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

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  • (PMID = 16776254.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Androgens; 78E4J5IB5J / Mitotane
  • [Number-of-references] 5
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2. Takehara K, Sakai H, Shono T, Irie J, Kanetake H: Proliferative activity and genetic changes in adrenal cortical tumors examined by flow cytometry, fluorescence in situ hybridization and immunohistochemistry. Int J Urol; 2005 Feb;12(2):121-7
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  • [Title] Proliferative activity and genetic changes in adrenal cortical tumors examined by flow cytometry, fluorescence in situ hybridization and immunohistochemistry.
  • BACKGROUND: To determine differences in biological features among different adrenal tumors, we investigated the DNA ploidy, numerical chromosomal aberration and proliferative activity in human adrenal cortical neoplasms.
  • METHODS: Our study included six adrenal cortical adenomas with Cushing syndrome, 12 adenomas with hyperaldosteronism, three non-functioning adenomas and three adrenal cortical carcinomas.
  • RESULTS: The mean Ki-67 labeling index (LI) of adrenal cortical carcinomas was markedly higher than that of adrenal cortical adenomas (209.4 vs 8.7).
  • In functional adrenal cortical adenomas, the LI was significantly lower in adenomas with hyperaldosteronism than in those with Cushing syndrome (P = 0.004), although FCM results indicated that tetraploid patterns were more frequently observed in the former type.
  • Tumor size was significantly smaller in adenomas with hyperaldosteronism than in those with Cushing syndrome (P = 0.004).
  • Chromosome 17 showed disomy in all adrenal cortical adenomas, whereas chromosome 17 abnormalities were found in two of three adrenal cortical carcinomas.
  • CONCLUSIONS: Our study characterized various biological features of benign and malignant adrenal cortical tumors.
  • The use of a combination of markers might provide additional information to assist our understanding of the clinical behavior of an individual adrenal cortical tumor.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / metabolism. Flow Cytometry. Immunohistochemistry. In Situ Hybridization, Fluorescence
  • [MeSH-minor] Adenoma / genetics. Adenoma / metabolism. Adenoma / pathology. Adult. Aged. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Carcinoma / genetics. Carcinoma / metabolism. Carcinoma / pathology. Cell Proliferation. Chromosomes, Human, Pair 17. Cushing Syndrome / genetics. Cushing Syndrome / metabolism. Cushing Syndrome / pathology. DNA, Neoplasm / genetics. Female. Humans. Hyperaldosteronism / genetics. Hyperaldosteronism / metabolism. Hyperaldosteronism / pathology. Ki-67 Antigen / metabolism. Male. Middle Aged. Ploidies. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 15733104.001).
  • [ISSN] 0919-8172
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
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3. Pianovski MA, Maluf EM, de Carvalho DS, Ribeiro RC, Rodriguez-Galindo C, Boffetta P, Zancanella P, Figueiredo BC: Mortality rate of adrenocortical tumors in children under 15 years of age in Curitiba, Brazil. Pediatr Blood Cancer; 2006 Jul;47(1):56-60
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  • [Title] Mortality rate of adrenocortical tumors in children under 15 years of age in Curitiba, Brazil.
  • BACKGROUND: Several reports refer to an increased frequency of adrenal cortex tumors (ACT) among children in Southern Brazil, yet all data have been derived from hospital-based registries.
  • PROCEDURE: We reviewed all death certificates that mentioned ACT or adrenal neuroblastoma (NB) and which were reported to the Paraná State Department of Health between 1998 and 2003, for individuals younger than 15 years who resided in the Curitiba metropolitan region.
  • The ratio of the adrenal NB and ACT age-adjusted mortality rates was 1.43.
  • CONCLUSIONS: Our investigation of population-based mortality confirms the evidence from hospital-based registries of a clustering of ACT in Southern Brazil.
  • [MeSH-major] Adrenal Cortex Neoplasms / mortality

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16200634.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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4. Beuschlein F, Reincke M: Adrenocortical tumorigenesis. Ann N Y Acad Sci; 2006 Nov;1088:319-34
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  • [Title] Adrenocortical tumorigenesis.
  • Through the widespread use of imaging techniques with great sensitivity adrenal tumors are often diagnosed as an incidental finding.
  • Although the majority of these adrenal lesions are benign and without evidence of endocrine activity or malignancy, hormone hypersecretion needs to be ruled out by specific tests.
  • In addition to the classical forms of overt adrenocortical hypersecretion, it has become evident over the recent years that modest adrenocortical steroid autonomy as present in normokalemic primary aldosteronism and subclinical Cushing's syndrome is also associated with a significant morbidity.
  • However, detection and differential diagnosis of these subtle changes in adrenal steroidogenesis can pose a diagnostic challenge to the clinician and is dependent on tests with reliable sensitivity and specificity.
  • Regulation of adrenocortical development and growth, which results in clinical symptoms if disrupted, is dependent upon the distinct spatiotemporal expression of a variety of transcription factors as well as stimulation by extra-adrenal peptide hormones.
  • Contributions to the elucidation of growth regulation of the adrenal cortex come from rare familiar syndromes associated with adrenocortical tumors, expression studies of adrenal tumor samples, in vitro studies on adrenocortical tumor cell lines, and mouse models displaying adrenal growth defects.
  • In this review, we will summarize the important molecular aspects of adrenal tumorigenesis and highlight some prospects for clinical applications.
  • [MeSH-major] Adrenal Cortex / pathology. Adrenal Cortex Neoplasms / pathology. Adrenal Cortex Neoplasms / physiopathology
  • [MeSH-minor] Animals. Genes, Tumor Suppressor. Humans. Hyperaldosteronism / genetics. Hyperaldosteronism / pathology. Hyperaldosteronism / physiopathology

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  • (PMID = 17192577.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 112
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5. Szekeres M, Turu G, Orient A, Szalai B, Süpeki K, Cserzo M, Várnai P, Hunyady L: Mechanisms of angiotensin II-mediated regulation of aldosterone synthase expression in H295R human adrenocortical and rat adrenal glomerulosa cells. Mol Cell Endocrinol; 2009 Apr 29;302(2):244-53
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  • [Title] Mechanisms of angiotensin II-mediated regulation of aldosterone synthase expression in H295R human adrenocortical and rat adrenal glomerulosa cells.
  • In adrenal zona glomerulosa cells angiotensin II (Ang II) is a key regulator of steroidogenesis.
  • Our purpose was to compare the mechanisms of Ang II-induced changes in the expression level of early transcription factors NR4A1 (NGFIB) and NR4A2 (Nurr1) genes, and the CYP11B2 gene encoding aldosterone synthase in H295R human adrenocortical tumor cells and in primary rat adrenal glomerulosa cells.
  • Real-time PCR studies have demonstrated that Ang II increased the expression levels of NR4A1 and NR4A2 in H295R cells within 1 h after stimulation, which persisted up to 6 h; whereas in rat adrenal glomerulosa cells the kinetics of the expression of these genes were more rapid and transient.
  • Studies using MEK inhibitor (PD98059, 20 microM), protein kinase C inhibitor (BIM1, 3 microM) and calmodulin kinase (CAMK) inhibitor (KN93, 10 microM) revealed that in rat adrenal glomerulosa cells CAMK-mediated mechanisms play a predominant role in the regulation of CYP11B2.
  • These data suggest that the previously reported CAMK-mediated stimulation of early transcription factors NGFIB and Nurr1 has a predominant role in Ang II-induced CYP11B2 activation in rat adrenal glomerulosa cells, whereas in H295R cells ERK activation and G protein-independent mechanisms also contribute to this process.
  • [MeSH-major] Adrenal Cortex / cytology. Angiotensin II / pharmacology. Cytochrome P-450 CYP11B2 / genetics. Gene Expression Regulation / drug effects. Zona Glomerulosa / cytology

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  • (PMID = 19418629.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Transcription Factors; 11128-99-7 / Angiotensin II; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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6. Al-Zaid T, Alroy J, Pfannl R, Strissel KJ, Powers JF, Layer A, Carpinito G, Tischler AS: Oncocytic adrenal cortical tumor with cytoplasmic inclusions and hyaline globules. Virchows Arch; 2008 Sep;453(3):301-6
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  • [Title] Oncocytic adrenal cortical tumor with cytoplasmic inclusions and hyaline globules.
  • Adrenal cortical tumors, particularly oncocytic tumors, have been reported to contain a variety of intracytoplasmic and intramitochondrial inclusions.
  • Oncocytic cortical tumors can also morphologically mimic pheochromocytomas.
  • We report an unusual, partially oncocytic cortical neoplasm with nesting architecture, intranuclear inclusions, and hyaline globules reminiscent of pheochromocytoma, together with numerous, small, brightly eosinophilic, periodic acid-Schiff-positive cytoplasmic inclusions and typical cytoplasmic lipid droplets.
  • Immunohistochemistry and immunoblots were utilized to further characterize the tumor.
  • Immunohistochemistry demonstrated immunoreactivity of both the eosinophilic inclusions and the hyaline globules for adipose differentiation-related protein (ADRP), which is one of a group of proteins associated with storage of neutral lipids in many cell types.
  • Immunoblots confirmed the presence of ADRP and demonstrated an imbalance between ADRP and perilipin, another neutral lipid-associated protein, in tumor tissue compared to normal adrenal cortex.
  • The findings suggest that mitochondrial dysfunction in oncocytic cortical tumors may lead to abnormal processing of proteins related to the lipid-storing functions of the adrenal cortex, resulting in unusual cytoplasmic inclusions and extracellular globules resembling the globules in pheochromocytomas.
  • The finding of ADRP as a constituent of inclusions in adrenal cortical tumors has not been previously reported.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Inclusion Bodies / pathology. Oxyphil Cells / pathology
  • [MeSH-minor] Adrenal Cortex / pathology. Humans. Hyalin / metabolism. Male. Membrane Proteins / metabolism. Microscopy, Electron. Middle Aged. Perilipin-2. Pheochromocytoma / pathology

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  • (PMID = 18688642.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Membrane Proteins; 0 / PLIN2 protein, human; 0 / Perilipin-2
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7. Mazzuco TL, Chabre O, Sturm N, Feige JJ, Thomas M: Ectopic expression of the gastric inhibitory polypeptide receptor gene is a sufficient genetic event to induce benign adrenocortical tumor in a xenotransplantation model. Endocrinology; 2006 Feb;147(2):782-90
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  • [Title] Ectopic expression of the gastric inhibitory polypeptide receptor gene is a sufficient genetic event to induce benign adrenocortical tumor in a xenotransplantation model.
  • Aberrant expression of ectopic G protein-coupled receptors (GPCRs) in adrenal cortex tissue has been observed in several cases of ACTH-independent macronodular adrenal hyperplasias and adenomas associated with Cushing's syndrome.
  • Although there is clear clinical evidence for the implication of these ectopic receptors in abnormal regulation of cortisol production, whether this aberrant GPCR expression is the cause or the consequence of the development of an adrenal hyperplasia is still an open question.
  • To answer it, we genetically engineered primary bovine adrenocortical cells to have them express the gastric inhibitory polypeptide receptor.
  • We observed the formation of an enlarged and hyperproliferative adenomatous adrenocortical tissue that secreted cortisol in a gastric inhibitory polypeptide-dependent manner and induced a mild Cushing's syndrome with hyperglycemia.
  • Moreover, we show that tumor development was ACTH independent.
  • Thus, a single genetic event, inappropriate expression of a nonmutated GPCR gene, is sufficient to initiate the complete phenotypic alterations that ultimately lead to the formation of a benign adrenocortical tumor.
  • [MeSH-major] Adenoma / genetics. Adrenal Cortex / metabolism. Adrenal Gland Neoplasms / genetics. Cell Transformation, Neoplastic / metabolism. Gene Expression Regulation, Neoplastic. Receptors, Gastrointestinal Hormone / metabolism

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  • (PMID = 16254030.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Gastrointestinal Hormone; 0 / gastric inhibitory polypeptide receptor; 128559-51-3 / RAG-1 protein; WI4X0X7BPJ / Hydrocortisone
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8. 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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9. 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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10. 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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11. 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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12. Assié G, Guillaud-Bataille M, Ragazzon B, Bertagna X, Bertherat J, Clauser E: The pathophysiology, diagnosis and prognosis of adrenocortical tumors revisited by transcriptome analyses. Trends Endocrinol Metab; 2010 May;21(5):325-34
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  • [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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13. Cotesta D, Petramala L, Serra V, Giustini S, Divona L, Calvieri S, De Toma G, Ciardi A, Corsi A, Massa R, Reale MG, Letizia C: Pheochromocytoma associated with adrenocortical tumor in the same gland. Two case reports and literature review. Minerva Endocrinol; 2006 Jun;31(2):183-9
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  • [Title] Pheochromocytoma associated with adrenocortical tumor in the same gland. Two case reports and literature review.
  • Pheochromocytomas are catecholamine-producing neuroendocrine tumours arising from chromaffin cells of the adrenal medulla or extra-adrenal paraganglionic system that show 2 distinctive features, rarity and clinical variability.
  • Pheochromocytoma occasionally is associated with pathological lesions of the adrenal cortex.
  • We present 2 cases of patients referred to our hospital with a finding of clinical suspected pheochromocytoma.
  • The diagnosis of pheochromocytoma was confirmed in both cases with laboratory analysis and the lesion was achieved by employing 3 imaging techniques: computed tomography (CT), magnetic resonance imaging (MRI) and scintigraphy with (123)I-metaiodobenzilguanidine (MIBG).
  • The patients underwent adrenalectomy and in the same adrenal gland we found a pheochromocytoma associated with a nonfunctioning cortical adenoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenal Gland Neoplasms / diagnosis. Adrenocortical Adenoma / diagnosis. Neoplasms, Multiple Primary / diagnosis. Pheochromocytoma / diagnosis
  • [MeSH-minor] 3-Iodobenzylguanidine. Adrenalectomy. Adult. Humans. Male. Middle Aged. Neurofibromatosis 1 / diagnosis. Radiopharmaceuticals. Treatment Outcome

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  • (PMID = 16682942.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 35MRW7B4AD / 3-Iodobenzylguanidine
  • [Number-of-references] 41
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14. Saeger W, Fassnacht M: [Effects of drugs on the adrenal cortex and its tumors]. Pathologe; 2006 Feb;27(1):61-4
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  • [Title] [Effects of drugs on the adrenal cortex and its tumors].
  • [Transliterated title] Wirkungen von Medikamenten auf die Nebennierenrinde und ihre Tumoren.
  • The structure of the normal adrenal cortex is changed by stimulating hormones (ACTH) and inhibiting hormonal drugs (especially glucocorticoids).
  • In the therapy of patients with adrenocortical cancer, mitotane can cause an increase in of necrosis and fibrosis, but also in intracellular lipid.
  • [MeSH-major] Adrenal Cortex / pathology. Adrenal Cortex Neoplasms / drug therapy. Antineoplastic Agents / therapeutic use

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  • (PMID = 16320017.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Hormonal; 0O54ZQ14I9 / Aminoglutethimide; 9002-60-2 / Adrenocorticotropic Hormone
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15. Gross MD, Gauger PG, Djekidel M, Rubello D: The role of PET in the surgical approach to adrenal disease. Eur J Surg Oncol; 2009 Nov;35(11):1137-45
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  • [Title] The role of PET in the surgical approach to adrenal disease.
  • BACKGROUND: Appropriate surgical approach to diseases of the adrenal requires a diagnosis sufficient to determine the biochemical status of adrenal dysfunction and anatomic evaluation sufficient to differentiate unilateral from bilateral disease, intra-adrenal from extra-adrenal neoplasm, adrenal tumor recurrence or adrenal metastases.
  • High resolution computed tomography (CT) and magnetic resonance have been the primary imaging modalities for the evaluation of anatomy, while scintigraphic studies have played a secondary role in diagnosis.
  • The recent availability of functional imaging provided by positron emission tomography (PET) with radiopharmaceuticals designed to depict substrate precursor uptake, cellular metabolism or receptor binding in neoplasms and CT as a single modality, hybrid PET/CT, to directly correlate function and anatomy has had a significant impact upon the diagnostic and therapeutic approach to many cancers and has been applied to adrenal disease with some early success that we describe in this review.
  • METHODS: In addition to the authors' experience, a search of Medline and PubMed databases was performed using search terms: 'adrenal scintigraphy', 'positron tomography', 'computed tomography', 'adrenal surgery', 'adrenal mass', '(18)F-fluorodeoxyglucose', 'adrenal carcinoma', 'adrenal medulla' and 'pheochromocytoma'.
  • CONCLUSIONS: Present PET radiopharmaceuticals and their use in hybrid PET/CT have demonstrated efficacy in the preoperative and follow-up evaluation of neoplasms of the adrenal cortex and medulla that hopefully will continue to improve with the development of newer tracers that continue to exploit unusual characteristics of the adrenals.
  • [MeSH-major] Adrenal Gland Neoplasms / radionuclide imaging. Adrenal Gland Neoplasms / surgery. Radiopharmaceuticals. Tomography, Emission-Computed
  • [MeSH-minor] Diagnosis, Differential. Humans. Tomography, X-Ray Computed

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  • (PMID = 19243910.001).
  • [ISSN] 1532-2157
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Radiopharmaceuticals
  • [Number-of-references] 75
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16. Rodriguez FJ, Scheithauer BW, Erickson LA, Jenkins RB, Giannini C: Ectopic low-grade adrenocortical carcinoma in the spinal region: immunohistochemical and molecular cytogenetic study of a pediatric case. Am J Surg Pathol; 2009 Jan;33(1):142-8
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  • [Title] Ectopic low-grade adrenocortical carcinoma in the spinal region: immunohistochemical and molecular cytogenetic study of a pediatric case.
  • Ectopic adrenocortical neoplasms arising in the nervous system are very rare.
  • We encountered an intradural, extramedullary case of an adrenocortical neoplasm of indeterminate malignant potential affecting a spinal nerve root in the distal lumbar region of a 5-month-old girl.
  • The tumor in both resections had increased mitotic activity (5/10 high power fields) and MIB-1 labeling indices of 23% and 33% at initial resection and recurrence, respectively.
  • Both tumors demonstrated gains of chromosomes 5 and 12 by interphase cytogenetics, whereas insulin growth factor 2 was identified in the recurrent tumor by immunohistochemistry.
  • This report demonstrates that ectopic adrenocortical tumors in the nervous system may exhibit clinicopathologic and cytogenetic features suggestive of adrenocortical carcinoma.

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  • (PMID = 18941403.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / T32 NS007494; United States / NINDS NIH HHS / NS / T32 NS07494-04
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS396174; NLM/ PMC3427599
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17. 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


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

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  • (PMID = 19717419.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AN 238; 0 / Aniline Compounds; 0 / Cytostatic Agents; 0 / Neuropeptides; 0 / Pyrroles; 0 / RNA, Messenger; 0 / Receptors, LHRH; 0 / Receptors, Neuropeptide; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 2PK59M9GFF / vapreotide; 33189-65-0 / N-(2-diethylaminoethyl)-N-(2-hydroxy-2-phenylethyl)-2,5-dichloroaniline; 51110-01-1 / Somatostatin; 7568-93-6 / 2-Hydroxyphenethylamine; 80168379AG / Doxorubicin
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19. 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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20. 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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21. 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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22. Puech-Bret N, Bret J, Bennet A, Huyghe E, Mazerolles C, Zabraniecki L, Fournie B: Maffucci syndrome and adrenal cortex tumor. Joint Bone Spine; 2009 Oct;76(5):556-8
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  • [Title] Maffucci syndrome and adrenal cortex tumor.
  • We report the second known case of Maffucci syndrome associated with an adrenal cortex tumor.
  • Endocrine tumors have been reported in patients with multiple enchondromas, although the underlying mechanism of this combination is unknown.
  • Therefore, routine evaluation for involvement of the adrenal cortex may be warranted to improve our knowledge of this syndrome and of its pathophysiology.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Enchondromatosis / complications
  • [MeSH-minor] Abdomen / pathology. Adrenocorticotropic Hormone / blood. Adult. Amputation. Bone Neoplasms / pathology. Bone Neoplasms / radiography. Female. Femoral Neoplasms / pathology. Femoral Neoplasms / radiography. Fingers / surgery. Hemangioma / complications. Hemangioma / pathology. Humans. Hydrocortisone / blood. Leg / pathology. Magnetic Resonance Imaging. Sarcoma / pathology. Sarcoma / surgery. Uterine Neoplasms / pathology

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  • (PMID = 19782627.001).
  • [ISSN] 1778-7254
  • [Journal-full-title] Joint, bone, spine : revue du rhumatisme
  • [ISO-abbreviation] Joint Bone Spine
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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23. 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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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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  • [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. 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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26. 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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27. 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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28. 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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29. Li Q, Zhang XQ, Nie L, Chen GS, Li H, Zhang F, Zhang LY, Hong L, Wang SF, Wang H: Expression of interferon-gamma in human adrenal gland and kidney tumours. Br J Cancer; 2007 Aug 6;97(3):420-5
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  • [Title] Expression of interferon-gamma in human adrenal gland and kidney tumours.
  • Our previous studies have shown that IFN-gamma-like immunoreactivity also appears in human adrenal cortical tumour and phaeochromocytoma.
  • To investigate whether human tumour cells can produce IFN-gamma, we examined 429 biopsy specimens of 30 kinds of tumour and tumour-surrounding tissues in adrenal glands and in kidneys by using immunohistochemistry and in situ hybridisation.
  • IFN-gamma immunoactivity was shown in 34.3% of the adrenal cortical adenomas, 50% of the adrenal cortical carcinomas, 26.7% of the phaeochromocytomas, 26.7% of the clear cell renal cell carcinomas (RCCs), 22% of the adrenal cortexes and 40% of medullas adjacent to tumours.
  • Western blot analysis has further confirmed the immunohistochemistry results by showing a distinct IFN-gamma band corresponding to 17.4 kDa in tissue extracts from adrenal cortical adenoma, phaeochromocytoma and clear cell RCCs.
  • These results indicate that IFN-gamma is produced by some types of tumour cells, suggesting it may play a dual role in the development of these tumours.
  • [MeSH-major] Adrenal Gland Neoplasms / metabolism. Interferon-gamma / metabolism. Kidney Neoplasms / metabolism

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

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  • (PMID = 18984295.001).
  • [ISSN] 0242-6498
  • [Journal-full-title] Annales de pathologie
  • [ISO-abbreviation] Ann Pathol
  • [Language] fre
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
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31. 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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32. Forti FL, Dias MH, Armelin HA: ACTH receptor: ectopic expression, activity and signaling. Mol Cell Biochem; 2006 Dec;293(1-2):147-60
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  • Failure in obtaining expression of functional adrenocorticotropic hormone receptor (ACTHR, or melanocortin 2 receptor, MC2R) in non-adrenal cells has hindered molecular analysis of ACTH signaling pathways.
  • Natural constitutive expression of the MC2R accessory protein (MRAP) in Balb3T3 and other mouse 3T3 fibroblasts (NIH, Swiss and 3T3-L1) renders these fibroblastic lines suitable for ectopic expression of ACTHR in its active form properly inserted into the plasma membrane at levels similar to those found in mouse Y1 adrenocortical tumor cells.
  • The Y1 cell line is a cultured cell system well known for stably displaying normal adrenal specific metabolic pathways, ACTHR expression and ACTH functional responses.
  • Fourteen 3T3-AR and four 3T3-0 clones were screened for response to ACTH(39) in comparison with Y1 adrenocortical cells.
  • Eight 3T3-AR clones responded to ACTH(39) with activation of adenylate cyclase and induction of c-Fos protein, but the levels of, respectively, activation and induction were not strictly correlated.
  • In Y1 cells, specific inhibitors (H89/PKA; PD98059/MEK; Go6983/PKC and SP600125/JNK) show that signals initiated in the ACTH/ACTHR-system activate 4 pathways to induce the c-fos gene, namely: (a) cAMP/PKA/CREB;.
  • On the other hand, SP600125 caused 85% inhibition of c-Fos induction by ACTH(39) and, in addition, ACTH(39) promotes JNK1/2 phosphorylation, suggesting that JNK is a major signaling pathway mediating c-Fos induction by ACTH(39) in these cells.
  • However, activation of cAMP/PKA/CREB and JNK pathways and induction of fos and jun genes are not yet sufficient to enable ACTH for interference in morphology, migration and proliferation of Balb3T3 fibroblasts as it does in Y1 adrenocortical cells.
  • [MeSH-minor] 3T3 Cells. Adenylyl Cyclases / metabolism. Adrenal Cortex / metabolism. Adrenocorticotropic Hormone / metabolism. Animals. Cell Line, Tumor. Enzyme Activation. Fluorescent Antibody Technique. Gene Expression. Genes, fos. Genes, jun. Mice. Models, Biological. Phosphorylation. Transfection


33. Mazzuco TL, Chabre O, Feige JJ, Thomas M: Aberrant GPCR expression is a sufficient genetic event to trigger adrenocortical tumorigenesis. Mol Cell Endocrinol; 2007 Feb;265-266:23-8
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  • [Title] Aberrant GPCR expression is a sufficient genetic event to trigger adrenocortical tumorigenesis.
  • Aberrant expression of G protein-coupled receptors (GPCR) in the adrenal cortex is observed in some cases of ACTH-independent macronodular adrenal hyperplasias and adenomas associated with Cushing syndrome (CS).
  • Although there is clinical evidence for the implication of these receptors in abnormal regulation of cortisol secretion, whether this aberrant expression also directly causes the development of a benign adrenocortical tumor is an open question.
  • Cell transplantation provides a way to study genes that may be important in human tumor development.
  • The system we developed uses genetically modified adrenocortical cells transplanted into adrenalectomized immunodeficient mice, which form a functional tissue structure.
  • We observed that enforcing expression of the gastric inhibitory polypeptide (GIP) receptor or the luteinizing hormone (LH) receptor genes (taken as canonical examples of aberrantly expressed GPCRs) in adrenocortical cells resulted in the formation of hyperplastic tissues and the development of Cushing syndrome features in transplanted mice.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Receptors, G-Protein-Coupled / genetics
  • [MeSH-minor] Adrenal Cortex / cytology. Adrenal Cortex / metabolism. Animals. Cell Transplantation. Cushing Syndrome / genetics. Humans

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  • (PMID = 17250952.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Receptors, G-Protein-Coupled
  • [Number-of-references] 35
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34. Sandrini F, Villani DP, Tucci S, Moreira AC, de Castro M, Elias LL: Inheritance of R337H p53 gene mutation in children with sporadic adrenocortical tumor. Horm Metab Res; 2005 Apr;37(4):231-5
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  • [Title] Inheritance of R337H p53 gene mutation in children with sporadic adrenocortical tumor.
  • Adrenocortical tumors (ACTs) are frequent in Brazil.
  • The mechanisms of adrenal tumorigenesis remain poorly established; the R337H germline mutation in the p53 gene has previously been associated with ACTs in Brazilian children.
  • DNA was extracted from peripheral blood cells and/or tumor tissue for sequencing exon 10 of the p53 gene.
  • Two members of the adult group showed asymptomatic adrenal incidentalomas, two showed virilization, and one presented with Cushing's syndrome.
  • The R337H mutation was found in fifteen samples of the nineteen tumor specimens available (78.9%).
  • None of the parents showed ACTs or any other neoplasia at the time of the study.
  • There was no association between the presence of germline or tissue R337H p53 mutation and malignancy at diagnosis.
  • The R337H p53 mutation was inherited from one of the parents of the patients, and there was no association between the presence of this mutation and tumor malignancy in children.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Genes, p53 / genetics. Mutation / genetics

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  • (PMID = 15952083.001).
  • [ISSN] 0018-5043
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Codon; 9007-49-2 / DNA
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35. Mann MW, Ellis SS, Mallory SB: Infantile acne as the initial sign of an adrenocortical tumor. J Am Acad Dermatol; 2007 Feb;56(2 Suppl):S15-8
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  • [Title] Infantile acne as the initial sign of an adrenocortical tumor.
  • Ultrasound and abdominal computed tomographic scan revealed a large adrenal mass consistent with an adrenocortical tumor.
  • The patient underwent surgical excision of the well-encapsulated tumor with normalization of his hormones and no subsequent recurrence.
  • Although rare, childhood adrenocortical tumors have a poor prognosis, with the majority of tumors having regional and metastatic disease.
  • Because early diagnosis and complete surgical excision improve prognosis, children with refractory infantile acne should be evaluated for signs of virilization and accelerated growth.
  • Elevated levels of DHEA and DHEA-S should prompt an aggressive diagnostic evaluation for an adrenocortical tumor.
  • [MeSH-major] Acne Vulgaris / etiology. Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications

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  • (PMID = 17097383.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 3XMK78S47O / Testosterone; 459AG36T1B / Dehydroepiandrosterone
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66. Palazzo FF, Sebag F, Sierra M, Ippolito G, Souteyrand P, Henry JF: Long-term outcome following laparoscopic adrenalectomy for large solid adrenal cortex tumors. World J Surg; 2006 May;30(5):893-8
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  • [Title] Long-term outcome following laparoscopic adrenalectomy for large solid adrenal cortex tumors.
  • INTRODUCTION: Laparoscopic adrenalectomy (LA) is the procedure of choice for small benign adrenal tumors.
  • In the absence of local invasion or metastases, the preoperative diagnosis of an adrenocortical carcinoma (ACC) is difficult, often leaving size as the principal predictor of malignancy.
  • Large tumors are resectable laparoscopically, but the long-term outcome and therefore appropriateness of LA for cortical tumors > 6 cm is not known.
  • METHODS: We reviewed the LA experience in our institution since its introduction in June 1994.
  • Patients who underwent LA for solid cortical tumors > or = 60 mm in diameter without preoperative or intraoperative evidence of malignancy were reviewed.
  • Follow-up data, including clinical examination, biochemical analysis, and repeat scans, were reviewed for evidence of local or systemic recurrent disease.
  • Among them, 19 were solid cortical tumors > or = 60 mm in diameter with no overt malignant preoperative or intraoperative characteristics: 9 nonsecreting tumors, 8 Cushing's syndrome tumors (including 2 virilizing variants), 1 virilizing tumor, and 1 aldosteronoma.
  • The mean age of the patients was 49.9 years (range 22-77 years), and the mean tumor size was 69.0 mm (range 60-80 mm).
  • Histology confirmed a cortical adenoma in eight patients, malignant tumors in three, and indeterminate tumors in eight.
  • Two patients died of systemic recurrent disease (liver metastases) at 10 and 19 months, respectively, following surgery; two other patients died 12 and 21 months, respectively following surgery owing to unrelated cardiovascular and cerebrovascular pathology.
  • One patient underwent surgery for local recurrence 54 months after primary surgery; the remaining 14 patients are well with no clinical or radiologic evidence of recurrent disease.
  • CONCLUSIONS: Laparoscopic adrenalectomy for large solid cortical tumors without pre- or intraoperative evidence of malignancy is not contraindicated, and it is unlikely to have a deleterious effect on long-term outcome.
  • We provide an algorithm for the approach to adrenocortical tumors > or = 6 cm.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenalectomy. Adrenocortical Adenoma / surgery. Adrenocortical Carcinoma / surgery
  • [MeSH-minor] Adult. Aged. Algorithms. Humans. Laparoscopy. Middle Aged. Neoplasm Staging. Retrospective Studies. Time Factors. Treatment Outcome

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  • (PMID = 16680605.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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67. 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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  • [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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68. 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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69. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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70. Lai P, Bomanji JB, Mahmood S, Nagabhushan N, Syed R, Gacinovic S, Lee SM, Ell PJ: Detection of tumour thrombus by 18F-FDG-PET/CT imaging. Eur J Cancer Prev; 2007 Feb;16(1):90-4
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  • [Title] Detection of tumour thrombus by 18F-FDG-PET/CT imaging.
  • Tumour thrombus is a rare complication of many solid cancers including renal cell carcinoma, Wilms' tumour, testicular tumour, adrenal cortical carcinoma, lymphoma, pancreatic cancer, osteosarcoma and Ewing's sarcoma.
  • We describe six patients who harboured occult tumour thrombus detected by fluorine-18 fluorodeoxyglucose (F-FDG) positron emission tomography (PET)/X-ray computerized tomography (CT) imaging as part of the staging investigations.
  • Recognition of this rare complication by PET/CT can change the management plan and prevent unnecessary long-term anti-coagulation treatment because of wrong diagnosis of cancer-related venous thrombus.
  • [MeSH-major] Neoplasms / complications. Positron-Emission Tomography. Thrombosis / diagnosis. Tomography, X-Ray Computed

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  • (PMID = 17220710.001).
  • [ISSN] 0959-8278
  • [Journal-full-title] European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP)
  • [ISO-abbreviation] Eur. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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71. 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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72. Komissarenko IV, Rybakov SI, Kvacheniuk AN, Lazar' SI, Fedorova TI, Kovalenko AE, Mel'nik ND, Negrienko KV: [The role of computer tomography in differential diagnosis of benign and malignant tumors of the adrenals cortex]. Klin Khir; 2005 Jul;(7):42-5
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  • [Title] [The role of computer tomography in differential diagnosis of benign and malignant tumors of the adrenals cortex].
  • Possibilities of computer tomography (CT) application for differential diagnosis of tumors of the adrenal cortex (TAC) were studied.
  • While the trustworthy signs of malignancy are absent, it is necessary to conduct morphological verification of the adrenal tumors nature using puncture biopsy and/or intraoperative express-cytological investigation.

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  • (PMID = 16255222.001).
  • [ISSN] 0023-2130
  • [Journal-full-title] Klinichna khirurhiia
  • [ISO-abbreviation] Klin Khir
  • [Language] RUS
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Ukraine
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73. 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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74. 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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75. 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


76. 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
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  • [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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77. Koga Y, Ohe K, Gondo S, Watanabe T, Sakamoto R, Nomura M, Okabe T, Kawazoe N, Sasano K, Yanase T: [MEN type I presenting hypokalemia and hypertension, complicated with acromegaly, adrenal cortical tumor and rectal carcinoid tumor]. Nihon Naika Gakkai Zasshi; 2006 Nov 10;95(11):2298-301
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  • [Title] [MEN type I presenting hypokalemia and hypertension, complicated with acromegaly, adrenal cortical tumor and rectal carcinoid tumor].
  • [MeSH-major] Acromegaly / etiology. Adrenocortical Adenoma / complications. Carcinoid Tumor / complications. Growth Hormone-Secreting Pituitary Adenoma / complications. Hypertension / etiology. Hypokalemia / etiology. Multiple Endocrine Neoplasia Type 1 / complications. Rectal Neoplasms / complications


78. 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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  • [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.


79. 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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80. Gonzalez RJ, Shapiro S, Sarlis N, Vassilopoulou-Sellin R, Perrier ND, Evans DB, Lee JE: Laparoscopic resection of adrenal cortical carcinoma: a cautionary note. Surgery; 2005 Dec;138(6):1078-85; discussion 1085-6
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  • [Title] Laparoscopic resection of adrenal cortical carcinoma: a cautionary note.
  • BACKGROUND: While laparoscopic removal of small, benign, functioning adrenal tumors is accepted, laparoscopic resection of adrenal tumors that may be adrenal cortical carcinoma (ACC) remains controversial.
  • Open adrenalectomy remains the standard of care for patients presenting with an adrenal cortical tumor for which ACC is in the differential diagnosis.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenalectomy. Carcinoma / surgery. Laparoscopy. Neoplasm Recurrence, Local / epidemiology

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  • (PMID = 16360394.001).
  • [ISSN] 0039-6060
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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81. 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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  • [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


82. Jarral OA, Todd C, Willson PD: Hemorrhagic shock secondary to spontaneous rupture of a non-secretory adrenal cortical tumour: A case report. Can Urol Assoc J; 2010 Dec;4(6):E161-3
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  • [Title] Hemorrhagic shock secondary to spontaneous rupture of a non-secretory adrenal cortical tumour: A case report.
  • After emergency laparotomy, angiography, embolisation and histological investigation, a diagnosis of spontaneous rupture of a benign non-secretory adrenal cortical tumour was made.
  • To our knowledge, this is the only reported case of this diagnosis.

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  • [Cites] Am J Surg. 2007 Jul;194(1):77-8 [17560914.001]
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  • (PMID = 21749812.001).
  • [ISSN] 1920-1214
  • [Journal-full-title] Canadian Urological Association journal = Journal de l'Association des urologues du Canada
  • [ISO-abbreviation] Can Urol Assoc J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Canada
  • [Other-IDs] NLM/ PMC3038376
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83. 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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  • [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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84. 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
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  • [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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85. 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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86. Komorowski J, Jurczynska J, Stepien T, Kolomecki K, Kuzdak K, Stepien H: Serum concentrations of TNF α and its soluble receptors in patients with adrenal tumors treated by surgery. Int J Mol Sci; 2010;11(6):2281-90
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  • [Title] Serum concentrations of TNF α and its soluble receptors in patients with adrenal tumors treated by surgery.
  • The peripheral blood levels of TNF alpha and its soluble receptors were studied in 39 patients with malignant and benign adrenal tumors treated by adrenalectomy.
  • The concentrations of TNF alpha were significantly elevated in patients with malignant tumors of the adrenal cortex and in patients with Conn's syndrome compared to control.
  • After adrenalectomy, the levels of TNF alpha were decreased in patients with malignant tumors and in patients with Conn's syndrome, nonfunctioniong adenomas and pheochromocytomas compared to the concentration before surgery.
  • However, to confirm practicality of the evaluation of TNF alpha and its soluble receptors in differential diagnosis in patients with adrenal tumors, a larger study group is needed.
  • [MeSH-major] Adrenal Gland Neoplasms / blood. Adrenal Gland Neoplasms / surgery. Receptors, Tumor Necrosis Factor / blood. Tumor Necrosis Factor-alpha / blood
  • [MeSH-minor] Adrenalectomy. Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Receptors, Tumor Necrosis Factor, Type I / blood. Receptors, Tumor Necrosis Factor, Type II / blood

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  • (PMID = 20640152.001).
  • [ISSN] 1422-0067
  • [Journal-full-title] International journal of molecular sciences
  • [ISO-abbreviation] Int J Mol Sci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Receptors, Tumor Necrosis Factor; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Receptors, Tumor Necrosis Factor, Type II; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC2904916
  • [Keywords] NOTNLM ; TNF α / TNF α R1 / TNF α R2 / adrenal tumors / adrenalectomy
  • [General-notes] NLM/ Original DateCompleted: 20110714
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87. Woods AM, McIlmoil CJ, Rankin EN, Packer AA, Stevens JC, Macievic JA, Brown AB, Porter JP, Judd AM: Leukemia inhibitory factor protein and receptors are expressed in the bovine adrenal cortex and increase cortisol and decrease adrenal androgen release. Domest Anim Endocrinol; 2008 Aug;35(2):217-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leukemia inhibitory factor protein and receptors are expressed in the bovine adrenal cortex and increase cortisol and decrease adrenal androgen release.
  • The release of adrenal steroids during acute stress is primarily regulated by adrenocorticotropic hormone (ACTH).
  • In contrast, during chronic inflammatory stress additional factors are involved in regulating adrenal function.
  • In addition, LIF and LIF receptors (LIFR) are expressed in the human adrenal cortex and the human adrenocortical tumor cell line H295R.
  • However, the expression of LIF and LIFR in non-human adrenal glands and the effects of LIF on the release of cortisol from adrenal cells of non-human species have not been determined.
  • Furthermore, the effects of LIF on adrenal androgen release from all species are unknown.
  • In this study, immunohistochemistry, Western blots, RT-PCR, and nucleotide sequencing was utilized to demonstrate that LIF and its receptor are expressed throughout the bovine adrenal cortex.
  • Although LIF did not modify basal cortisol release from dispersed cells isolated from the bovine adrenal zona fasciculate, this cytokine increased ACTH-stimulated release of cortisol from these cells in a manner dependent on the LIF concentration and exposure interval.
  • In contrast, LIF in a concentration-dependent and time-dependent manner decreased basal and ACTH-stimulated adrenal androgen release from dispersed cells isolated from the bovine adrenal zona reticularis.
  • Because LIF release increases during inflammatory stress and this cytokine stimulates adrenal cortisol release and inhibits adrenal androgen release, this cytokine may play an important role in regulating the release of adrenal steroids during inflammatory stress.
  • [MeSH-major] Adrenal Cortex / metabolism. Androgens / metabolism. Cattle / metabolism. Hydrocortisone / metabolism. Leukemia Inhibitory Factor / metabolism. Receptors, OSM-LIF / metabolism

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  • (PMID = 18638665.001).
  • [ISSN] 0739-7240
  • [Journal-full-title] Domestic animal endocrinology
  • [ISO-abbreviation] Domest. Anim. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Leukemia Inhibitory Factor; 0 / RNA, Messenger; 0 / Receptors, OSM-LIF; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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88. Georgiadou D, Sergentanis TN, Papastratis G: Estrogen receptor alpha to beta ratio: a counterpart also in adrenal cortical neoplasia? Med Hypotheses; 2008;70(6):1225
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  • [Title] Estrogen receptor alpha to beta ratio: a counterpart also in adrenal cortical neoplasia?
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenal Cortex Neoplasms / pathology. Estrogen Receptor alpha / analysis. Estrogen Receptor beta / analysis. Models, Biological

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  • (PMID = 18226862.001).
  • [ISSN] 0306-9877
  • [Journal-full-title] Medical hypotheses
  • [ISO-abbreviation] Med. Hypotheses
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta
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89. 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
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  • [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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90. 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


91. Rossbach HC, Baschinsky D, Wynn T, Obzut D, Sutcliffe M, Tebbi C: Composite adrenal anaplastic neuroblastoma and virilizing adrenocortical tumor with germline TP53 R248W mutation. Pediatr Blood Cancer; 2008 Mar;50(3):681-3
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  • [Title] Composite adrenal anaplastic neuroblastoma and virilizing adrenocortical tumor with germline TP53 R248W mutation.
  • Composite tumors are extremely rare.
  • Such tumors in adrenal glands are usually of neuroendocrine-neural type and occur mostly in adults.
  • We report a patient with composite neuroblastoma (NB), adrenocortical tumor (ACT), and Li-Fraumeni syndrome (LFS) with germline TP53 R248W mutation.
  • LFS predisposes to the development of leukemia, sarcomas, adrenocortical and breast carcinomas, brain tumors and, questionably, NB.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenal Gland Neoplasms / pathology. Adrenocortical Adenoma / pathology. Genes, p53. Germ-Line Mutation. Li-Fraumeni Syndrome / genetics. Mutation, Missense. Neoplasms, Multiple Primary / pathology. Neuroblastoma / pathology. Point Mutation. Virilism / etiology
  • [MeSH-minor] Amino Acid Substitution. Aneuploidy. Brain Neoplasms / genetics. Breast Neoplasms / genetics. Carcinoma / genetics. Choroid Plexus Neoplasms / genetics. Female. Glioblastoma / genetics. Humans. Infant. Loss of Heterozygosity. Male. Pedigree


92. 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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93. 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
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  • [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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94. 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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95. 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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96. Markou A, Tsigou K, Papadogias D, Kossyvakis K, Vamvakidis K, Kounadi T, Piaditis G: A unique case of a benign adrenocortical tumor with triple secretion of cortisol, androgens, and aldosterone: development of multiple sclerosis after surgical removal of the tumor. Hormones (Athens); 2005 Oct-Dec;4(4):226-30
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  • [Title] A unique case of a benign adrenocortical tumor with triple secretion of cortisol, androgens, and aldosterone: development of multiple sclerosis after surgical removal of the tumor.
  • We present a 39-year old female with a benign adrenal tumor characterized by autonomous secretion of cortisol, androgens, and aldosterone.
  • CT of the adrenals revealed a 2.5 x 3.0 cm tumor with characteristics of an adenoma on the left adrenal gland.
  • Further investigations revealed suppressed basal ACTH levels, loss of diurnal rhythm of cortisol, and failure to suppress on low dose dexamethasone suppression test, suggesting autonomous cortisol secretion by the tumor.
  • Complete clinical and biochemical remission of the disease was observed after left adrenalectomy.
  • Histology confirmed the presence of an adrenocortical adenoma.
  • The flare-up of an autoimmune disease (multiple sclerosis) postoperatively could be coincidental or possibly related to the high normalization of the high cortisol levels acting as a precipitating factor.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenal Cortex Neoplasms / surgery. Adrenalectomy / adverse effects. Adrenocortical Adenoma / pathology. Adrenocortical Adenoma / surgery. Multiple Sclerosis / etiology
  • [MeSH-minor] Adult. Aldosterone / secretion. Androgens / secretion. Biopsy, Needle. Female. Follow-Up Studies. Humans. Hydrocortisone / secretion. Immunohistochemistry. Neoplasm Staging. Risk Assessment

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  • (PMID = 16613821.001).
  • [ISSN] 1109-3099
  • [Journal-full-title] Hormones (Athens, Greece)
  • [ISO-abbreviation] Hormones (Athens)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Androgens; 4964P6T9RB / Aldosterone; WI4X0X7BPJ / Hydrocortisone
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97. 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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98. Doghman M, Madoux F, Hodder P, Lalli E: Identification and characterization of steroidogenic factor-1 inverse agonists. Methods Enzymol; 2010;485:3-23
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  • 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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99. Stephenson TJ: Prognostic and predictive factors in endocrine tumours. Histopathology; 2006 May;48(6):629-43
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  • [Title] Prognostic and predictive factors in endocrine tumours.
  • This review encompasses the diagnostic features of malignancy, the routinely observable prognostic features and the prognostic and predictive features emerging from research techniques in the principal endocrine neoplasms: pancreatic and extrapancreatic endocrine cell tumours, thyroid and parathyroid neoplasia, adrenal cortical neoplasms and adrenal and extra-adrenal paragangliomas.
  • While each endocrine tissue has its own set of diagnostic features for malignancy, and prognostic features once a diagnosis of malignancy has been established, there are a few common themes.
  • For several endocrine neoplasms, definite recognition of malignancy can be difficult and may depend upon frank invasive or metastatic growth at presentation.
  • The accurate documentation of routinely observable histological features interpreted in the light of current literature has not been superseded by special techniques in the statement of diagnosis or prognosis in the vast majority of endocrine neoplasms.
  • [MeSH-major] Endocrine Gland Neoplasms / pathology. Peptide Hormones / analysis
  • [MeSH-minor] Diagnosis, Differential. Glucagon / analysis. Humans. Insulin / analysis. Predictive Value of Tests. Prognosis

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  • (PMID = 16681678.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Insulin; 0 / Peptide Hormones; 9007-92-5 / Glucagon
  • [Number-of-references] 123
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100. 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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