, Spain : 1984)
  • [ISO-abbreviation] An Med Interna
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
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23. Sahin U, Alkan A, Altundag K: Bone morphogenetic proteins and zoledronic acid. Ann Oncol; 2009 Dec;20(12):2019; author reply 2019
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  • [Title] Bone morphogenetic proteins and zoledronic acid.

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  • [CommentOn] Ann Oncol. 2009 Oct;20(10):1747 [19633056.001]
  • (PMID = 19752002.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Comment; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bone Density Conservation Agents; 0 / Bone Morphogenetic Proteins; 0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid
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24. Figueiredo BC, Sandrini R, Zambetti GP, Pereira RM, Cheng C, Liu W, Lacerda L, Pianovski MA, Michalkiewicz E, Jenkins J, Rodriguez-Galindo C, Mastellaro MJ, Vianna S, Watanabe F, Sandrini F, Arram SB, Boffetta P, Ribeiro RC: Penetrance of adrenocortical tumours associated with the germline TP53 R337H mutation. J Med Genet; 2006 Jan;43(1):91-6
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  • [Title] Penetrance of adrenocortical tumours associated with the germline TP53 R337H mutation.
  • BACKGROUND: An inherited germline P53 mutation has been identified in cases of childhood adrenocortical carcinoma (ACT), a neoplasm with a high incidence in southern Brazil.

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  • (PMID = 16033918.001).
  • [ISSN] 1468-6244
  • [Journal-full-title] Journal of medical genetics
  • [ISO-abbreviation] J. Med. Genet.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / CA-71907
  • [Publication-type] Letter; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ PMC2564508
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25. Korzeniewska M, Kołomecki K, Stepień H, Naze M, Stepień T, Kuzdak K: [Assessment of pro- and antiangiogenic factors blood serum concentrations in patients with hormonal inactive adrenal tumors]. Endokrynol Pol; 2005 Jan-Feb;56(1):39-44
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  • [Title] [Assessment of pro- and antiangiogenic factors blood serum concentrations in patients with hormonal inactive adrenal tumors].
  • INTRODUCTION: The growth and persistence of solid tumors and their metastases is connected with angiogenesis.
  • THE AIM OF THE STUDY: Evaluation the value of serum VEGF and soluble forms of VEGF receptors concentration as a marker of malignancy in patients with hormonal inactive adrenal tumors.
  • MATERIAL AND METHODS: Twenty seven patients (18 female, 9 male; mean age 48+/-4.3 years) with adrenocortical carcinoma (N=8), adrenal metastases (N=4) and adrenocortical adenoma (N=15) were included in this study.
  • Patients with adrenocortical carcinoma had the levels of VEGF (1263.8 pg/ml) significantly higher and of sVEGFR-2 (5893.7 pg/ml) significantly lower in comparison to control group (p<0.05).
  • On the other hand the mean VEGF (334.2 pg/ml) concentration in patients with benign adrenocortical adenoma wasn't significant different than in control group (p>0.05) but mean sVEGFR-1 (21.7 pg/ml) and sVEGFR-2 (7106.4 pg/ml) concentrations were significantly lower than in the control (p<0.05).
  • CONCLUSION: These data suggest that determination of VEGF and sVEGFR concentration in the serum of patients with hormonal inactive adrenal tumors may be applied as an additional marker of malignancy.
  • [MeSH-major] Adrenal Cortex Neoplasms / blood. Adrenal Cortex Neoplasms / pathology. Biomarkers, Tumor / blood. Vascular Endothelial Growth Factor A / blood
  • [MeSH-minor] Adrenocortical Adenoma / blood. Adrenocortical Adenoma / pathology. Adrenocortical Carcinoma / blood. Adrenocortical Carcinoma / pathology. Adrenocortical Carcinoma / secondary. Adult. Aged. Female. Humans. Male. Middle Aged. Neoplasm Staging. Vascular Endothelial Growth Factor Receptor-1 / blood. Vascular Endothelial Growth Factor Receptor-2 / blood

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  • (PMID = 16335673.001).
  • [ISSN] 0423-104X
  • [Journal-full-title] Endokrynologia Polska
  • [ISO-abbreviation] Endokrynol Pol
  • [Language] pol
  • [Publication-type] Controlled Clinical Trial; English Abstract; 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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26. 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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27. Fassnacht M, Johanssen S, Fenske W, Weismann D, Agha A, Beuschlein F, Führer D, Jurowich C, Quinkler M, Petersenn S, Spahn M, Hahner S, Allolio B, German ACC Registry Group: Improved survival in patients with stage II adrenocortical carcinoma followed up prospectively by specialized centers. J Clin Endocrinol Metab; 2010 Nov;95(11):4925-32
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  • [Title] Improved survival in patients with stage II adrenocortical carcinoma followed up prospectively by specialized centers.
  • CONTEXT: Median survival in stage II adrenocortical carcinoma (ACC) differs widely in published series ranging between 23 and more than 60 months.
  • OBJECTIVE: The objective of the study was a comparison of outcome in patients with stage II ACC who were followed up prospectively early after surgery and were counseled by a specialized center (prospective group) with patients who registered with the German ACC registry later than 4 months after diagnosis (retrospective group).
  • In the retrospective group, 67% of the patients had registered only after disease recurrence.
  • [MeSH-major] Adrenal Cortex Neoplasms / mortality. Adrenocortical Carcinoma / mortality
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Agents, Hormonal / therapeutic use. Chemotherapy, Adjuvant. Chi-Square Distribution. Female. Follow-Up Studies. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Mitotane / therapeutic use. Neoplasm Recurrence, Local. Neoplasm Staging. Prognosis. Referral and Consultation. Registries. Statistics, Nonparametric. Treatment Outcome

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  • (PMID = 20668036.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 78E4J5IB5J / Mitotane
  • [Investigator] Willenberg H; Morcos M; Fehm HL; Behrend M; Reisch N; Brauckhoff M; Arlt W; Beuschlein F; Saeger W; Müssig K; Denecke H; Hengst K
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28. Strosberg JR, Hammer GD, Doherty GM: Management of adrenocortical carcinoma. J Natl Compr Canc Netw; 2009 Jul;7(7):752-8; quiz 759
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  • [Title] Management of adrenocortical carcinoma.
  • Adrenocortical carcinomas (ACCs) are rare tumors that arise from the cortex of the adrenal gland with an incidence 1 to 2 per million.
  • The rarity of this tumor translates into a paucity of experience in managing patients in most medical centers.
  • This article describes the basic diagnostic and prognostic issues in adrenal cancer management, and presents detailed rationales for therapeutic management.
  • [MeSH-major] Adrenal Cortex Neoplasms / therapy. Adrenocortical Carcinoma / therapy
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Catecholamines / analysis. Chemotherapy, Adjuvant. Cushing Syndrome / drug therapy. Cushing Syndrome / etiology. Diagnostic Imaging. Humans. Hydrocortisone / analysis. Metanephrine / analysis. Mitotane / therapeutic use. Neoplasm Metastasis. Neoplasm Staging. Prognosis

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  • (PMID = 19635227.001).
  • [ISSN] 1540-1405
  • [Journal-full-title] Journal of the National Comprehensive Cancer Network : JNCCN
  • [ISO-abbreviation] J Natl Compr Canc Netw
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Catecholamines; 5001-33-2 / Metanephrine; 78E4J5IB5J / Mitotane; WI4X0X7BPJ / Hydrocortisone
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29. Fassnacht M, Allolio B: What is the best approach to an apparently nonmetastatic adrenocortical carcinoma? Clin Endocrinol (Oxf); 2010 Nov;73(5):561-5
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  • [Title] What is the best approach to an apparently nonmetastatic adrenocortical carcinoma?
  • In suspected nonmetastatic adrenocortical carcinoma (ACC) a careful preoperative diagnostic work up is needed including comprehensive endocrine analysis as recommended by the European Network for the Study of Adrenal Tumors (http://www.ENSAT.org/ACC.htm).
  • As many patients will suffer from tumor recurrence after seemingly complete removal of ACC, adjuvant treatment based on the individual risk status is recommended.
  • Key factors for risk assessment are tumor stage, resection status and the proliferation marker Ki67.
  • R1 resection) we recommend additional radiotherapy of the tumor bed.
  • In low/intermediate risk patients who cannot be included in this trial observation only can be justified in cases with a tumor diameter of <8 cm and no microscopic evidence for invasion of blood vessels or tumor capsule.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology
  • [MeSH-minor] Humans. Ki-67 Antigen / metabolism. Mitotane / therapeutic use. Neoplasm Recurrence, Local / pathology. Neoplasm Recurrence, Local / surgery. Neoplasm Staging. Treatment Outcome

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  • [Copyright] © 2010 Blackwell Publishing Ltd.
  • (PMID = 20738315.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 78E4J5IB5J / Mitotane
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30. Zancanella P, Pianovski MA, Oliveira BH, Ferman S, Piovezan GC, Lichtvan LL, Voss SZ, Stinghen ST, Callefe LG, Parise GA, Santana MH, Figueiredo BC: Mitotane associated with cisplatin, etoposide, and doxorubicin in advanced childhood adrenocortical carcinoma: mitotane monitoring and tumor regression. J Pediatr Hematol Oncol; 2006 Aug;28(8):513-24
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  • [Title] Mitotane associated with cisplatin, etoposide, and doxorubicin in advanced childhood adrenocortical carcinoma: mitotane monitoring and tumor regression.
  • PURPOSE: To define a mitotane dose for pediatric patients with adrenocortical cancer (ACC) that maintains therapeutic plasma levels (TL) between 14 and 20 microg/mL and to verify its antitumor efficacy in association with 8 cycles of cisplatin, etoposide, and doxorubicin (CED).
  • Minor to partial tumor remission was found in 5 patients (<1 y) and complete remission was found in 2 patients.
  • Of the 3 patients who are alive at the time of report, 1 patient has been without disease for 16 months, and 2 patients have progressive disease.
  • All patients had recurrent metastatic disease (2 to 9 times).
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Adrenocortical Carcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cisplatin / administration & dosage. Doxorubicin / administration & dosage. Etoposide / administration & dosage. Mitotane / administration & dosage
  • [MeSH-minor] Administration, Oral. Child. Child, Preschool. Disease Progression. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug Monitoring / methods. Drug Therapy, Combination. Female. Follow-Up Studies. Humans. Male. Neoplasm Staging. Prospective Studies. Remission Induction. Survival Rate. Time Factors. Treatment Outcome

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  • (PMID = 16912591.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 6PLQ3CP4P3 / Etoposide; 78E4J5IB5J / Mitotane; 80168379AG / Doxorubicin; Q20Q21Q62J / Cisplatin
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31. Huang H, Fojo T: Adjuvant mitotane for adrenocortical cancer--a recurring controversy. J Clin Endocrinol Metab; 2008 Oct;93(10):3730-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adjuvant mitotane for adrenocortical cancer--a recurring controversy.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Carcinoma / drug therapy. Mitotane / adverse effects. Mitotane / therapeutic use
  • [MeSH-minor] Antineoplastic Agents, Hormonal / adverse effects. Antineoplastic Agents, Hormonal / therapeutic use. Chemotherapy, Adjuvant. Dose-Response Relationship, Drug. Humans. Neoplasm Metastasis. Recurrence

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  • (PMID = 18842984.001).
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  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
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32. Cotesta D, Petramala L, Serra V, Giustini S, Divona L, Calvieri S, De Toma G, Ciardi A, Corsi A, Massa R, Reale MG, Letizia C: Pheochromocytoma associated with adrenocortical tumor in the same gland. Two case reports and literature review. Minerva Endocrinol; 2006 Jun;31(2):183-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pheochromocytoma associated with adrenocortical tumor in the same gland. Two case reports and literature review.
  • Pheochromocytomas are catecholamine-producing neuroendocrine tumours arising from chromaffin cells of the adrenal medulla or extra-adrenal paraganglionic system that show 2 distinctive features, rarity and clinical variability.
  • Pheochromocytoma occasionally is associated with pathological lesions of the adrenal cortex.
  • We present 2 cases of patients referred to our hospital with a finding of clinical suspected pheochromocytoma.
  • The diagnosis of pheochromocytoma was confirmed in both cases with laboratory analysis and the lesion was achieved by employing 3 imaging techniques: computed tomography (CT), magnetic resonance imaging (MRI) and scintigraphy with (123)I-metaiodobenzilguanidine (MIBG).
  • The patients underwent adrenalectomy and in the same adrenal gland we found a pheochromocytoma associated with a nonfunctioning cortical adenoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenal Gland Neoplasms / diagnosis. Adrenocortical Adenoma / diagnosis. Neoplasms, Multiple Primary / diagnosis. Pheochromocytoma / diagnosis
  • [MeSH-minor] 3-Iodobenzylguanidine. Adrenalectomy. Adult. Humans. Male. Middle Aged. Neurofibromatosis 1 / diagnosis. Radiopharmaceuticals. Treatment Outcome

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  • (PMID = 16682942.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 35MRW7B4AD / 3-Iodobenzylguanidine
  • [Number-of-references] 41
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33. 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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34. Boudou-Rouquette P, Alexandre J, Soubrane O, Bertagna X, Goldwasser F: Antitumoral effect of the bisphosphonate zoledronic acid against visceral metastases in an adrenocortical cancer patient. Ann Oncol; 2009 Oct;20(10):1747
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  • [Title] Antitumoral effect of the bisphosphonate zoledronic acid against visceral metastases in an adrenocortical cancer patient.

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  • [CommentIn] Ann Oncol. 2009 Dec;20(12):2019; author reply 2019 [19752002.001]
  • (PMID = 19633056.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid
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35. Topf S, Lüftl M, Neisius U, Brabletz T, Simon M Jr, Schuler G, Schultz ES: Mycosis fungoides palmaris et plantaris--an unusual variant of cutaneous T-cell lymphoma. Eur J Dermatol; 2006 Jan-Feb;16(1):84-6
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  • Sometimes the clinical diversity makes the diagnosis of MF, and especially its atypical forms, challenging.
  • [MeSH-major] Lymphoma, T-Cell, Cutaneous / pathology. Mycosis Fungoides / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adrenal Cortex Hormones / therapeutic use. Biopsy, Needle. Combined Modality Therapy. Follow-Up Studies. Hand Dermatoses / pathology. Hand Dermatoses / therapy. Humans. Immunohistochemistry. Male. Neoplasm Staging. PUVA Therapy / methods. Risk Assessment. Treatment Outcome

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  • (PMID = 16436350.001).
  • [ISSN] 1167-1122
  • [Journal-full-title] European journal of dermatology : EJD
  • [ISO-abbreviation] Eur J Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
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36. Doghman M, Arhatte M, Thibout H, Rodrigues G, De Moura J, Grosso S, West AN, Laurent M, Mas JC, Bongain A, Zambetti GP, Figueiredo BC, Auberger P, Martinerie C, Lalli E: Nephroblastoma overexpressed/cysteine-rich protein 61/connective tissue growth factor/nephroblastoma overexpressed gene-3 (NOV/CCN3), a selective adrenocortical cell proapoptotic factor, is down-regulated in childhood adrenocortical tumors. J Clin Endocrinol Metab; 2007 Aug;92(8):3253-60
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  • [Title] Nephroblastoma overexpressed/cysteine-rich protein 61/connective tissue growth factor/nephroblastoma overexpressed gene-3 (NOV/CCN3), a selective adrenocortical cell proapoptotic factor, is down-regulated in childhood adrenocortical tumors.
  • CONTEXT: Childhood adrenocortical tumors (ACTs) have a fetal adrenal phenotype and overexpress steroidogenic factor-1 (SF-1).
  • OBJECTIVE: The objective of the study was to measure NOV protein levels in childhood ACTs and characterize NOV expression regulation and biological function in human adrenocortical cells.
  • DESIGN AND SETTING: Protein extracts from ACT and normal adrenal cortex samples, human adrenocortical carcinoma H295R, primary adrenocortical tumors and fetal adrenal cultures, tissue culture supernatants, and cell lysates from H295R cells overexpressing SF-1 in an inducible fashion were used.
  • RESULTS: NOV mRNA and protein expression is lower in childhood ACTs than in normal adrenal cortex.
  • NOV has a selective proapoptotic activity toward human adrenocortical cells.
  • The C-terminal domain of NOV is responsible for its proapoptotic effect.
  • NOV protein is expressed in DAX-1-positive human fetal adrenal cells.
  • CONCLUSIONS: NOV is a selective proapoptotic factor for human adrenocortical cells.
  • Reduced expression of NOV in ACTs may play an important role in the process of childhood ACT tumorigenesis, accounting at least in part for the defect of apoptotic regression of the fetal adrenal that has been proposed to be responsible for tumor formation.
  • [MeSH-major] Adenoma / metabolism. Adrenal Cortex / cytology. Adrenal Cortex Neoplasms / metabolism. Apoptosis / genetics. Apoptosis / physiology. Carcinoma / metabolism. Gene Expression Regulation, Neoplastic / genetics. Immediate-Early Proteins / genetics. Intercellular Signaling Peptides and Proteins / genetics
  • [MeSH-minor] Caspases / metabolism. Cell Line, Tumor. Child. Connective Tissue Growth Factor. DNA, Complementary / biosynthesis. DNA, Complementary / genetics. Down-Regulation / genetics. Down-Regulation / physiology. Enzyme Activation / physiology. Flow Cytometry. Fluorescent Antibody Technique. Homeodomain Proteins / biosynthesis. Homeodomain Proteins / genetics. Humans. Immunoblotting. Luciferases / biosynthesis. Luciferases / genetics. Nephroblastoma Overexpressed Protein. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. RNA, Neoplasm / biosynthesis. RNA, Neoplasm / genetics. Receptors, Cytoplasmic and Nuclear / biosynthesis. Receptors, Cytoplasmic and Nuclear / genetics. Reverse Transcriptase Polymerase Chain Reaction. Steroidogenic Factor 1. Transcription Factors / biosynthesis. Transcription Factors / genetics. Transfection

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  • (PMID = 17566092.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA63230
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CTGF protein, human; 0 / DNA, Complementary; 0 / Homeodomain Proteins; 0 / Immediate-Early Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / NOV protein, human; 0 / NR5A1 protein, human; 0 / Nephroblastoma Overexpressed Protein; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Steroidogenic Factor 1; 0 / Transcription Factors; 139568-91-5 / Connective Tissue Growth Factor; EC 1.13.12.- / Luciferases; EC 3.4.22.- / Caspases
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37. Gaujoux S, Tissier F, Groussin L, Libé R, Ragazzon B, Launay P, Audebourg A, Dousset B, Bertagna X, Bertherat J: Wnt/beta-catenin and 3',5'-cyclic adenosine 5'-monophosphate/protein kinase A signaling pathways alterations and somatic beta-catenin gene mutations in the progression of adrenocortical tumors. J Clin Endocrinol Metab; 2008 Oct;93(10):4135-40
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  • [Title] Wnt/beta-catenin and 3',5'-cyclic adenosine 5'-monophosphate/protein kinase A signaling pathways alterations and somatic beta-catenin gene mutations in the progression of adrenocortical tumors.
  • BACKGROUND: The Wnt/beta-catenin and cAMP signaling pathways play an important role in adrenal cortex tumorigenesis.
  • Somatic activating mutations of the beta-catenin gene (CTNNB1) are the most frequent genetic defects identified both in adrenocortical adenomas (ACAs) and adrenocortical cancers (ACCs).
  • PRKAR1A mutations leading to cAMP pathway dysregulation are observed in primary pigmented nodular adrenocortical diseases (PPNADs) and some sporadic ACAs.
  • OBJECTIVE: The objective of the investigation was to study Wnt/beta-catenin dysregulation in adrenocortical tumors (ACTs) with cAMP pathway genetic alteration and search for secondary CTNNB1 somatic mutations in heterogeneous tumors.
  • PATIENTS AND METHODS: Nine PPNADs, including five with macronodules, three ACAs with PRKAR1A somatic mutations, and one heterogeneous tumor with ACC developed within an ACA, were studied by immunohistochemistry and DNA sequencing.
  • RESULTS: beta-Catenin accumulation was observed in all PPNADs, ACAs with PRKAR1A mutations, and the ACC component of the heterogeneous tumor.
  • In addition, the occurrence as an additional hit of a CTNNB1 somatic mutation is associated with larger or more aggressive ACTs.
  • This underlines the importance of the Wnt/beta-catenin pathway in adrenal cortex tumorigenesis and the importance of genetic accumulation in the progression of ACTs.
  • [MeSH-major] Adenoma / genetics. Adrenal Cortex Neoplasms / genetics. Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / genetics. Mutation. Signal Transduction / genetics. Wnt Proteins / genetics. beta Catenin / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Cyclic AMP / metabolism. DNA Mutational Analysis. Disease Progression. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Neoplasm Invasiveness. Tumor Burden / genetics

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  • (PMID = 18647815.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human; 0 / Wnt Proteins; 0 / beta Catenin; E0399OZS9N / Cyclic AMP
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38. Shimony A, Bereza S, Shalev A, Gilutz H, Ilia R, Zahger D: Ventricular fibrillation as the presenting manifestation of adrenocortical carcinoma. Am Heart Hosp J; 2009;7(1):65-6
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  • [Title] Ventricular fibrillation as the presenting manifestation of adrenocortical carcinoma.
  • We describe a case of a young adult in whom sudden cardiac death due to ventricular fibrillation was the presenting manifestation of an adrenocortical carcinoma.
  • The arrhythmia was precipitated by severe hypokalemia induced by the aldosterone-secreting tumor.
  • Sudden death has not been previously described as a manifestation of this adrenal neoplasm.
  • Unexplained persistent hypokalemia after resuscitated sudden death (especially when combined with hypertension( should prompt investigation for an underlying secondary hypertension, particularly adrenal pathology.
  • Adrenocortical carcinoma should be considered in the differential diagnosis of unexplained sudden death associated with unexplained hypokalemia.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenocortical Carcinoma / complications. Ventricular Fibrillation / etiology

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  • (PMID = 19742438.001).
  • [ISSN] 1751-7168
  • [Journal-full-title] The American heart hospital journal
  • [ISO-abbreviation] Am Heart Hosp J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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39. Lee JO, Lee KW, Kim CJ, Kim YJ, Lee HE, Kim H, Kim JH, Bang SM, Kim JS, Lee JS: Metastatic adrenocortical carcinoma treated with sunitinib: a case report. Jpn J Clin Oncol; 2009 Mar;39(3):183-5
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  • [Title] Metastatic adrenocortical carcinoma treated with sunitinib: a case report.
  • Adrenocortical carcinoma (ACC) is a rare malignancy with poor prognosis.
  • Palliative chemotherapy can be considered in patients with metastatic disease.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Adrenal Cortex Neoplasms / pathology. Antineoplastic Agents / therapeutic use. Carcinoma / drug therapy. Carcinoma / secondary. Indoles / therapeutic use. Pyrroles / therapeutic use
  • [MeSH-minor] Angiogenesis Inhibitors / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drug Resistance, Neoplasm. Humans. Male. Mitotane / administration & dosage. Radiotherapy, Adjuvant. Treatment Failure. Treatment Outcome. Young Adult

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  • (PMID = 19168875.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Indoles; 0 / Pyrroles; 0 / sunitinib; 78E4J5IB5J / Mitotane
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40. Sundberg AK, Roskopf JA, Hartmann EL, Farney AC, Rohr MS, Stratta RJ: Pilot study of rapid steroid elimination with alemtuzumab induction therapy in kidney and pancreas transplantation. Transplant Proc; 2005 Mar;37(2):1294-6
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  • [MeSH-major] Adrenal Cortex Hormones / administration & dosage. Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Immunosuppressive Agents / therapeutic use. Kidney Transplantation / immunology. Pancreas Transplantation / immunology


41. van't Sant HP, Bouvy ND, Kazemier G, Bonjer HJ, Hop WC, Feelders RA, de Herder WW, de Krijger RR: The prognostic value of two different histopathological scoring systems for adrenocortical carcinomas. Histopathology; 2007 Aug;51(2):239-45
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  • [Title] The prognostic value of two different histopathological scoring systems for adrenocortical carcinomas.
  • AIMS: To compare two different multiparameter histopathological scoring indices and determine their prognostic value in patients presenting with adrenocortical carcinoma (ACC).
  • METHODS AND RESULTS: Seventy-nine adrenal cortical tumours were divided into adenomas (n = 17), non-metastatic carcinomas (n = 24) and carcinomas with metastatic disease and/or local recurrence during follow-up (n = 19) or at time of presentation (n = 19).
  • Time from diagnosis of ACC to development of metastatic disease was correlated with the WRI (P = 0.036, r = -0.350).
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology
  • [MeSH-minor] Adenoma / pathology. Adolescent. Adult. Aged. Aged, 80 and over. Carcinoma / pathology. Carcinoma / secondary. Diagnosis, Differential. Disease-Free Survival. Female. Humans. Male. Middle Aged. Neoplasm Recurrence, Local / pathology. Prognosis

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  • (PMID = 17593212.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
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42. Terzolo M, Angeli A, Fassnacht M, Daffara F, Tauchmanova L, Conton PA, Rossetto R, Buci L, Sperone P, Grossrubatscher E, Reimondo G, Bollito E, Papotti M, Saeger W, Hahner S, Koschker AC, Arvat E, Ambrosi B, Loli P, Lombardi G, Mannelli M, Bruzzi P, Mantero F, Allolio B, Dogliotti L, Berruti A: Adjuvant mitotane treatment for adrenocortical carcinoma. N Engl J Med; 2007 Jun 7;356(23):2372-80
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  • [Title] Adjuvant mitotane treatment for adrenocortical carcinoma.
  • BACKGROUND: Adrenocortical carcinoma is a rare neoplasm characterized by a high risk of recurrence after radical resection.
  • METHODS: We performed a retrospective analysis involving 177 patients with adrenocortical cancer who had undergone radical surgery at 8 centers in Italy and 47 centers in Germany between 1985 and 2005.
  • RESULTS: Baseline features in the mitotane group and the control group from Italy were similar; the German patients were significantly older (P=0.03) and had more stage I or II adrenocortical carcinomas (P=0.02) than did patients in the mitotane group.
  • CONCLUSIONS: Adjuvant mitotane may prolong recurrence-free survival in patients with radically resected adrenocortical carcinoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Adrenocortical Carcinoma / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Mitotane / therapeutic use
  • [MeSH-minor] Chemotherapy, Adjuvant. Humans. Multivariate Analysis. Neoplasm Recurrence, Local / epidemiology. Neoplasm Recurrence, Local / prevention & control. Retrospective Studies. Survival Analysis


43. Blanes A, Diaz-Cano SJ: Histologic criteria for adrenocortical proliferative lesions: value of mitotic figure variability. Am J Clin Pathol; 2007 Mar;127(3):398-408
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  • [Title] Histologic criteria for adrenocortical proliferative lesions: value of mitotic figure variability.
  • This study compared 3 systems and a newly designed stepwise discriminant diagnostic system (SDDS) to assess accuracy, reproducibility, and reliability in adrenocortical nodular hyperplasia (ACNH; n = 82), adenoma (ACA; n = 78), and carcinoma (ACC; n = 32) (diagnoses according to World Health Organization criteria; median follow-up, 135 months).
  • In cross-validations, we studied cortex appearance, growth pattern, cytoplasmic features, nuclear parameters, mitotic figure counting (MFC), necrosis, invasion, and stromal-inflammatory reactions.
  • The SDDS independent predictors were MFC/high-power field SD, anisokaryosis, cortex appearance, and stromal reaction, correctly classifying 100% of ACNH, 91% of ACA, and 88% of ACC cases.
  • MFC variability is the most important adrenocortical malignancy criterion.
  • Accurate malignancy diagnosis requires multiple variable evaluations, provided by SDDS (the most specific system) and the Weiss or van Slooten system (the most sensitive).
  • SDDS is the most useful system for distinguishing tumors from ACNH (myxoid stroma and anisokaryosis).
  • [MeSH-major] Adrenal Cortex / pathology. Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / pathology. Adrenocortical Carcinoma / pathology
  • [MeSH-minor] Adult. Aged. Algorithms. Diagnosis, Differential. Disease-Free Survival. Female. Humans. Hyperplasia. Male. Middle Aged. Mitosis. Necrosis. Neoplasm Staging. Prognosis. Reproducibility of Results

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  • (PMID = 17276949.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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44. Chamberlain MC: 10 Questions about the use of bevacizumab in the management of recurrent malignant gliomas. Neurologist; 2010 Jan;16(1):56-60
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  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antibodies, Monoclonal / therapeutic use. Brain Neoplasms / drug therapy. Glioma / drug therapy. Neoplasm Recurrence, Local / drug therapy
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Antibodies, Monoclonal, Humanized. Antineoplastic Combined Chemotherapy Protocols. Bevacizumab. Disease Progression. Drug Approval. Humans. Treatment Outcome. United States. United States Food and Drug Administration

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  • (PMID = 20065801.001).
  • [ISSN] 2331-2637
  • [Journal-full-title] The neurologist
  • [ISO-abbreviation] Neurologist
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 2S9ZZM9Q9V / Bevacizumab
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45. Chen TW, Tsai CH, Chou SJ, Yu CY, Shih ML, Yu JC, Hsieh CB: Intrapericardial isolation of the inferior vena cava through a transdiaphragmatic pericardial window for tumor resection without sternotomy or thoracotomy. Eur J Surg Oncol; 2007 Mar;33(2):239-42
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  • [Title] Intrapericardial isolation of the inferior vena cava through a transdiaphragmatic pericardial window for tumor resection without sternotomy or thoracotomy.
  • AIMS: The prognosis for patients with advanced tumors invading the inferior vena cava (IVC) is dismal and surgical treatments for these tumors are challenging.
  • A surgical approach that avoids sternotomy and thoracotomy for tumors invading the IVC even to the level of the hepatocaval junction would be extremely helpful.
  • We removed the primary tumor, the liver portion involved and the tumor thrombi, with segmental resection of the IVC.
  • RESULTS: Four patients with tumors invading the IVC were treated with this method.
  • All underwent gross en-bloc tumor resections and all survived.
  • CONCLUSION: This method for the resection of IVC tumors could avoid emboli dislodging from the tumor thrombi, prevent the complications of sternotomy, cardiopulmonary bypass and shorten operative times.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Leiomyosarcoma / pathology. Liver Neoplasms / pathology. Pericardium / surgery. Vascular Surgical Procedures / methods. Vena Cava, Inferior / surgery
  • [MeSH-minor] Adrenocortical Carcinoma / pathology. Adrenocortical Carcinoma / radiography. Adrenocortical Carcinoma / surgery. Carcinoma, Hepatocellular / pathology. Carcinoma, Hepatocellular / radiography. Carcinoma, Hepatocellular / surgery. Hepatectomy. Humans. Neoplasm Invasiveness. Sternum / surgery. Thoracotomy / contraindications. Treatment Outcome

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  • (PMID = 17174512.001).
  • [ISSN] 0748-7983
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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46. Papewalis C, Fassnacht M, Willenberg HS, Domberg J, Fenk R, Rohr UP, Schinner S, Bornstein SR, Scherbaum WA, Schott M: Dendritic cells as potential adjuvant for immunotherapy in adrenocortical carcinoma. Clin Endocrinol (Oxf); 2006 Aug;65(2):215-22
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  • [Title] Dendritic cells as potential adjuvant for immunotherapy in adrenocortical carcinoma.
  • OBJECTIVE: Adrenocortical carcinoma (ACC) is a rare malignancy associated with a dismal prognosis.
  • DESIGN/PATIENTS: Autologous DCs were pulsed with autologous tumour lysate (TL).
  • Fusion of DCs with tumour cells was based on a polyethylene glycol method.
  • Clinical response was monitored by CT scan of tumour mass and measurement of angiogenic factors.
  • The DC/tumour cell fusion efficacy was approximately 45% as shown by double positive staining for ACTH receptor and DC-specific CD83.
  • Although angiogenic serum markers could be stabilized, no impact on tumour growth could be observed.
  • CONCLUSION: Our data demonstrate that autologous dendritic cells induce antigen-specific Th1 immunity in adrenocortical carcinoma.
  • [MeSH-major] Adjuvants, Immunologic / administration & dosage. Adrenal Cortex Neoplasms / therapy. Adrenocortical Carcinoma / therapy. Cancer Vaccines / administration & dosage. Dendritic Cells / transplantation
  • [MeSH-minor] Adult. Antigens, Neoplasm / immunology. Antineoplastic Agents / therapeutic use. Fatal Outcome. Flow Cytometry. Humans. Hybridomas. Hypersensitivity, Delayed / immunology. Injections. Male. Microscopy, Electron. Middle Aged. Mitotane / therapeutic use. Treatment Failure

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  • (PMID = 16886963.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Cancer Vaccines; 78E4J5IB5J / Mitotane
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47. 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


48. Tan HS, Thai AC, Nga ME, Mukherjee JJ: Development of ipsilateral adrenocortical carcinoma sixteen years after resection of an adrenal tumour causing Cushing's syndrome. Ann Acad Med Singapore; 2005 Apr;34(3):271-4
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  • [Title] Development of ipsilateral adrenocortical carcinoma sixteen years after resection of an adrenal tumour causing Cushing's syndrome.
  • INTRODUCTION: At times, it may be difficult to differentiate early stage, low-grade adrenocortical carcinoma from benign adrenal adenoma.
  • CLINICAL PICTURE: A 53-year-old lady underwent right adrenalectomy for a 4-cm adrenocortical tumour causing Cushing's syndrome.
  • Histology revealed an adrenocortical adenoma.
  • Sixteen years later, she presented with a 14-cm adrenal tumour, again on the right side.
  • TREATMENT: She underwent surgical removal of the tumour.
  • Histology confirmed adrenocortical carcinoma.
  • OUTCOME: She died of metastatic disease 17 months later.
  • CONCLUSIONS: This case highlights the importance of long-term, systematic follow-up of patients treated for benign adrenal adenomas, especially if the tumour size exceeds 4 cm.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Cushing Syndrome / etiology. Neoplasm Recurrence, Local / pathology
  • [MeSH-minor] Adrenocortical Adenoma / pathology. Diagnosis, Differential. Fatal Outcome. Female. Humans. Middle Aged


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

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  • [Copyright] Copyright © 2010 European Association of Urology. Published by Elsevier B.V. All rights reserved.
  • (PMID = 20137850.001).
  • [ISSN] 1873-7560
  • [Journal-full-title] European urology
  • [ISO-abbreviation] Eur. Urol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
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50. Williams TA, Monticone S, Morello F, Liew CC, Mengozzi G, Pilon C, Asioli S, Sapino A, Veglio F, Mulatero P: Teratocarcinoma-derived growth factor-1 is upregulated in aldosterone-producing adenomas and increases aldosterone secretion and inhibits apoptosis in vitro. Hypertension; 2010 Jun;55(6):1468-75
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  • However, the molecular mechanisms involved in adrenal tumorigenesis and deregulated aldosterone secretion are currently unknown.
  • In vitro studies and Western blot analysis using the NCI H295R adrenocortical cell line showed that TDGF-1 increased Akt phosphorylation on Thr308 and Ser473, consistent with activation of phosphatidylinositol 3-kinase/Akt signaling, and also demonstrated a concomitant inactivation of the Akt substrate glycogen synthesis kinase-3beta via Ser9 phosphorylation.
  • Taken together, our data suggest that TDGF-1, which is significantly upregulated in APA and mediates aldosterone hypersecretion and deregulated growth in adrenocortical cells in vitro, may represent a key player in the development and pathophysiology of primary aldosteronism.
  • [MeSH-major] Adenoma / secretion. Adrenal Cortex Neoplasms / secretion. Aldosterone / secretion. Apoptosis / physiology. Biomarkers, Tumor / metabolism. Caspase 3 / metabolism. Epidermal Growth Factor / metabolism. Membrane Glycoproteins / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Adrenalectomy. Adult. Aged. Biopsy, Needle. Blotting, Western. Cell Proliferation. Female. GPI-Linked Proteins. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Intercellular Signaling Peptides and Proteins. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. RNA, Neoplasm / analysis. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Tissue Culture Techniques. Tumor Cells, Cultured. Up-Regulation

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  • [CommentIn] Hypertension. 2010 Jun;55(6):1306-7 [20385966.001]
  • (PMID = 20385969.001).
  • [ISSN] 1524-4563
  • [Journal-full-title] Hypertension (Dallas, Tex. : 1979)
  • [ISO-abbreviation] Hypertension
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / GPI-Linked Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Glycoproteins; 0 / Neoplasm Proteins; 0 / RNA, Neoplasm; 0 / TDGF1 protein, human; 4964P6T9RB / Aldosterone; 62229-50-9 / Epidermal Growth Factor; EC 3.4.22.- / Caspase 3
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51. 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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52. Soga H, Takenaka A, Ooba T, Nakano Y, Miyake H, Takeda M, Tanaka K, Hara I, Fujisawa M: A twelve-year experience with adrenal cortical carcinoma in a single institution: long-term survival after surgical treatment and transcatheter arterial embolization. Urol Int; 2009;82(2):222-6
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  • [Title] A twelve-year experience with adrenal cortical carcinoma in a single institution: long-term survival after surgical treatment and transcatheter arterial embolization.
  • INTRODUCTION: We retrospectively analyzed 6 cases of adrenal cortical carcinoma (ACC) treated during a 12-year period at a single institution.
  • The mean age at diagnosis was 53.3 years (range 36-72).
  • [MeSH-major] Adrenal Cortex Neoplasms / therapy. Adrenalectomy. Adrenocortical Carcinoma / therapy. Chemoembolization, Therapeutic
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Neoplasms / secondary. Bone Neoplasms / therapy. Female. Humans. Japan. Liver Neoplasms / secondary. Liver Neoplasms / therapy. Male. Middle Aged. Neoplasm Staging. Reoperation. Retrospective Studies. Survival Analysis. Time Factors. Tomography, X-Ray Computed. Treatment Outcome

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19322014.001).
  • [ISSN] 1423-0399
  • [Journal-full-title] Urologia internationalis
  • [ISO-abbreviation] Urol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
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53. Ziegler CG, Brown JW, Schally AV, Erler A, Gebauer L, Treszl A, Young L, Fishman LM, Engel JB, Willenberg HS, Petersenn S, Eisenhofer G, Ehrhart-Bornstein M, Bornstein SR: Expression of neuropeptide hormone receptors in human adrenal tumors and cell lines: antiproliferative effects of peptide analogues. Proc Natl Acad Sci U S A; 2009 Sep 15;106(37):15879-84
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  • [Title] Expression of neuropeptide hormone receptors in human adrenal tumors and cell lines: antiproliferative effects of peptide analogues.
  • A hallmark of adrenocortical tumor formation is the aberrant expression of peptide receptors relating to uncontrolled cell proliferation and hormone overproduction.
  • Our microarray results have also demonstrated a differential expression of neuropeptide hormone receptors in tumor subtypes of human pheochromocytoma.
  • In light of these findings, we performed a comprehensive analysis of relevant receptors in both human adrenomedullary and adrenocortical tumors and tested the antiproliferative effects of peptide analogues targeting these receptors.
  • Specifically, we examined the receptor expression of somatostatin-type-2 receptor, growth hormone-releasing hormone (GHRH) receptor or GHRH receptor splice variant-1 (SV-1) and luteinizing hormone-releasing hormone (LHRH) receptor at the mRNA and protein levels in normal human adrenal tissues, adrenocortical and adrenomedullary tumors, and cell lines.
  • Cytotoxic derivatives of somatostatin AN-238 and, to a lesser extent, AN-162, reduced cell numbers of uninduced and NGF-induced adrenomedullary pheochromocytoma cells and adrenocortical cancer cells.
  • Both the splice variant of GHRH receptor SV-1 and the LHRH receptor were also expressed in adrenocortical cancer cell lines but not in the pheochromocytoma cell line.
  • The GHRH receptor antagonist MZ-4-71 and LHRH antagonist Cetrorelix both significantly reduced cell growth in the adrenocortical cancer cell line.
  • In conclusion, the expression of receptors for somatostatin, GHRH, and LHRH in the normal human adrenal and in adrenal tumors, combined with the growth-inhibitory effects of the antitumor peptide analogues, may make possible improved treatment approaches to adrenal tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / drug therapy. Adrenal Gland Neoplasms / metabolism. Neuropeptides / pharmacology. Receptors, Neuropeptide / metabolism
  • [MeSH-minor] 2-Hydroxyphenethylamine / analogs & derivatives. 2-Hydroxyphenethylamine / pharmacology. Adrenal Glands / metabolism. Aniline Compounds / pharmacology. Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Cytostatic Agents / pharmacology. Doxorubicin / analogs & derivatives. Doxorubicin / pharmacology. Gene Expression. Humans. Oligonucleotide Array Sequence Analysis. PC12 Cells. Pyrroles / pharmacology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Receptors, LHRH / genetics. Receptors, LHRH / metabolism. Receptors, Somatostatin / genetics. Receptors, Somatostatin / metabolism. Somatostatin / analogs & derivatives. Somatostatin / pharmacology

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  • (PMID = 19717419.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AN 238; 0 / Aniline Compounds; 0 / Cytostatic Agents; 0 / Neuropeptides; 0 / Pyrroles; 0 / RNA, Messenger; 0 / Receptors, LHRH; 0 / Receptors, Neuropeptide; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 2PK59M9GFF / vapreotide; 33189-65-0 / N-(2-diethylaminoethyl)-N-(2-hydroxy-2-phenylethyl)-2,5-dichloroaniline; 51110-01-1 / Somatostatin; 7568-93-6 / 2-Hydroxyphenethylamine; 80168379AG / Doxorubicin
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54. Berthon A, Sahut-Barnola I, Lambert-Langlais S, de Joussineau C, Damon-Soubeyrand C, Louiset E, Taketo MM, Tissier F, Bertherat J, Lefrançois-Martinez AM, Martinez A, Val P: Constitutive beta-catenin activation induces adrenal hyperplasia and promotes adrenal cancer development. Hum Mol Genet; 2010 Apr 15;19(8):1561-76
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  • [Title] Constitutive beta-catenin activation induces adrenal hyperplasia and promotes adrenal cancer development.
  • Adrenocortical carcinoma is a rare but aggressive cancer with unknown aetiology.
  • Constitutive activation of beta-catenin is the most frequent alteration in benign and malignant adrenocortical tumours in patients.
  • Here, we show that constitutive activation of beta-catenin in the adrenal cortex of transgenic mice resulted in progressive steroidogenic and undifferentiated spindle-shaped cells hyperplasia as well as dysplasia of the cortex and medulla.
  • Altogether these observations demonstrate that constitutively active beta-catenin is an adrenal oncogene which triggers benign aldosterone-secreting tumour development and promotes malignancy.
  • [MeSH-major] Adrenal Cortex / pathology. Adrenal Gland Neoplasms / metabolism. Adrenal Gland Neoplasms / pathology. beta Catenin / metabolism
  • [MeSH-minor] Aldosterone / metabolism. Animals. Cell Proliferation. Disease Models, Animal. Humans. Hyperplasia. Mice. Mice, Inbred C57BL. Mice, Transgenic. Neoplasm Metastasis


55. 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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56. Berthelot C, Rivera A, Duvic M: Skin directed therapy for mycosis fungoides: a review. J Drugs Dermatol; 2008 Jul;7(7):655-66
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  • Mycosis fungoides (MF) is a rare neoplasm of epidermotropic CD4+ lymphocytes and represents a majority of all cutaneous T cell lymphomas.
  • More aggressive systemic treatment of early disease does not alter survival or cure the disease and could accelerate progression by causing immunosuppression.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Mycosis Fungoides / drug therapy. Photochemotherapy. Photosensitizing Agents / therapeutic use. Skin Neoplasms / drug therapy
  • [MeSH-minor] Administration, Topical. Adrenal Cortex Hormones / therapeutic use. Calcineurin Inhibitors. Combined Modality Therapy. Humans. Lasers, Excimer / therapeutic use. Retinoids / therapeutic use

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  • (PMID = 18664158.001).
  • [ISSN] 1545-9616
  • [Journal-full-title] Journal of drugs in dermatology : JDD
  • [ISO-abbreviation] J Drugs Dermatol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / K24-CA86815
  • [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 / Adrenal Cortex Hormones; 0 / Antineoplastic Agents; 0 / Calcineurin Inhibitors; 0 / Photosensitizing Agents; 0 / Retinoids
  • [Number-of-references] 163
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57. Pan CC, Lee WL: Vaginal obliteration in a woman with a history of cutaneous T-cell lymphoma: the results of combined chemotherapy-induced gonadal toxicity and lymphoma relapse. Taiwan J Obstet Gynecol; 2010 Mar;49(1):69-71
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  • In this case, vaginal obliteration was an early sign of tumor recurrence, although menopause may have contributed to the vaginal obliteration.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Lymphoma, T-Cell, Cutaneous / pathology. Neoplasm Recurrence, Local. Surgically-Created Structures. Vagina / surgery. Vaginal Neoplasms / pathology
  • [MeSH-minor] Adrenal Cortex Hormones / administration & dosage. Adrenal Cortex Hormones / adverse effects. Adult. Bleomycin / administration & dosage. Bleomycin / adverse effects. Cyclophosphamide / administration & dosage. Cyclophosphamide / adverse effects. Doxorubicin / administration & dosage. Doxorubicin / adverse effects. Female. Humans. Prednisolone / administration & dosage. Prednisolone / adverse effects. Vincristine / administration & dosage. Vincristine / adverse effects

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  • (PMID = 20466296.001).
  • [ISSN] 1875-6263
  • [Journal-full-title] Taiwanese journal of obstetrics & gynecology
  • [ISO-abbreviation] Taiwan J Obstet Gynecol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 11056-06-7 / Bleomycin; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone
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58. Amo Trillo V, Vera García P, Pinto I, Olmedo Martín R, Romero Blasco B: [Extramedullary plasmacytoma of the colon]. Gastroenterol Hepatol; 2007 May;30(5):277-9
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  • [Transliterated title] Plasmocitoma extramedular de localización colónica.
  • We report the case of a 68 year-old man in whom a tumour of the colon was identified by colonoscopy, during diagnostic studies for lower gastrointestinal bleeding as an outpatient.
  • Diagnosis of plasmacytoma of the colon was made.
  • We have carried out a review of the literature in relation to this unusual disorder.
  • [MeSH-major] Plasmacytoma / diagnosis. Sigmoid Neoplasms / diagnosis
  • [MeSH-minor] Adrenal Cortex Hormones / administration & dosage. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Colonoscopy. Combined Modality Therapy. Diverticulum / complications. Fatal Outcome. Gastrointestinal Hemorrhage / etiology. Hemorrhoids / complications. Humans. Lymphatic Metastasis. Male. Melphalan / administration & dosage. Neoplasm Recurrence, Local / drug therapy. Rectum

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  • (PMID = 17493438.001).
  • [ISSN] 0210-5705
  • [Journal-full-title] Gastroenterología y hepatología
  • [ISO-abbreviation] Gastroenterol Hepatol
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; Q41OR9510P / Melphalan
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59. Chiche L, Dousset B, Kieffer E, Chapuis Y: Adrenocortical carcinoma extending into the inferior vena cava: presentation of a 15-patient series and review of the literature. Surgery; 2006 Jan;139(1):15-27
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  • [Title] Adrenocortical carcinoma extending into the inferior vena cava: presentation of a 15-patient series and review of the literature.
  • BACKGROUND: Involvement of the inferior vena cava (IVC) is a controversial risk factor for surgical treatment of adrenocortical carcinoma (ACC).
  • Long-term prognosis is poor owing to delay in diagnosis, frequent associated metastatic disease and lack of effective adjuvant treatment.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / surgery. Adrenocortical Carcinoma / diagnosis. Adrenocortical Carcinoma / surgery
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Angiography. Female. Follow-Up Studies. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Invasiveness / pathology. Neoplasm Invasiveness / radiography. Neoplasm Recurrence, Local. Prognosis. Reoperation. Survival Analysis. Tomography, X-Ray Computed. Treatment Outcome. Vena Cava, Inferior / pathology. Vena Cava, Inferior / radiography

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  • (PMID = 16364713.001).
  • [ISSN] 0039-6060
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 78
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60. Gottschling S, Schneider G, Meyer S, Reinhard H, Dill-Mueller D, Graf N: Two infants with life-threatening diffuse neonatal hemangiomatosis treated with cyclophosphamide. Pediatr Blood Cancer; 2006 Feb;46(2):239-42
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  • Diffuse neonatal hemangiomatosis (DNH) is a rare, frequently fatal disorder characterized by multiple cutaneous and visceral hemangiomas.
  • [MeSH-major] Angiomatosis / drug therapy. Antineoplastic Agents, Alkylating / administration & dosage. Cyclophosphamide / administration & dosage. Hemangioma / drug therapy. Liver Neoplasms / drug therapy
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Disseminated Intravascular Coagulation / etiology. Drug Resistance, Neoplasm / drug effects. Female. Heart Diseases / etiology. Humans. Infant, Newborn. Male. Remission Induction. Treatment Outcome

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  • [CommentIn] Pediatr Blood Cancer. 2006 Dec;47(7):972-3 [16609951.001]
  • (PMID = 16369922.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Antineoplastic Agents, Alkylating; 8N3DW7272P / Cyclophosphamide
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61. Montone KT, Rosen M, Siegelman ES, Fogt F, Livolsi VA: Adrenocortical neoplasms with myelolipomatous and lipomatous metaplasia: report of 3 cases. Endocr Pract; 2009 Mar;15(2):128-33
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  • [Title] Adrenocortical neoplasms with myelolipomatous and lipomatous metaplasia: report of 3 cases.
  • OBJECTIVE: To present pathologic and radiographic features of 3 patients with adrenocortical neoplasms-2 with uncertain malignant potential and 1 adenoma with areas of myelolipomatous and lipomatous metaplasia.
  • METHODS: We describe 3 patients who had adrenocortical neoplasms with foci of myelolipomatous and lipomatous metaplasia.
  • Two patients showed imaging findings compatible with adrenal myelolipoma.
  • Pathologically, 2 of the lesions were classified as adrenocortical neoplasms of uncertain malignant potential, and 1 lesion was classified as an adrenocortical adenoma.
  • All 3 lesions contained myelolipomatous foci throughout the neoplasm, and 2 of the tumors contained several pure lipomatous foci.
  • CONCLUSION: Adrenocortical neoplasms, including those associated with an uncertain malignant potential, may be associated with areas of myelolipomatous and lipomatous metaplasia.
  • Imaging studies may result in a false diagnosis of a benign adrenal myelolipoma and potential undertreatment in such patients.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / pathology. Lipomatosis / diagnosis. Metaplasia / diagnosis. Myelolipoma / diagnosis

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  • (PMID = 19289323.001).
  • [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
  • [Publication-country] United States
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62. Wen MJ, Lin YF, Chen JS: Newly developed hypertension as an early marker of recurrence of adrenocortical carcinoma with high renin expression. Int J Urol; 2008 Jun;15(6):540-2
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  • [Title] Newly developed hypertension as an early marker of recurrence of adrenocortical carcinoma with high renin expression.
  • Adrenocortical carcinoma can recur frequently after successful surgery but no adequate markers can detect this recurrence.
  • Here, we present a recurrence of adrenocortical carcinoma with a high renin expression, after successful surgery, where hypertension has developed again.
  • Tumor recurrence was observed via (18)F-fluorodeoxyglucose positron emission tomography and coregistered computed tomography.
  • Based on our findings, follow-up blood pressure assessment may effectively predict the recurrence of adrenocortical carcinoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenal Cortex Neoplasms / metabolism. Adrenocortical Carcinoma / complications. Adrenocortical Carcinoma / metabolism. Hypertension / etiology. Neoplasm Recurrence, Local / complications. Neoplasm Recurrence, Local / metabolism. Renin / biosynthesis

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  • (PMID = 18489644.001).
  • [ISSN] 1442-2042
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] EC 3.4.23.15 / Renin
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63. Gur C, Salmon A, Silvetski N, Gross DJ: [Adrenocortical carcinoma]. Harefuah; 2008 Jun;147(6):520-5, 574
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  • [Title] [Adrenocortical carcinoma].
  • Adrenocortical carcinoma (ACC) is a rare cancer with a generally poor prognosis.
  • In approximately 60% of cases the initial clinical manifestations are due to hypersecretion of adrenocortical hormones.
  • In the remainder of the cases the tumor is identified after imaging procedures for nonspecific complaints such as abdominal pain and nausea.
  • Medical therapy is employed in patients with unresectable or partially resected tumor and metastatic disease.
  • The current accepted treatment is a combination of Mitotane with chemotherapy, aimed at controlling hormonal hypersecretion and reduction of tumor mass.
  • In ACC patients there is wide variability in the course of the disease: some with metastatic disease will survive for more than 10 years, others succumb to the disease within months.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Cushing Syndrome / etiology. Humans. Nausea / etiology. Neoplasm Staging. Pain / etiology. Survival Analysis

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  • (PMID = 18693629.001).
  • [ISSN] 0017-7768
  • [Journal-full-title] Harefuah
  • [ISO-abbreviation] Harefuah
  • [Language] heb
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Israel
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 36
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64. Vivarelli M, Dazzi A, Zanello M, Cucchetti A, Cescon M, Ravaioli M, Del Gaudio M, Lauro A, Grazi GL, Pinna AD: Effect of different immunosuppressive schedules on recurrence-free survival after liver transplantation for hepatocellular carcinoma. Transplantation; 2010 Jan 27;89(2):227-31
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  • BACKGROUND: Tumor recurrence represents the main limitation of liver transplantation in patients with hepatocellular carcinoma (HCC) and can be favored by exposure to calcineurin inhibitors.
  • METHODS: We investigated the effect of an immunosuppressant schedule that minimizes the exposure to calcineurin inhibitors on patients transplanted for HCC to ascertain whether this can reduce the tumor recurrence rate.
  • [MeSH-major] Carcinoma, Hepatocellular / surgery. Immunosuppressive Agents / therapeutic use. Liver Neoplasms / surgery. Liver Transplantation / immunology. Neoplasm Recurrence, Local / epidemiology. Sirolimus / therapeutic use. Tacrolimus / therapeutic use
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Adult. Aged. Cohort Studies. Disease-Free Survival. Drug Administration Schedule. Female. Hepatitis B / complications. Hepatitis C / complications. Humans. Male. Middle Aged. Risk Factors. Survivors. Young Adult

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  • (PMID = 20098287.001).
  • [ISSN] 1534-6080
  • [Journal-full-title] Transplantation
  • [ISO-abbreviation] Transplantation
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Immunosuppressive Agents; W36ZG6FT64 / Sirolimus; WM0HAQ4WNM / Tacrolimus
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65. Tucci S Jr, Martins AC, Suaid HJ, Cologna AJ, Reis RB: The impact of tumor stage on prognosis in children with adrenocortical carcinoma. J Urol; 2005 Dec;174(6):2338-42, discussion 2342
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  • [Title] The impact of tumor stage on prognosis in children with adrenocortical carcinoma.
  • PURPOSE: We evaluated treatment outcomes in children with adrenocortical carcinoma.
  • In 27 of 28 patients without intracaval extension complete surgical excision was accomplished, while tumor resection combined with thrombectomy was carried out in 5 of 6 children with vascular invasion.
  • Children with incomplete excision of the tumor and/or stage IV disease received adjuvant chemotherapy.
  • RESULTS: Ultrasonography, computerized tomography and magnetic resonance imaging exhibited specificity of 100% in the diagnosis of vascular invasion, and sensitivity of 50%, 66% and 100%, respectively.
  • Patient age, tumor stage or size and vascular invasion were associated with survival in univariate analysis.
  • Tumor stage was the only independent factor associated with survival in multivariate analysis.
  • The overall 5-year survival rates according to tumor stage were 100% in stage I, 85% in stage II, 40% in stage III and 0% in stage IV.
  • Of 11 children with local recurrence only 2 were alive without disease at 96 and 204 months after reoperation with complete tumor excision.
  • Only 2 of 6 patients with vascular invasion were disease-free at 17 and 50 months.
  • A total of 10 children with stage IV disease treated with chemotherapy died within a median of 6 months.
  • CONCLUSIONS: Tumor stage was the most relevant prognostic factor for children with adrenocortical carcinoma.
  • Reoperation for local tumor recurrence and thrombectomy for inferior vena caval tumor invasion should be attempted whenever possible.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenocortical Carcinoma / diagnosis
  • [MeSH-minor] Adolescent. Cardiopulmonary Bypass. Child. Child, Preschool. Female. Follow-Up Studies. Humans. Infant. Magnetic Resonance Imaging. Male. Multivariate Analysis. Neoplasm Invasiveness. Neoplasm Recurrence, Local / epidemiology. Neoplasm Recurrence, Local / etiology. Neoplasm Staging. Prognosis. Retrospective Studies. Sensitivity and Specificity. Survival Analysis. Thrombectomy. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 16280838.001).
  • [ISSN] 0022-5347
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
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66. Mishima S, Mizuta Y, Yamao T, Yamakawa M, Akazawa Y, Mishima R, Ohba K, Masuda JI, Ohnita K, Isomoto H, Shikuwa S, Omagari K, Kohno S: Autoimmune pancreatitis with extreme elevation of DUPAN-2. Intern Med; 2007;46(7):377-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Antigens, Neoplasm / blood. Autoimmune Diseases / blood. Autoimmune Diseases / diagnosis. Pancreatitis / blood. Pancreatitis / diagnosis
  • [MeSH-minor] Acute Disease. Adrenal Cortex Hormones / therapeutic use. Aged, 80 and over. Biomarkers / blood. Cholangiopancreatography, Endoscopic Retrograde / methods. Diagnosis, Differential. Female. Humans. Pancreatic Function Tests. Pancreatic Neoplasms / diagnosis. Risk Assessment. Severity of Illness Index. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 17409601.001).
  • [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
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Antigens, Neoplasm; 0 / Biomarkers; 0 / DU-PAN-2 antigen, human
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67. Gonçalves FT, Feibelmann TC, Mendes CM, Fernandes ML, Miranda GH, Gouvêa AP, Jorge PT: Primary pigmented nodular adrenocortical disease associated with Carney complex: case report and literature review. Sao Paulo Med J; 2006 Nov 7;124(6):336-9
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  • [Title] Primary pigmented nodular adrenocortical disease associated with Carney complex: case report and literature review.
  • CONTEXT: Carney complex (CNC), a familial multiple neoplasm syndrome with dominant autosomal transmission, is characterized by tumors of the heart, skin, endocrine and peripheral nervous system, and also cutaneous lentiginosis.
  • This is a rare syndrome and its main endocrine manifestation, primary pigmented nodular adrenal disease (PPNAD), is an uncommon cause of adrenocorticotropic hormone-independent Cushing's syndrome.
  • CASE REPORT: We report the case of a 20-year-old patient with a history of weight gain, hirsutism, acne, secondary amenorrhea and facial lentiginosis.
  • Screening was also performed for other tumors related to this syndrome.
  • [MeSH-major] Adrenal Cortex Diseases / pathology. Cushing Syndrome / complications. Lentigo / complications. Multiple Endocrine Neoplasia / diagnosis


68. Shen WT, Grogan R, Vriens M, Clark OH, Duh QY: One hundred two patients with pheochromocytoma treated at a single institution since the introduction of laparoscopic adrenalectomy. Arch Surg; 2010 Sep;145(9):893-7
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  • Six operations were bilateral; 3 were subtotal cortex-sparing resections.
  • Thirty-four patients (33%) presented with adrenal incidentaloma and minimal symptoms, 28 within the past decade.
  • The mean (SD) tumor size was 5.3 (2.8) cm.
  • [MeSH-major] Adrenal Gland Neoplasms / surgery. Adrenalectomy / methods. Pheochromocytoma / surgery
  • [MeSH-minor] Adult. Female. Humans. Incidental Findings. Intra-Aortic Balloon Pumping. Laparoscopy. Male. Middle Aged. Neoplasm Recurrence, Local / epidemiology. Retrospective Studies. Shock, Cardiogenic / epidemiology. Shock, Cardiogenic / therapy


69. 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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70. Terzolo M, Berruti A: Adjunctive treatment of adrenocortical carcinoma. Curr Opin Endocrinol Diabetes Obes; 2008 Jun;15(3):221-6
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  • [Title] Adjunctive treatment of adrenocortical carcinoma.
  • PURPOSE OF REVIEW: Description of the adjunctive treatment strategies in patients with adrenocortical carcinoma after complete surgical resection.
  • RECENT FINDINGS: A retrospective analysis showing that adjuvant mitotane may prolong recurrence-free survival in a large cohort of patients with radically resected adrenocortical carcinoma has recently been published.
  • SUMMARY: Radical surgical resection of adrenocortical carcinoma offers the best chance for prolonged recurrence-free survival; however, a significant number of patients without objective and biochemical evidence of residual tumor after surgery are destined to relapse.
  • Mitotane, an analogue of the insecticide dichlorodiphenyltrichloroethane, has been used for treatment of advanced adrenocortical carcinoma since the 1960s, but its use as an adjunctive postoperative measure has remained controversial.
  • The recent demonstration that mitotane treatment following macroscopically complete removal of adrenocortical carcinoma was associated with beneficial effects on outcome in a well designed, multicenter, international study should renew interest in adjuvant mitotane therapy.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Adrenocortical Carcinoma / drug therapy. Mitotane / adverse effects. Neoplasm Recurrence, Local / prevention & control
  • [MeSH-minor] Adrenalectomy. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Chemotherapy, Adjuvant / adverse effects. Chemotherapy, Adjuvant / methods. Disease-Free Survival. Humans


71. 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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72. Fine SW, Pindzola JA, Uhlman EJ, Epstein JI: Pathologic quiz case: a 64-year-old man with an adrenal mass. Myxoid adrenal cortical neoplasm. Arch Pathol Lab Med; 2005 Apr;129(4):541-2
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  • [Title] Pathologic quiz case: a 64-year-old man with an adrenal mass. Myxoid adrenal cortical neoplasm.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology

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  • (PMID = 15794685.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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73. Antoniu SA: Novel therapies for hypereosinophilic syndromes. Neth J Med; 2010 Aug;68(1):304-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Adrenal Cortex Hormones / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Hypereosinophilic Syndrome / drug therapy. Immunologic Factors / therapeutic use. Interferon-alpha / therapeutic use
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / therapeutic use. Antigens, CD / immunology. Antigens, Neoplasm / immunology. Benzamides. Benzenesulfonates / therapeutic use. Bone Marrow Transplantation. Glycoproteins / antagonists & inhibitors. Glycoproteins / immunology. Humans. Imatinib Mesylate. Interleukin-5 / antagonists & inhibitors. Interleukin-5 / immunology. Niacinamide / analogs & derivatives. Phenylurea Compounds. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyridines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 20739727.001).
  • [ISSN] 1872-9061
  • [Journal-full-title] The Netherlands journal of medicine
  • [ISO-abbreviation] Neth J Med
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Benzenesulfonates; 0 / CD52 antigen; 0 / Glycoproteins; 0 / Immunologic Factors; 0 / Interferon-alpha; 0 / Interleukin-5; 0 / Phenylurea Compounds; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 0 / Pyrimidines; 25X51I8RD4 / Niacinamide; 3A189DH42V / alemtuzumab; 8A1O1M485B / Imatinib Mesylate; 9ZOQ3TZI87 / sorafenib; EC 2.7.10.1 / Protein-Tyrosine Kinases
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74. Li D, Mukai K, Suzuki T, Suzuki R, Yamashita S, Mitani F, Suematsu M: Adrenocortical zonation factor 1 is a novel matricellular protein promoting integrin-mediated adhesion of adrenocortical and vascular smooth muscle cells. FEBS J; 2007 May;274(10):2506-22
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  • [Title] Adrenocortical zonation factor 1 is a novel matricellular protein promoting integrin-mediated adhesion of adrenocortical and vascular smooth muscle cells.
  • Expression of a previously cloned secretory protein named adrenocortical zonation factor 1 (AZ-1, also called Tin-ag-RP or lipocalin 7) is tightly linked with the zonal differentiation of adrenocortical cells.
  • In this study, the location of AZ-1 was specified to the basal laminae along adrenocortical sinusoidal capillaries and surrounding VSM cells in the arterial system, consistent with the fact that AZ-1 was extractable under denaturing conditions as a 52 kDa polypeptide.
  • AZ-1 immobilized on substratum or bound to collagens or anastellin promoted adhesion and spreading of adrenocortical cells.
  • Collectively with the putative role of AZ-1 in the adrenocortical zonation, we propose that AZ-1 potentially regulates functions of adrenocortical and VSM cells by modulating cell-matrix interactions.
  • [MeSH-major] Adrenal Cortex / cytology. Carrier Proteins / physiology. Cell Adhesion / physiology. Integrins / physiology. Muscle, Smooth, Vascular / cytology. Neoplasm Proteins / physiology

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  • (PMID = 17425658.001).
  • [ISSN] 1742-464X
  • [Journal-full-title] The FEBS journal
  • [ISO-abbreviation] FEBS J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Fibronectins; 0 / Integrin alpha1beta1; 0 / Integrin alpha2beta1; 0 / Integrin alpha5beta1; 0 / Integrins; 0 / Lipocalins; 0 / Neoplasm Proteins; 0 / Tinagl protein, mouse; 9007-34-5 / Collagen
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75. Namour F, Ayav A, Lu X, Klein M, Muresan M, Bresler L, Tramoy D, Guéant JL, Brunaud L: Lack of association between microsatellite instability and benign adrenal tumors. World J Surg; 2006 Jul;30(7):1240-6
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  • [Title] Lack of association between microsatellite instability and benign adrenal tumors.
  • BACKGROUND: The adrenal gland may give rise to pheochromocytomas, which are catecholamine-producing tumors originating from the adrenal medulla, or to adrenocortical tumors, which derive from the adrenocortical cortex and may be secreting or not.
  • The genetic mechanisms underlying the formation of these tumors include somatic mutations in susceptibility genes, especially in the familial forms, and allelic loss, especially in chromosome 1.
  • Microsatellite loci were analyzed in 32 benign tumors, including 11 pheochromocytomas and 21 adrenocortical tumors, in patients with and without familial syndrome.
  • No microsatellite instability was detected in any tumor.
  • A second patient with a MEN-2A syndrome and a two-sided pheochromocytoma exhibited a loss of heterozygosity for D2S123 in the right tumor only and a retention of heterozygosity for all markers in the left tumor.
  • CONCLUSIONS: These results suggest that microsatellite instability, evaluated by the five reference markers of the National Cancer Institute, is not a feature of benign adrenal tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Microsatellite Repeats / genetics. Pheochromocytoma / genetics
  • [MeSH-minor] Adult. Aged. Alleles. DNA, Neoplasm / analysis. Female. Humans. Loss of Heterozygosity. Male. Middle Aged. Polymerase Chain Reaction. Proto-Oncogene Proteins / genetics

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  • (PMID = 16715450.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Proto-Oncogene Proteins
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76. 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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77. Aspinall SR, Imisairi AH, Bliss RD, Scott-Coombes D, Harrison BJ, Lennard TW: How is adrenocortical cancer being managed in the UK? Ann R Coll Surg Engl; 2009 Sep;91(6):489-93
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  • [Title] How is adrenocortical cancer being managed in the UK?
  • INTRODUCTION: Adrenocortical carcinomas are rare.
  • This case series is reported to give an overview of how adrenocortical carcinoma is currently managed in the UK.
  • PATIENTS AND METHODS: A retrospective review was made of case notes from patients with adrenocortical carcinomas presenting to the authors (TWJL, RDB, BJH, and DS-C) over the past 10 years in Newcastle, Sheffield and Cardiff.
  • All tumours were greater than 5 cm in diameter.
  • CONCLUSIONS: The size of tumour, stage and mode of presentation, age and overall survival of patients in this study are comparable to published series of adrenocortical carcinomas from major endocrine surgical centres world-wide.
  • The exact role of adjuvant therapy in the management of adrenocortical carcinoma is not as well established as for other more common malignancies.
  • Establishing a database for adrenocortical carcinomas in the UK would contribute to our understanding of the management of this disease.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Adrenocortical Carcinoma / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Mitotane / therapeutic use
  • [MeSH-minor] Adrenalectomy / methods. Antineoplastic Combined Chemotherapy Protocols. Chemotherapy, Adjuvant. Cytotoxins / therapeutic use. Great Britain. Humans. Neoplasm Recurrence, Local. Retrospective Studies. Survival Analysis

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  • (PMID = 19558758.001).
  • [ISSN] 1478-7083
  • [Journal-full-title] Annals of the Royal College of Surgeons of England
  • [ISO-abbreviation] Ann R Coll Surg Engl
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Cytotoxins; 78E4J5IB5J / Mitotane
  • [Other-IDs] NLM/ PMC2966201
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78. Pianovski MA, Cavalli LR, Figueiredo BC, Santos SC, Doghman M, Ribeiro RC, Oliveira AG, Michalkiewicz E, Rodrigues GA, Zambetti G, Haddad BR, Lalli E: SF-1 overexpression in childhood adrenocortical tumours. Eur J Cancer; 2006 May;42(8):1040-3
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  • [Title] SF-1 overexpression in childhood adrenocortical tumours.
  • We have recently shown that SF-1 is amplified in childhood adrenocortical tumours (ACT).
  • Conversely, the SF-1 protein was found to be overexpressed in all cases, compared to normal age-matched adrenal glands.
  • Furthermore, no significant correlation existed with histological grade or with the clinical manifestation or evolution of disease.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Homeodomain Proteins / genetics. Neoplasm Proteins / genetics. Receptors, Cytoplasmic and Nuclear / genetics. Transcription Factors / genetics

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  • (PMID = 16574405.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA21765; 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] England
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / NR5A1 protein, human; 0 / Neoplasm Proteins; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Steroidogenic Factor 1; 0 / Transcription Factors
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79. Fenske W, Völker HU, Adam P, Hahner S, Johanssen S, Wortmann S, Schmidt M, Morcos M, Müller-Hermelink HK, Allolio B, Fassnacht M: Glucose transporter GLUT1 expression is an stage-independent predictor of clinical outcome in adrenocortical carcinoma. Endocr Relat Cancer; 2009 Sep;16(3):919-28
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  • [Title] Glucose transporter GLUT1 expression is an stage-independent predictor of clinical outcome in adrenocortical carcinoma.
  • Owing to the rarity of adrenocortical carcinoma (ACC) no prognostic markers have been established beyond stage and resection status.
  • Accelerated glycolysis is a characteristic feature of cancer cells and in a variety of tumour entities key factors in glucose metabolism like glucose transporter 1 and 3 (GLUT1 and -3), transketolase like-1 enzyme (TKTL1) and pyruvate kinase type M2 (M2-PK) are overexpressed and of prognostic value.
  • Immunohistochemical analysis was performed on tissue microarrays of paraffin-embedded tissue samples from 167 ACCs, 15 adrenal adenomas and 4 normal adrenal glands.
  • GLUT1 and -3 were expressed in 33 and 17% of ACC samples respectively, but in none of the benign tumours or normal adrenals glands.
  • When analysing patients in their early stages and advanced disease separately, similar results were obtained.
  • HR for survival was 5.31 (1.80-15.62) in patients with metastatic ACC and in patients after radical resection the HR for disease-free survival was 6.10 (2.16-16.94).
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / metabolism. Adrenocortical Carcinoma / diagnosis. Adrenocortical Carcinoma / metabolism. Glucose Transporter Type 1 / metabolism
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / metabolism. Biomarkers, Tumor / physiology. Female. Glucose / metabolism. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis

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  • (PMID = 19465749.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glucose Transporter Type 1; 0 / SLC2A1 protein, human; IY9XDZ35W2 / Glucose
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80. Markou A, Tsigou K, Papadogias D, Kossyvakis K, Vamvakidis K, Kounadi T, Piaditis G: A unique case of a benign adrenocortical tumor with triple secretion of cortisol, androgens, and aldosterone: development of multiple sclerosis after surgical removal of the tumor. Hormones (Athens); 2005 Oct-Dec;4(4):226-30
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  • [Title] A unique case of a benign adrenocortical tumor with triple secretion of cortisol, androgens, and aldosterone: development of multiple sclerosis after surgical removal of the tumor.
  • We present a 39-year old female with a benign adrenal tumor characterized by autonomous secretion of cortisol, androgens, and aldosterone.
  • CT of the adrenals revealed a 2.5 x 3.0 cm tumor with characteristics of an adenoma on the left adrenal gland.
  • Further investigations revealed suppressed basal ACTH levels, loss of diurnal rhythm of cortisol, and failure to suppress on low dose dexamethasone suppression test, suggesting autonomous cortisol secretion by the tumor.
  • Complete clinical and biochemical remission of the disease was observed after left adrenalectomy.
  • Histology confirmed the presence of an adrenocortical adenoma.
  • The flare-up of an autoimmune disease (multiple sclerosis) postoperatively could be coincidental or possibly related to the high normalization of the high cortisol levels acting as a precipitating factor.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenal Cortex Neoplasms / surgery. Adrenalectomy / adverse effects. Adrenocortical Adenoma / pathology. Adrenocortical Adenoma / surgery. Multiple Sclerosis / etiology
  • [MeSH-minor] Adult. Aldosterone / secretion. Androgens / secretion. Biopsy, Needle. Female. Follow-Up Studies. Humans. Hydrocortisone / secretion. Immunohistochemistry. Neoplasm Staging. Risk Assessment

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  • (PMID = 16613821.001).
  • [ISSN] 1109-3099
  • [Journal-full-title] Hormones (Athens, Greece)
  • [ISO-abbreviation] Hormones (Athens)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Androgens; 4964P6T9RB / Aldosterone; WI4X0X7BPJ / Hydrocortisone
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81. Gołkowski F, Buziak-Bereza M, Huszno B, Bałdys-Waligórska A, Stefańska A, Budzyński A, Okoń K, Chrzan R, Urbanik A: The unique case of adrenocortical malignant and functioning oncocytic tumour. Exp Clin Endocrinol Diabetes; 2007 Jun;115(6):401-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The unique case of adrenocortical malignant and functioning oncocytic tumour.
  • Adrenocortical oncocytoma is extremely rarely found.
  • Only a little more than thirty cases of adrenal oncocytoma, mainly nonfunctioning and benign, have been reported in the literature.
  • Adrenal mass 150 x 160 x 172 mm in size and enlarged periarterial lymph nodes were found in CT examination performed in 51-year-old male.
  • On laparotomy, the lesion was considered unresectable because of evident - confirmed by intraoperative ultrasound - tumour infiltration of the inferior caval vein.
  • The large biopsy specimen was obtained for histological examination in which tumour fulfilled criteria proposed by Bisceglia et al. for adrenocortical oncocytic borderline tumour.
  • The presented case appears to be the first malignant and functioning adrenocortical oncocytic tumour reported and confirms the complexity of its biology.
  • [MeSH-major] Adenoma, Oxyphilic / pathology. Adrenal Cortex Neoplasms / pathology
  • [MeSH-minor] Antineoplastic Agents, Hormonal / administration & dosage. Humans. Male. Middle Aged. Mitotane / administration & dosage. Neoplasm Proteins / metabolism. Venae Cavae / pathology

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  • (PMID = 17701888.001).
  • [ISSN] 0947-7349
  • [Journal-full-title] Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
  • [ISO-abbreviation] Exp. Clin. Endocrinol. Diabetes
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Neoplasm Proteins; 78E4J5IB5J / Mitotane
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82. 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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83. Fulmer BR: Diagnosis and management of adrenal cortical carcinoma. Curr Urol Rep; 2007 Jan;8(1):77-82
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  • [Title] Diagnosis and management of adrenal cortical carcinoma.
  • Adrenal cortical carcinoma is a relatively uncommon malignancy that represents a significant clinical challenge for the development of optimal treatment strategies.
  • Although the framework of a successful treatment paradigm still relies on these steps, advances in diagnostic imaging have led to increased accuracy in diagnosis, and advances in laparoscopic surgical technique have served to reduce morbidity for patients facing treatment.
  • This review focuses on a discussion of advances in modalities for the diagnosis and treatment of adrenal cortical carcinoma amenable to curative therapy.
  • Patients that present with metastatic or locally advanced disease generally are treated with mitotane-based chemotherapy with or without the addition of cytotoxic drugs.
  • Contemporary results of this treatment approach are presented in this review as well as a discussion of further directions for the treatment of patients with advanced disease.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / therapy. Adrenocortical Carcinoma / diagnosis. Adrenocortical Carcinoma / therapy
  • [MeSH-minor] Adrenalectomy / methods. Chemotherapy, Adjuvant. Combined Modality Therapy. Female. Humans. Laparoscopy / methods. Male. Neoplasm Staging. Prognosis. Radiotherapy, Adjuvant. Risk Assessment. Survival Analysis

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  • (PMID = 17239320.001).
  • [ISSN] 1534-6285
  • [Journal-full-title] Current urology reports
  • [ISO-abbreviation] Curr Urol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 50
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84. Zhang H, Bu H, Chen H, Wei B, Liu W, Guo J, Li F, Liao D, Tang Y, Zhang Z: Comparison of immunohistochemical markers in the differential diagnosis of adrenocortical tumors: immunohistochemical analysis of adrenocortical tumors. Appl Immunohistochem Mol Morphol; 2008 Jan;16(1):32-9
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  • [Title] Comparison of immunohistochemical markers in the differential diagnosis of adrenocortical tumors: immunohistochemical analysis of adrenocortical tumors.
  • Most adrenocortical tumors (ACTs) can be diagnosed directly by a combination of morphologic features and clinical findings.
  • However, sometimes it may be difficult to distinguish ACTs from other neoplasms such as pheochromocytomas and some metastatic tumors, particularly for small biopsy specimens because they may be morphologically similar.
  • Expression of calretinin has recently been suggested as a valuable immunomarker for the differential diagnosis between ACTs and other tumors; however, its diagnostic value is still under debate.
  • To determine the diagnostic value of calretinin in Chinese patients with adrenocortical and non-ACTs, we employed both polyclonal and monoclonal anticalretinin to characterize the expression of calretinin in adrenal tissues and compared its expression with that of inhibin alpha, Melan-A, cytokeratin, or CD99 by immunohistochemistry in tissue microarrays and standard tissue sections of 414 specimens.
  • Our results revealed that calretinin was expressed by adrenocortical cells, but not by the other cells tested and the percentage of calretinin-positive ACTs reached 99% when stained with polyclonal antibodies, which was higher than that with monoclonal anticalretinin (91.3%), anti-Melan-A (90.3%), antiinhibin alpha (81.6%).
  • Furthermore, unlike anti-Melan-A that stained all metastatic malignant melanoma, anticalretinin did not recognize other tested tumors.
  • Therefore, immunohistologic staining with polyclonal anticalretinin is more sensitive than other antibodies tested for the diagnosis of ACTs.
  • Importantly, our data suggested that the fried-egg-like staining pattern, but not the mere cytoplasmic staining, was characteristic of anticalretinin staining in adrenocortical tissues.
  • Thus, the combinational characterization of calretinin (either by polyclonal or monoclonal antibody), inhibin alpha, and Melan-A expression is of great significance in the differential diagnosis of ACTs.

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  • (PMID = 18091323.001).
  • [ISSN] 1541-2016
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / CALB2 protein, human; 0 / Calbindin 2; 0 / MART-1 Antigen; 0 / MLANA protein, human; 0 / Neoplasm Proteins; 0 / S100 Calcium Binding Protein G; 57285-09-3 / Inhibins
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85. 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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86. Weismann D, Briese J, Niemann J, Grüneberger M, Adam P, Hahner S, Johanssen S, Liu W, Ezzat S, Saeger W, Bamberger AM, Fassnacht M, Schulte HM, Asa SL, Allolio B, Bamberger CM: Osteopontin stimulates invasion of NCI-h295 cells but is not associated with survival in adrenocortical carcinoma. J Pathol; 2009 Jun;218(2):232-40
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  • [Title] Osteopontin stimulates invasion of NCI-h295 cells but is not associated with survival in adrenocortical carcinoma.
  • Gene array studies indicated that osteopontin (OPN) mRNA is highly expressed in adrenocortical carcinomas (ACCs).
  • In this study, we demonstrated OPN and integrin alphavbeta3 expression in normal adrenal glands and benign adenomas, with staining seen exclusively in adrenocortical cells as well as even stronger staining in ACC.
  • However, no association with survival was seen in Kaplan-Meier analysis including 111 patients with primary tumours graded for OPN staining and follow-up data available.
  • In conclusion, our in vitro data indicate that OPN and integrin alphavbeta3 may act as a functional complex facilitating the invasiveness of adrenocortical tumours.
  • This relationship remains of relevance to our understanding of carcinogenesis, but further studies are needed to address the physiological and pathological function of OPN in adrenal tissue.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenocortical Carcinoma / metabolism. Osteopontin / analysis
  • [MeSH-minor] Adenoma / chemistry. Adrenal Glands / chemistry. Blotting, Western / methods. Cell Line, Tumor. Gene Expression Profiling. Humans. Immunohistochemistry. Integrin alphaVbeta3 / analysis. Integrin alphaVbeta3 / genetics. Integrin alphaVbeta3 / metabolism. Kaplan-Meier Estimate. Neoplasm Invasiveness. Oligonucleotide Array Sequence Analysis. Reverse Transcriptase Polymerase Chain Reaction. Statistics, Nonparametric. Transfection / methods

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  • (PMID = 19326399.001).
  • [ISSN] 1096-9896
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Integrin alphaVbeta3; 106441-73-0 / Osteopontin
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87. Gross MD, Gauger PG, Djekidel M, Rubello D: The role of PET in the surgical approach to adrenal disease. Eur J Surg Oncol; 2009 Nov;35(11):1137-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of PET in the surgical approach to adrenal disease.
  • BACKGROUND: Appropriate surgical approach to diseases of the adrenal requires a diagnosis sufficient to determine the biochemical status of adrenal dysfunction and anatomic evaluation sufficient to differentiate unilateral from bilateral disease, intra-adrenal from extra-adrenal neoplasm, adrenal tumor recurrence or adrenal metastases.
  • High resolution computed tomography (CT) and magnetic resonance have been the primary imaging modalities for the evaluation of anatomy, while scintigraphic studies have played a secondary role in diagnosis.
  • The recent availability of functional imaging provided by positron emission tomography (PET) with radiopharmaceuticals designed to depict substrate precursor uptake, cellular metabolism or receptor binding in neoplasms and CT as a single modality, hybrid PET/CT, to directly correlate function and anatomy has had a significant impact upon the diagnostic and therapeutic approach to many cancers and has been applied to adrenal disease with some early success that we describe in this review.
  • METHODS: In addition to the authors' experience, a search of Medline and PubMed databases was performed using search terms: 'adrenal scintigraphy', 'positron tomography', 'computed tomography', 'adrenal surgery', 'adrenal mass', '(18)F-fluorodeoxyglucose', 'adrenal carcinoma', 'adrenal medulla' and 'pheochromocytoma'.
  • CONCLUSIONS: Present PET radiopharmaceuticals and their use in hybrid PET/CT have demonstrated efficacy in the preoperative and follow-up evaluation of neoplasms of the adrenal cortex and medulla that hopefully will continue to improve with the development of newer tracers that continue to exploit unusual characteristics of the adrenals.
  • [MeSH-major] Adrenal Gland Neoplasms / radionuclide imaging. Adrenal Gland Neoplasms / surgery. Radiopharmaceuticals. Tomography, Emission-Computed
  • [MeSH-minor] Diagnosis, Differential. Humans. Tomography, X-Ray Computed

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  • (PMID = 19243910.001).
  • [ISSN] 1532-2157
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Radiopharmaceuticals
  • [Number-of-references] 75
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88. Cardoso CC, Bornstein SR, Hornsby PJ: Optimizing orthotopic cell transplantation in the mouse adrenal gland. Cell Transplant; 2010;19(5):565-72
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  • [Title] Optimizing orthotopic cell transplantation in the mouse adrenal gland.
  • Orthotopic cell transplantation models are important for a complete understanding of cell-cell interactions as well as tumor biology.
  • In published studies of orthotopic transplantation in the mouse adrenal gland, human neuroblastoma cells have been shown to invade and occupy the adrenal, but in these investigations a true orthotopic model was not established.
  • Here we show an orthotopic model in which transplanted cells are retained within the adrenal gland by formation of a fibrin clot.
  • To establish an appropriate technique, we used brightly fluorescent 10 microm polystyrene microspheres injected into the mouse adrenal gland.
  • When the microspheres were injected in a fibrinogen/thrombin mixture, fluorescence was confined to the adrenal gland.
  • As a model neoplastic cell originating from the cortex of the gland, we used a tumorigenic bovine adrenocortical cell line.
  • When 3 x 10(5) cells were implanted orthotopically, by 16 days the cell mass had expanded and had invaded the cortex, whereas when 1 x 10(5) cells were used, tumor masses were much smaller.
  • When mice were sacrificed at different time points, we found that tumor growth resulting was progressive and that by 26 days cells there was extensive invasion into the cortex or almost complete replacement of the cortex with tumor cells.
  • In summary, the present orthotopic model for intra-adrenal cell transplantation is valuable for investigation of growth of neoplastic cells of both cortical and medullary origin and should be useful for future studies of cortex-medulla interactions.

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  • (PMID = 20525431.001).
  • [ISSN] 1555-3892
  • [Journal-full-title] Cell transplantation
  • [ISO-abbreviation] Cell Transplant
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / AG012287-14; United States / NIA NIH HHS / AG / P01 AG020752-020006; United States / NIA NIH HHS / AG / AG020752-020006; United States / NIA NIH HHS / AG / P01 AG020752; United States / NIA NIH HHS / AG / R37 AG012287-14; United States / NIA NIH HHS / AG / R37 AG012287
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 9001-31-4 / Fibrin; 9001-32-5 / Fibrinogen; EC 3.4.21.5 / Thrombin
  • [Other-IDs] NLM/ NIHMS246503; NLM/ PMC3735364
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89. 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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90. Coli A, Di Giorgio A, Castri F, Destito C, Marin AW, Bigotti G: Sarcomatoid carcinoma of the adrenal gland: A case report and review of literature. Pathol Res Pract; 2010 Jan 15;206(1):59-65
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  • [Title] Sarcomatoid carcinoma of the adrenal gland: A case report and review of literature.
  • Reports about adrenocortical carcinomas (AC) mixed with sarcomatous areas are very rare.
  • The terminology and pathogenesis of such biphasic tumors remain controversial.
  • Herein, we report a case of sarcomatoid carcinoma of the adrenal gland in a 75-year-old woman who presented with left abdominal pain of one month's standing.
  • The results of abdominal ultrasonography and computed tomography (CT) showed the presence of a large heterogeneous adrenal mass.
  • Histologically, the neoplasm showed areas of adrenocortical carcinoma and areas of sarcomatoid spindle cell proliferation.
  • Twelve months after removal of the primary tumor, the patient died of her disease.
  • To the best of our knowledge, only seven cases of adrenal sarcomatoid carcinoma have been reported in the medical literature.
  • We review the reported cases according to the 2004 classification of the World Health Organization (WHO) of lung tumors, and highlight the histogenesis, diagnosis, and clinical course of this very aggressive tumor.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Carcinosarcoma / secondary. Liver Neoplasms / secondary
  • [MeSH-minor] Adrenalectomy. Aged. Fatal Outcome. Female. Humans. Neoplasm Proteins. Splenectomy

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  • [Copyright] Copyright 2009 Elsevier GmbH. All rights reserved.
  • (PMID = 19369012.001).
  • [ISSN] 1618-0631
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Neoplasm Proteins
  • [Number-of-references] 16
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91. Hahner S, Fassnacht M, Hammer F, Schammann M, Weismann D, Hansen IA, Allolio B: Evidence against a role of human airway trypsin-like protease--the human analogue of the growth-promoting rat adrenal secretory protease--in adrenal tumourigenesis. Eur J Endocrinol; 2005 Jan;152(1):143-53
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  • [Title] Evidence against a role of human airway trypsin-like protease--the human analogue of the growth-promoting rat adrenal secretory protease--in adrenal tumourigenesis.
  • OBJECTIVE: A serine protease from rat adrenal cortex was recently characterized and named adrenal secretory protease (AsP).
  • AsP is expressed in the adrenal cortex and is capable of cleaving pro-gamma-melanocyte-stimulating hormone (1-76 N-terminus of pro-opiomelanocortin) into fragments that act as adrenal mitogens.
  • AsP may therefore play a crucial role in adrenal growth and tumourigenesis.
  • The aim of this study was to further characterize the human homologue of AsP and its possible role in adrenal tumourigenesis.
  • Further analysis revealed that the HAT gene is the human homologue of a long splice variant of AsP, which we recently described as rat airway trypsin-like serine protease 1.
  • In contrast to rodents, no short isoform of HAT was found in humans due to a stop codon in exon 6 which prevents the expression of a short isoform.
  • While high expression of HAT mRNA was found in the trachea and in the gastrointestinal tract, expression in the adrenal was only very weak.
  • We further investigated HAT expression in five normal adrenal glands, 15 adrenocortical adenomas (five hormonally inactive adenomas, five aldosterone-producing adenomas and five cortisol-producing adenomas), nine adrenocortical carcinomas, five phaeochromocytomas and two adrenal hyperplasias.
  • Weak HAT expression was detectable in only two out of five normal adrenal glands, in one out of twenty-four adrenocortical tumours and four out of five phaeochromocytomas.
  • However, the expression in the adrenal tissue was several orders of magnitude lower than in the trachea.
  • In addition, we could not detect any HAT transcripts in a sample of fetal adrenal.
  • CONCLUSION: Gene structure and tissue distribution of HAT, the human homologue of the rat adrenal secretory protease AsP, reveal major interspecies differences.
  • The observation of very low expression levels in normal adrenal tissue and adrenocortical tumours casts doubt about a role for HAT in the physiological and pathological growth of adrenocortical cells.

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  • (PMID = 15762198.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / RNA, Neoplasm; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / human airway trypsin-like protease
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92. 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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93. Inoue Y, True LD, Martins RG: Thymic carcinoma associated with paraneoplastic polymyositis. J Clin Oncol; 2009 Aug 1;27(22):e33-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Paraneoplastic Syndromes / etiology. Polymyositis / etiology. Thymoma / complications. Thymoma / pathology. Thymus Neoplasms / complications. Thymus Neoplasms / pathology
  • [MeSH-minor] Adrenal Cortex Hormones / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biopsy, Needle. Disease Progression. Drug Therapy, Combination. Follow-Up Studies. Humans. Immunoglobulins, Intravenous / administration & dosage. Immunohistochemistry. Male. Neoplasm Invasiveness / pathology. Neoplasm Staging. Positron-Emission Tomography. Radiotherapy, Adjuvant. Rare Diseases. Risk Assessment. Tomography, X-Ray Computed. Young Adult

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  • [CommentIn] J Clin Oncol. 2010 Aug 1;28(22):e378 [20458028.001]
  • (PMID = 19506156.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Immunoglobulins, Intravenous
  • [Number-of-references] 13
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94. 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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95. 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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96. 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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97. 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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98. 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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99. Schlosser KA: Infantile hemangioma: how to treat this benign neoplasm of childhood. JAAPA; 2009 May;22(5):46-9
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  • [Title] Infantile hemangioma: how to treat this benign neoplasm of childhood.
  • [MeSH-major] Hemangioma / therapy. Skin Neoplasms / therapy
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Aminoquinolines / therapeutic use. Antineoplastic Agents / therapeutic use. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Interferon-alpha / therapeutic use. Laser Therapy. Male

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  • (PMID = 19469391.001).
  • [ISSN] 1547-1896
  • [Journal-full-title] JAAPA : official journal of the American Academy of Physician Assistants
  • [ISO-abbreviation] JAAPA
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Aminoquinolines; 0 / Antineoplastic Agents; 0 / Interferon-alpha; 99011-02-6 / imiquimod
  • [Number-of-references] 11
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100. 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






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