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

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  • (PMID = 16444357.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] por
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Brazil
  • [Number-of-references] 36
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3. Delhanty PJ, van Koetsveld PM, Gauna C, van de Zande B, Vitale G, Hofland LJ, van der Lely AJ: Ghrelin and its unacylated isoform stimulate the growth of adrenocortical tumor cells via an anti-apoptotic pathway. Am J Physiol Endocrinol Metab; 2007 Jul;293(1):E302-9
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  • [Title] Ghrelin and its unacylated isoform stimulate the growth of adrenocortical tumor cells via an anti-apoptotic pathway.
  • Ghrelin is expressed in normal human adrenocortical cells and induces their proliferation through growth hormone secretagogue receptor 1a (GHS-R1a).
  • Consequently, it was of interest to us to determine whether acylated ghrelin and its predominant serum isoform, unacylated ghrelin, also act as factors for adrenocortical carcinoma cell growth.
  • To examine a potential ghrelin-regulated system in adrenocortical tumors, we measured proliferative effects of acylated and unacylated ghrelin in the adrenocortical carcinoma cell lines SW-13 and NCI-H295R.
  • Acylated and unacylated ghrelin in the nanomolar range dose-dependently induced adrenocortical cell growth up to 200% of untreated controls, as measured by thymidine uptake and WST1 assay.
  • Acylated and unacylated ghrelin are potential auto/paracrine factors acting through an antiapoptotic pathway to stimulate adrenocortical tumor cell growth.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Apoptosis / drug effects. Cell Proliferation / drug effects. Peptide Hormones / pharmacology
  • [MeSH-minor] Acetylation. Cell Cycle / drug effects. Ghrelin. Humans. Protein Isoforms / pharmacology. Receptors, Corticotropin-Releasing Hormone / antagonists & inhibitors. Receptors, Corticotropin-Releasing Hormone / genetics. Receptors, Corticotropin-Releasing Hormone / metabolism. Receptors, G-Protein-Coupled / antagonists & inhibitors. Receptors, G-Protein-Coupled / genetics. Receptors, G-Protein-Coupled / metabolism. Receptors, Ghrelin. Signal Transduction / drug effects. Tumor Cells, Cultured

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  • (PMID = 17405826.001).
  • [ISSN] 0193-1849
  • [Journal-full-title] American journal of physiology. Endocrinology and metabolism
  • [ISO-abbreviation] Am. J. Physiol. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CRF receptor type 2; 0 / Ghrelin; 0 / Peptide Hormones; 0 / Protein Isoforms; 0 / Receptors, Corticotropin-Releasing Hormone; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Ghrelin
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4. 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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5. Castellano JJ, Warren MW, Arroyo MR, Cendan JC: Laparoscopic resection of a virilizing adrenocortical tumor. JSLS; 2008 Jul-Sep;12(3):343-6
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  • [Title] Laparoscopic resection of a virilizing adrenocortical tumor.
  • Virilizing adrenocortical tumors are rare.
  • Herein, we describe a case of laparoscopic resection of a testosterone-producing adrenal tumor in a sixteen-year-old female.

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  • (PMID = 18765068.001).
  • [ISSN] 1086-8089
  • [Journal-full-title] JSLS : Journal of the Society of Laparoendoscopic Surgeons
  • [ISO-abbreviation] JSLS
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3015862
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6. 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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7. Mann MW, Ellis SS, Mallory SB: Infantile acne as the initial sign of an adrenocortical tumor. J Am Acad Dermatol; 2007 Feb;56(2 Suppl):S15-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Infantile acne as the initial sign of an adrenocortical tumor.
  • Ultrasound and abdominal computed tomographic scan revealed a large adrenal mass consistent with an adrenocortical tumor.
  • The patient underwent surgical excision of the well-encapsulated tumor with normalization of his hormones and no subsequent recurrence.
  • Although rare, childhood adrenocortical tumors have a poor prognosis, with the majority of tumors having regional and metastatic disease.
  • Because early diagnosis and complete surgical excision improve prognosis, children with refractory infantile acne should be evaluated for signs of virilization and accelerated growth.
  • Elevated levels of DHEA and DHEA-S should prompt an aggressive diagnostic evaluation for an adrenocortical tumor.
  • [MeSH-major] Acne Vulgaris / etiology. Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications

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  • (PMID = 17097383.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 3XMK78S47O / Testosterone; 459AG36T1B / Dehydroepiandrosterone
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8. Rossbach HC, Baschinsky D, Wynn T, Obzut D, Sutcliffe M, Tebbi C: Composite adrenal anaplastic neuroblastoma and virilizing adrenocortical tumor with germline TP53 R248W mutation. Pediatr Blood Cancer; 2008 Mar;50(3):681-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Composite adrenal anaplastic neuroblastoma and virilizing adrenocortical tumor with germline TP53 R248W mutation.
  • Composite tumors are extremely rare.
  • Such tumors in adrenal glands are usually of neuroendocrine-neural type and occur mostly in adults.
  • We report a patient with composite neuroblastoma (NB), adrenocortical tumor (ACT), and Li-Fraumeni syndrome (LFS) with germline TP53 R248W mutation.
  • LFS predisposes to the development of leukemia, sarcomas, adrenocortical and breast carcinomas, brain tumors and, questionably, NB.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenal Gland Neoplasms / pathology. Adrenocortical Adenoma / pathology. Genes, p53. Germ-Line Mutation. Li-Fraumeni Syndrome / genetics. Mutation, Missense. Neoplasms, Multiple Primary / pathology. Neuroblastoma / pathology. Point Mutation. Virilism / etiology
  • [MeSH-minor] Amino Acid Substitution. Aneuploidy. Brain Neoplasms / genetics. Breast Neoplasms / genetics. Carcinoma / genetics. Choroid Plexus Neoplasms / genetics. Female. Glioblastoma / genetics. Humans. Infant. Loss of Heterozygosity. Male. Pedigree

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17427234.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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9. Sethi D, Arora MK, Sinha R, Bose S: Anesthetic management of a child with functional adrenocortical tumor for resection. Paediatr Anaesth; 2008 Nov;18(11):1142-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anesthetic management of a child with functional adrenocortical tumor for resection.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Anesthesia, General / methods

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  • (PMID = 18950363.001).
  • [ISSN] 1460-9592
  • [Journal-full-title] Paediatric anaesthesia
  • [ISO-abbreviation] Paediatr Anaesth
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] France
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10. Libé R, Tissier F, Bienvenu M, Groussin L, Joannidis S, Hignette C, Dousset B, Legmann P, Faraggi M, Richard B, Bertagna X, Tenenbaum F: Adrenocortical tumor with two distinct elements revealed by combined (18)F-fluorodeoxyglucose positron emission tomography and (131)I nor-cholesterol scintigraphy. J Clin Endocrinol Metab; 2009 Oct;94(10):3631-2

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenocortical tumor with two distinct elements revealed by combined (18)F-fluorodeoxyglucose positron emission tomography and (131)I nor-cholesterol scintigraphy.
  • [MeSH-major] Adenoma / radionuclide imaging. Adosterol. Adrenal Cortex Neoplasms / pathology. Adrenal Cortex Neoplasms / radionuclide imaging. Carcinoma / radionuclide imaging. Fluorodeoxyglucose F18. Positron-Emission Tomography

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  • (PMID = 19808858.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18; 55623-03-5 / Adosterol
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11. Katsumata N: [Feminizing adrenocortical tumor]. Nihon Rinsho; 2006 May 28;Suppl 1:708-9
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  • [Title] [Feminizing adrenocortical tumor].
  • [MeSH-major] Adrenal Cortex Neoplasms. Feminization
  • [MeSH-minor] Adrenal Cortex / metabolism. Adrenalectomy. Combined Modality Therapy. Diagnosis, Differential. Estrogens / biosynthesis. Humans. Male. Mitotane / therapeutic use. Prognosis

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  • (PMID = 16776255.001).
  • [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 / Estrogens; 78E4J5IB5J / Mitotane
  • [Number-of-references] 10
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12. 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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13. Müller-Vieira U, Angotti M, Hartmann RW: The adrenocortical tumor cell line NCI-H295R as an in vitro screening system for the evaluation of CYP11B2 (aldosterone synthase) and CYP11B1 (steroid-11beta-hydroxylase) inhibitors. J Steroid Biochem Mol Biol; 2005 Aug;96(3-4):259-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The adrenocortical tumor cell line NCI-H295R as an in vitro screening system for the evaluation of CYP11B2 (aldosterone synthase) and CYP11B1 (steroid-11beta-hydroxylase) inhibitors.
  • For studies of the effects of CYP11B2 inhibitors on the adrenal cortex, we selected the NCI-H295R cell line which expresses most of the key enzymes necessary for steroidogenesis.
  • [MeSH-major] Cell Line, Tumor. Cytochrome P-450 CYP11B2 / antagonists & inhibitors. Enzyme Inhibitors / pharmacology. Steroid 11-beta-Hydroxylase / antagonists & inhibitors
  • [MeSH-minor] Adrenal Cortex / cytology. Adrenal Cortex / drug effects. Adrenal Cortex / enzymology. Aldosterone / metabolism. Aromatase Inhibitors / pharmacology. Drug Evaluation, Preclinical. Fadrozole / pharmacology. Humans. Steroids / analysis. Steroids / metabolism

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  • (PMID = 15985365.001).
  • [ISSN] 0960-0760
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aromatase Inhibitors; 0 / Enzyme Inhibitors; 0 / Steroids; 4964P6T9RB / Aldosterone; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase; H3988M64PU / Fadrozole
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14. Betz MJ, Shapiro I, Fassnacht M, Hahner S, Reincke M, Beuschlein F, German and Austrian Adrenal Network: Peroxisome proliferator-activated receptor-gamma agonists suppress adrenocortical tumor cell proliferation and induce differentiation. J Clin Endocrinol Metab; 2005 Jul;90(7):3886-96
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  • [Title] Peroxisome proliferator-activated receptor-gamma agonists suppress adrenocortical tumor cell proliferation and induce differentiation.
  • Moreover, recent evidence has suggested that TZDs might have favorable effects in the treatment of a variety of tumors as differentiation-inducing agents.
  • Adrenocortical carcinoma (ACC) is a rare tumor entity with poor prognosis due to its highly malignant phenotype and lack of effective treatment options.
  • OBJECTIVE: The purpose of this study was to investigate effects of TZDs on adrenocortical cancer cells.
  • RESULTS: PPARgamma mRNA expression was detectable in all adrenocortical tumors including ACCs at similar levels.
  • Furthermore, incubation of the adrenocortical tumor cell line NCI h295 with the PPARgamma agonist rosiglitazone led to a decrease in cell viability, a decrease of cellular proliferation, and an increase in apoptosis as well as steroidogenesis.
  • On the molecular level, NCI h295 cells expressed higher levels of ACTH receptor (melanocortin receptor-2) mRNA upon treatment, whereas cyclin E mRNA was reduced, thus reflecting a shift toward an expression pattern found in less aggressive adrenocortical tumors in vivo.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. PPAR gamma / agonists. Thiazolidinediones / pharmacology
  • [MeSH-minor] Adult. Aged. Anilides / pharmacology. Apoptosis / drug effects. Cell Differentiation. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin E / genetics. Dose-Response Relationship, Drug. Female. Humans. Insulin-Like Growth Factor II / genetics. Male. Middle Aged. Promoter Regions, Genetic. RNA, Messenger / analysis. Receptor, Melanocortin, Type 2 / genetics

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  • (PMID = 15886257.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-chloro-5-nitrobenzanilide; 0 / Anilides; 0 / Cyclin E; 0 / PPAR gamma; 0 / RNA, Messenger; 0 / Receptor, Melanocortin, Type 2; 0 / Thiazolidinediones; 05V02F2KDG / rosiglitazone; 67763-97-7 / Insulin-Like Growth Factor II
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15. Alsultan A, Lovell MA, Hayes KL, Allshouse MJ, Garrington TP: Simultaneous occurrence of right adrenocortical tumor and left adrenal neuroblastoma in an infant with Beckwith-Wiedemann syndrome. Pediatr Blood Cancer; 2008 Nov;51(5):695-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Simultaneous occurrence of right adrenocortical tumor and left adrenal neuroblastoma in an infant with Beckwith-Wiedemann syndrome.
  • Children with Beckwith-Wiedemann syndrome (BWS) have increased risk for development of embryonal tumors.
  • We present the case of an infant with BWS who has hypomethylation of LIT1 gene in the 11p15.5 chromosomal region and at 6 months of age presented with simultaneous occurrence of neuroblastoma arising from the left adrenal gland and a right adrenocortical tumor.
  • She underwent surgical resection of both tumors and remains tumor free 18 months after surgery.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenal Gland Neoplasms / complications. Beckwith-Wiedemann Syndrome / complications. Neoplasms, Multiple Primary / complications. Neuroblastoma / complications


16. Lindsay CR, Chan E, Evans TR, Campbell S, Bell P, Stephens AW, Franke A, Poondru S, Rothenberg ML, Puzanov I: Phase I dose escalation study of continuous oral dosing of OSI-906, an insulin like growth factor-1 receptor (IGF-1R) tyrosine kinase inhibitor, in patients with advanced solid tumors. J Clin Oncol; 2009 May 20;27(15_suppl):2559

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I dose escalation study of continuous oral dosing of OSI-906, an insulin like growth factor-1 receptor (IGF-1R) tyrosine kinase inhibitor, in patients with advanced solid tumors.
  • Study objectives included assessment of: safety; determination of MTD; pharmacokinetics (PK), pharmacodynamics (PD) including IGF-1R levels in peripheral blood cells; and tumor response (RECIST).
  • Stable disease > 12 weeks was seen in 7/20 pts (range 12-34 weeks), including 1 pt each with thymic (27 w), adrenocortical (28w), and colorectal (34w) cancer.
  • PD target modulation and preliminary anti-tumor activity have been observed.

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  • (PMID = 27961869.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Carden CP, Frentzas S, Langham M, Casamayor I, Stephens AW, Poondru S, Wheaton J, Lippman SM, Kaye SB, Kim ES: Preliminary activity in adrenocortical tumor (ACC) in phase I dose escalation study of intermittent oral dosing of OSI-906, a small-molecule insulin-like growth factor-1 receptor (IGF-1R) tyrosine kinase inhibitor in patients with advanced solid tumors. J Clin Oncol; 2009 May 20;27(15_suppl):3544

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

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  • (PMID = 27961354.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. 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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19. Mazzuco TL, Chabre O, Sturm N, Feige JJ, Thomas M: Ectopic expression of the gastric inhibitory polypeptide receptor gene is a sufficient genetic event to induce benign adrenocortical tumor in a xenotransplantation model. Endocrinology; 2006 Feb;147(2):782-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ectopic expression of the gastric inhibitory polypeptide receptor gene is a sufficient genetic event to induce benign adrenocortical tumor in a xenotransplantation model.
  • Aberrant expression of ectopic G protein-coupled receptors (GPCRs) in adrenal cortex tissue has been observed in several cases of ACTH-independent macronodular adrenal hyperplasias and adenomas associated with Cushing's syndrome.
  • Although there is clear clinical evidence for the implication of these ectopic receptors in abnormal regulation of cortisol production, whether this aberrant GPCR expression is the cause or the consequence of the development of an adrenal hyperplasia is still an open question.
  • To answer it, we genetically engineered primary bovine adrenocortical cells to have them express the gastric inhibitory polypeptide receptor.
  • We observed the formation of an enlarged and hyperproliferative adenomatous adrenocortical tissue that secreted cortisol in a gastric inhibitory polypeptide-dependent manner and induced a mild Cushing's syndrome with hyperglycemia.
  • Moreover, we show that tumor development was ACTH independent.
  • Thus, a single genetic event, inappropriate expression of a nonmutated GPCR gene, is sufficient to initiate the complete phenotypic alterations that ultimately lead to the formation of a benign adrenocortical tumor.
  • [MeSH-major] Adenoma / genetics. Adrenal Cortex / metabolism. Adrenal Gland Neoplasms / genetics. Cell Transformation, Neoplastic / metabolism. Gene Expression Regulation, Neoplastic. Receptors, Gastrointestinal Hormone / metabolism

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  • (PMID = 16254030.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Gastrointestinal Hormone; 0 / gastric inhibitory polypeptide receptor; 128559-51-3 / RAG-1 protein; WI4X0X7BPJ / Hydrocortisone
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20. Assié G, Guillaud-Bataille M, Ragazzon B, Bertagna X, Bertherat J, Clauser E: The pathophysiology, diagnosis and prognosis of adrenocortical tumors revisited by transcriptome analyses. Trends Endocrinol Metab; 2010 May;21(5):325-34

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The pathophysiology, diagnosis and prognosis of adrenocortical tumors revisited by transcriptome analyses.
  • Accumulating data on adrenal cortex and adrenocortical tumor transcriptomes have already identified striking transcriptome differences not only between adenoma and carcinoma but also between two sets of carcinoma, which have very different prognoses.
  • These transcriptome data observing adrenocortical tumor phenotype in great but complex detail, combined with genomic and proteomic information, will function for future research investigating the pathophysiology of their tumorigenesis and hormonal secretion.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / physiopathology. Gene Expression Profiling
  • [MeSH-minor] Adenoma / genetics. Adenoma / pathology. Adenoma / physiopathology. Adrenal Cortex / metabolism. Animals. Carcinoma / genetics. Carcinoma / pathology. Carcinoma / physiopathology. Humans. Hyperaldosteronism / physiopathology. Oligonucleotide Array Sequence Analysis. Prognosis

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  • [Copyright] 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20097573.001).
  • [ISSN] 1879-3061
  • [Journal-full-title] Trends in endocrinology and metabolism: TEM
  • [ISO-abbreviation] Trends Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 39
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21. 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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22. Sandrini F, Villani DP, Tucci S, Moreira AC, de Castro M, Elias LL: Inheritance of R337H p53 gene mutation in children with sporadic adrenocortical tumor. Horm Metab Res; 2005 Apr;37(4):231-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inheritance of R337H p53 gene mutation in children with sporadic adrenocortical tumor.
  • Adrenocortical tumors (ACTs) are frequent in Brazil.
  • The mechanisms of adrenal tumorigenesis remain poorly established; the R337H germline mutation in the p53 gene has previously been associated with ACTs in Brazilian children.
  • DNA was extracted from peripheral blood cells and/or tumor tissue for sequencing exon 10 of the p53 gene.
  • Two members of the adult group showed asymptomatic adrenal incidentalomas, two showed virilization, and one presented with Cushing's syndrome.
  • The R337H mutation was found in fifteen samples of the nineteen tumor specimens available (78.9%).
  • None of the parents showed ACTs or any other neoplasia at the time of the study.
  • There was no association between the presence of germline or tissue R337H p53 mutation and malignancy at diagnosis.
  • The R337H p53 mutation was inherited from one of the parents of the patients, and there was no association between the presence of this mutation and tumor malignancy in children.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Genes, p53 / genetics. Mutation / genetics

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  • (PMID = 15952083.001).
  • [ISSN] 0018-5043
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Codon; 9007-49-2 / DNA
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23. De Groot PC, Van Kamp IL, Zweers EJ, De Kroon CD, Van Wijngaarden WJ: Oligohydramnios in a pregnant woman with Cushing's syndrome caused by an adrenocortical adenoma. J Matern Fetal Neonatal Med; 2007 May;20(5):431-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oligohydramnios in a pregnant woman with Cushing's syndrome caused by an adrenocortical adenoma.
  • A 28-year-old primigravida with severe oligohydramnios and pre-eclamptic symptoms was found to have Cushing's syndrome caused by an adrenocortical tumor.
  • As clinical features of pre-eclampsia and Cushing's syndrome may overlap, diagnosis can be delayed or even missed.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Cushing Syndrome / diagnosis. Oligohydramnios / diagnosis. Pregnancy Complications, Neoplastic / diagnosis
  • [MeSH-minor] Adenoma / complications. Adenoma / diagnosis. Adenoma / surgery. Adrenalectomy. Adult. Diagnosis, Differential. Female. Fetal Death. Humans. Hydrocortisone / therapeutic use. Pre-Eclampsia. Pregnancy

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  • (PMID = 17674251.001).
  • [ISSN] 1476-7058
  • [Journal-full-title] The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians
  • [ISO-abbreviation] J. Matern. Fetal. Neonatal. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] WI4X0X7BPJ / Hydrocortisone
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24. Wright CB, Brennan L, Brophy P, Kirsh G, Shapiro M, Potter B, Giss S, Lindeman KE, Obial R, Fannin E: Adrenocortical tumor with left renal vein, vena cava and intrahepatic venous extension. J Cardiovasc Surg (Torino); 2008 Feb;49(1):79-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenocortical tumor with left renal vein, vena cava and intrahepatic venous extension.
  • She proved, however, to have an adrenal cortical carcinoma which displaced the kidney, exhibiting vascular invasion within the gland and non-adherent extension into the vena cava, atrium, common hepatic vein and left renal vein, where some adherence was present.
  • This unusual tumor required extensive surgery for removal, including use of cardiopulmonary bypass, with good results.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Carcinoma, Renal Cell / diagnosis. Hepatic Veins / pathology. Kidney Neoplasms / diagnosis. Renal Veins / pathology. Vena Cava, Inferior / pathology
  • [MeSH-minor] Adrenalectomy. Adult. Cardiopulmonary Bypass. Diagnosis, Differential. Female. Heart Atria / pathology. Humans. Neoplasm Invasiveness. Nephrectomy. Treatment Outcome. Vascular Surgical Procedures

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  • (PMID = 18212691.001).
  • [ISSN] 0021-9509
  • [Journal-full-title] The Journal of cardiovascular surgery
  • [ISO-abbreviation] J Cardiovasc Surg (Torino)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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25. Behrend EN, Weigand CM, Whitley EM, Refsal KR, Young DW, Kemppainen RJ: Corticosterone- and aldosterone-secreting adrenocortical tumor in a dog. J Am Vet Med Assoc; 2005 May 15;226(10):1662-6, 1659
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Corticosterone- and aldosterone-secreting adrenocortical tumor in a dog.
  • An adrenal gland tumor was visualized via ultrasonography and computed tomography.
  • Histologic examination confirmed that the mass was an adrenocortical carcinoma.
  • Excess adrenal secretion of corticosterone was hypothesized to be the cause of the signs of glucocorticoid excess.
  • Treatment with mitotane was instituted and successful for a period of 4-months until the dog was euthanatized for neurologic problems that were most likely unrelated to endocrine disease.
  • [MeSH-major] Adrenal Cortex Neoplasms / veterinary. Aldosterone / secretion. Antineoplastic Agents, Hormonal / therapeutic use. Corticosterone / secretion. Dog Diseases / diagnosis. Mitotane / therapeutic use

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  • (PMID = 15906564.001).
  • [ISSN] 0003-1488
  • [Journal-full-title] Journal of the American Veterinary Medical Association
  • [ISO-abbreviation] J. Am. Vet. Med. Assoc.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 4964P6T9RB / Aldosterone; 78E4J5IB5J / Mitotane; W980KJ009P / Corticosterone
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26. Kumar S, Mandal AK, Acharya N, Thingnam SK, Bhalla V, Singh SK: Superior mesenteric artery injury during en bloc excision of a massive left adrenal tumor. Urol Int; 2007;78(2):182-4

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

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  • [Copyright] 2007 S. Karger AG, Basel
  • (PMID = 17293663.001).
  • [ISSN] 0042-1138
  • [Journal-full-title] Urologia internationalis
  • [ISO-abbreviation] Urol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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27. Lee R, Al-Ahmadie HA, Boorjian SA, Gonzalez RR, Badillo C, Badillo F, Reuter VE, Steckel J: A case of incidental adrenocortical oncocytoma. Nat Clin Pract Urol; 2006 Nov;3(11):618-21

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of incidental adrenocortical oncocytoma.
  • BACKGROUND: A 39-year-old female presented with an incidentally discovered left adrenal mass.
  • DIAGNOSIS: Oncocytic adrenocortical tumor, or adrenal oncocytoma.
  • [MeSH-major] Adenoma, Oxyphilic / diagnosis. Adenoma, Oxyphilic / surgery. Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / surgery

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  • (PMID = 17088930.001).
  • [ISSN] 1743-4289
  • [Journal-full-title] Nature clinical practice. Urology
  • [ISO-abbreviation] Nat Clin Pract Urol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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28. Doghman M, Madoux F, Hodder P, Lalli E: Identification and characterization of steroidogenic factor-1 inverse agonists. Methods Enzymol; 2010;485:3-23

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Furthermore, SF-1 is amplified and overexpressed in most cases of adrenocortical tumor occurring in children; studies performed in transgenic mice have shown that an increased SF-1 dosage triggers tumor formation in the adrenal cortex.
  • For these reasons, drugs interfering with SF-1 action would represent a promising tool to be added to the current pharmacological protocols in the therapy of adrenocortical cancer.
  • These compounds have the attributes to inhibit the increase in proliferation triggered by an augmented SF-1 dosage in adrenocortical tumor cells and to reduce their steroid production.
  • This latter property may also reveal beneficial for drugs used in the therapy of adrenocortical tumors to alleviate symptoms of virilization and Cushing often associated with tumor burden.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 21050908.001).
  • [ISSN] 1557-7988
  • [Journal-full-title] Methods in enzymology
  • [ISO-abbreviation] Meth. Enzymol.
  • [Language] ENG
  • [Grant] United States / NIMH NIH HHS / MH / U54 MH084512; United States / NIMH NIH HHS / MH / MH077624; United States / NIMH NIH HHS / MH / MH084512
  • [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 / Antineoplastic Agents; 0 / Isoquinolines; 0 / Steroidogenic Factor 1; 0 / Steroids
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29. Horvath A, Stratakis CA: Unraveling the molecular basis of micronodular adrenal hyperplasia. Curr Opin Endocrinol Diabetes Obes; 2008 Jun;15(3):227-33

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

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  • (PMID = 18438169.001).
  • [ISSN] 1752-2978
  • [Journal-full-title] Current opinion in endocrinology, diabetes, and obesity
  • [ISO-abbreviation] Curr Opin Endocrinol Diabetes Obes
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / Z01 HD000642; United States / Intramural NIH HHS / / Z99 HD999999
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] England
  • [Number-of-references] 53
  • [Other-IDs] NLM/ NIHMS101741; NLM/ PMC2671149
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30. Lerario AM, Mendonça BB, Lin CJ: [Molecular mechanisms involved in adrenocortical tumorigenesis]. Arq Bras Endocrinol Metabol; 2005 Oct;49(5):753-68

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Molecular mechanisms involved in adrenocortical tumorigenesis].
  • [Transliterated title] Avanços recentes no conhecimento dos mecanismos moleculares envolvidos na tumorigênese adrenocortical.
  • The adrenocortical tumorigenesis is a complex process, which involves multiple genetic changes.
  • A better knowledge on the mechanisms involved in tumor development would enable an early identification of malignant disease and also lead to the development of new treatment strategies.
  • Although in the recent years a large amount of data was produced, the exact mechanisms that lead to adrenocortical tumor development remains poorly understood.
  • A genome-wide approach, such as microarrays, will surely shed some light into the mechanisms responsible for adrenocortical tumorigenesis.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics

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  • (PMID = 16444358.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] por
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Genetic Markers
  • [Number-of-references] 125
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31. Fragoso MC, Kohek MB, Martin RM, Latronico AC, Lucon AM, Zerbini MC, Longui CA, Mendonca BB, Domenice S: An inhibin B and estrogen-secreting adrenocortical carcinoma leading to selective FSH suppression. Horm Res; 2007;67(1):7-11
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  • [Title] An inhibin B and estrogen-secreting adrenocortical carcinoma leading to selective FSH suppression.
  • OBJECTIVE: Hormone-secreting adrenocortical tumors are frequently associated with endocrine syndromes.
  • Abdominal magnetic resonance imaging revealed a very large tumor in the right adrenal gland.
  • Cortisol and adrenal androgen levels were normal.
  • The unusual finding of selective FSH suppression suggested secretion of inhibin B by the adrenocortical tumor.
  • Right adrenalectomy and nephrectomy were performed and the tumor was classified as a malignant tumor (Weiss score: 7.0) and unilateral mastectomy disclosed a lipoma.
  • Immunohistochemical analysis with anti-B-inhibin antibody revealed intense staining in the adrenocortical tumor cells.
  • One month after surgery, an abdominal magnetic resonance imaging revealed a local recurrence of the tumor and a second surgery was performed with partial resection of the tumor and the patient died 1 year after the first surgery.
  • CONCLUSION: We herein report the first inhibin B and estradiol-secreting adrenocortical carcinoma.
  • The unusual selective inhibition of FSH secretion should be considered a valuable hormonal finding for the diagnosis of inhibin B-secreting adrenocortical tumors.
  • [MeSH-major] Adrenal Cortex Neoplasms / blood. Carcinoma / blood. Estradiol / blood. Follicle Stimulating Hormone / blood. Inhibins / blood

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  • [Copyright] Copyright (c) 2007 S. Karger AG, Basel.
  • (PMID = 16974107.001).
  • [ISSN] 0301-0163
  • [Journal-full-title] Hormone research
  • [ISO-abbreviation] Horm. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / inhibin B; 4TI98Z838E / Estradiol; 57285-09-3 / Inhibins; 9002-68-0 / Follicle Stimulating Hormone
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32. Almeida MQ, Fragoso MC, Lotfi CF, Santos MG, Nishi MY, Costa MH, Lerario AM, Maciel CC, Mattos GE, Jorge AA, Mendonca BB, Latronico AC: Expression of insulin-like growth factor-II and its receptor in pediatric and adult adrenocortical tumors. J Clin Endocrinol Metab; 2008 Sep;93(9):3524-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of insulin-like growth factor-II and its receptor in pediatric and adult adrenocortical tumors.
  • BACKGROUND: Adrenocortical tumors are heterogeneous neoplasms with incompletely understood pathogenesis.
  • IGF-II overexpression has been consistently demonstrated in adult adrenocortical carcinomas.
  • OBJECTIVES: The objective of the study was to analyze expression of IGF-II and its receptor (IGF-IR) in pediatric and adult adrenocortical tumors and the effects of a selective IGF-IR kinase inhibitor (NVP-AEW541) on adrenocortical tumor cells.
  • PATIENTS: Fifty-seven adrenocortical tumors (37 adenomas and 20 carcinomas) from 23 children and 34 adults were studied.
  • Cell proliferation and apoptosis were analyzed in NCI H295 cells and a new cell line established from a pediatric adrenocortical adenoma.
  • RESULTS: IGF-II transcripts were overexpressed in both pediatric adrenocortical carcinomas and adenomas.
  • Otherwise, IGF-II was mainly overexpressed in adult adrenocortical carcinomas (270.5 +/- 130.2 vs. 16.1 +/- 13.3; P = 0.0001).
  • IGF-IR expression was significantly higher in pediatric adrenocortical carcinomas than adenomas (9.1 +/- 3.1 vs. 2.6 +/- 0.3; P = 0.0001), whereas its expression was similar in adult adrenocortical carcinomas and adenomas.
  • IGF-IR expression was a predictor of metastases in pediatric adrenocortical tumors in univariate analysis (hazard ratio 1.84; 95% confidence interval 1.28-2.66; P = 0.01).
  • CONCLUSION: IGF-IR overexpression was a biomarker of pediatric adrenocortical carcinomas.
  • Additionally, a selective IGF-IR kinase inhibitor had antitumor effects in adult and pediatric adrenocortical tumor cell lines, suggesting that IGF-IR inhibitors represent a promising therapy for human adrenocortical carcinoma.
  • [MeSH-major] Adenoma / genetics. Adrenal Cortex Neoplasms / genetics. Carcinoma / genetics. Insulin-Like Growth Factor II / genetics. Receptor, IGF Type 2 / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Female. Gene Expression Regulation, Neoplastic. Humans. Infant. Male. Middle Aged. Neoplasm Metastasis. Tumor Cells, Cultured

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  • (PMID = 18611974.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptor, IGF Type 2; 67763-97-7 / Insulin-Like Growth Factor II
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33. 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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34. Beuschlein F, Reincke M: Adrenocortical tumorigenesis. Ann N Y Acad Sci; 2006 Nov;1088:319-34

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenocortical tumorigenesis.
  • Through the widespread use of imaging techniques with great sensitivity adrenal tumors are often diagnosed as an incidental finding.
  • Although the majority of these adrenal lesions are benign and without evidence of endocrine activity or malignancy, hormone hypersecretion needs to be ruled out by specific tests.
  • In addition to the classical forms of overt adrenocortical hypersecretion, it has become evident over the recent years that modest adrenocortical steroid autonomy as present in normokalemic primary aldosteronism and subclinical Cushing's syndrome is also associated with a significant morbidity.
  • However, detection and differential diagnosis of these subtle changes in adrenal steroidogenesis can pose a diagnostic challenge to the clinician and is dependent on tests with reliable sensitivity and specificity.
  • Regulation of adrenocortical development and growth, which results in clinical symptoms if disrupted, is dependent upon the distinct spatiotemporal expression of a variety of transcription factors as well as stimulation by extra-adrenal peptide hormones.
  • Contributions to the elucidation of growth regulation of the adrenal cortex come from rare familiar syndromes associated with adrenocortical tumors, expression studies of adrenal tumor samples, in vitro studies on adrenocortical tumor cell lines, and mouse models displaying adrenal growth defects.
  • In this review, we will summarize the important molecular aspects of adrenal tumorigenesis and highlight some prospects for clinical applications.
  • [MeSH-major] Adrenal Cortex / pathology. Adrenal Cortex Neoplasms / pathology. Adrenal Cortex Neoplasms / physiopathology
  • [MeSH-minor] Animals. Genes, Tumor Suppressor. Humans. Hyperaldosteronism / genetics. Hyperaldosteronism / pathology. Hyperaldosteronism / physiopathology

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  • (PMID = 17192577.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 112
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35. Wagner S, Kiupel M, Peterson RA 2nd, Heikinheimo M, Wilson DB: Cytochrome b5 expression in gonadectomy-induced adrenocortical neoplasms of the domestic ferret (Mustela putorius furo). Vet Pathol; 2008 Jul;45(4):439-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytochrome b5 expression in gonadectomy-induced adrenocortical neoplasms of the domestic ferret (Mustela putorius furo).
  • Whereas the adrenal glands of healthy ferrets produce only limited amounts of androgenic steroids, adrenocortical neoplasms that arise in neutered ferrets typically secrete androgens or their derivative, estrogen.
  • The 17,20-lyase activity of cytochrome P450 17alpha-hydroxylase/17,20-lyase (P450c17) must increase to permit androgen biosynthesis in neoplastic adrenal tissue.
  • We screened ferret adrenocortical tumor specimens for expression of cytochrome b(5) (cyt b(5)), an allosteric regulator that selectively enhances the 17,20-lyase activity of P450c17.
  • Cyt b(5) immunoreactivity was evident in 24 of 25 (96%) adrenocortical adenomas/carcinomas from ferrets with signs of ectopic sex steroid production.
  • Normal adrenocortical cells lacked cyt b(5), which may account for the low production of adrenal androgens in healthy ferrets.
  • Other markers characteristic of gonadal somatic cells, such as luteinizing hormone receptor, aromatase, and GATA4, were coexpressed with cyt b(5) in some of the tumors.
  • We concluded that cyt b(5) is upregulated during gonadectomy-induced adrenocortical neoplasia and is a marker of androgen synthetic potential in these tumors.

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  • (PMID = 18587089.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK075618-02; United States / NIDDK NIH HHS / DK / P30 DK052574-09; United States / NIDDK NIH HHS / DK / R01 DK075618-02; United States / NIDDK NIH HHS / DK / DK52574; United States / NIDDK NIH HHS / DK / DK075618; United States / NIDDK NIH HHS / DK / P30 DK052574; United States / NIDDK NIH HHS / DK / R01 DK075618
  • [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 / GATA4 Transcription Factor; 0 / Receptors, LH; 0 / inhibin-alpha subunit; 57285-09-3 / Inhibins; 9035-39-6 / Cytochromes b5
  • [Other-IDs] NLM/ NIHMS45245; NLM/ PMC2497446
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36. Oki K, Yamane K, Sakashita Y, Kamei N, Watanabe H, Toyota N, Shigeta M, Sasano H, Kohno N: Primary aldosteronism and hypercortisolism due to bilateral functioning adrenocortical adenomas. Clin Exp Nephrol; 2008 Oct;12(5):382-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary aldosteronism and hypercortisolism due to bilateral functioning adrenocortical adenomas.
  • A 50-year-old male patient with a 15-year history of hypertension was referred to our hospital for evaluation of bilateral adrenal tumors.
  • Computed tomographic scan showed 10-mm masses in each adrenal gland.
  • The results of a subsequent adrenal venous catheterization study were consistent with the presence of a left cortisol-producing tumor and a right aldosterone-producing tumor.
  • This is an extremely rare case of bilateral adrenal tumors, in which the left adrenocortical tumor produced and secreted cortisol or both cortisol and aldosterone and the right one produced and secreted both aldosterone and cortisol, as confirmed by clinical findings and pathological studies using immunohistochemical analysis.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications. Cushing Syndrome / etiology. Hyperaldosteronism / etiology
  • [MeSH-minor] Aldosterone / metabolism. Diagnosis, Differential. Humans. Hydrocortisone / metabolism. Male. Middle Aged

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  • (PMID = 18543063.001).
  • [ISSN] 1342-1751
  • [Journal-full-title] Clinical and experimental nephrology
  • [ISO-abbreviation] Clin. Exp. Nephrol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone; WI4X0X7BPJ / Hydrocortisone
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37. Mazzuco TL, Chabre O, Feige JJ, Thomas M: Aberrant GPCR expression is a sufficient genetic event to trigger adrenocortical tumorigenesis. Mol Cell Endocrinol; 2007 Feb;265-266:23-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant GPCR expression is a sufficient genetic event to trigger adrenocortical tumorigenesis.
  • Aberrant expression of G protein-coupled receptors (GPCR) in the adrenal cortex is observed in some cases of ACTH-independent macronodular adrenal hyperplasias and adenomas associated with Cushing syndrome (CS).
  • Although there is clinical evidence for the implication of these receptors in abnormal regulation of cortisol secretion, whether this aberrant expression also directly causes the development of a benign adrenocortical tumor is an open question.
  • Cell transplantation provides a way to study genes that may be important in human tumor development.
  • The system we developed uses genetically modified adrenocortical cells transplanted into adrenalectomized immunodeficient mice, which form a functional tissue structure.
  • We observed that enforcing expression of the gastric inhibitory polypeptide (GIP) receptor or the luteinizing hormone (LH) receptor genes (taken as canonical examples of aberrantly expressed GPCRs) in adrenocortical cells resulted in the formation of hyperplastic tissues and the development of Cushing syndrome features in transplanted mice.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Receptors, G-Protein-Coupled / genetics
  • [MeSH-minor] Adrenal Cortex / cytology. Adrenal Cortex / metabolism. Animals. Cell Transplantation. Cushing Syndrome / genetics. Humans

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  • (PMID = 17250952.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Receptors, G-Protein-Coupled
  • [Number-of-references] 35
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38. Mathonnet M: [Management of adrenal incidentaloma combined with high blood pressure]. Ann Chir; 2005 Jun;130(5):303-8
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  • [Title] [Management of adrenal incidentaloma combined with high blood pressure].
  • Hypertension (HTA) is a very common disease but its origin is well known only in 1 to 5% of the cases.
  • HTA is present in half of the patients who have an adrenal incidentaloma.
  • Clinical data, hormonal sampling, computed tomography and adrenal scintigraphies are necessary to identify hyperfunctioning adrenal tumors.
  • Adrenalectomy is indicated in case of potential malignant tumors and hyperfunctioning tumors.
  • If HTA seems to be not in relation with the adrenal mass, it is recommended to recognize a congenital enzymatic block in order to ovoid an unnecessary adrenalectomy and to search for a preclinical Cushing's syndrome.
  • The removal of the adrenal mass improves the HTA for half of the patients.
  • If the adrenocortical tumor is nonfunctioning, patients have to be followed during a long time.
  • [MeSH-major] Adrenal Gland Neoplasms / therapy. Cushing Syndrome / therapy

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  • (PMID = 15935786.001).
  • [ISSN] 0003-3944
  • [Journal-full-title] Annales de chirurgie
  • [ISO-abbreviation] Ann Chir
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antihypertensive Agents
  • [Number-of-references] 36
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39. Hantel C, Beuschlein F: Mouse models of adrenal tumorigenesis. Best Pract Res Clin Endocrinol Metab; 2010 Dec;24(6):865-75
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  • [Title] Mouse models of adrenal tumorigenesis.
  • Adrenocortical carcinomas (ACCs) are heterogeneous tumors with a poor prognosis.
  • The rarity of this disorder causes a lack of treatment experience and material availability which is necessary to optimize existing treatments and to develop novel therapeutic strategies.
  • Although surgery is still the treatment of choice, adjuvant therapies are urgently needed as the rate of recurrence for these tumors is high.
  • In recent years molecular characterization of surgical tumor specimen has aided in the understanding of disease mechanisms and definition of therapeutic targets also in adrenocortical carcinoma.
  • Here we give an overview on rodent models that have been described to either have adrenocortical tumors as part of their phenotype or have been utilized for therapeutic screens as adrenocortical tumor models.
  • [MeSH-major] Adrenal Cortex Neoplasms / therapy. Adrenal Gland Neoplasms / physiopathology. Adrenal Gland Neoplasms / therapy. Disease Models, Animal
  • [MeSH-minor] Animals. Animals, Genetically Modified. Mice. Neoplasm Transplantation

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  • [Copyright] 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 21115155.001).
  • [ISSN] 1878-1594
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
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40. Horvath A, Boikos S, Giatzakis C, Robinson-White A, Groussin L, Griffin KJ, Stein E, Levine E, Delimpasi G, Hsiao HP, Keil M, Heyerdahl S, Matyakhina L, Libè R, Fratticci A, Kirschner LS, Cramer K, Gaillard RC, Bertagna X, Carney JA, Bertherat J, Bossis I, Stratakis CA: A genome-wide scan identifies mutations in the gene encoding phosphodiesterase 11A4 (PDE11A) in individuals with adrenocortical hyperplasia. Nat Genet; 2006 Jul;38(7):794-800
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  • [Title] A genome-wide scan identifies mutations in the gene encoding phosphodiesterase 11A4 (PDE11A) in individuals with adrenocortical hyperplasia.
  • Increased cyclic AMP (cAMP) signaling has been associated with PRKAR1A or GNAS mutations and leads to adrenocortical tumors and Cushing syndrome.
  • We investigated the genetic source of Cushing syndrome in individuals with adrenocortical hyperplasia that was not caused by known defects.
  • We performed genome-wide SNP genotyping, including the adrenocortical tumor DNA.
  • Tumor tissues showed 2q31-2q35 LOH, decreased protein expression and high cyclic nucleotide levels and cAMP-responsive element binding protein (CREB) phosphorylation.
  • PDE11A codes for a dual-specificity PDE that is expressed in adrenal cortex and is partially inhibited by tadalafil and other PDE inhibitors; its germline inactivation is associated with adrenocortical hyperplasia, suggesting another means by which dysregulation of cAMP signaling causes endocrine tumors.
  • [MeSH-major] Adrenal Glands / enzymology. Adrenal Glands / pathology. Mutation. Phosphoric Diester Hydrolases / genetics


41. Murao K, Imachi H, Cao W, Yu X, Li J, Yoshida K, Ahmed RA, Matsumoto K, Nishiuchi T, Wong NC, Ishida T: High-density lipoprotein is a potential growth factor for adrenocortical cells. Biochem Biophys Res Commun; 2006 May 26;344(1):226-32
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  • [Title] High-density lipoprotein is a potential growth factor for adrenocortical cells.
  • The entry of cholesterol contained within high-density lipoprotein (HDL) into adrenocortical cells is mediated by a human homologue of SR-BI, CD36, and LIMPII Analogous-1 (CLA-1) and thus augmenting their growth.
  • To address the role of CLA-1, we created a mutant mCLA that lacked the C-terminal tail.
  • Expression of mCLA inhibited the proliferation of an adrenocortical cell line and the incorporation of [(3)H]thymidine into the cells.
  • These findings raise the possibility that the inhibitors of the effects of HDL may be of therapeutic value for adrenocortical tumor.
  • [MeSH-major] Adrenal Cortex / drug effects. Growth Substances / physiology. Lipoproteins, HDL / pharmacology. Scavenger Receptors, Class B / physiology. Transcription Factor AP-1 / antagonists & inhibitors
  • [MeSH-minor] Androstadienes / pharmacology. Animals. Cell Line, Tumor. Cell Proliferation. Mice. Mutation. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / metabolism. Promoter Regions, Genetic. Proto-Oncogene Proteins c-akt / antagonists & inhibitors. Proto-Oncogene Proteins c-akt / metabolism. Transcriptional Activation / drug effects

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  • (PMID = 16600185.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androstadienes; 0 / Growth Substances; 0 / Lipoproteins, HDL; 0 / Scarb1 protein, mouse; 0 / Scavenger Receptors, Class B; 0 / Transcription Factor AP-1; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; XVA4O219QW / wortmannin
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42. Geller JL, Azer PC, Weiss LM, Mertens RB: Pigmented adrenocortical carcinoma: case report and review. Endocr Pathol; 2006;17(3):297-304
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  • [Title] Pigmented adrenocortical carcinoma: case report and review.
  • Darkly pigmented adrenocortical neoplasms are rare tumors that are often referred to as "black adenomas," indicative of both their pigmented nature and their invariably benign clinical behavior in previously reported cases.
  • We herein describe an exceptional case of a malignant pigmented adrenocortical neoplasm, with late recurrence and metastasis.
  • At age 53, this female patient was diagnosed with Cushing's syndrome and underwent a laparoscopic right adrenalectomy, revealing a 3 cm well-circumscribed, darkly pigmented adrenocortical tumor.
  • The tumor exhibited several atypical histologic features and was diagnosed as an atypical pigmented adrenal cortical neoplasm of uncertain malignant potential.
  • At subsequent exploratory laparotomy, three separate tumor nodules exhibiting varying degrees of pigmentation and ranging from 2.2 to 3.3 cm maximum dimension were excised.
  • Histologically, the tumor nodules were consistent with local recurrence/metastasis of the patient's previously excised pigmented adrenocortical neoplasm.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / secondary. Pigmentation. Retroperitoneal Neoplasms / secondary
  • [MeSH-minor] Adrenalectomy. Cushing Syndrome / etiology. Female. Humans. Middle Aged. Neoplasm Recurrence, Local / pathology. Neoplasm Recurrence, Local / surgery

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  • (PMID = 17308367.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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43. 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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44. 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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45. Ide H, Terado Y, Tokiwa S, Nishio K, Saito K, Isotani S, Kamiyama Y, Muto S, Imamura T, Horie S: Novel germ line mutation p53-P177R in adult adrenocortical carcinoma producing neuron-specific enolase as a possible marker. Jpn J Clin Oncol; 2010 Aug;40(8):815-8
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  • [Title] Novel germ line mutation p53-P177R in adult adrenocortical carcinoma producing neuron-specific enolase as a possible marker.
  • Adrenocortical cancer (ACC) is a rare and aggressive endocrine tumor.
  • The patient presented with a large retroperitoneum tumor and lung metastases.
  • Removal of the adrenocortical tumor with part of the transverse colon and tail of the pancreas, spleen and kidney was successfully performed following chemotherapy.
  • Levels of serum neuron-specific enolase (NSE) were found to be markedly high before surgery and may be clinically useful markers for monitoring tumor status during management.
  • [MeSH-major] Adrenal Gland Neoplasms / enzymology. Adrenal Gland Neoplasms / genetics. Adrenocortical Carcinoma / enzymology. Adrenocortical Carcinoma / genetics. Biomarkers, Tumor / blood. Genes, p53 / genetics. Germ-Line Mutation. Phosphopyruvate Hydratase / blood
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chemotherapy, Adjuvant. Combined Modality Therapy. Female. Humans. Lung Neoplasms / secondary. Nephrectomy. Retroperitoneal Neoplasms / secondary

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  • (PMID = 20421238.001).
  • [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 / Biomarkers, Tumor; EC 4.2.1.11 / Phosphopyruvate Hydratase
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46. 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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47. Chevalier N, Carrier P, Piche M, Chevallier A, Wagner K, Tardy V, Benchimol D, Fénichel P: Adrenocortical incidentaloma with uncertain prognosis associated with an inadequately treated congenital adrenal hyperplasia. Ann Endocrinol (Paris); 2010 Feb;71(1):56-9
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  • [Title] Adrenocortical incidentaloma with uncertain prognosis associated with an inadequately treated congenital adrenal hyperplasia.
  • Large adrenal tumors are rarely associated with adrenal enzymatic deficiency, except in 11-ss-hydroxylase insufficiency.
  • These tumors are exceptionally malignant.
  • We report here the case of a patient with a congenital 21-hydroxylase deficiency (compound heterozygote for two severe mutations in the CYP21A2 gene) untreated for 20 years.
  • His evaluation at 36 years of age showed a four-centimeter mass in the left adrenal gland, with most characteristics suggestive of malignancy (CT and positron emission tomography [PET] scan).
  • We performed a surgical resection that established the diagnosis of adrenocortical tumor of uncertain prognosis (Weiss's score: 3).
  • Even though malignant tumors are unusual in adrenal deficiency, our observation shows the need for a replacement therapy during adulthood, with a regular CT scan follow up in order to diagnose early isolated adrenal adenoma and remove it in case of malignancy suspicion.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenal Hyperplasia, Congenital / complications
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Adrenal Glands / pathology. Adrenal Glands / radionuclide imaging. Adrenalectomy. Adult. Cushing Syndrome / etiology. Heterozygote. Humans. Male. Positron-Emission Tomography. Prognosis. Steroid 21-Hydroxylase / genetics. Tomography, X-Ray Computed

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  • [Copyright] Copyright (c) 2009 Elsevier Masson SAS. All rights reserved.
  • (PMID = 19942208.001).
  • [ISSN] 0003-4266
  • [Journal-full-title] Annales d'endocrinologie
  • [ISO-abbreviation] Ann. Endocrinol. (Paris)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; EC 1.14.99.10 / CYP21A2 protein, human; EC 1.14.99.10 / Steroid 21-Hydroxylase
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48. 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

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  • (PMID = 15741269.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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49. Rodriguez-Galindo C, Figueiredo BC, Zambetti GP, Ribeiro RC: Biology, clinical characteristics, and management of adrenocortical tumors in children. Pediatr Blood Cancer; 2005 Sep;45(3):265-73
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  • [Title] Biology, clinical characteristics, and management of adrenocortical tumors in children.
  • Childhood adrenocortical tumors (ACT) are very aggressive endocrine neoplasms whose incidence is quite low.
  • In recent years, however, new information has been derived from the International Pediatric Adrenocortical Tumor Registry (IPACTR), and new clues to its pathogenesis have emerged.
  • Two-thirds of patients have resectable tumors.
  • Cisplatin-based chemotherapy with mitotane is indicated for unresectable or metastatic disease, although its impact on overall outcome is slight.
  • In childhood ACT, age, tumor size, and tumor resectability are the most important prognostic indicators.
  • Outcome is stage-dependent; patients with small, resectable tumors have survival rates in excess of 80%, whereas the outcome for patients with unresectable disease is dismal.
  • Patients with large, resectable tumors have an intermediate outcome.
  • [MeSH-major] Adrenal Cortex Neoplasms
  • [MeSH-minor] Adolescent. Antineoplastic Agents, Hormonal / therapeutic use. Child. Child, Preschool. Genes, p53 / genetics. Humans. Infant. Mitotane / therapeutic use. Mutation. Neoplasm Staging. Research. Survival Rate

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15747338.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 21765; United States / NCI NIH HHS / CA / CA 71907
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 78E4J5IB5J / Mitotane
  • [Number-of-references] 83
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50. Fon WP, Li PH: Dexamethasone-induced suppression of steroidogenic acute regulatory protein gene expression in mouse Y-1 adrenocortical cells is associated with reduced histone H3 acetylation. Endocrine; 2007 Oct;32(2):155-65
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  • [Title] Dexamethasone-induced suppression of steroidogenic acute regulatory protein gene expression in mouse Y-1 adrenocortical cells is associated with reduced histone H3 acetylation.
  • In this study, we investigated the effect of dexamethasone on the expression of steroidogenic acute regulatory protein (StAR) and the acetylation of histone H3 in mouse Y-1 adrenocortical tumor cells.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenocortical Carcinoma / metabolism. Dexamethasone / pharmacology. Glucocorticoids / pharmacology. Histones / metabolism. Phosphoproteins / metabolism
  • [MeSH-minor] 8-Bromo Cyclic Adenosine Monophosphate / pharmacology. Acetylation / drug effects. Animals. Cell Line, Tumor. Dose-Response Relationship, Drug. Gene Expression Regulation / drug effects. Mice. Progesterone / metabolism. Promoter Regions, Genetic / genetics. RNA, Messenger / metabolism. Receptors, Glucocorticoid / genetics. Receptors, Glucocorticoid / metabolism

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  • (PMID = 18040891.001).
  • [ISSN] 1355-008X
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / Histones; 0 / Phosphoproteins; 0 / RNA, Messenger; 0 / Receptors, Glucocorticoid; 0 / steroidogenic acute regulatory protein; 23583-48-4 / 8-Bromo Cyclic Adenosine Monophosphate; 4G7DS2Q64Y / Progesterone; 7S5I7G3JQL / Dexamethasone
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51. Mazzuco TL, Chabre O, Feige JJ, Thomas M: Aberrant expression of human luteinizing hormone receptor by adrenocortical cells is sufficient to provoke both hyperplasia and Cushing's syndrome features. J Clin Endocrinol Metab; 2006 Jan;91(1):196-203
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  • [Title] Aberrant expression of human luteinizing hormone receptor by adrenocortical cells is sufficient to provoke both hyperplasia and Cushing's syndrome features.
  • CONTEXT: Aberrant expression of LH/human chorionic gonadotropin (hCG) receptor has been suggested in several cases of bilateral macronodular adrenal hyperplasia with Cushing's syndrome.
  • OBJECTIVE: The aim of this study was to explore the action of LH/hCG receptor on the development of adrenal hyperplasia.
  • RESULTS: The ectopic expression of this single nonmutated gene transduced into bovine adrenocortical cells was sufficient to induce not only the aberrant cortisol secretion but also hyperproliferation and benign transformation.
  • CONCLUSIONS: These results demonstrate that a single genetic event such as the inappropriate expression of the nonmutated LH/hCG receptor gene is sufficient to initiate the phenotypic changes that cause the development of a benign adrenocortical tumor.
  • [MeSH-major] Adrenal Cortex / metabolism. Adrenal Hyperplasia, Congenital / genetics. Cushing Syndrome / genetics. Receptors, LH / biosynthesis

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  • (PMID = 16249277.001).
  • [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 / DNA, Complementary; 0 / DNA-Binding Proteins; 0 / Rag2 protein, mouse; 0 / Receptors, LH
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52. Fernandez-Ranvier GG, Weng J, Yeh RF, Shibru D, Khafnashar E, Chung KW, Hwang J, Duh QY, Clark OH, Kebebew E: Candidate diagnostic markers and tumor suppressor genes for adrenocortical carcinoma by expression profile of genes on chromosome 11q13. World J Surg; 2008 May;32(5):873-81
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  • [Title] Candidate diagnostic markers and tumor suppressor genes for adrenocortical carcinoma by expression profile of genes on chromosome 11q13.
  • BACKGROUND: The most common genetic change observed in adrenocortical carcinoma is loss of heterozygozity on chromosome 11q13.
  • As genes on this chromosome may be important in the pathogenesis of adrenocortical carcinoma, we compared their expression profile between benign and malignant adrenocortical tissue.
  • METHODS: We used the Affymetrix GeneChip (U133 plus 2.0) array in 54 adrenocortical tumors (11 carcinoma and 43 benign).
  • The area under the receiver operating characteristic (ROC) curve (AUC) was used to determined the diagnostic accuracy of the differently expressed genes for distinguishing benign from malignant tumors.
  • RESULTS: We found 25 of the 314 genes on chromosome 11q13 to be differentially expressed between adrenocortical carcinoma and benign adrenocortical tumor.
  • All 25 were downregulated in adrenocortical carcinoma by 2-fold to 4.8-fold; 21 were validated to be differentially expressed by RT-PCR (Pearson's coefficient>0.5).
  • Six genes (SERPING1, MRPL48, TM7SF2, DDB1, NDUSF8, PRDX5) validated by RT-PCR were significantly differentially expressed between benign and malignant adrenocortical tumors (p<0.05) with an overall accuracy of 89% for SERPING1, 91% for MRPL48, 87% for TM7SF2, 88% for DDB1, 91% for NDUFS8, and 89% for PRDX5.
  • CONCLUSIONS: We have identified 25 genes located on chromosome 11q13 that are downregulated in adrenocortical carcinoma and may be candidate tumor suppressor genes.
  • Six of these genes were good diagnostic markers for distinguishing adrenocortical carcinoma from adenoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Chromosomes, Human, Pair 11 / genetics. Genes, Tumor Suppressor / physiology. Loss of Heterozygosity / genetics

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  • (PMID = 18324346.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers
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53. 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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54. Szabó PM, Wiener Z, Tömböl Z, Kovács A, Pócza P, Horányi J, Kulka J, Riesz P, Tóth M, Patócs A, Gaillard RC, Falus A, Rácz K, Igaz P: Differences in the expression of histamine-related genes and proteins in normal human adrenal cortex and adrenocortical tumors. Virchows Arch; 2009 Aug;455(2):133-42
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  • [Title] Differences in the expression of histamine-related genes and proteins in normal human adrenal cortex and adrenocortical tumors.
  • Histamine is involved in the pathogenesis of several tumors; however, there are no data on its possible involvement in human adrenocortical tumorigenesis.
  • The expression of genes and proteins involved in the biosynthesis (histidine decarboxylase, HDC), action (histamine receptors: HRH1-HRH4), and metabolism of histamine is largely unknown both in the normal human adrenal cortex and in adrenocortical tumors.
  • In this study, we examined the expression of histamine-related genes and proteins and histamine content in normal adrenal cortex, benign adrenocortical adenomas, and malignant adrenocortical cancer (ACC).
  • Fifteen normal adrenals and 43 tumors were studied. mRNA expression was examined by real time RT-PCR.
  • We found that all proteins involved in histamine biosynthesis and action are present both in the normal adrenal cortex and in the tumors studied.
  • HDC expression and histamine content was highest in the normal tissues and lower in benign tumors, whereas it was significantly less in ACCs.
  • Adrenocortical tumorigenesis might, thus, be characterized by reduced histamine biosynthesis; furthermore, different adrenocortical tumor subtypes may show unique histamine receptor expression profiles.
  • [MeSH-major] Adrenal Cortex / metabolism. Adrenal Cortex Neoplasms / metabolism. Adrenocortical Adenoma / metabolism. Histamine / metabolism. Histidine Decarboxylase / metabolism. Receptors, Histamine / metabolism

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  • (PMID = 19568768.001).
  • [ISSN] 1432-2307
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / HRH4 protein, human; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Histamine; 0 / Receptors, Histamine H1; 0 / Receptors, Histamine H2; 0 / Receptors, Histamine H3; 820484N8I3 / Histamine; EC 4.1.1.22 / Histidine Decarboxylase
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55. 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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56. Woods AM, McIlmoil CJ, Rankin EN, Packer AA, Stevens JC, Macievic JA, Brown AB, Porter JP, Judd AM: Leukemia inhibitory factor protein and receptors are expressed in the bovine adrenal cortex and increase cortisol and decrease adrenal androgen release. Domest Anim Endocrinol; 2008 Aug;35(2):217-30
Hazardous Substances Data Bank. Corticotropin .

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  • [Title] Leukemia inhibitory factor protein and receptors are expressed in the bovine adrenal cortex and increase cortisol and decrease adrenal androgen release.
  • The release of adrenal steroids during acute stress is primarily regulated by adrenocorticotropic hormone (ACTH).
  • In contrast, during chronic inflammatory stress additional factors are involved in regulating adrenal function.
  • In addition, LIF and LIF receptors (LIFR) are expressed in the human adrenal cortex and the human adrenocortical tumor cell line H295R.
  • However, the expression of LIF and LIFR in non-human adrenal glands and the effects of LIF on the release of cortisol from adrenal cells of non-human species have not been determined.
  • Furthermore, the effects of LIF on adrenal androgen release from all species are unknown.
  • In this study, immunohistochemistry, Western blots, RT-PCR, and nucleotide sequencing was utilized to demonstrate that LIF and its receptor are expressed throughout the bovine adrenal cortex.
  • Although LIF did not modify basal cortisol release from dispersed cells isolated from the bovine adrenal zona fasciculate, this cytokine increased ACTH-stimulated release of cortisol from these cells in a manner dependent on the LIF concentration and exposure interval.
  • In contrast, LIF in a concentration-dependent and time-dependent manner decreased basal and ACTH-stimulated adrenal androgen release from dispersed cells isolated from the bovine adrenal zona reticularis.
  • Because LIF release increases during inflammatory stress and this cytokine stimulates adrenal cortisol release and inhibits adrenal androgen release, this cytokine may play an important role in regulating the release of adrenal steroids during inflammatory stress.
  • [MeSH-major] Adrenal Cortex / metabolism. Androgens / metabolism. Cattle / metabolism. Hydrocortisone / metabolism. Leukemia Inhibitory Factor / metabolism. Receptors, OSM-LIF / metabolism

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  • (PMID = 18638665.001).
  • [ISSN] 0739-7240
  • [Journal-full-title] Domestic animal endocrinology
  • [ISO-abbreviation] Domest. Anim. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Leukemia Inhibitory Factor; 0 / RNA, Messenger; 0 / Receptors, OSM-LIF; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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57. Benchekroun G, de Fornel-Thibaud P, Rodríguez Piñeiro MI, Rault D, Besso J, Cohen A, Hernandez J, Stambouli F, Gomes E, Garnier F, Begon D, Maurey-Guenec C, Rosenberg D: Ultrasonography criteria for differentiating ACTH dependency from ACTH independency in 47 dogs with hyperadrenocorticism and equivocal adrenal asymmetry. J Vet Intern Med; 2010 Sep-Oct;24(5):1077-85
Hazardous Substances Data Bank. Corticotropin .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ultrasonography criteria for differentiating ACTH dependency from ACTH independency in 47 dogs with hyperadrenocorticism and equivocal adrenal asymmetry.
  • BACKGROUND: Adrenal ultrasonography (US) in dogs with hyperadrenocorticism (HAC) is commonly used to distinguish adrenocorticotropic hormone (ACTH)-independent (AIHAC) and ACTH-dependent hyperadrenocorticism (ADHAC).
  • To date, no cut-off values for defining adrenal atrophy in cases of adrenal asymmetry have been determined.
  • Given that asymmetrical hyperplasia is sometimes observed in ADHAC, adrenal asymmetry without ultrasonographic proof of adrenocortical tumor such as vascular invasion or metastasis can be equivocal.
  • OBJECTIVE: The purpose of this study was to compare adrenal US findings between cases of ADHAC and AIHAC in dogs with equivocal adrenal asymmetry (EAA), and to identify useful criteria for their distinction.
  • METHODS: Ultrasound reports of HAC dogs with adrenal asymmetry without obvious vascular invasion or metastases were reviewed.
  • The thickness, shape, and echogenicity of both adrenal glands and presence of adjacent vascular compression were compared between AIHAC and ADHAC groups.
  • The 95% confidence intervals for estimated sensitivity and specificity of a SDV cut-off set at 5.0 mm in the diagnosis of AIHAC were 82-100 and 82-99%, respectively.
  • CONCLUSION AND CLINICAL IMPORTANCE: In EAA cases, an SDV ≤5.0 mm is an appropriate cut-off for AIHAC ultrasonographic diagnosis.

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  • [Copyright] Copyright © 2010 by the American College of Veterinary Internal Medicine.
  • (PMID = 20666982.001).
  • [ISSN] 0891-6640
  • [Journal-full-title] Journal of veterinary internal medicine
  • [ISO-abbreviation] J. Vet. Intern. Med.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 7S5I7G3JQL / Dexamethasone; 9002-60-2 / Adrenocorticotropic Hormone
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58. 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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59. Hahner S, Stuermer A, Kreissl M, Reiners C, Fassnacht M, Haenscheid H, Beuschlein F, Zink M, Lang K, Allolio B, Schirbel A: [123 I]Iodometomidate for molecular imaging of adrenocortical cytochrome P450 family 11B enzymes. J Clin Endocrinol Metab; 2008 Jun;93(6):2358-65
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [123 I]Iodometomidate for molecular imaging of adrenocortical cytochrome P450 family 11B enzymes.
  • BACKGROUND: Due to advances in conventional imaging, adrenal tumors are detected with increasing frequency.
  • Furthermore, four patients with known adrenal tumors (two metastatic adrenal adenocarcinomas, one bilateral adrenocortical adenoma, and one melanoma metastasis) were investigated with [(123)I]iodometomidate-SPECT.
  • In patients, adrenocortical tissue showed high and specific tracer uptake in both primary tumor and metastases with short investigation time and low radiation exposure, whereas the non-adrenocortical tumor did not exhibit any tracer uptake.
  • CONCLUSION: We have successfully completed the development of an in vivo detection system of adrenal Cyp11B enzymes by [(123)I]IMTO scintigraphy in both experimental animals and humans.
  • Our findings suggest that [(123)I]IMTO is a highly specific radiotracer for imaging of adrenocortical tissue.
  • Due to the general availability of SPECT technology, we anticipate that [(123)I]IMTO scintigraphy may become a widely used tool to characterize adrenal lesions.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenocortical Carcinoma / diagnosis. Cytochrome P-450 CYP11B2 / analysis. Iodine Radioisotopes. Steroid 11-beta-Hydroxylase / analysis
  • [MeSH-minor] Adrenal Cortex / enzymology. Adrenal Cortex / metabolism. Aged. Animals. Cells, Cultured. Etomidate / analogs & derivatives. Etomidate / chemistry. Female. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Humans. Male. Mice. Middle Aged. Molecular Diagnostic Techniques. Multigene Family. Radioactive Tracers. Whole Body Imaging / methods

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  • (PMID = 18397978.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Iodine Radioisotopes; 0 / Radioactive Tracers; 5377-20-8 / metomidate; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase; Z22628B598 / Etomidate
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60. Toledo RA, Mendonca BB, Fragoso MC, Soares IC, Almeida MQ, Moraes MB, Lourenço DM Jr, Alves VA, Bronstein MD, Toledo SP: Isolated familial somatotropinoma: 11q13-loh and gene/protein expression analysis suggests a possible involvement of aip also in non-pituitary tumorigenesis. Clinics (Sao Paulo); 2010 Apr;65(4):407-15
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  • OBJECTIVE: Non-pituitary tumors have been reported in a subset of patients harboring germline mutations in the aryl hydrocarbon receptor-interacting protein (AIP) gene.
  • However, no detailed investigations of non-pituitary tumors of AIP-mutated patients have been reported so far.
  • Subsequently, the mother developed a large virilizing adrenocortical carcinoma and a grade II B-cell non-Hodgkin's lymphoma.
  • Analyzing the tumoral DNA revealed that the AIP wild-type allele was lost in the daughter's somatotropinoma and the mother's adrenocortical carcinoma.
  • Both tumors displayed low AIP protein expression levels.
  • Low AIP gene expression was confirmed by qPCR in the adrenocortical carcinoma.
  • No evidence of LOH was observed in the DNA sample from the mother's B-cell lymphoma, and this tumor displayed normal AIP immunostaining.
  • CONCLUSIONS: Our study presents the first molecular analysis of non-pituitary tumors in AIP-mutated patients.
  • The finding of AIP inactivation in the adrenocortical tumor suggests that further investigation of the potential role of this recently identified tumor suppressor gene in non-pituitary tumors, mainly in those tumors in which the cAMP and the 11q13 locus are implicated, is likely to be worthwhile.
  • [MeSH-major] Acromegaly / genetics. Adenoma / genetics. Adrenocortical Carcinoma / genetics. Growth Hormone-Secreting Pituitary Adenoma / genetics. Intracellular Signaling Peptides and Proteins / genetics. Pituitary Neoplasms / genetics
  • [MeSH-minor] Adolescent. Adult. Female. Gene Expression. Genes, p53. Germ-Line Mutation. Humans. Loss of Heterozygosity / genetics. Multiple Endocrine Neoplasia Type 1 / genetics. Polymerase Chain Reaction

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  • (PMID = 20454499.001).
  • [ISSN] 1980-5322
  • [Journal-full-title] Clinics (São Paulo, Brazil)
  • [ISO-abbreviation] Clinics (Sao Paulo)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / aryl hydrocarbon receptor-interacting protein
  • [Other-IDs] NLM/ PMC2862671
  • [Keywords] NOTNLM ; AIP / Acromegaly / Adrenocortical tumor / FIPA / pituitary tumor
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61. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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62. Else T, Giordano TJ, Hammer GD: Evaluation of telomere length maintenance mechanisms in adrenocortical carcinoma. J Clin Endocrinol Metab; 2008 Apr;93(4):1442-9
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  • [Title] Evaluation of telomere length maintenance mechanisms in adrenocortical carcinoma.
  • CONTEXT: Adrenocortical cancer (ACC) is a rare disease with an often fatal outcome.
  • The clinical and pathological diagnosis of a malignant vs. benign adrenocortical tumor is sometimes challenging.
  • Telomere maintenance mechanisms (TMMs) are critical for the persistence of the malignant phenotype, but little is known about these mechanisms or their diagnostic value in adrenocortical lesions.
  • OBJECTIVE: Tissue samples of diagnostically known adrenocortical neoplasms were evaluated for parameters of known TMMs, telomerase activity (TA), and alternative telomere lengthening (ALT).
  • DESIGN: The study analyzed retrospectively collected frozen adrenocortical tissue samples from the University of Michigan Health System.
  • PATIENT SAMPLES: Samples included 24 ACCs, 11 adrenocortical adenomas (ACAs), and three normal adrenal tissues.
  • None of the normal adrenal tissues (none of three) or ACA (none of 11) samples had signs of an active TMM.
  • Determination of telomere maintenance mechanisms in diagnostically challenging adrenocortical tumors might be of additional diagnostic value in the pathological diagnosis of malignant vs. benign lesions.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Telomere

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  • (PMID = 18198226.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.7.49 / Telomerase
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63. Forti FL, Costa ET, Rocha KM, Moraes MS, Armelin HA: c-Ki-ras oncogene amplification and FGF2 signaling pathways in the mouse Y1 adrenocortical cell line. An Acad Bras Cienc; 2006 Jun;78(2):231-9
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  • [Title] c-Ki-ras oncogene amplification and FGF2 signaling pathways in the mouse Y1 adrenocortical cell line.
  • The mouse Y1 adrenocortical tumor cell line is highly responsive to FGF2-(Fibroblast Growth Factor 2) and possesses amplified and over-expressed c-Ki-ras proto-oncogene.
  • On the other hand, activation levels of another important pathway downstream of c-Ki-Ras-GTP, namely, Raf-->MEK-->ERK, remain strictly dependent on FGF2 stimulation (Rocha et al. 2003).
  • Here we show that, first, FGF2 transiently up-regulates the c-Ki-Ras-GTP-->PI3K-->Akt pathway, in spite of its high basal levels.
  • But, Y1 cells, expressing dominant negative mutant RasN17, display a rapid and transient up-regulation of c-H-Ras-GTP upon FGF2 treatment.
  • Elucidation of FGF2-signaling pathways in Y1 tumor cells can uncover new targets for drug development of interest in cancer therapy.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Fibroblast Growth Factor 2 / genetics. Genes, ras / genetics. Signal Transduction / genetics
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Transformation, Neoplastic. Gene Amplification. Gene Expression Regulation, Neoplastic. Mice


64. 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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  • [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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65. Galac S, Kars VJ, Klarenbeek S, Teerds KJ, Mol JA, Kooistra HS: Expression of receptors for luteinizing hormone, gastric-inhibitory polypeptide, and vasopressin in normal adrenal glands and cortisol-secreting adrenocortical tumors in dogs. Domest Anim Endocrinol; 2010 Jul;39(1):63-75
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  • [Title] Expression of receptors for luteinizing hormone, gastric-inhibitory polypeptide, and vasopressin in normal adrenal glands and cortisol-secreting adrenocortical tumors in dogs.
  • Hypercortisolism caused by an adrenocortical tumor (AT) results from adrenocorticotropic hormone (ACTH)-independent hypersecretion of glucocorticoids.
  • Normal adrenal glands served as control tissues.
  • In both normal adrenal glands and ATs, mRNA encoding for all receptors was present, although the expression abundance of the V(1b) receptor was very low.
  • The mRNA expression abundance for GIP and V(2) receptors in ATs were significantly lower (0.03 and 0.01, respectively) than in normal adrenal glands.
  • The zona fasciculata of normal adrenal glands stained immunonegative for the GIP receptor.
  • The zona fasciculata of both normal adrenal glands and AT tissue were immunopositive for LH receptor; in ATs in a homogenous or heterogenous pattern.
  • In normal adrenal glands, no immunolabeling for V(1b)R and V(2) receptor was present, but in ATs, V(2) receptor-immunopositive cells were detected.
  • [MeSH-major] Adrenal Cortex Neoplasms / veterinary. Dog Diseases / metabolism. Hydrocortisone / secretion. Receptors, Gastrointestinal Hormone / genetics. Receptors, LH / genetics. Receptors, Vasopressin / genetics
  • [MeSH-minor] Adrenal Glands / chemistry. Adrenalectomy. Animals. Dogs. Gene Expression. Immunohistochemistry. Polymerase Chain Reaction. RNA, Messenger / analysis. Zona Fasciculata / chemistry

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  • (PMID = 20399066.001).
  • [ISSN] 1879-0054
  • [Journal-full-title] Domestic animal endocrinology
  • [ISO-abbreviation] Domest. Anim. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptors, Gastrointestinal Hormone; 0 / Receptors, LH; 0 / Receptors, Vasopressin; 0 / gastric inhibitory polypeptide receptor; WI4X0X7BPJ / Hydrocortisone
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66. Okayama S, Imagawa K, Naya N, Iwama H, Somekawa S, Kawata H, Horii M, Nakajima T, Uemura S, Saito Y: Blocking T-type Ca2+ channels with efonidipine decreased plasma aldosterone concentration in healthy volunteers. Hypertens Res; 2006 Jul;29(7):493-7
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  • In a previous in vitro study, we clarified that efonidipine dramatically suppresses aldosterone secretion from human adrenocortical tumor cells during angiotensin II (Ang II)- and K+-stimulation, whereas nifedipine, a dominant L-type Ca2+ channel antagonist, does not.

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  • (PMID = 17044661.001).
  • [ISSN] 0916-9636
  • [Journal-full-title] Hypertension research : official journal of the Japanese Society of Hypertension
  • [ISO-abbreviation] Hypertens. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Calcium Channel Blockers; 0 / Calcium Channels, T-Type; 0 / Dihydropyridines; 0 / Neurotransmitter Agents; 0 / Nitrophenols; 0 / Organophosphorus Compounds; 0214FUT37J / nilvadipine; 11128-99-7 / Angiotensin II; 40ZTP2T37Q / efonidipine; 4964P6T9RB / Aldosterone; 9002-60-2 / Adrenocorticotropic Hormone; EC 3.4.23.15 / Renin; I9ZF7L6G2L / Nifedipine
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67. 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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68. Louiset E, Isvi K, Gasc JM, Duparc C, Cauliez B, Laquerrière A, Kuhn JM, Lefebvre H: Ectopic expression of serotonin7 receptors in an adrenocortical carcinoma co-secreting renin and cortisol. Endocr Relat Cancer; 2008 Dec;15(4):1025-34
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  • [Title] Ectopic expression of serotonin7 receptors in an adrenocortical carcinoma co-secreting renin and cortisol.
  • Abnormal expression of membrane receptors has been previously described in benign adrenocortical neoplasms causing Cushing's syndrome.
  • In particular, we have observed that, in some adreno corticotropic hormone (ACTH)-independent macronodular adrenal hyperplasia tissues, cortisol secretion is controlled by ectopic serotonin(7) (5-HT(7)) receptors.
  • The objective of the present study was to investigate in vitro the effect of serotonin (5-hydroxy tryptamine; 5-HT) on cortisol and renin production by a left adrenocortical carcinoma removed from a 48-year-old female patient with severe Cushing's syndrome and elevated plasma renin levels.
  • Tumor explants were obtained at surgery and processed for immunohistochemistry, in situ hybridization and cell culture studies.
  • In addition, immunohistochemistry showed the occurrence of 5-HT(7) receptor-like immunoreactivity in carcinoma cells. mRNAs encoding renin as well as renin-like immunoreactivity were detected in endothelial and tumor cells.
  • Cell incubation studies revealed that the adrenocortical tissue also released renin.
  • 5-HT(7) receptors, in an adrenocortical carcinoma.
  • Our results also indicate that 5-HT can influence the secretory activity of malignant adrenocortical tumors in an autocrine/paracrine manner.
  • The effects of 5-HT on adrenocortical tumor cells included a paradoxical inhibitory action on renin production and a stimulatory action on cortisol secretion involving 5-HT(7) receptors.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenocortical Carcinoma / metabolism. Hydrocortisone / metabolism. Receptors, Serotonin / metabolism. Renin / metabolism
  • [MeSH-minor] Adrenocorticotropic Hormone / pharmacology. Angiotensin II / pharmacology. Cushing Syndrome / metabolism. Cushing Syndrome / pathology. Female. Hormones / pharmacology. Humans. Immunoenzyme Techniques. In Situ Hybridization. Mast Cells / drug effects. Mast Cells / metabolism. Middle Aged. Phenols / pharmacology. Serotonin / pharmacology. Sulfonamides / pharmacology. Tumor Cells, Cultured / drug effects. Vasoconstrictor Agents / pharmacology

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  • (PMID = 18708508.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hormones; 0 / Phenols; 0 / Receptors, Serotonin; 0 / SB 269970; 0 / Sulfonamides; 0 / Vasoconstrictor Agents; 0 / serotonin 7 receptor; 11128-99-7 / Angiotensin II; 333DO1RDJY / Serotonin; 9002-60-2 / Adrenocorticotropic Hormone; EC 3.4.23.15 / Renin; WI4X0X7BPJ / Hydrocortisone
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69. Lichtenauer UD, Shapiro I, Geiger K, Quinkler M, Fassnacht M, Nitschke R, Rückauer KD, Beuschlein F: Side population does not define stem cell-like cancer cells in the adrenocortical carcinoma cell line NCI h295R. Endocrinology; 2008 Mar;149(3):1314-22
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  • [Title] Side population does not define stem cell-like cancer cells in the adrenocortical carcinoma cell line NCI h295R.
  • Recent evidence suggests the existence of a stem cell-like subpopulation of cells in hematological and solid tumor entities, which determine the malignant phenotype of a given tumor through their proliferative potential and chemotherapy resistance.
  • Herein we demonstrate the presence of SP cells in a variety of adrenal specimens, including primary cultures of human adrenocortical tumors and normal adrenal glands as well as established human and murine adrenocortical cancer cell lines by fluorescence-activated cell sorter analysis and confocal microscopy.
  • On a functional level, SP cells from the human adrenocortical tumor cell line NCI h295R revealed an expression pattern consistent with a less differentiated phenotype, including lower expression of steroidogenic enzymes such as steroid acute regulatory protein (StAR) and side-chain cleavage enzyme (P450scc) in comparison with non-SP cells.
  • Similarly to the baseline growth kinetics, no survival benefit was evident in SP cells after treatment with cytotoxic agents commonly used in adrenocortical carcinomas.
  • Taken together, these findings provide evidence that Hoechst dye exclusion, in contrast to what has been reported for other tumor entities, is not a major tumor stem cell defining marker in adrenocortical NCI h295R tumor cells.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Neoplastic Stem Cells / cytology
  • [MeSH-minor] Adrenal Glands / cytology. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Cell Cycle / physiology. Cell Differentiation / physiology. Cell Line, Tumor. Cell Proliferation. Cholesterol Side-Chain Cleavage Enzyme / metabolism. Coloring Agents. Drug Resistance, Neoplasm / physiology. Humans. Phenotype. Phosphoproteins / metabolism. Tumor Cells, Cultured

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  • (PMID = 18063677.001).
  • [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 / Antineoplastic Agents; 0 / Coloring Agents; 0 / Phosphoproteins; 0 / steroidogenic acute regulatory protein; EC 1.14.15.6 / Cholesterol Side-Chain Cleavage Enzyme
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70. 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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71. Doghman M, Karpova T, Rodrigues GA, Arhatte M, De Moura J, Cavalli LR, Virolle V, Barbry P, Zambetti GP, Figueiredo BC, Heckert LL, Lalli E: Increased steroidogenic factor-1 dosage triggers adrenocortical cell proliferation and cancer. Mol Endocrinol; 2007 Dec;21(12):2968-87
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  • [Title] Increased steroidogenic factor-1 dosage triggers adrenocortical cell proliferation and cancer.
  • Steroidogenic factor-1 (SF-1/Ad4BP; NR5A1), a nuclear receptor transcription factor, has a pivotal role in adrenal and gonadal development in humans and mice.
  • A frequent feature of childhood adrenocortical tumors is SF-1 amplification and overexpression.
  • Here we show that an increased SF-1 dosage can by itself augment human adrenocortical cell proliferation through concerted actions on the cell cycle and apoptosis.
  • Consistent with these results, increased SF-1 levels selectively modulate the steroid secretion profile of adrenocortical cells, reducing cortisol and aldosterone production and maintaining dehydroepiandrosterone sulfate secretion.
  • On the other hand, sphingosine, which can compete with phospholipids for binding to SF-1, had no effect on the SF-1 dosage-dependent increase of adrenocortical cell proliferation and expression of the FATE1 promoter.
  • In mice, increased Sf-1 dosage produces adrenocortical hyperplasia and formation of tumors expressing gonadal markers (Amh, Gata-4), which originate from the subcapsular region of the adrenal cortex.
  • Our studies reveal a critical role for SF-1 dosage in adrenocortical tumorigenesis and constitute a rationale for the development of drugs targeting SF-1 transcriptional activity for adrenocortical tumor therapy.

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  • (PMID = 17761949.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE5911/ GSE5912
  • [Grant] United States / NICHD NIH HHS / HD / R01 HD038498; United States / NCI NIH HHS / CA / CA63230; United States / NCI NIH HHS / CA / CA71907; United States / NICHD NIH HHS / HD / U54-HD28934
  • [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 / STAT3 Transcription Factor; 0 / Steroidogenic Factor 1; 0 / Steroids; 4QD397987E / Histidine
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72. 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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73. Zwermann O, Schulte DM, Reincke M, Beuschlein F: ACTH 1-24 inhibits proliferation of adrenocortical tumors in vivo. Eur J Endocrinol; 2005 Sep;153(3):435-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ACTH 1-24 inhibits proliferation of adrenocortical tumors in vivo.
  • OBJECTIVES: Although several lines of evidence suggest that the overall effects of the ACTH receptor, melanocortin 2 receptor (MC2-R), mediated signal transduction on adrenocortical growth and tumorigenesis are anti-proliferative, activation of MC2-R induces mitogens like jun, fos, and myc and activates the MAPK pathway.
  • In vivo, potential effects of endogenous ACTH on adrenal tumori-genesis can not be separated from effects of other POMC derived peptides.
  • METHODS: Murine adrenocortical tumor cells that lack MC2-R expression (Y6(pcDNA)) and Y6 cells stablely transfected with MC2-R (Y6(MC2-R)) were generated.
  • As a syngenic tumor model, LaHeF1/J mice simultaneously received 10(7) Y6(MC2-R) and Y6(pcDNA) subcutaneously, giving rise to MC2-R positive and negative tumors within the same animal.
  • Animals were treated for 3 weeks in groups of 12 according to the following schedule: group A, control animals receiving saline injection; group B, animals receiving 5.7 ng/injection of a slow release formula of ACTH 1-24 administered i.p. three times a week (aiming at a low physiologic dose); and group C, animals receiving 57 ng/injection of ACTH 1-24 (high physiological dose).
  • RESULTS: Twenty days of ACTH 1-24 treatment did not significantly affect corticosterone levels, endogenous ACTH levels or adrenal and thymus weight compared with saline injection.
  • However, ACTH 1-24 treatment of group B and C mice significantly reduced tumor weight in MC2-R positive tumors in a dose dependent manner (P = 0.03), while no significant difference in tumor mass was observed in MC2-R negative tumors.
  • PCNA and TUNEL staining, together with morphological characterization, demonstrated that these in vivo effects were due to reduced proliferation, while apoptosis and cellular hypertrophy within the tumor remained unchanged.
  • CONCLUSION: MC2-R expression is associated with a less aggressive adrenal tumor phenotype and anti-proliferative effects can be amplified through stimulation with physiological doses of ACTH.

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  • (PMID = 16131607.001).
  • [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 / Delayed-Action Preparations; 0 / Proliferating Cell Nuclear Antigen; 0 / Receptor, Melanocortin, Type 2; 16960-16-0 / Cosyntropin; 63231-63-0 / RNA; W980KJ009P / Corticosterone
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74. Matyakhina L, Freedman RJ, Bourdeau I, Wei MH, Stergiopoulos SG, Chidakel A, Walther M, Abu-Asab M, Tsokos M, Keil M, Toro J, Linehan WM, Stratakis CA: Hereditary leiomyomatosis associated with bilateral, massive, macronodular adrenocortical disease and atypical cushing syndrome: a clinical and molecular genetic investigation. J Clin Endocrinol Metab; 2005 Jun;90(6):3773-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hereditary leiomyomatosis associated with bilateral, massive, macronodular adrenocortical disease and atypical cushing syndrome: a clinical and molecular genetic investigation.
  • Hereditary leiomyomatosis and renal cell cancer (HLRCC) is an autosomal dominant disorder caused by mutations in the fumarate hydratase (FH) gene on chromosome 1q42.3-43.
  • Massive macronodular adrenocortical disease (MMAD) is a heterogeneous condition associated with Cushing syndrome (CS) and bilateral hyperplasia of the adrenal glands.
  • In MMAD, cortisol secretion is often mediated by ectopic, adrenocortical expression of receptors for a variety of substances; however, to date, no consistent genetic defects have been identified.
  • In a patient with HLRCC caused by a germline-inactivating FH mutation, we diagnosed atypical (subclinical) CS due to bilateral, ACTH-independent adrenocortical hyperplasia.
  • The tumor tissue harbored the germline FH mutation and demonstrated allelic losses of the 1q42.3-43 FH locus.
  • We then searched the National Institutes of Health (NIH) databases of patients with MMAD or HLRCC and found at least three other cases with MMAD that had a history of tumors that could be part of HLRCC; among patients with HLRCC, there were several with some adrenal nodularity noted on computed tomography but none with imaging findings consistent with MMAD.
  • From two of the three MMAD patients, adrenocortical tumor DNA was available and sequenced for coding FH mutations; there were none.
  • We conclude that in a patient with HLRCC, adrenal hyperplasia and CS were due to MMAD.
  • The latter was likely due to the FH germline mutation because in tumor cells, only the mutant allele was retained.
  • However, other patients with MMAD and HLRCC, or HLRCC patients with adrenal imaging findings consistent with MMAD, or MMAD patients with somatic FH mutations were not found among the NIH series.
  • Although a fortuitous association cannot be excluded, HLRCC may be added to the short list of monogenic disorders that have been reported to be associated with the development of adrenal tumors; FH may be considered a candidate gene for MMAD.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Cushing Syndrome / genetics. Leiomyomatosis / genetics
  • [MeSH-minor] Adrenal Glands / pathology. Aged. Chromosome Mapping. Chromosomes, Human, Pair 1. DNA / blood. DNA / genetics. DNA / isolation & purification. Female. Functional Laterality. Humans. In Situ Hybridization, Fluorescence. Skin / pathology. Treatment Outcome

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  • (PMID = 15741255.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9007-49-2 / DNA
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75. Galac S, Kooistra HS, Voorhout G, van den Ingh TS, Mol JA, van den Berg G, Meij BP: Hyperadrenocorticism in a dog due to ectopic secretion of adrenocorticotropic hormone. Domest Anim Endocrinol; 2005 Apr;28(3):338-48
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Spontaneous hyperadrenocorticism in dogs is known to be the result of excessive secretion of adrenocorticotropic hormone (ACTH) by the pituitary gland or excessive autonomous glucocorticoid secretion by an adrenocortical tumor.
  • Here, we report on an 8-year-old German shepherd dog in which ACTH-dependent hyperadrenocorticism was a result of ectopic ACTH secretion and could be related to an abdominal neuroendocrine tumor.
  • Ultrasonography revealed two equivalently enlarged adrenal glands, consistent with adrenocortical hyperplasia.
  • Histological examination of the pituitary gland revealed no neoplasia.
  • Histological examination revealed a metastasized neuroendocrine tumor.
  • In conclusion, the combination of (1) severe dexamethasone-resistant hyperadrenocorticism with elevated circulating ACTH levels, (2) definitive demonstration of the absence of pituitary neoplasia, and (3) an abdominal neuroendocrine tumor allowed the diagnosis of ectopic ACTH secretion.
  • [MeSH-major] ACTH Syndrome, Ectopic / veterinary. Adrenocortical Hyperfunction / veterinary. Adrenocorticotropic Hormone / secretion. Dog Diseases / etiology
  • [MeSH-minor] Abdominal Neoplasms / secretion. Abdominal Neoplasms / veterinary. Animals. Corticotropin-Releasing Hormone / pharmacology. Dogs. Hydrocortisone / blood. Liver / ultrasonography. Male. Neuroendocrine Tumors / secretion. Neuroendocrine Tumors / veterinary. Tomography, X-Ray Computed / veterinary. Ultrasonography / veterinary

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  • (PMID = 15760674.001).
  • [ISSN] 0739-7240
  • [Journal-full-title] Domestic animal endocrinology
  • [ISO-abbreviation] Domest. Anim. Endocrinol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone; WI4X0X7BPJ / Hydrocortisone
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76. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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


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


78. Szajerka A, Dziegiel P, Szajerka T, Zabel M, Winowski J, Grzebieniak Z: Immunohistochemical evaluation of metallothionein, Mcm-2 and Ki-67 antigen expression in tumors of the adrenal cortex. Anticancer Res; 2008 Sep-Oct;28(5B):2959-65

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

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  • (PMID = 19031940.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / Ki-67 Antigen; 0 / Nuclear Proteins; 9038-94-2 / Metallothionein; EC 3.6.4.12 / MCM2 protein, human; EC 3.6.4.12 / Minichromosome Maintenance Complex Component 2
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79. Jain M, Kapoor S, Mishra A, Gupta S, Agarwal A: Weiss criteria in large adrenocortical tumors: a validation study. Indian J Pathol Microbiol; 2010 Apr-Jun;53(2):222-6

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

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  • (PMID = 20551521.001).
  • [ISSN] 0974-5130
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] India
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80. Tissier F: [Sporadic adrenocortical tumors: genetics and perspectives for the pathologist]. Ann Pathol; 2008 Oct;28(5):409-16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Sporadic adrenocortical tumors: genetics and perspectives for the pathologist].
  • [Transliterated title] Tumeurs corticosurrénaliennes sporadiques de l'adulte : aspects génétiques et perspectives pour le pathologiste.
  • Most adrenocortical tumors are benign; adrenocortical carcinomas are rare but their prognosis is poor and few therapeutic options are available.
  • In most adrenocortical tumors, the morphological approach provides enough elements to establish the differential diagnosis between a benign and a malignant tumor but in few cases, it is insufficient.
  • Moreover, morphology is limited for predicting prognosis of adrenocortical carcinomas.
  • The comprehension of the genetic syndromes associated with adrenocortical tumors led to progress in the identification of genetic abnormalities involved in sporadic adrenocortical tumorigenesis.
  • Thus, in sporadic adrenocortical tumorigenesis, IGF-II overexpression and cyclin E overproduction have been associated with 11p15 alterations which are observed in Bethwith-Wiedemann syndrome and TP53 inactivating mutations and 17p13 locus abnormalities which are observed in Li-Fraumeni syndrome.
  • Activation of the Wnt/ss-catenin signaling pathway which is observed in familial adenomatous polyposis has been found in adrenocortical adenomas and carcinomas associated to mutations of CTNNB1, the gene coding ss-catenin, suggesting a central role for this pathway in adrenocortical tumorigenesis.
  • These genetics findings already have had repercussions for patients via the development of molecular markers for diagnosis and prognosis; in the future they should be helpful in the development of new therapeutics.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / pathology

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  • (PMID = 19068395.001).
  • [ISSN] 0242-6498
  • [Journal-full-title] Annales de pathologie
  • [ISO-abbreviation] Ann Pathol
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human; 67763-97-7 / Insulin-Like Growth Factor II; EC 3.1.4.- / Phosphoric Diester Hydrolases; EC 3.1.4.35 / PDE11A protein, human
  • [Number-of-references] 73
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81. Gur C, Salmon A, Silvetski N, Gross DJ: [Adrenocortical carcinoma]. Harefuah; 2008 Jun;147(6):520-5, 574
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Adrenocortical carcinoma].
  • 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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82. Misić M, Vidas Z, Skegro D, Kocman B, Jelić-Puskarić B, Kardum-Skelin I: Fine needle aspiration cytology of adrenocortical carcinoma--case report. Coll Antropol; 2010 Jun;34(2):665-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fine needle aspiration cytology of adrenocortical carcinoma--case report.
  • Ultrasonography (US) revealed a solitary tumor mass, eight cm in size, of the right adrenal gland.
  • Laboratory tests showed it to be a hormonally active, androgen secreting tumor (elevated testosterone level), which was consistent with the clinical picture of the disease.
  • After histopathological analysis tumor was signed out as adrenocortical carcinoma, a low risk carcinoma according to Weiss' classification.
  • The finding was verified by computerized tomography and the patient was reoperated on.
  • Cytologic opinion was recidive of primary malignant disease.
  • ACC is a rare malignant epithelial tumor of adrenal cortical cells, with high malignant potential.
  • Morphologically (histopathology and cytology), differential diagnosis includes adenoma on the one hand, and renal cell carcinoma (RCC) and hepatocellular carcinoma (HCC) on the other hand.
  • A combined evaluation of clinical features, size or weight, microscopic appearance, immunohistochemical and molecular genetic data is necessary to ensure a correct diagnosis.
  • The purpose of this case report is to present clinical and cytomorphologic features of our case of adrenocortical carcinoma which is very rare in cytology practice.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Carcinoma / pathology

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  • (PMID = 20698150.001).
  • [ISSN] 0350-6134
  • [Journal-full-title] Collegium antropologicum
  • [ISO-abbreviation] Coll Antropol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Croatia
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83. Tissier F: [Pathology of adrenocortical tumors: review and recent data]. Ann Endocrinol (Paris); 2009 Jun;70(3):179-85

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Pathology of adrenocortical tumors: review and recent data].
  • [Transliterated title] Anatomie pathologique des tumeurs corticosurrénaliennes de l'adulte : état des lieux et données récentes.
  • Most adrenocortical tumors are benign; adrenocortical carcinomas are rare but their prognosis is poor and their therapeutic is sparse.
  • In most adrenocortical tumors, the morphological approach brings sufficient elements to establish the differential diagnosis between a benign and a malignant tumor but in few cases, it is insufficient.
  • Moreover, morphology is limited for predicting prognosis of adrenocortical carcinomas.
  • These genetics findings already have repercussions for the patients in the development of molecular markers for diagnosis and prognosis and in the future they could help in the development of new morphological approaches, in particular immunohistochemical approaches.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology
  • [MeSH-minor] Cyclin E / genetics. Gene Expression Regulation, Neoplastic. Insulin-Like Growth Factor II / genetics. Mitosis. Mutation. Necrosis / pathology. Neoplasm Metastasis / pathology. Pheochromocytoma / genetics. Pheochromocytoma / pathology. Prognosis. Tumor Suppressor Protein p53 / genetics. beta Catenin / genetics

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  • (PMID = 19298951.001).
  • [ISSN] 0003-4266
  • [Journal-full-title] Annales d'endocrinologie
  • [ISO-abbreviation] Ann. Endocrinol. (Paris)
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Cyclin E; 0 / Tumor Suppressor Protein p53; 0 / beta Catenin; 67763-97-7 / Insulin-Like Growth Factor II
  • [Number-of-references] 77
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84. Ohtake H, Kawamura H, Matsuzaki M, Yokoyama E, Kitajima M, Onizuka S, Yamakawa M: Oncocytic adrenocortical carcinoma. Ann Diagn Pathol; 2010 Jun;14(3):204-8
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  • [Title] Oncocytic adrenocortical carcinoma.
  • Only 17 cases of oncocytic adrenocortical carcinoma have been reported in the English literature.
  • Here, we report an incidental case of oncocytic adrenocortical carcinoma.
  • Abdominal computed tomography revealed a left adrenal tumor.
  • The excised tumor was whitish, encapsulated, and 75 x 60 x 45 mm in size.
  • Large polygonal tumor cells were arranged in a generally diffuse architecture and exhibited abundant eosinophilic granular cytoplasm.
  • The tumor cells were immunopositive for vimentin, neuron-specific enolase, and synaptophysin but not for alpha-inhibin, melan A, or p53.
  • Diffuse and strong immunopositivity with an antimitochondrial antibody proved that this tumor was truly oncocytic.
  • Upon review of previous cases of oncocytic adrenocortical tumors, we reconsidered the diagnostic findings of the potential for malignancy.
  • [MeSH-major] Adenoma, Oxyphilic / pathology. Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology
  • [MeSH-minor] Aged. Autoantibodies / analysis. Biomarkers, Tumor / metabolism. Cell Nucleus / metabolism. Cell Nucleus / pathology. Humans. Incidental Findings. Male. Mitochondria / immunology

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  • (PMID = 20471567.001).
  • [ISSN] 1532-8198
  • [Journal-full-title] Annals of diagnostic pathology
  • [ISO-abbreviation] Ann Diagn Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Biomarkers, Tumor
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85. Opocher G, Schiavi F, Cicala MV, Patalano A, Mariniello B, Boaretto F, Zovato S, Pignataro V, Macino B, Negro I, Mantero F: Genetics of adrenal tumors. Minerva Endocrinol; 2009 Jun;34(2):107-21
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  • [Title] Genetics of adrenal tumors.
  • Endocrinology pioneered the development of molecular medicine, but also the study of adrenal tumors had a great impact in this field.
  • Particularly important was the detection of genetics of tumors derived from the adrenal medulla, as well as that of those derived from the sympathetic and parasympathetic paraganglia.
  • Less well understood is the genetics of adrenal cortex tumors, in particular adrenocortical carcinoma, a rare and particularly aggressive disease.
  • There are only a few examples of hereditary transmission of adrenocortical carcinoma, but the analysis of low penetrance genes by genome wide association study may enable us to discover new genetic mechanisms responsible for adrenocortical-derived tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Biomarkers, Tumor / genetics. Mutation. Pheochromocytoma / genetics
  • [MeSH-minor] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Genetic Predisposition to Disease. Genomics. Humans. Neoplasm Proteins / genetics. Paraganglioma / genetics

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  • (PMID = 19471236.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
  • [Number-of-references] 81
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86. West AN, Neale GA, Pounds S, Figueredo BC, Rodriguez Galindo C, Pianovski MA, Oliveira Filho AG, Malkin D, Lalli E, Ribeiro R, Zambetti GP: Gene expression profiling of childhood adrenocortical tumors. Cancer Res; 2007 Jan 15;67(2):600-8
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  • [Title] Gene expression profiling of childhood adrenocortical tumors.
  • Pediatric adrenocortical tumors (ACT) are rare and often fatal malignancies; little is known regarding their etiology and biology.
  • To provide additional insight into the nature of ACT, we determined the gene expression profiles of 24 pediatric tumors (five adenomas, 18 carcinomas, and one undetermined) and seven normal adrenal glands.
  • Distinct patterns of gene expression, validated by quantitative real-time PCR and Western blot analysis, were identified that distinguish normal adrenal cortex from tumor.
  • Differences in gene expression were also identified between adrenocortical adenomas and carcinomas.
  • In addition, pediatric adrenocortical carcinomas were found to share similar patterns of gene expression when compared with those published for adult ACT.
  • Our findings lay the groundwork for establishing gene expression profiles that may aid in the diagnosis and prognosis of pediatric ACT, and in the identification of signaling pathways that contribute to this disease.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics. Adrenocortical Carcinoma / genetics

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  • (PMID = 17234769.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / CA63230; United States / NCI NIH HHS / CA / CA71907
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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87. Akatsu T, Kameyama K, Araki K, Ashizawa T, Wakabayashi G, Kitajima M: Functioning adrenocortical oncocytoma: the first documented case producing interleukin-6 and review of the literature. J Endocrinol Invest; 2008 Jan;31(1):68-73
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  • [Title] Functioning adrenocortical oncocytoma: the first documented case producing interleukin-6 and review of the literature.
  • Adrenocortical oncocytoma is an extremely rare and predominantly non-functioning tumor.
  • We herein report the first case of an adrenocortical oncocytoma that produces interleukin (IL)-6.
  • A 38-yr-old woman was referred for treatment of a 4-cm adrenal mass.
  • Microscopic examination showed that the tumor was an adrenocortical oncocytoma with a unique peripheral lymphoid cuff with germinal centers.
  • Three observations lead us to consider that this tumor was the primary source of serum IL-6.
  • First, the IL-6 level in blood collected from the right adrenal vein was highest (527 pg/ml) among intra-operative blood samples.
  • [MeSH-major] Adenoma, Oxyphilic / secretion. Adrenal Cortex Neoplasms / secretion. Interleukin-6 / secretion

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  • (PMID = 18296908.001).
  • [ISSN] 1720-8386
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Interleukin-6
  • [Number-of-references] 43
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88. Guerrero MA, Kebebew E: Adrenocortical carcinoma and synchronous malignancies. J Cancer; 2010;1:108-11
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  • [Title] Adrenocortical carcinoma and synchronous malignancies.
  • OBJECTIVE: Adrenocortical carcinoma (ACC) is an aggressive tumor that accounts for 0.02% of all reported cancers.
  • ACC commonly arises in a sporadic manner, but may also manifest as part of a familial syndrome.
  • Regardless of the setting, ACC rarely arises concurrent with other malignant tumors.
  • We also provide a literature review of the past 20 years to identify other patients with ACC and synchronous malignant tumors, and those with familial syndromes associated with an increased risk of developing ACC.
  • RESULTS AND CONCLUSIONS: To our knowledge this is the first report of a patient with synchronous malignant tumors of the uterus, ovary and adrenal gland.
  • Review of the literature revealed only 5 other cases in which a patient had concurrent ACC and malignant tumors in other organs.

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  • (PMID = 20842232.001).
  • [ISSN] 1837-9664
  • [Journal-full-title] Journal of Cancer
  • [ISO-abbreviation] J Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Other-IDs] NLM/ PMC2938073
  • [Keywords] NOTNLM ; Adrenocortical carcinoma / Ovarian cancer / Synchronous malignancies / Uterine cancer / and Hereditary syndrome
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89. Ali AE, Raphael SJ: Functional oncocytic adrenocortical carcinoma. Endocr Pathol; 2007;18(3):187-9
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  • [Title] Functional oncocytic adrenocortical carcinoma.
  • We present a case of oncocytic adrenocortical carcinoma in a 25-year-old man who presented with persistent hypertension, hypokalemia, and a large right adrenal mass.
  • Histologically the tumor showed several features of malignancy and electron microscopy confirmed oncocytic differentiation.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / physiopathology. Adrenocortical Carcinoma / diagnosis. Adrenocortical Carcinoma / physiopathology

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  • (PMID = 18058268.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone; WI4X0X7BPJ / Hydrocortisone
  • [Number-of-references] 13
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90. Lee JA, Duh QY: Reoperation for adrenocortical neoplasms. Curr Treat Options Oncol; 2006 Jul;7(4):320-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reoperation for adrenocortical neoplasms.
  • Adrenocortical cancer is a highly lethal malignancy.
  • Surgical resection remains the only potential modality for cure or appreciable disease-free intervals.
  • Even with radical resection, most patients will recur or have metastatic disease.
  • For these patients, surgical re-resection of local recurrence and metastases is the best chance of controlling disease and prolonging survival.
  • Patients with widely metastatic disease or those with tumors not amenable to re-resection may benefit from tumor debulking to help control symptoms associated with oversecretion syndromes.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery

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  • (PMID = 16916492.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 35
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91. 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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92. Rodriguez FJ, Scheithauer BW, Erickson LA, Jenkins RB, Giannini C: Ectopic low-grade adrenocortical carcinoma in the spinal region: immunohistochemical and molecular cytogenetic study of a pediatric case. Am J Surg Pathol; 2009 Jan;33(1):142-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ectopic low-grade adrenocortical carcinoma in the spinal region: immunohistochemical and molecular cytogenetic study of a pediatric case.
  • Ectopic adrenocortical neoplasms arising in the nervous system are very rare.
  • We encountered an intradural, extramedullary case of an adrenocortical neoplasm of indeterminate malignant potential affecting a spinal nerve root in the distal lumbar region of a 5-month-old girl.
  • The tumor in both resections had increased mitotic activity (5/10 high power fields) and MIB-1 labeling indices of 23% and 33% at initial resection and recurrence, respectively.
  • Both tumors demonstrated gains of chromosomes 5 and 12 by interphase cytogenetics, whereas insulin growth factor 2 was identified in the recurrent tumor by immunohistochemistry.
  • This report demonstrates that ectopic adrenocortical tumors in the nervous system may exhibit clinicopathologic and cytogenetic features suggestive of adrenocortical carcinoma.

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  • [Cites] Am J Clin Pathol. 1999 Dec;112(6):801-9 [10587703.001]
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  • (PMID = 18941403.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / T32 NS007494; United States / NINDS NIH HHS / NS / T32 NS07494-04
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS396174; NLM/ PMC3427599
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93. Dundr P, Povýsil C, Zelinka T, Tvrdík D, Ciprová V, Novák K: Adrenocortical adenoma with rhabdoid features. Pathol Res Pract; 2006;202(3):177-81
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  • [Title] Adrenocortical adenoma with rhabdoid features.
  • We report a case of an aldosterone producing adrenocortical adenoma with rhabdoid features in a 16-year-old girl.
  • Grossly, the tumor measured 30 mm in diameter and weighed 24 g.
  • Histologically, the tumor was composed of approximately equal parts of tumor cells with rhabdoid features arranged in a solid and trabecular pattern and cells characterized by compact eosinophilic cytoplasm, solid growth with focal necroses, and increased mitotic activity.
  • The lipid-rich tumor cells with ample clear vacuolized cytoplasm represent a minor component.
  • Immunohistochemically, all the tumor cells showed the same results and were positive for vimentin, synaptophysin, Melan A, and alpha-inhibin.
  • Rhabdoid features have been described in many tumors of variable histogenesis; however, to the best of our knowledge, the presence of rhabdoid phenotype has never been described in either adrenocortical adenoma or carcinoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / pathology. Rhabdoid Tumor / metabolism
  • [MeSH-minor] Adolescent. Adrenalectomy. Aldosterone / metabolism. Biomarkers, Tumor / analysis. Female. Follow-Up Studies. Humans. Treatment Outcome

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  • (PMID = 16448785.001).
  • [ISSN] 0344-0338
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 4964P6T9RB / Aldosterone
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94. Suyama K, Beppu T, Isiko T, Sugiyama S, Matsumoto K, Doi K, Masuda T, Ohara C, Takamori H, Kanemitsu K, Hirota M, Baba H: Spontaneous rupture of adrenocortical carcinoma. Am J Surg; 2007 Jul;194(1):77-8
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  • [Title] Spontaneous rupture of adrenocortical carcinoma.
  • Massive hemorrhage from an adrenocortical carcinoma seldom occurs in the retroperitoneal or abdominal cavity.
  • We report a case of spontaneous rupture of primary adrenocortical carcinoma occurring in an adolescent.
  • A right adrenalectomy with complete removal of the tumor was performed successfully.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenocortical Carcinoma / surgery

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  • (PMID = 17560914.001).
  • [ISSN] 1879-1883
  • [Journal-full-title] American journal of surgery
  • [ISO-abbreviation] Am. J. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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95. Soon PS, Sidhu SB: Molecular basis of adrenocortical carcinomas. Minerva Endocrinol; 2009 Jun;34(2):137-47
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular basis of adrenocortical carcinomas.
  • Adrenocortical carcinomas (ACCs) are rare tumors associated with poor prognosis.
  • Although surgery is the mainstay of treatment for this cancer, most patients will experience a recurrence of their tumor.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Mutation. Neoplastic Syndromes, Hereditary / genetics
  • [MeSH-minor] Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Genes, Tumor Suppressor. Humans. Loss of Heterozygosity. Prognosis. Treatment Outcome

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  • (PMID = 19471238.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Number-of-references] 88
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96. Rodgers SE, Evans DB, Lee JE, Perrier ND: Adrenocortical carcinoma. Surg Oncol Clin N Am; 2006 Jul;15(3):535-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenocortical carcinoma.
  • ACC is a rare clinical entity that carries a poor prognosis; early diagnosis and complete surgical resection are associated with the improvement in patient survival.
  • Even with appropriated diagnosis and treatment, most patients will develop recurrence and succumb to ACC because of the underlying tumor biology, the difficulty of achieving a complete resection, and the lack of effective systemic therapies.
  • Despite its many drawbacks, mitotane continues to be a mainstay in the treatment of high-risk patients with ACC, especially those with recurrent or metastatic disease.
  • [MeSH-major] Adrenal Cortex Neoplasms. Adrenocortical Carcinoma
  • [MeSH-minor] Beckwith-Wiedemann Syndrome / genetics. Biopsy, Needle. Humans. Hydrocortisone / blood. Insulin-Like Growth Factor II. Magnetic Resonance Imaging. Neoplasm Staging. Proteins / genetics

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  • (PMID = 16882496.001).
  • [ISSN] 1055-3207
  • [Journal-full-title] Surgical oncology clinics of North America
  • [ISO-abbreviation] Surg. Oncol. Clin. N. Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / IGF2 protein, human; 0 / Proteins; 67763-97-7 / Insulin-Like Growth Factor II; WI4X0X7BPJ / Hydrocortisone
  • [Number-of-references] 85
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97. Schittenhelm J, Ebner FH, Harter P, Bornemann A: Symptomatic intraspinal oncocytic adrenocortical adenoma. Endocr Pathol; 2009;20(1):73-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Symptomatic intraspinal oncocytic adrenocortical adenoma.
  • Most intraspinal neoplasms of epithelial origin are metastases from primary carcinomas.
  • Benign epithelial tumors are rarely found at this site.
  • We here present the case of a 44-year-old woman with a lesion in the cauda equina that fulfilled the radiologic criteria of schwannoma and caused clinical symptoms for 3 years.
  • The excised tumor was composed of nests of large polygonal cells with eosinophilic partial granular cytoplasm.
  • The tumor showed diffuse positivity for melan-A, synaptophysin, and alpha-inhibin.
  • This immunoprofile indicated adrenocortical origin.
  • Ultrastructural examination showed abundant mitochondria, suggesting an oncocytic tumor.
  • The diagnosis of an oncocytic adrenal cortical adenoma was made.
  • These extraadrenal tumors are thought to arise from heterotopic adrenocortical tissue in the spinal cavity.
  • Oncocytic tumors are rare neoplasms and they comprise non-functioning variants of adrenal cortical adenomas.
  • To date, only five such intraspinal tumors have been observed.
  • Immunohistochemistry excluded oncocytic paraganglioma, oncocytic meningioma, renal cell carcinoma, alveolar soft part sarcoma, and granular cell tumor.
  • A view of the literature of these rare but probably underdiagnosed intraspinal tumors is given.
  • [MeSH-major] Adenoma, Oxyphilic / pathology. Adrenocortical Adenoma / pathology. Spinal Cord Neoplasms / pathology

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  • (PMID = 19039533.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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98. Bacchetta J, Droz JP: [Practical use of o,p'DDD in adrenocortical carcinoma]. Bull Cancer; 2005 Mar;92(3):273-9
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  • [Title] [Practical use of o,p'DDD in adrenocortical carcinoma].
  • Adrenocortical carcinoma (AC) is a rare tumor of poor prognosis.
  • Five patients (four with AC and one with a metastatic Leydig cell tumor of the testis) were treated by Lysodren.
  • Surgery is an important part of metastatic disease treatment.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Adrenocortical Carcinoma / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Mitotane / therapeutic use

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  • (PMID = 15820922.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 78E4J5IB5J / Mitotane
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99. Xu Y, Yu RM, Zhang X, Murphy MB, Giesy JP, Lam MH, Lam PK, Wu RS, Yu H: Effects of PCBs and MeSO2-PCBs on adrenocortical steroidogenesis in H295R human adrenocortical carcinoma cells. Chemosphere; 2006 May;63(5):772-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of PCBs and MeSO2-PCBs on adrenocortical steroidogenesis in H295R human adrenocortical carcinoma cells.
  • In this study, the potential effects of four selected polychlorinated biphenyl (PCB) congeners (PCB101, PCB110, PCB126 and PCB149) as well as several of their environmentally-relevant methylsulfonyl-(MeSO(2)-) PCB metabolites (3'-MeSO(2)-CB101, 4'-MeSO(2)-CB101, 4'-MeSO(2)-CB110, 3'-MeSO(2)-CB149 and 4'-MeSO(2)-CB149) on adrenocortical steroidogenesis were evaluated by in vitro bioassay based on the human adrenocortical carcinoma H295R cell line.
  • Overall, these findings suggest that PCBs and PCB metabolites can affect regulation of adrenocortical steroidogenesis.
  • [MeSH-major] Adrenocortical Carcinoma / metabolism. Cytochrome P-450 Enzyme System / biosynthesis. Hydroxysteroid Dehydrogenases / drug effects. Polychlorinated Biphenyls / toxicity. Steroids / biosynthesis
  • [MeSH-minor] Enzyme Activation / drug effects. Humans. Tumor Cells, Cultured

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  • (PMID = 16216300.001).
  • [ISSN] 0045-6535
  • [Journal-full-title] Chemosphere
  • [ISO-abbreviation] Chemosphere
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Steroids; 9035-51-2 / Cytochrome P-450 Enzyme System; DFC2HB4I0K / Polychlorinated Biphenyls; EC 1.1.- / Hydroxysteroid Dehydrogenases
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100. Modi P, Goel R, Kadam G: Retroperitoneoscopic partial adrenalectomy for large adrenocortical oncocytoma. J Endourol; 2007 Apr;21(4):419-22
MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Retroperitoneoscopic partial adrenalectomy for large adrenocortical oncocytoma.
  • A young woman had mild hypertension, and on evaluation, a large tumor arising from the right adrenal gland was found.
  • The tumor was hormonally inactive.
  • The histopathology report described adrenocortical oncocytoma.

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  • (PMID = 17451335.001).
  • [ISSN] 0892-7790
  • [Journal-full-title] Journal of endourology
  • [ISO-abbreviation] J. Endourol.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media; 0 / Vimentin
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