[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 591
1. Shigematsu K, Nakagaki T, Yamaguchi N, Kawai K, Sakai H, Takahara O: Analysis of mRNA expression for steroidogenic enzymes in the remaining adrenal cortices attached to adrenocortical adenomas. Eur J Endocrinol; 2008 Jun;158(6):867-78

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of mRNA expression for steroidogenic enzymes in the remaining adrenal cortices attached to adrenocortical adenomas.
  • DESIGN AND METHODS: We have recently demonstrated that the adrenal cortices attached to aldosterone-producing adenoma (APA) contained microscopic subcapsular micronodules suggestive of active aldosterone production.
  • In this study, we used in situ hybridization to investigate the mRNA expression of steroidogenic enzymes in the adrenal cortices attached to cortisol-producing adenoma (CPA) and clinically silent adenoma (non-functioning adenoma; NFA), in addition to APA.
  • Most of the cortical nodules in zona fasciculata to zona reticularis showed a suppressed steroidogenesis in the cortices attached to adenoma, but some expressed intensely all necessary steroidogenic enzyme mRNAs for cortisol synthesis.
  • CONCLUSIONS: It is thus necessary to keep in mind, on the occasion of subtotal adrenalectomy, that lesions with the potential to later develop into functional adrenocortical nodules may be present in other parts of the ipsilateral or contralateral adrenal cortices.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18505908.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / RNA, Messenger; 0 / SPATA7 protein, human; EC 1.14.15.6 / Cholesterol Side-Chain Cleavage Enzyme; EC 1.14.99.9 / CYP17A1 protein, human; EC 1.14.99.9 / Steroid 17-alpha-Hydroxylase; EC 2.8.2.- / Sulfotransferases; EC 2.8.2.2 / alcohol sulfotransferase
  •  go-up   go-down


2. Tissier F, Cavard C, Groussin L, Perlemoine K, Fumey G, Hagneré AM, René-Corail F, Jullian E, Gicquel C, Bertagna X, Vacher-Lavenu MC, Perret C, Bertherat J: Mutations of beta-catenin in adrenocortical tumors: activation of the Wnt signaling pathway is a frequent event in both benign and malignant adrenocortical tumors. Cancer Res; 2005 Sep 1;65(17):7622-7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mutations of beta-catenin in adrenocortical tumors: activation of the Wnt signaling pathway is a frequent event in both benign and malignant adrenocortical tumors.
  • Adrenocortical cancer is a rare cancer with a very poor prognosis.
  • The genetic alterations identified to date in adrenocortical tumors are limited.
  • We investigated whether Wnt pathway activation is involved in adrenocortical tumorigenesis.
  • In a series of 39 adrenocortical tumors, immunohistochemistry revealed abnormal cytoplasmic and/or nuclear accumulation of beta-catenin in 10 of 26 adrenocortical adenomas and in 11 of 13 adrenocortical carcinomas.
  • An activating somatic mutation of the beta-catenin gene was shown in 7 of 26 adrenocortical adenomas and in 4 of 13 adrenocortical carcinomas; these mutations were observed only in adrenocortical tumors with abnormal beta-catenin accumulation and most were point mutations altering the Ser45 of exon 3 (in the consensus GSK3-beta/CK1 phosphorylation site).
  • Functional studies showed that the activating Ser45 beta-catenin mutation found in the adrenocortical cancer H295R cell line leads to constitutive activation of T-cell factor-dependent transcription.
  • This is the first molecular defect to be reported with the same prevalence in both benign (27%) and malignant (31%) adrenocortical tumors. beta-Catenin mutations are also the most frequent genetic defect currently known in adrenocortical adenomas.
  • In adrenocortical adenomas, beta-catenin alterations are more frequent in nonfunctioning tumors, suggesting that beta-catenin pathway activation might be mostly involved in the development of nonsecreting adrenocortical adenomas and adrenocortical carcinomas.
  • The very frequent and substantial accumulation of beta-catenin in adrenocortical carcinomas suggests that other alterations might also be involved.
  • This finding may contribute to new therapeutic approaches targeting the Wnt pathway in malignant adrenocortical tumors, for which limited medical therapy is available.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Cytoskeletal Proteins / genetics. Intercellular Signaling Peptides and Proteins / genetics. Trans-Activators / genetics
  • [MeSH-minor] Adult. Aged. Cell Line, Tumor. Female. Humans. Immunohistochemistry. Male. Middle Aged. Mutation. Signal Transduction. Wnt Proteins. beta Catenin

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16140927.001).
  • [ISSN] 0008-5472
  • [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 / CTNNB1 protein, human; 0 / Cytoskeletal Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Trans-Activators; 0 / Wnt Proteins; 0 / beta Catenin
  •  go-up   go-down


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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical evaluation of metallothionein, Mcm-2 and Ki-67 antigen expression in tumors of the adrenal cortex.
  • BACKGROUND: The aim of this study was to assess the metallothionein (MT), maintenance protein 2 (Mcm-2) and Ki-67 expressions in adrenocortical adenomas and carcinomas in comparison to normal tissue and evaluate the correlations between these markers of proliferation and between these markers and tumor diameter.
  • MATERIALS AND METHODS: The expression of MT, Mcm-2 and Ki-67 was assessed by immunochemistry in forty-eight adrenocortical adenomas, six adrenocortical carcinomas and eleven normal adrenal cortex tissue samples.
  • RESULTS: The expressions of MT, Mcm-2 and Ki-67 in the adrenocortical carcinomas were significantly higher than in the adenomas and normal tissue (p<0.05).
  • The levels of Mcm-2 were also higher in the adrenocortical adenomas compared to the normal tissue (p<0.05).
  • The Mcm-2 expression showed a positive correlation to the expression of MT in the adrenocortical carcinomas (r=0.773; p<0.05) and to the expression of Ki-67 in the adrenocortical adenomas (r=0.432; p<0.05).
  • 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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


Advertisement
4. Boyle B, Butz H, Liko I, Zalatnai A, Toth M, Feldman K, Horanyi J, Igaz P, Racz K, Patocs A: Expression of glucocorticoid receptor isoforms in human adrenocortical adenomas. Steroids; 2010 Oct;75(10):695-700

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of glucocorticoid receptor isoforms in human adrenocortical adenomas.
  • INTRODUCTION: Glucocorticoid receptor (GR) is expressed in the normal human adrenal gland, however, no study has been performed to evaluate the separate expression of alpha- and beta-isoforms (GRalpha and GRbeta) in normal human adrenals and in adrenocortical adenomas.
  • EXPERIMENTAL: GRalpha and GRbeta mRNA expression was examined by quantitative real-time PCR in 31 adrenal tissues including 19 non-functioning adenomas (NFA), 6 cortisol-producing adenomas (CPA) and 6 normal adrenocortical tissues.
  • In addition, the presence and cellular localization of GRalpha and GRbeta proteins in adrenal tissues were studied by immunohistochemistry.
  • RESULTS: Compared to normal adrenocortical tissues, both GRalpha and GRbeta mRNAs were significantly increased in CPA but not in NFA.
  • Using anti-GRalpha antibody a strong nuclear staining was observed in NFA and CPA, and a less remarkable immunoreactivity was detected in some nuclei of normal adrenocortical cells.
  • GRbeta immunostaining was absent in normal adrenal tissues and NFA, while a strong cytoplasmic and nuclear immunoreaction was found in CPA.
  • CONCLUSIONS: Altered expression of GRalpha and GRbeta in CPA raises their possible role in the pathophysiology of these adrenal tumors, although further studies are needed to elucidate the potential significance of these findings.
  • [MeSH-major] Adrenocortical Adenoma / metabolism. Protein Isoforms / metabolism. Receptors, Glucocorticoid / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20438742.001).
  • [ISSN] 1878-5867
  • [Journal-full-title] Steroids
  • [ISO-abbreviation] Steroids
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / Receptors, Glucocorticoid
  •  go-up   go-down


5. Volante M, Sperone P, Bollito E, Frangipane E, Rosas R, Daffara F, Terzolo M, Berruti A, Papotti M: Matrix metalloproteinase type 2 expression in malignant adrenocortical tumors: Diagnostic and prognostic significance in a series of 50 adrenocortical carcinomas. Mod Pathol; 2006 Dec;19(12):1563-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Matrix metalloproteinase type 2 expression in malignant adrenocortical tumors: Diagnostic and prognostic significance in a series of 50 adrenocortical carcinomas.
  • The differential diagnosis of adrenocortical carcinoma from adrenocortical adenoma is based on different pathological parameters, usually incorporated in scoring systems, which unfortunately lack a 100% sensitivity and specificity.
  • Little is known on the molecular mechanisms leading to the malignant phenotype in adrenocortical tumors.
  • Therefore, we aimed to investigate metalloproteinases and their inhibitors expression in a series of 50 adrenocortical carcinomas and 50 control adrenocortical adenomas, diagnosed according to the Weiss histological criteria.
  • Metalloproteinase type 2 gave the most significant result, being detected in neoplastic cells in 1/50 adrenocortical adenomas (2%) and 37/50 adrenocortical carcinomas (74%) (P < 0.001), with a focal (score 1, <20% of positive cells--two-thirds of cases) or diffuse (score 2, >20% of positive cells--one-third of cases) pattern.
  • In addition, diffuse (score 2) metalloproteinase type 2 protein expression, as compared to focal or negative immunostaining, correlated with shorter survival (P < 0.02) and disease-free interval (P = 0.05).
  • Our data indicate that metalloproteinase type 2 immunohistochemical localization in tumor cells is significantly restricted to malignant adrenocortical tumors, with high specificity but low sensitivity.
  • In addition, a strong metalloproteinase type 2 expression in adrenocortical carcinoma was for the first time recognized as an unfavorable prognostic factor.
  • [MeSH-major] Adrenal Cortex Neoplasms / enzymology. Adrenocortical Adenoma / enzymology. Adrenocortical Carcinoma / enzymology. Matrix Metalloproteinase 2 / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Diagnosis, Differential. Female. Humans. Immunoenzyme Techniques. Male. Middle Aged. Prognosis. Reproducibility of Results. Sensitivity and Specificity. Survival Rate

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16980949.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 3.4.24.24 / Matrix Metalloproteinase 2
  •  go-up   go-down


6. Tadjine M, Lampron A, Ouadi L, Horvath A, Stratakis CA, Bourdeau I: Detection of somatic beta-catenin mutations in primary pigmented nodular adrenocortical disease (PPNAD). Clin Endocrinol (Oxf); 2008 Sep;69(3):367-73

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of somatic beta-catenin mutations in primary pigmented nodular adrenocortical disease (PPNAD).
  • BACKGROUND: Primary pigmented nodular adrenocortical disease (PPNAD) leads to Cushing syndrome (CS) and is often associated with Carney complex (CNC).
  • Recent studies have demonstrated that beta-catenin mutations are frequent in adrenocortical adenomas and carcinomas and that the Wnt-signalling pathway is involved in PPNAD tumorigenesis.
  • We hypothesized that adrenocortical adenomas that form in the context of PPNAD may harbour beta-catenin mutations.
  • Tumor DNA was extracted from pigmented adrenocortical adenoma and nodular adrenal hyperplasia.
  • In both cases, the mutations occurred in relatively large adenomas that had formed in the background of PPNAD.
  • Nuclear translocation of beta-catenin protein in the PPNAD adenoma suggests activation of the Wnt-beta-catenin pathway in PPNAD.
  • CONCLUSIONS: We report, for the first time, beta-catenin mutations in adenomas associated with PPNAD, further implicating Wnt-beta-catenin signalling in tumorigenesis linked to bilateral adrenal hyperplasias.
  • [MeSH-major] Adrenal Cortex Diseases / genetics. beta Catenin / genetics
  • [MeSH-minor] Adenoma / complications. Adenoma / genetics. Adenoma / pathology. Adolescent. Adrenal Cortex Neoplasms / complications. Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / pathology. Adult. Child. Child, Preschool. Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / genetics. DNA Mutational Analysis. Female. Genetic Testing. Humans. Male. Middle Aged. Mutation. Phosphoric Diester Hydrolases / genetics. Pigmentation Disorders / complications. Pigmentation Disorders / genetics. Young Adult

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Genes Dev. 2000 Aug 1;14(15):1837-51 [10921899.001]
  • [Cites] Nat Genet. 2006 Jul;38(7):794-800 [16767104.001]
  • [Cites] Hum Mol Genet. 2000 Dec 12;9(20):3037-46 [11115848.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Sep;86(9):4041-6 [11549623.001]
  • [Cites] Biochem Biophys Res Commun. 2002 Jun 7;294(2):324-8 [12051714.001]
  • [Cites] Am J Pathol. 2003 Feb;162(2):521-31 [12547710.001]
  • [Cites] Cancer Sci. 2003 Mar;94(3):225-9 [12824913.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Aug;88(8):3931-7 [12915689.001]
  • [Cites] Oncogene. 2004 Feb 26;23(8):1575-85 [14767469.001]
  • [Cites] Nat Rev Genet. 2004 Sep;5(9):691-701 [15372092.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Sep 16;94(19):10330-4 [9294210.001]
  • [Cites] Science. 1998 Sep 4;281(5382):1509-12 [9727977.001]
  • [Cites] Nature. 1999 Apr 1;398(6726):422-6 [10201372.001]
  • [Cites] Ann Intern Med. 1999 Oct 19;131(8):585-91 [10523219.001]
  • [Cites] Nature. 2005 Jan 20;433(7023):317-22 [15568017.001]
  • [Cites] Endocr Res. 2004 Nov;30(4):575-83 [15666794.001]
  • [Cites] J Clin Pathol. 2005 Mar;58(3):225-36 [15735151.001]
  • [Cites] Nature. 2005 Apr 14;434(7035):843-50 [15829953.001]
  • [Cites] Genes Dev. 2005 Apr 15;19(8):877-90 [15833914.001]
  • [Cites] Endocrinol Metab Clin North Am. 2005 Jun;34(2):441-58, x [15850852.001]
  • [Cites] Cancer Res. 2005 Sep 1;65(17):7622-7 [16140927.001]
  • [Cites] Oncogene. 2006 Dec 4;25(57):7482-91 [17143292.001]
  • [Cites] Cancer Res. 2006 Dec 15;66(24):11571-5 [17178847.001]
  • [Cites] Horm Metab Res. 2007 Jun;39(6):467-73 [17578766.001]
  • [Cites] Curr Opin Endocrinol Diabetes Obes. 2007 Jun;14(3):219-25 [17940443.001]
  • [Cites] Clin Endocrinol (Oxf). 2008 Feb;68(2):264-70 [17854394.001]
  • [Cites] Nat Genet. 2000 Sep;26(1):89-92 [10973256.001]
  • (PMID = 18419788.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / ZIA HD000642-13
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human; 0 / beta Catenin; EC 3.1.4.- / Phosphoric Diester Hydrolases; EC 3.1.4.35 / PDE11A protein, human
  • [Other-IDs] NLM/ NIHMS307371; NLM/ PMC3138207
  •  go-up   go-down


7. Adam P, Hahner S, Hartmann M, Heinrich B, Quinkler M, Willenberg HS, Saeger W, Sbiera S, Schmull S, Voelker HU, Ströbel P, Allolio B, Fassnacht M: Epidermal growth factor receptor in adrenocortical tumors: analysis of gene sequence, protein expression and correlation with clinical outcome. Mod Pathol; 2010 Dec;23(12):1596-604
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epidermal growth factor receptor in adrenocortical tumors: analysis of gene sequence, protein expression and correlation with clinical outcome.
  • Adrenocortical carcinoma is a rare but highly malignant neoplasm with still limited treatment options.
  • Epidermal growth factor receptor (EGFR) has been shown to be overexpressed in many solid tumors, but its expression in adrenocortical carcinoma has been studied only in a limited number of cases.
  • Therefore, we analyzed the expression of EGFR in 169 adrenocortical carcinoma samples and compared it with 31 adrenocortical adenomas.
  • Additionally, in 30 cases of adrenocortical carcinoma, exons 18-21 of the EGFR gene were cloned and sequenced.
  • EGFR expression was found in 128 of 169 adrenocortical carcinoma samples (76%), and in 60 of these samples (=36%) strong membrane staining was detected.
  • In contrast, only 1 out of 31 adrenocortical adenomas weakly expressed the EGFR (3%).
  • In summary, EGFR was overexpressed in more than three-quarters of adrenocortical carcinoma cases of this series.
  • As EGFR is hardly expressed in adrenocortical adenomas, our results suggest that its expression in adrenocortical tumors indicates a malignant phenotype, which may be used in the differential diagnosis between adrenocortical adenomas and carcinomas.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / metabolism. Adrenocortical Adenoma / pathology. Receptor, Epidermal Growth Factor / biosynthesis

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20693985.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  •  go-up   go-down


8. Contesse V, Reznik Y, Louiset E, Duparc C, Cartier D, Sicard F, Laquerriere A, Parmentier F, Kuhn JM, Vaudry H, Lefebvre H: Abnormal sensitivity of cortisol-producing adrenocortical adenomas to serotonin: in vivo and in vitro studies. J Clin Endocrinol Metab; 2005 May;90(5):2843-50
Hazardous Substances Data Bank. HYDROCORTISONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Abnormal sensitivity of cortisol-producing adrenocortical adenomas to serotonin: in vivo and in vitro studies.
  • Two patients with incidentally discovered adrenocortical adenomas underwent a series of pharmacological and physiological tests after pretreatment with dexamethasone.
  • In the two cases, 5-HT stimulated cortisol secretion from tumor cells with increased efficacy and/or potency to activate steroidogenesis by comparison with normal adrenocortical cells.
  • In the two adenoma tissues, immunohistochemical studies revealed the presence of 5-HT-like immunoreactivity within clusters of steroidogenic cells, suggesting that 5-HT acted through an autocrine/paracrine mechanism to stimulate steroidogenesis.
  • In conclusion, this study provides the first observation of adrenocortical cortisol-producing adenomas hypersensitive in vivo and in vitro to serotonergic agonists.
  • Our results also show that cortisol-producing adenomas can express simultaneously several illegitimate receptors.
  • [MeSH-major] Adenoma / metabolism. Adrenocortical Adenoma / metabolism. Hydrocortisone / secretion. Serotonin / pharmacology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Horm Metab Res. 2005 Aug;37(8):528-9 [16138268.001]
  • (PMID = 15705918.001).
  • [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] 158165-40-3 / Receptors, Serotonin, 5-HT4; 333DO1RDJY / Serotonin; WI4X0X7BPJ / Hydrocortisone
  •  go-up   go-down


9. Satoh F, Abe T, Tanemoto M, Nakamura M, Abe M, Uruno A, Morimoto R, Sato A, Takase K, Ishidoya S, Arai Y, Suzuki T, Sasano H, Ishibashi T, Ito S: Localization of aldosterone-producing adrenocortical adenomas: significance of adrenal venous sampling. Hypertens Res; 2007 Nov;30(11):1083-95
Hazardous Substances Data Bank. Corticotropin .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Localization of aldosterone-producing adrenocortical adenomas: significance of adrenal venous sampling.
  • Accurate localization of aldosterone-producing adenoma (APA) is essential for the treatment of primary aldosteronism (PA).
  • In order to confirm the clinical usefulness of adrenal venous sampling (AVS), we retrospectively studied 87 cases of PA in whom AVS was conducted.
  • We collected right and left adrenal venous effluents simultaneously before and after adrenocorticotropic hormone (ACTH) stimulation for measurements of aldosterone concentration (A) and cortisol concentration (C).
  • Of the above 66 subjects, 61 underwent laparoscopic removal of the adrenal gland through a retroperitoneal approach.
  • The receiver operator characteristics (ROC) curve analysis between the operated and no-apparent-laterality groups revealed that the ratio of A/C on the higher side to A/C on the lower side (A/C ratio) after ACTH stimulation is a useful index, with a cutoff value of 2.6, a sensitivity of 0.98 and a specificity of 1.0.
  • The ROC curve analysis between the APA side and contralateral side within the operated patients revealed that the cutoff value of A was 1,340 ng/dL, with a sensitivity of 0.92 and a specificity of 1.00.
  • [MeSH-major] Adenoma / diagnosis. Adrenal Cortex Neoplasms / diagnosis. Aldosterone / blood. Blood Specimen Collection / methods. Hydrocortisone / blood

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. HYDROCORTISONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Hypertens Res. 2007 Nov;30(11):1009-10 [18250546.001]
  • (PMID = 18250558.001).
  • [ISSN] 0916-9636
  • [Journal-full-title] Hypertension research : official journal of the Japanese Society of Hypertension
  • [ISO-abbreviation] Hypertens. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
  •  go-up   go-down


10. Hirose A, Okada Y, Fukushima A, Tanaka Y: [A rare case of primary aldosteronism caused by bilateral functioning adrenocortical adenomas with renal cell carcinoma]. J UOEH; 2005 Dec 1;27(4):315-23
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A rare case of primary aldosteronism caused by bilateral functioning adrenocortical adenomas with renal cell carcinoma].
  • We report a rare case of bilateral primary aldosteronism with renal cell carcinoma.
  • Abdominal CT and MRI revealed tumor masses in both adrenal glands, and a large left renal mass.
  • The preoperative diagnosis was primary aldosteronism due to bilateral functioning adrenocortical adenomas and left renal cell carcinoma.
  • The Pathological diagnosis was left renal cell carcinoma and bilateral functioning adrenocortical adenomas.
  • Primary aldosteronism due to bilateral functioning adrenocortical adenomas is relatively rare and its complication with renal cell carcinoma is an extremely rare case.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications. Carcinoma, Renal Cell / complications. Hyperaldosteronism / etiology. Kidney Neoplasms / complications


11. Ziaja J, Cholewa K, Mazurek U, Cierpka L: [Molecular basics of aldosterone and cortisol synthesis in normal adrenals and adrenocortical adenomas]. Endokrynol Pol; 2008 Jul-Aug;59(4):330-9
Hazardous Substances Data Bank. HYDROCORTISONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Molecular basics of aldosterone and cortisol synthesis in normal adrenals and adrenocortical adenomas].
  • [Transliterated title] Molekularne podstawy syntezy aldosteronu i kortyzolu w prawidlowych nadnerczach i w gruczolakach kory nadnerczy.
  • The aim of the study is to present genes encoding enzymatic proteins of aldosterone and cortisol synthesis pathway, methods of their transcriptional activity measurement, mRNA expression of the genes in normal adrenal cortex, in adrenocortical adenomas excised from patients with Conn and Cushing syndromes, as well as in adrenocortical adenomas excised from patients, in which hormonal activity of the tumour was not confirmed.
  • According to presented papers mRNA expression of analyzed genes is best known in tissue obtained from tumours excised from patients with Conn syndrome.
  • On the other hand transcriptional activity of the genes within the other adrenocortical adenomas is documented in lesser degree.
  • It concerns particularly analyses of tissue material obtained from patients, in which hormonal activity of adrenal tumours was not confirmed with biochemical tests.
  • It should be also considered, that the frame of reference for the majority of molecular analyses of adrenocortical tumour tissues was material obtained from little number of normal adrenals, what decreases in some degree credibility of obtained results.
  • Mentioned above remarks may be the basis for conduction of further investigations based on larger material, obtained both from normal adrenals and adrenocortical adenomas.
  • [MeSH-major] Adrenal Cortex Neoplasms / enzymology. Adrenal Glands / metabolism. Adrenocortical Adenoma / enzymology. Aldosterone / biosynthesis. Gene Expression Regulation, Enzymologic. Hydrocortisone / biosynthesis. Mixed Function Oxygenases / genetics
  • [MeSH-minor] Adrenal Cortex / metabolism. Cushing Syndrome / genetics. Cushing Syndrome / metabolism. Cytochrome P-450 CYP11B2 / genetics. Humans. Hyperaldosteronism / genetics. Hyperaldosteronism / metabolism. RNA, Messenger / analysis. Reference Values. Transcription, Genetic

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18777504.001).
  • [ISSN] 0423-104X
  • [Journal-full-title] Endokrynologia Polska
  • [ISO-abbreviation] Endokrynol Pol
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / RNA, Messenger; 4964P6T9RB / Aldosterone; EC 1.- / Mixed Function Oxygenases; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; WI4X0X7BPJ / Hydrocortisone
  • [Number-of-references] 76
  •  go-up   go-down


12. Tadjine M, Lampron A, Ouadi L, Bourdeau I: Frequent mutations of beta-catenin gene in sporadic secreting adrenocortical adenomas. Clin Endocrinol (Oxf); 2008 Feb;68(2):264-70

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequent mutations of beta-catenin gene in sporadic secreting adrenocortical adenomas.
  • OBJECTIVE: Molecular alterations remain largely unknown in most sporadic adrenocortical tumours and hyperplasias.
  • In our previous work, we demonstrated the differential expression of several Wnt/beta-catenin signalling-related genes implicated in ACTH-independent macronodular adrenal hyperplasias (AIMAH).
  • To better understand the role of Wnt/beta-catenin signalling in adrenocortical tumours, we performed mutational analysis of the beta-catenin gene.
  • METHODS: We studied 53 human adrenocortical samples (33 adenomas, 4 carcinomas, 13 AIMAH, 3 ACTH-dependent adrenal hyperplasias) and the human adrenocortical cancer cell line NCI-H295R.
  • RESULTS: No mutations were detected in adrenocortical carcinomas, AIMAH and ACTH-dependent hyperplasias.
  • Genetic alterations were found in 5 (15%) out of 33 adenomas: three cortisol-secreting adenomas, one aldosterone-secreting adenoma and one nonfunctional adenoma.
  • In addition, cytoplasmic and/or nuclear accumulation of beta-catenin was observed in mutated adenomas by immunohistochemistry.
  • CONCLUSIONS: Activating mutations of exon 3 of the beta-catenin gene are frequent in adrenocortical adenomas, and further characterization of the Wnt/beta-catenin signalling pathway should lead to a better understanding of adrenal tumourigenesis.
  • [MeSH-major] Adrenocortical Adenoma / genetics. Adrenocortical Adenoma / metabolism. beta Catenin / genetics. beta Catenin / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17854394.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / beta Catenin
  •  go-up   go-down


13. Inoue T, Ishiguro K, Suda T, Ito N, Suzuki Y, Taniguchi Y, Ohgi S: Laparoscopic bilateral partial adrenalectomy for adrenocortical adenomas causing Cushing's syndrome: report of a case. Surg Today; 2006;36(1):94-7
MedlinePlus Health Information. consumer health - Cushing's Syndrome.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Laparoscopic bilateral partial adrenalectomy for adrenocortical adenomas causing Cushing's syndrome: report of a case.
  • Laparoscopic total adrenalectomy has become a standard technique for small adrenal tumors; however, bilateral adrenalectomy results in postoperative adrenal insufficiency, necessitating lifelong steroid replacement.
  • To preserve adrenocortical function in a 41-year-old woman with bilateral adrenocortical adenoma (BAA) causing Cushing's syndrome, we performed laparoscopic bilateral partial adrenalectomy.
  • We based our preoperative diagnosis of bilateral adrenocortical tumors causing Cushing's syndrome on the results of endocrinological investigations and imaging findings.
  • Thus, we performed lateral transperitoneal laparoscopic bilateral partial adrenalectomy, preserving the adrenal glands, which were normal.
  • Pathological examination of both tumors confirmed the diagnosis of adrenocortical adenoma.
  • The patient had no postoperative complications, and her adrenocortical function was normal without steroid replacement at her 10-month follow-up.
  • This report shows that Cushing's syndrome resulting from bilateral adenomas can be effectively treated by laparoscopic bilateral partial adrenalectomy as a minimally invasive, adrenocortical-preserving operation.
  • [MeSH-major] Adrenalectomy / methods. Adrenocortical Adenoma / surgery. Cushing Syndrome / etiology. Laparoscopy

  • Genetic Alliance. consumer health - Cushing's Syndrome.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] World J Surg. 2000 Jan;24(1):108-13 [10594213.001]
  • [Cites] Surgery. 2003 Dec;134(6):1066-72; discussion 1072-3 [14668742.001]
  • [Cites] Endocr J. 1997 Aug;44(4):533-40 [9447286.001]
  • [Cites] J Endourol. 2002 Oct;16(8):591-7 [12470468.001]
  • [Cites] Urology. 2002 Dec;60(6):1100-3 [12475679.001]
  • [Cites] J Urol. 2000 Jul;164(1):14-7 [10840414.001]
  • [Cites] ANZ J Surg. 2003 Aug;73(8):664-6 [12887546.001]
  • [Cites] Surg Today. 1994;24(6):538-43 [7919738.001]
  • [Cites] Eur Urol. 2000 Sep;38(3):344-8 [10940711.001]
  • [Cites] Endocr J. 2003 Apr;50(2):155-62 [12803235.001]
  • [Cites] Acta Endocrinol (Copenh). 1985 Feb;108(2):245-54 [3969816.001]
  • (PMID = 16378204.001).
  • [ISSN] 0941-1291
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


14. Spinazzi R, Rucinski M, Neri G, Malendowicz LK, Nussdorfer GG: Preproorexin and orexin receptors are expressed in cortisol-secreting adrenocortical adenomas, and orexins stimulate in vitro cortisol secretion and growth of tumor cells. J Clin Endocrinol Metab; 2005 Jun;90(6):3544-9
Hazardous Substances Data Bank. HYDROCORTISONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preproorexin and orexin receptors are expressed in cortisol-secreting adrenocortical adenomas, and orexins stimulate in vitro cortisol secretion and growth of tumor cells.
  • We previously found that orexin-A, via the OX1-R, stimulates cortisol secretion from dispersed human adrenocortical cells.
  • In this study, we demonstrate that six of eight cortisol-secreting adenomas expressed preproorexin mRNA, and seven of 10 adenomas contained measurable amounts of orexin-A but not orexin-B.
  • Normal adrenal cortexes neither expressed preproorexin nor contained orexins.
  • All adenomas expressed OX1-R and OX2-R mRNAs, and real-time PCR showed that the expression of both receptors was up-regulated in adenomas, compared with normal adrenal cortex.
  • Orexin-A concentration-dependently raised basal cortisol secretion from freshly dispersed normal and adenomatous cells, minimal and maximal effective concentrations being 10(-10) and 10(-8) m, and the peptide efficacy (percent increase elicited by 10(-8) m orexin-A) was significantly higher in adenomas than in the normal adrenal cortex.
  • Collectively, our findings allow us to conclude that the orexin system is overexpressed in cortisol-secreting adenomas and suggest that orexin-A may act as an autocrine-paracrine regulator of the secretory activity and growth of some of these adrenal tumors.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics. Hydrocortisone / secretion. Receptors, Neuropeptide / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15797953.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA, Complementary; 0 / HCRT protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / Neuropeptides; 0 / Orexin Receptors; 0 / Orexins; 0 / RNA, Messenger; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Neuropeptide; WI4X0X7BPJ / Hydrocortisone
  •  go-up   go-down


15. Lachenmayer A, Lichtenauer UD, Cox T, Schott M, Malendowicz LK, Goretzki PE, Cupisti K, Scherbaum WA, Bornstein SR, Willenberg HS: Nestin as a marker in the classification of adrenocortical tumors. Horm Metab Res; 2009 May;41(5):397-401
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nestin as a marker in the classification of adrenocortical tumors.
  • Since adrenocortical carcinoma, a tumor entity still very difficult to classify, may gain the ability to aberrantly express neuroectodermal proteins including chromogranin A and synaptophysin, we asked the question whether nestin might also be detected in adrenocortical carcinomas, and if so, whether it might serve as a tool for clinical pathology.
  • Therefore, we studied the expression of nestin in normal adrenal glands, adrenocortical adenomas, and adrenocortical cancers using specific immunohistochemistry and semi-quantitative reverse transcriptase-polymerase chain reaction.
  • Immunostaining was nestin-positive in 1 out of 9 normal adrenal glands (11%), 2 out of 20 adrenocortical adenomas (10%), and 13 out of 16 adrenocortical carcinomas (81%).
  • We conclude that our findings provide further evidence that nestin, as a marker, is not restricted to neuronal stem cells and nestin expression is worth to be studied in adrenocortical tumors.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / classification. Adrenocortical Carcinoma / pathology. Biomarkers, Tumor / metabolism. Intermediate Filament Proteins / metabolism. Nerve Tissue Proteins / metabolism
  • [MeSH-minor] Adrenal Glands / metabolism. Adult. Aged. Aged, 80 and over. Female. Gene Expression. Humans. Male. Middle Aged. Nestin

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19294612.001).
  • [ISSN] 1439-4286
  • [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 / Biomarkers, Tumor; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin
  •  go-up   go-down


16. Velázquez-Fernández D, Laurell C, Geli J, Höög A, Odeberg J, Kjellman M, Lundeberg J, Hamberger B, Nilsson P, Bäckdahl M: Expression profiling of adrenocortical neoplasms suggests a molecular signature of malignancy. Surgery; 2005 Dec;138(6):1087-94
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression profiling of adrenocortical neoplasms suggests a molecular signature of malignancy.
  • BACKGROUND: Distinguishing between adrenocortical adenomas and carcinomas is often difficult.
  • Our aim was to investigate the differences in transcriptional profiles between benign and malignant adrenocortical neoplasms using complementary DNA microarray techniques.
  • METHODS: We studied 7 patients with adrenocortical carcinomas and 13 with adenomas.
  • RESULTS: Transcriptional profiles were homogeneous among adenomas, while carcinomas were much more heterogeneous.
  • Hierarchical clustering and self-organizing maps could separate clearly carcinomas from adenomas.
  • Among genes that were most significantly downregulated in carcinomas were a cytokine gene (CXCL10), several genes related to cell metabolism (RARRES2, ALDH1A1, CYBRD1 and GSTA4), and the cadherin 2 gene (CDH2).
  • CONCLUSIONS: Through the use of cDNA arrays, adrenocortical adenomas and carcinomas appear to be clearly distinguishable on the basis of their specific molecular signature.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics. Adrenocortical Carcinoma / genetics

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16360395.001).
  • [ISSN] 0039-6060
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


17. Fuller PJ, Alexiadis M, Jobling T, McNeilage J: Seladin-1/DHCR24 expression in normal ovary, ovarian epithelial and granulosa tumours. Clin Endocrinol (Oxf); 2005 Jul;63(1):111-5
MedlinePlus Health Information. consumer health - Ovarian Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: The human DIMINUTO/DWARF1 homolog seladin-1/DHCR24 has been recently reported to be up-regulated in adrenocortical adenomas.
  • Granulosa cell tumours of the ovary (GCT) as with adrenocortical adenomas arise from a steroidogenic tissue, respond to pituitary hormone stimulation and synthesize steroid hormones.
  • [MeSH-major] Granulosa Cell Tumor / genetics. Neoplasm Proteins / genetics. Nerve Tissue Proteins / genetics. Ovarian Neoplasms / genetics. Ovary / metabolism. Oxidoreductases Acting on CH-CH Group Donors / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15963070.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Nerve Tissue Proteins; 0 / Receptors, LH; EC 1.3.- / Oxidoreductases Acting on CH-CH Group Donors; EC 1.3.1.- / 3beta-hydroxysterol delta24-reductase; EC 1.3.1.- / DHCR24 protein, human
  •  go-up   go-down


18. Bourdeau I, Lampron A, Costa MH, Tadjine M, Lacroix A: Adrenocorticotropic hormone-independent Cushing's syndrome. Curr Opin Endocrinol Diabetes Obes; 2007 Jun;14(3):219-25
Hazardous Substances Data Bank. Corticotropin .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Primary Cushing's syndrome is most often secondary to adrenocortical adenomas or carcinomas, and more rarely to bilateral adrenal hyperplasias.
  • Corticotropin-independent cortisol-producing hyperplasia is caused by micronodular diseases, including primary pigmented nodular adrenocortical disease and nonpigmented micronodular hyperplasia and adrenocorticotropic hormone-independent macronodular adrenal hyperplasia.
  • Primary pigmented nodular adrenocortical disease can be found either alone or in the context of Carney complex, a multiple endocrine neoplasia syndrome.
  • RECENT FINDINGS: In recent years, the pathophysiology of adrenocortical tumors and hyperplasias became better understood following the identification of genes responsible for syndromes associated with corticotropin-independent Cushing's syndrome and the demonstration of aberrant expression and function of various hormone receptors in adrenocortical adenomas and adrenocorticotropic hormone-independent macronodular adrenal hyperplasia.
  • This article reviews findings on the molecular and genetic aspects of corticotropin-independent Cushing's syndrome including recent gene expression profiling studies of adrenocortical tumors and hyperplasias and animal models that provided clues on the pathogenesis of primary Cushing's syndrome.
  • SUMMARY: A better understanding of molecular mechanisms involved in adrenocortical tumors and hyperplasias may lead to improved diagnostic and prognostic markers and treatment strategies to assist clinicians in the management of corticotropin-independent Cushing's syndrome.
  • [MeSH-major] Adrenal Cortex Diseases / complications. Adrenal Cortex Neoplasms / complications. Adrenocorticotropic Hormone / metabolism. Cushing Syndrome / etiology

  • Genetic Alliance. consumer health - Cushing's Syndrome.
  • MedlinePlus Health Information. consumer health - Cushing's Syndrome.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17940443.001).
  • [ISSN] 1752-2978
  • [Journal-full-title] Current opinion in endocrinology, diabetes, and obesity
  • [ISO-abbreviation] Curr Opin Endocrinol Diabetes Obes
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
  • [Number-of-references] 63
  •  go-up   go-down


19. Adissu HA, Hayes G, Wood GA, Caswell JL: Cardiac myxosarcoma with adrenal adenoma and pituitary hyperplasia resembling Carney complex in a dog. Vet Pathol; 2010 Mar;47(2):354-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cardiac myxosarcoma with adrenal adenoma and pituitary hyperplasia resembling Carney complex in a dog.
  • The pathological evaluation revealed a left atrial ossifying myxosarcoma, bilateral adrenocortical adenomas, multifocal pituitary hyperplasia with expression of adrenocorticotrophic hormone, and multiple pituitary Rathke's cleft cysts.
  • [MeSH-major] Adrenal Cortex Neoplasms / veterinary. Dog Diseases / pathology. Heart Neoplasms / veterinary. Myxosarcoma / veterinary. Pituitary Neoplasms / veterinary
  • [MeSH-minor] Animals. Diagnosis, Differential. Dogs. Fatal Outcome. Female

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20110224.001).
  • [ISSN] 1544-2217
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


20. Cotesta D, Caliumi C, Alò P, Petramala L, Reale MG, Masciangelo R, Signore A, Cianci R, D'Erasmo E, Letizia C: High plasma levels of human chromogranin A and adrenomedullin in patients with pheochromocytoma. Tumori; 2005 Jan-Feb;91(1):53-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS AND STUDY DESIGN: We collected blood samples for measurement of plasma CgA and AM in 21 patients with pheochromocytomas, 43 healthy subjects and 26 patients with solid non-functioning adrenocortical adenomas.
  • CgA and AM were measured by means of a novel solid-phase two-site immunoradiometric assay based on monoclonal antibodies (CgA-RIA CT, CIS bio international) and by a specific radioimmunoassay (RIA, Phoenix Pharm. Inc.
  • RESULTS: The mean plasma CgA level (+/- SD) in patients with pheochromocytomas (204 +/- 147.9 ng/mL) was significantly higher (P < 0.001) than that in healthy subjects (41.6 +/- 10.7 ng/mL) and in patients with non-functioning adrenocortical adenomas (47.3 +/- 17.6 ng/mL).
  • The mean plasma AM concentration (+/- SD) in patients with pheochromocytomas (27.5 +/- 10.4 pg/mL) was significantly higher (P < 0.001) than that in HS (13.8 +/- 4.5 pg/mL) and in patients with non-functioning adrenocortical adenomas (16.6 +/- 7.3 pg/mL).
  • CONCLUSION: This study demonstrates that circulating CgA and AM levels are increased in pheochromocytoma patients compared with healthy subjects and patients with non-functioning adrenocortical adenomas.
  • Moreover, at the time of diagnosis plasma CgA levels correlated with plasma AM levels and with plasma metanephrine levels in all patients with pheochromocytomas.
  • [MeSH-major] Adrenal Gland Neoplasms / blood. Biomarkers, Tumor / blood. Chromogranins / blood. Peptides / blood. Pheochromocytoma / blood
  • [MeSH-minor] Adrenal Cortex Neoplasms / blood. Adrenocortical Adenoma / blood. Adrenomedullin. Adult. Antibodies, Monoclonal. Chromogranin A. Female. Humans. Immunohistochemistry. Male. Middle Aged. Radioimmunoassay. Sensitivity and Specificity. Tissue Distribution

  • Genetic Alliance. consumer health - Pheochromocytoma.
  • MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.
  • MedlinePlus Health Information. consumer health - Pheochromocytoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15850005.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Biomarkers, Tumor; 0 / CHGA protein, human; 0 / Chromogranin A; 0 / Chromogranins; 0 / Peptides; 148498-78-6 / Adrenomedullin
  •  go-up   go-down


21. Pena FJ, Quirce R, Allende RH, Banzo I, Carril JM: Bilateral adrenocortical uptake of Ga-67 SPECT during septicemia in a heart transplant patient. Clin Nucl Med; 2005 May;30(5):349-50
Hazardous Substances Data Bank. GALLIUM .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bilateral adrenocortical uptake of Ga-67 SPECT during septicemia in a heart transplant patient.
  • Ga-67 SPECT showed bilateral abnormal adrenal gland uptake that disappeared after intensive antibiotic therapy as assessed by a new Ga-67 scintigraphy obtained 3 months later.
  • Unilateral and bilateral adrenal uptake of gallium has been reported in several clinical settings, ranging from adrenocortical adenomas to malignant disease such as lymphoma or adrenal metastases.
  • Only one similar case, septicemia with transient adrenal uptake of gallium, has been previously reported.
  • [MeSH-major] Adrenal Cortex / radionuclide imaging. Bacteremia / radionuclide imaging. Citrates. Gallium. Heart Transplantation / adverse effects. Heart Transplantation / radionuclide imaging. Staphylococcal Infections / radionuclide imaging. Tomography, Emission-Computed, Single-Photon / methods
  • [MeSH-minor] Fever of Unknown Origin / diagnosis. Fever of Unknown Origin / etiology. Humans. Male. Middle Aged. Radiopharmaceuticals / pharmacokinetics. Sepsis. Staphylococcus haemolyticus

  • Genetic Alliance. consumer health - Heart Transplant.
  • MedlinePlus Health Information. consumer health - Heart Transplantation.
  • MedlinePlus Health Information. consumer health - Staphylococcal Infections.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15827412.001).
  • [ISSN] 0363-9762
  • [Journal-full-title] Clinical nuclear medicine
  • [ISO-abbreviation] Clin Nucl Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Citrates; 0 / Radiopharmaceuticals; 27905-02-8 / gallium citrate; CH46OC8YV4 / Gallium
  •  go-up   go-down


22. Takahashi K, Shoji I, Shibasaki A, Kato I, Hiraishi K, Yamamoto H, Kaneko K, Murakami O, Morimoto R, Satoh F, Ito S, Totsune K: Presence of kisspeptin-like immunoreactivity in human adrenal glands and adrenal tumors. J Mol Neurosci; 2010 May;41(1):138-44
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Presence of kisspeptin-like immunoreactivity in human adrenal glands and adrenal tumors.
  • Kisspeptins have also been reported to stimulate the aldosterone secretion from the adrenal cortex.
  • However, the expression of kisspeptins in human adrenal glands and adrenal tumors has not been clarified yet.
  • We, therefore, studied the presence of kisspeptin-like immunoreactivity (LI) in human adrenal glands and adrenal tumors (adrenocortical adenomas, adrenocortical carcinomas, and pheochromocytomas) by radioimmunoassay and immunocytochemistry.
  • Kisspeptin-LI was detected in all the tissues examined; normal portions of adrenal glands (3.0 +/- 2.3 pmol/g wet weight, n = 21, mean +/- SD), aldosterone-producing adenomas (4.6 +/- 3.3 pmol/g wet weight, n = 10), cortisol-producing adenomas (2.7 +/- 1.4 pmol/g wet weight, n = 14), adrenocortical carcinomas (1.7 +/- 0.2 pmol/g wet weight, n = 4), and pheochromocytomas (1.8 +/- 0.8 pmol/g wet weight, n = 6).
  • Immunocytochemistry showed positive kisspeptin-immunostaining in normal adrenal glands, with stronger immunostaining found in the medulla.
  • Furthermore, positive kisspeptin-immunostaining was found in all types of adrenal tumors examined; adrenocortical adenomas, adrenocortical carcinomas, and pheochromocytomas.
  • The intensity of kisspeptin-immunostaining in these adrenal tumors was, however, not so strong as that in normal adrenal medulla.
  • The present study has shown for the first time the presence of kisspeptin-LI in adrenal glands and adrenal tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / metabolism. Adrenal Glands / metabolism. Tumor Suppressor Proteins / metabolism

  • MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Diabetologia. 2009 May;52(5):855-62 [19221709.001]
  • [Cites] N Engl J Med. 2003 Oct 23;349(17):1614-27 [14573733.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Apr;89(4):1897-903 [15070962.001]
  • [Cites] Peptides. 1992 Jan-Feb;13(1):121-3 [1535705.001]
  • [Cites] Proc Natl Acad Sci U S A. 1979 Aug;76(8):4079-83 [386355.001]
  • [Cites] Peptides. 2003 Feb;24(2):301-6 [12668216.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Aug;90(8):4671-8 [15914529.001]
  • [Cites] Am J Surg Pathol. 1989 Mar;13(3):202-6 [2919718.001]
  • [Cites] J Biol Chem. 2001 Sep 14;276(37):34631-6 [11457843.001]
  • [Cites] J Cell Sci. 2004 Mar 15;117(Pt 8):1319-28 [15020672.001]
  • [Cites] J Natl Cancer Inst. 1996 Dec 4;88(23):1731-7 [8944003.001]
  • [Cites] Reprod Sci. 2007 Dec;14(8):836-45 [18089602.001]
  • [Cites] Peptides. 2008 May;29(5):873-80 [17686550.001]
  • [Cites] Endocr J. 2008 Mar;55(1):49-55 [18187873.001]
  • [Cites] Neurosci Lett. 1996 Jan 26;203(3):207-10 [8742029.001]
  • [Cites] Endocrinology. 2007 Jan;148(1):140-7 [17023533.001]
  • [Cites] Peptides. 2000 Feb;21(2):251-6 [10764953.001]
  • [Cites] J Biol Chem. 2001 Aug 3;276(31):28969-75 [11387329.001]
  • [Cites] Diabetologia. 2006 Sep;49(9):2131-5 [16826407.001]
  • [Cites] Nature. 2001 May 31;411(6837):613-7 [11385580.001]
  • [Cites] Endocrinology. 2004 Sep;145(9):4073-7 [15217982.001]
  • [Cites] Lancet. 1983 Sep 3;2(8349):540-2 [6136694.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Dec;90(12):6609-15 [16174713.001]
  • [Cites] Endocrinology. 2004 Oct;145(10):4565-74 [15242985.001]
  • [Cites] J Neuroendocrinol. 2009 Mar;21(4):299-304 [19210293.001]
  • [Cites] J Endocrinol. 2008 Jul;198(1):175-83 [18460550.001]
  • [Cites] Am J Surg Pathol. 1984 Mar;8(3):163-9 [6703192.001]
  • (PMID = 19898965.001).
  • [ISSN] 1559-1166
  • [Journal-full-title] Journal of molecular neuroscience : MN
  • [ISO-abbreviation] J. Mol. Neurosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KISS1 protein, human; 0 / Kisspeptins; 0 / Tumor Suppressor Proteins
  •  go-up   go-down


23. Broome JT, Gauger P: Surgical techniques for adrenal tumors. Minerva Endocrinol; 2009 Jun;34(2):185-93
MedlinePlus Health Information. consumer health - Pheochromocytoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Surgical techniques for adrenal tumors.
  • As technology has advanced, the options for the surgical management of adrenal disorders have also increased.
  • An understanding of the basic evaluation of adrenal tumors, patient specific factors, and the risks and benefits of available techniques will allow the clinician to select an appropriate treatment for each individual.
  • Surgery remains the mainstay of treatment for functional adrenocortical adenomas including aldosteronomas, cortisol-producing adenomas, and pheochromocytomas.
  • While minimally-invasive techniques offer shorter recovery times and less potential morbidity, more traditional approaches remain necessary for management of known or suspected adrenocortical carcinoma.
  • Except in the case of pheochromocytoma, large adrenal tumors >6 cm should not be removed laparoscopically due to the risk of adrenocortical carcinoma.
  • This article will review basic surgical adrenal disorders, operative approaches, and delineate principles of patient and procedure selection.
  • [MeSH-major] Adrenal Gland Neoplasms / surgery. Adrenalectomy / methods. Pheochromocytoma / surgery
  • [MeSH-minor] Adrenal Cortex Neoplasms / surgery. Adrenocortical Adenoma / surgery. Adrenocortical Carcinoma / surgery. Humans. Laparoscopy / methods. Length of Stay. Patient Selection. Risk Assessment. Risk Factors. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19471241.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 30
  •  go-up   go-down


24. Weismann D, Fassnacht M, Weinberger F, Hamelmann W, Diehl S, Lorenz K, Baerlehner E, Reincke M, Beuschlein F, Knoefel W, Nies C, Hahner S, Allolio B: Intraoperative haemodynamic stability in patients with phaeochromocytoma--minimally invasive vs conventional open surgery. Clin Endocrinol (Oxf); 2006 Sep;65(3):352-8
Hazardous Substances Data Bank. PHENOXYBENZAMINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Patients undergoing MA for adrenocortical adenomas (aldosteronomas n = 15, inactive adenomas n = 13) served as controls.
  • In comparison to adrenocortical adenomas, MA in phaeochromocytomas was associated with a significantly higher maximum systolic BP (188 +/- 29 vs 154 +/- 22 mmHg, P < 0.001), more frequent hypertensive episodes (1[0-4]vs 0[0-1], P < 0.001), more episodes of systolic BP > 200 mmHg (0[0-4]vs 0[0-1], P = 0.03) and a higher demand for intraoperative fluids (3194 ml vs 1750 ml, P < 0.001).
  • CONCLUSION: There is no significant difference in haemodynamic stability between MA and CA in phaeochromocytomas, but it is significantly inferior when compared to MA for cortical adenomas.
  • [MeSH-major] Adrenal Gland Neoplasms / surgery. Adrenalectomy / methods. Pheochromocytoma / surgery
  • [MeSH-minor] Adenoma / physiopathology. Adenoma / surgery. Adrenergic alpha-Antagonists / therapeutic use. Adult. Blood Pressure. Case-Control Studies. Chi-Square Distribution. Drug Administration Schedule. Female. Heart Rate. Humans. Male. Middle Aged. Minimally Invasive Surgical Procedures. Monitoring, Intraoperative. Phenoxybenzamine / therapeutic use. Preoperative Care. Retrospective Studies. Statistics, Nonparametric

  • MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.
  • MedlinePlus Health Information. consumer health - Pheochromocytoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Clin Endocrinol (Oxf). 2007 Mar;66(3):455-6 [17302884.001]
  • (PMID = 16918955.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenergic alpha-Antagonists; 0TTZ664R7Z / Phenoxybenzamine
  •  go-up   go-down


25. Libé R, Mantovani G, Bondioni S, Lania AG, Pedroni C, Beck-Peccoz P, Spada A: Mutational analysis of PRKAR1A and Gs(alpha) in sporadic adrenocortical tumors. Exp Clin Endocrinol Diabetes; 2005 May;113(5):248-51

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mutational analysis of PRKAR1A and Gs(alpha) in sporadic adrenocortical tumors.
  • Little is known about the pathogenesis of adrenocortical tumors.
  • The cAMP-dependent pathway is physiologically activated by ACTH in adrenocortical cells and different components of this cascade may be altered in some functioning adrenocortical tumors.
  • Recently, mutations of the gene encoding the PKA type 1 A regulatory subunit (R1 A), PRKAR1A, associated with loss of heterozygosity (LOH) at PRKAR1A locus, have been demonstrated in primary pigmented nodular adrenocortical disease (PPNAD), either isolated or associated with Carney complex.
  • Moreover, activating mutations of the Gs(alpha) gene (the gsp oncogene) have also been found in a small number of adrenocortical cortisol-secreting adenomas.
  • Aim of this study was to investigate the presence of such genetic alterations on a series of 10 ACTH-independent Cushing syndrome due to non-PPNAD adrenocortical adenomas.
  • In one single adenoma gsp mutation was detected.
  • PRKAR1A mutations and gsp oncogene, are a rare event in adrenocortical tumors.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. DNA Mutational Analysis. GTP-Binding Protein alpha Subunits, Gs / genetics. Proteins / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15926108.001).
  • [ISSN] 0947-7349
  • [Journal-full-title] Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
  • [ISO-abbreviation] Exp. Clin. Endocrinol. Diabetes
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human; 0 / Proteins; E0399OZS9N / Cyclic AMP; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
  •  go-up   go-down


26. Vezzosi D, Bertherat J, Groussin L: Pathogenesis of benign adrenocortical tumors. Best Pract Res Clin Endocrinol Metab; 2010 Dec;24(6):893-905

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pathogenesis of benign adrenocortical tumors.
  • Most adrenocortical tumors (ACT) are benign unilateral adrenocortical adenomas, often discovered incidentally.
  • The identification of the genetics of familial diseases associated with benign ACT has been helpful to define somatic alterations in sporadic ACT: for example, identification of PRKAR1A mutations in Carney complex or alterations of the Wnt/β-catenin pathway in Familial Adenomatous Polyposis Coli.
  • Components of the cAMP signaling pathway-for example, adrenocorticotropic-hormone receptors and other membrane receptors, Gs protein, phosphodiesterases and protein kinase A-can be altered to various degrees in benign cortisol-secreting ACT.
  • These progress have been important for the understanding of the pathogenesis of benign ACT, but already have profound implications for clinical management, for example in unraveling the genetic origin of disease in some patients with ACT.
  • [MeSH-major] Adrenal Cortex Neoplasms / etiology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 21115158.001).
  • [ISSN] 1878-1594
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  •  go-up   go-down


27. Soon PS, McDonald KL, Robinson BG, Sidhu SB: Molecular markers and the pathogenesis of adrenocortical cancer. Oncologist; 2008 May;13(5):548-61
Hazardous Substances Data Bank. Corticotropin .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular markers and the pathogenesis of adrenocortical cancer.
  • Adrenal tumors are common, with an estimated incidence of 7.3% in autopsy cases, while adrenocortical carcinomas (ACCs) are rare, with an estimated prevalence of 4-12 per million population.
  • Because the prognoses for adrenocortical adenomas (ACAs) and ACCs are vastly different, it is important to be able to accurately differentiate the two tumor types.
  • Advancement in the understanding of the pathophysiology of ACCs is essential for the development of more sensitive means of diagnosis and treatment, resulting in better clinical outcome.
  • Adrenocortical tumors (ACTs) occur as a component of several hereditary tumor syndromes, which include the Li-Fraumeni syndrome, Beckwith-Wiedemann syndrome, multiple endocrine neoplasia 1, Carney complex, and congenital adrenal hyperplasia.
  • The adrenocorticotropic hormone-cAMP-protein kinase A and Wnt pathways are also implicated in adrenocortical tumorigenesis.
  • The aim of this review is to summarize the current knowledge on the molecular mechanisms involved in adrenocortical tumorigenesis, including results of comparative genomic hybridization, loss of heterozygosity, and microarray gene-expression profiling studies.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics. Adrenocortical Carcinoma / genetics. Neoplastic Syndromes, Hereditary / genetics

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18515740.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
  • [Number-of-references] 135
  •  go-up   go-down


28. Papotti M, Volante M, Duregon E, Delsedime L, Terzolo M, Berruti A, Rosai J: Adrenocortical tumors with myxoid features: a distinct morphologic and phenotypical variant exhibiting malignant behavior. Am J Surg Pathol; 2010 Jul;34(7):973-83
University of Turin Instituional Repository AperTO. Full Text from .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenocortical tumors with myxoid features: a distinct morphologic and phenotypical variant exhibiting malignant behavior.
  • Myxoid changes have been rarely reported both in adrenocortical adenomas and carcinomas.
  • The recent observation by our group of an adrenal myxoid tumor with morphologically borderline features, but aggressive clinical behavior prompted us to review a series of 196 adrenocortical lesions, comprising 122 carcinomas and 74 adenomas, to define the morphologic, phenotypical and clinical characteristics of adrenocortical tumors with myxoid features.
  • Fourteen cases, including 12 carcinomas and 2 borderline tumors, formed the basis of this report, and were characterized by a variably abundant myxoid component (from 5% to 90% of tumor) and 2 distinct cellular growth patterns: the first (10 cases), mostly associated with a predominant myxoid stromal component, was made of small cells with mild atypia arranged in cords and microcysts; the second (4 cases) was characterized by focal myxoid changes in tumors otherwise similar to conventional adrenocortical carcinoma, with large atypical cells having an eosinophilic cytoplasm and a diffuse or nodular architecture.
  • The above mentioned patterns were absent in all adenomas reviewed.
  • A peculiar reactivity to neurofilaments was seen, mostly associated to the presence of predominant rather that focal myxoid stromal changes, and in 40% of conventional adrenocortical carcinomas, thus representing an undescribed potential pitfall in the differential diagnosis of adrenal lesions.
  • Myxoid adrenocortical tumors probably represent a rare but histologically and phenotipically distinct entity and, although rare cases of benign lesions are on record, they seem to be generally associated to morphologic and clinical features of malignancy.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / pathology. Adrenocortical Carcinoma / secondary. Mucins / metabolism
  • [MeSH-minor] Adrenal Glands / embryology. Adrenal Glands / metabolism. Adult. Aged. Biomarkers, Tumor / metabolism. Fatal Outcome. Female. Fetal Development. Humans. Male. Middle Aged

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20534995.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Mucins
  •  go-up   go-down


29. Bertherat J, Bertagna X: Pathogenesis of adrenocortical cancer. Best Pract Res Clin Endocrinol Metab; 2009 Apr;23(2):261-71
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pathogenesis of adrenocortical cancer.
  • The study of the clonality of adrenocortical tumours (ACTs) has shown that adrenocortical cancers (ACCs) are of monoclonal origin.
  • Numerous chromosomal alterations have been observed in ACCs, and they are much more frequent than in adrenocortical adenomas.
  • This recent progress in the molecular genetics of ACC has led to the development of new molecular markers for the diagnosis of malignancy; these might also help to identify prognostic markers of ACC and may ultimately lead to novel therapeutic approaches.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19500768.001).
  • [ISSN] 1878-1594
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 67
  •  go-up   go-down


30. Masi G, Lavezzo E, Iacobone M, Favia G, Palù G, Barzon L: Investigation of BRAF and CTNNB1 activating mutations in adrenocortical tumors. J Endocrinol Invest; 2009 Jul;32(7):597-600
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Investigation of BRAF and CTNNB1 activating mutations in adrenocortical tumors.
  • BACKGROUND: Activating mutations of the BRAF oncogene play a central role in the development of various cancer types, but their role in human adrenocortical tumors is unknown.
  • At variance, activating mutations of another oncogene, CTNNB1, which encodes beta-catenin, have been shown to be common events in both benign and malignant adrenocortical tumors.
  • AIM: To investigate the prevalence of BRAF and CTNNB1 activating mutations in sporadic adrenocortical tumors.
  • MATERIALS AND METHODS: Tissue samples from 15 adrenocortical carcinomas and 41 adrenocortical adenomas were investigated for the presence of BRAF and CTNNB1 activating mutations by PCR amplification and direct sequencing.
  • RESULTS: An advanced invasive non-functioning adrenocortical carcinoma carried a somatic heterozygous BRAF V600E mutation, while 4 functioning and 4 non-functioning adenomas and 3 functioning carcinomas carried different CTNNB1 activating mutations.
  • CONCLUSIONS: Activating BRAF somatic mutations may be occasionally found in advanced adrenocortical carcinomas, while CTNNB1 activating mutations are early and common events in adrenal tumorigenesis.
  • [MeSH-major] Adrenal Cortex Neoplasms. Cell Transformation, Neoplastic / genetics. Mutation. Proto-Oncogene Proteins B-raf / genetics. beta Catenin / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Endocr Relat Cancer. 2009 Jun;16(2):565-72 [19190079.001]
  • [Cites] Endocr Relat Cancer. 2007 Mar;14(1):13-28 [17395972.001]
  • [Cites] Endocr Rev. 2007 Dec;28(7):742-62 [17940185.001]
  • [Cites] Cancer Res. 2005 Sep 1;65(17):7622-7 [16140927.001]
  • [Cites] Eur J Endocrinol. 2002 Jan;146(1):61-6 [11751069.001]
  • [Cites] Endocr Relat Cancer. 2004 Dec;11(4):855-60 [15613458.001]
  • [Cites] Nature. 2002 Jun 27;417(6892):949-54 [12068308.001]
  • [Cites] Genes Dev. 2000 Aug 1;14 (15):1837-51 [10921899.001]
  • [Cites] Clin Cancer Res. 2008 May 1;14(9):2551-9 [18451216.001]
  • [Cites] Exp Clin Endocrinol Diabetes. 2000;108(8):513-4 [11149627.001]
  • [Cites] Am J Surg Pathol. 2002 Dec;26(12):1612-9 [12459628.001]
  • [Cites] Eur J Endocrinol. 2008 Jul;159(1):77-80 [18426810.001]
  • [Cites] Curr Opin Genet Dev. 2007 Feb;17(1):31-9 [17208430.001]
  • [Cites] Am J Surg Pathol. 1989 Mar;13(3):202-6 [2919718.001]
  • [Cites] Br J Cancer. 1998 Apr;77(7):1060-5 [9569040.001]
  • [Cites] J Endocrinol Invest. 2007 Jan;30(1):RC1-3 [17318013.001]
  • [Cites] Clin Endocrinol (Oxf). 2008 Feb;68(2):264-70 [17854394.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Oct;93(10):4135-40 [18647815.001]
  • [Cites] Eur J Endocrinol. 2003 Oct;149(4):273-85 [14514341.001]
  • [Cites] Oncogene. 2008 Feb 7;27(7):877-95 [17724477.001]
  • [Cites] Br J Cancer. 2006 Aug 21;95(4):496-505 [16880792.001]
  • [Cites] Development. 2008 Aug;135(15):2593-602 [18599507.001]
  • [Cites] Nature. 2005 Aug 4;436(7051):720-4 [16079850.001]
  • [Cites] J Urol. 1993 Jun;149(6):1389-94 [8501773.001]
  • (PMID = 19498322.001).
  • [ISSN] 1720-8386
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / beta Catenin; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
  •  go-up   go-down


31. Wagner S, Kiupel M, Peterson RA 2nd, Heikinheimo M, Wilson DB: Cytochrome b5 expression in gonadectomy-induced adrenocortical neoplasms of the domestic ferret (Mustela putorius furo). Vet Pathol; 2008 Jul;45(4):439-42
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytochrome b5 expression in gonadectomy-induced adrenocortical neoplasms of the domestic ferret (Mustela putorius furo).
  • Whereas the adrenal glands of healthy ferrets produce only limited amounts of androgenic steroids, adrenocortical neoplasms that arise in neutered ferrets typically secrete androgens or their derivative, estrogen.
  • The 17,20-lyase activity of cytochrome P450 17alpha-hydroxylase/17,20-lyase (P450c17) must increase to permit androgen biosynthesis in neoplastic adrenal tissue.
  • We screened ferret adrenocortical tumor specimens for expression of cytochrome b(5) (cyt b(5)), an allosteric regulator that selectively enhances the 17,20-lyase activity of P450c17.
  • Cyt b(5) immunoreactivity was evident in 24 of 25 (96%) adrenocortical adenomas/carcinomas from ferrets with signs of ectopic sex steroid production.
  • Normal adrenocortical cells lacked cyt b(5), which may account for the low production of adrenal androgens in healthy ferrets.
  • We concluded that cyt b(5) is upregulated during gonadectomy-induced adrenocortical neoplasia and is a marker of androgen synthetic potential in these tumors.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Vet Pathol. 2003 Mar;40(2):136-42 [12637752.001]
  • [Cites] J Endocrinol. 1983 Dec;99(3):361-8 [6417256.001]
  • [Cites] J Clin Endocrinol Metab. 1993 May;76(5):1286-90 [8496319.001]
  • [Cites] Mol Cell Endocrinol. 2007 Feb;265-266:93-101 [17222503.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Jan;78(1):36-40 [8288710.001]
  • [Cites] J Am Vet Med Assoc. 1996 Sep 15;209(6):1097-102 [8800255.001]
  • [Cites] Semin Reprod Med. 2004 Nov;22(4):281-8 [15635496.001]
  • [Cites] J Endocrinol. 2005 Nov;187(2):267-74 [16293774.001]
  • [Cites] Vet Pathol. 2006 Mar;43(2):97-117 [16537928.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Nov 7;92(23):10619-23 [7479852.001]
  • (PMID = 18587089.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK075618-02; United States / NIDDK NIH HHS / DK / P30 DK052574-09; United States / NIDDK NIH HHS / DK / R01 DK075618-02; United States / NIDDK NIH HHS / DK / DK52574; United States / NIDDK NIH HHS / DK / DK075618; United States / NIDDK NIH HHS / DK / P30 DK052574; United States / NIDDK NIH HHS / DK / R01 DK075618
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GATA4 Transcription Factor; 0 / Receptors, LH; 0 / inhibin-alpha subunit; 57285-09-3 / Inhibins; 9035-39-6 / Cytochromes b5
  • [Other-IDs] NLM/ NIHMS45245; NLM/ PMC2497446
  •  go-up   go-down


32. Tissier F: [Sporadic adrenocortical tumors: genetics and perspectives for the pathologist]. Ann Pathol; 2008 Oct;28(5):409-16
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19068395.001).
  • [ISSN] 0242-6498
  • [Journal-full-title] Annales de pathologie
  • [ISO-abbreviation] Ann Pathol
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human; 67763-97-7 / Insulin-Like Growth Factor II; EC 3.1.4.- / Phosphoric Diester Hydrolases; EC 3.1.4.35 / PDE11A protein, human
  • [Number-of-references] 73
  •  go-up   go-down


33. Iihara M, Obara T: [Diagnosis and surgical treatment of adrenal tumors]. Nihon Geka Gakkai Zasshi; 2005 Aug;106(8):479-83
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Diagnosis and surgical treatment of adrenal tumors].
  • Adrenal surgery is necessary for the management of functioning adrenal tumors, such as aldosterone-producing adenoma, cortisol-producing adenoma, and pheochromocytoma.
  • The role of adrenal imaging in primary hyperaldosteronism is to separate the surgically resectable unilateral aldosteronoma from bilateral hyperplasia.
  • Once the clinical diagnosis of primary hyperaldosteronism is confirmed, adrenal computed tomography (CT) with 3-mm sections should be the first imaging study.
  • If the results of CT and NP-59 scintigraphy are equivocal, adrenal venous sampling is necessary.
  • Cortisol-producing adrenocortical adenomas are seen as adrenal masses 2.5 cm or larger in diameter in CT scanning.
  • When an adrenal mass measures more than 5 cm in diameter, a functioning adrenal carcinoma should be considered.
  • In the past decade, laparoscopic adrenalectomy has replaced open adrenalectomy as a standard operative procedure for benign adrenal tumors.
  • Adrenal-sparing laparoscopic surgery has recently become a feasible option in patients with hereditary bilateral pheochromocytomas.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis. Adrenal Gland Neoplasms / surgery
  • [MeSH-minor] Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / surgery. Adrenal Medulla. Humans

  • MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16119111.001).
  • [ISSN] 0301-4894
  • [Journal-full-title] Nihon Geka Gakkai zasshi
  • [ISO-abbreviation] Nihon Geka Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 17
  •  go-up   go-down


34. Barzon L, Masi G, Pacenti M, Trevisan M, Fallo F, Remo A, Martignoni G, Montanaro D, Pezzi V, Palù G: Expression of aromatase and estrogen receptors in human adrenocortical tumors. Virchows Arch; 2008 Feb;452(2):181-91
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of aromatase and estrogen receptors in human adrenocortical tumors.
  • We recently demonstrated that adrenocortical carcinoma cells express aromatase and estrogen receptors (ERs) and that 17beta-estradiol enhances adrenocortical cell proliferation.
  • To provide a clue to the role of estrogens in adrenal tumorigenesis, we investigated the expression profile of genes involved in sex steroid hormone production and activity in a large series of normal and neoplastic human adrenocortical tissues.
  • Quantitative reverse transcriptase-polymerase chain reaction, Western blotting, and immunohistochemistry showed that ERalpha and ERbeta, androgen receptor (AR), and aromatase were expressed in the adrenal cortex and in adrenocortical tumors.
  • ERbeta was the predominant ER subtype and was mainly expressed in the zona glomerulosa and fasciculata.
  • Western blot analysis revealed the presence of a truncated form of AR in adrenocortical tissues.
  • With respect to the normal adrenal cortex and adrenocortical adenomas, carcinomas were characterized by significantly lower ERbeta levels, ERalpha upregulation, and aromatase overexpression.
  • In agreement with our in vitro findings, the results of this study suggest that estrogens, locally produced by aromatase, could enhance adrenocortical cell proliferation though autocrine/paracrine mechanisms.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenocortical Adenoma / metabolism. Adrenocortical Carcinoma / metabolism. Aromatase / metabolism. Receptors, Estrogen / metabolism
  • [MeSH-minor] Adrenal Cortex / embryology. Adrenal Cortex / metabolism. Adult. Aged. Biomarkers, Tumor / metabolism. Blotting, Western. Female. Gene Expression. Humans. Male. Middle Aged. RNA, Messenger / metabolism. RNA, Neoplasm / analysis

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Virchows Arch. 2008 Aug;453(2):221-2 [18553103.001]
  • [Cites] Eur J Endocrinol. 2002 Dec;147(6):795-802 [12457455.001]
  • [Cites] J Mol Endocrinol. 2005 Oct;35(2):245-56 [16216906.001]
  • [Cites] Endocrinology. 2005 Dec;146(12 ):5474-84 [16150902.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Jun;92(6):2215-22 [17405842.001]
  • [Cites] J Endocrinol Invest. 2005 May;28(5):459-63 [16075931.001]
  • [Cites] J Steroid Biochem Mol Biol. 2003 Nov;87(2-3):181-9 [14672738.001]
  • [Cites] J Biol Chem. 2002 Jun 7;277(23):20591-7 [11927588.001]
  • [Cites] Comp Biochem Physiol B Biochem Mol Biol. 1997 Sep;118(1):217-27 [9418012.001]
  • [Cites] J Biol Chem. 1999 Jan 1;274(1):345-53 [9867849.001]
  • [Cites] Endocr Relat Cancer. 2006 Jun;13(2):327-34 [16728566.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Oct;82(10):3509-12 [9329394.001]
  • [Cites] Mol Genet Metab. 2001 Sep-Oct;74(1-2):206-16 [11592817.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Feb;85(2):847-52 [10690900.001]
  • [Cites] Am J Surg Pathol. 2002 Dec;26(12):1612-9 [12459628.001]
  • [Cites] Cancer Res. 2007 Oct 1;67(19):9001-5 [17909000.001]
  • [Cites] J Biol Chem. 2003 Sep 19;278(38):36418-29 [12842887.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Aug;80(8):2378-80 [7629233.001]
  • [Cites] Endocrinology. 2002 Mar;143(3):853-67 [11861507.001]
  • [Cites] Mol Endocrinol. 2002 Mar;16(3):515-28 [11875111.001]
  • [Cites] Endocr Relat Cancer. 2004 Sep;11(3):537-51 [15369453.001]
  • [Cites] J Clin Endocrinol Metab. 2001 May;86(5):2258-62 [11344236.001]
  • [Cites] J Steroid Biochem. 1986 Jul;25(1):1-9 [3747509.001]
  • [Cites] Am J Surg Pathol. 1989 Mar;13(3):202-6 [2919718.001]
  • [Cites] Cancer Res. 2005 Jan 15;65(2):657-63 [15695411.001]
  • [Cites] J Endocrinol. 2002 Sep;174(3):R13-7 [12208674.001]
  • [Cites] J Biol Chem. 2000 Dec 22;275(51):39855-9 [11053406.001]
  • [Cites] Mol Endocrinol. 2006 Oct;20(10):2326-42 [16709599.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Jun;89(6):3010-9 [15181092.001]
  • [Cites] J Endocrinol. 1998 Dec;159(3):373-80 [9834454.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Jul;83(7):2597-600 [9661652.001]
  • [Cites] Am J Obstet Gynecol. 1984 Oct 1;150(3):326-7 [6486196.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Dec;83(12 ):4520-3 [9851803.001]
  • [Cites] Eur J Endocrinol. 2003 Oct;149(4):273-85 [14514341.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Feb;86(2):649-52 [11158024.001]
  • [Cites] Int J Cancer. 1996 Feb 8;65(4):432-6 [8621222.001]
  • [Cites] Mol Cell Endocrinol. 1991 Jun;78(1-2):25-32 [1936523.001]
  • [Cites] Oncogene. 2005 Dec 8;24(55):8167-75 [16091743.001]
  • (PMID = 18157729.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Estrogen; EC 1.14.14.1 / Aromatase
  •  go-up   go-down


35. Feng C, Li HZ, Yan WG, Luo YF, Cao JL: [The expression and significance of chromogranin A and synaptophysin in adrenal gland tumors]. Zhonghua Zhong Liu Za Zhi; 2005 Aug;27(8):486-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [The expression and significance of chromogranin A and synaptophysin in adrenal gland tumors].
  • OBJECTIVE: To investigate the expression of chromogranin A (CgA) and synaptophysin (Syn) for differential diagnosis of different kinds of adrenal gland tumors.
  • METHODS: The samples of 69 adrenal gland tumors and 4 normal adrenal glands were immunohistochemically analyzed for the expression of chromogranin A and synaptophysin.
  • RESULTS: In the normal adrenal gland, CgA and Syn was exclusively detected in the medulla.
  • CgA was detected in all pheochromocytomas 25/25 (100%), and gave less or no expression in adrenocortical tumors.
  • Syn was detected in adrenocortical adenomas 27/28 (96.4%), adrenocortical carcinoma 7/8 (87.5%), pheochromocytoma 24/25 (96.0%) and adrenal metastatic carcinoma 6/8 (75.0%), respectively.
  • CONCLUSION: There is statistically significant difference of CgA expression between adrenalcortical and adrenal medullary tumors, and also between benign and malignant pheochromocytomas.
  • CgA and Syn are immunohistochemically reliable markers in the differential diagnosis of various kinds of adrenal gland tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / metabolism. Chromogranin A / biosynthesis. Pheochromocytoma / metabolism. Synaptophysin / biosynthesis
  • [MeSH-minor] Adrenocortical Adenoma / diagnosis. Adrenocortical Adenoma / metabolism. Adrenocortical Carcinoma / diagnosis. Adrenocortical Carcinoma / metabolism. Diagnosis, Differential. Female. Humans. Male

  • MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.
  • MedlinePlus Health Information. consumer health - Pheochromocytoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16188147.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Chromogranin A; 0 / Synaptophysin
  •  go-up   go-down


36. Barzon L, Maffei P, Sonino N, Pilon C, Baldazzi L, Balsamo A, Del Maschio O, Masi G, Trevisan M, Pacenti M, Fallo F: The role of 21-hydroxylase in the pathogenesis of adrenal masses: review of the literature and focus on our own experience. J Endocrinol Invest; 2007 Jul-Aug;30(7):615-23
Hazardous Substances Data Bank. 17ALPHA-HYDROXYPROGESTERONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of 21-hydroxylase in the pathogenesis of adrenal masses: review of the literature and focus on our own experience.
  • An exaggerated response of 17- hydroxyprogesterone (17-OHP) to exogenous ACTH stimulation has been found in 30 to 70% of patients with incidentally discovered adrenal tumors, supporting the concept that congenital 21- hydroxylase deficiency may be a predisposing factor for adrenocortical tumorigenesis.
  • Decreased expression of 21-hydroxylase gene has been observed in sporadic non-functioning adrenocortical adenomas and adrenocortical carcinomas, in agreement with the reduced steroidogenic activity found in these types of tumors.
  • Screening studies for the presence of mutations in CYP21A2 gene, encoding 21-hydroxylase, in patients with sporadic adrenocortical tumors yielded discordant results.
  • Overall, a higher frequency of germline 21-hydroxylase mutation carriers has been found among patients with adrenal tumors, including incidentalomas, than in the general population.
  • However, the presence of mutations did not correlate with endocrine test results and tumor mass features, suggesting that 21-hydroxylase deficiency does not represent a relevant mechanism in adrenal tumorigenesis.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Adrenal Hyperplasia, Congenital / genetics. Adrenocortical Carcinoma / genetics. Steroid 21-Hydroxylase / physiology

  • MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Endocrinol Metab. 1998 Jan;83(1):55-62 [9435416.001]
  • [Cites] J Mol Endocrinol. 2005 Oct;35(2):245-56 [16216906.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Sep;90(9):5446-55 [15985477.001]
  • [Cites] J Clin Endocrinol Metab. 1992 Mar;74(3):685-9 [1311000.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Sep;82(9):3054-8 [9284742.001]
  • [Cites] Proc Natl Acad Sci U S A. 1986 Jul;83(13):4715-9 [3014507.001]
  • [Cites] Clin Endocrinol (Oxf). 1996 Jan;44(1):111-6 [8706282.001]
  • [Cites] Eur J Endocrinol. 1997 Feb;136(2):196-200 [9116915.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Dec;90(12):6638-49 [16204365.001]
  • [Cites] Hum Pathol. 1993 Apr;24(4):397-404 [8491480.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Jul;88(7):3035-42 [12843140.001]
  • [Cites] JAMA. 1982 Dec 17;248(23):3140-1 [7143691.001]
  • [Cites] J Clin Endocrinol Metab. 1993 Sep;77(3):677-82 [8370688.001]
  • [Cites] J Steroid Biochem Mol Biol. 2003 Nov;87(2-3):181-9 [14672738.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Aug 3;285(5):1361-8 [11478808.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Jul;83(7):2585-8 [9661649.001]
  • [Cites] Mol Cell Biol. 1990 Jun;10(6):2950-9 [2342464.001]
  • [Cites] Nature. 1983 Nov 3-9;306(5938):70-3 [6633660.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Feb;82(2):479-85 [9024240.001]
  • [Cites] Hum Mol Genet. 1995 Nov;4(11):2109-16 [8589688.001]
  • [Cites] Endocrinology. 1981 May;108(5):1769-79 [6260464.001]
  • [Cites] J Endocrinol Invest. 1996 Dec;19(11):745-52 [9061508.001]
  • [Cites] Endocr Rev. 2004 Dec;25(6):947-70 [15583024.001]
  • [Cites] J Mol Endocrinol. 2004 Dec;33(3):651-62 [15591025.001]
  • [Cites] Cell Tissue Res. 1990 Apr;260(1):161-6 [2340580.001]
  • [Cites] Mol Endocrinol. 1993 Nov;7(11):1463-71 [8114760.001]
  • [Cites] J Endocrinol Invest. 1991 Nov;14 (10 ):831-7 [1687042.001]
  • [Cites] South Med J. 1998 Aug;91(8):775-9 [9715230.001]
  • [Cites] J Clin Endocrinol Metab. 1996 May;81(5):1776-9 [8626833.001]
  • [Cites] J Endocrinol. 2002 Sep;174(3):R13-7 [12208674.001]
  • [Cites] Lancet. 2005 Jun 18-24;365(9477):2125-36 [15964450.001]
  • [Cites] Mol Cell Endocrinol. 1998 Feb;137(1):13-9 [9607724.001]
  • [Cites] Endocr Rev. 1995 Aug;16(4):460-84 [8521790.001]
  • [Cites] Clin Endocrinol (Oxf). 2002 Jun;56(6):811-6 [12072053.001]
  • [Cites] J Pediatr Endocrinol Metab. 2003 Dec;16(9):1311-4 [14714757.001]
  • [Cites] Eur Radiol. 1996;6(4):470-2 [8798026.001]
  • [Cites] Am J Dis Child. 1993 Dec;147(12):1274-6 [8249939.001]
  • [Cites] Eur J Endocrinol. 2005 Sep;153(3):435-44 [16131607.001]
  • [Cites] J Urol. 2000 Feb;163(2):398-407 [10647642.001]
  • [Cites] Neuroendocrinology. 2005;82(5-6):274-81 [16721033.001]
  • [Cites] Endocr Rev. 1998 Dec;19(6):828-43 [9861547.001]
  • [Cites] J Endocrinol Invest. 2005 May;28(5):449-53 [16075929.001]
  • [Cites] Clin Endocrinol (Oxf). 2000 Jul;53(1):117-25 [10931088.001]
  • [Cites] Eur J Endocrinol. 2003 Oct;149(4):273-85 [14514341.001]
  • [Cites] Am J Med Sci. 1997 Nov;314(5):338-41 [9365337.001]
  • [Cites] Trends Endocrinol Metab. 2005 Dec;16(10):478-88 [16275121.001]
  • [Cites] Clin Endocrinol (Oxf). 1994 Oct;41(4):445-51 [7955456.001]
  • [Cites] Eur J Endocrinol. 1995 Apr;132(4):422-8 [7711879.001]
  • [Cites] J Clin Endocrinol Metab. 1996 Feb;81(2):740-4 [8636297.001]
  • [Cites] Eur J Endocrinol. 1999 Sep;141(3):238-45 [10474121.001]
  • [Cites] Horm Res. 2002;57(5-6):192-6 [12053092.001]
  • [Cites] J Endocrinol Invest. 2000 May;23(5):287-94 [10882146.001]
  • [Cites] Endocr Rev. 2000 Jun;21(3):245-91 [10857554.001]
  • [Cites] Mol Cell Endocrinol. 2001 Mar 28;174(1-2):111-20 [11306177.001]
  • [Cites] Eur J Endocrinol. 2002 Sep;147(3):349-55 [12213672.001]
  • [Cites] Endocrinology. 1998 Dec;139(12 ):5144-50 [9832454.001]
  • [Cites] J Assoc Physicians India. 1981 Jun;29(6):491-3 [7320006.001]
  • [Cites] Clin Endocrinol (Oxf). 1999 Mar;50(3):343-6 [10435060.001]
  • [Cites] Can J Urol. 2002 Jun;9(3):1563-4 [12121582.001]
  • [Cites] J Clin Endocrinol Metab. 1998 May;83(5):1592-7 [9589661.001]
  • [Cites] J Biol Chem. 1999 Dec 31;274(53):38097-106 [10608879.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Feb;84(2):520-6 [10022410.001]
  • [Cites] Arch Intern Med. 1993 Jun 14;153(11):1389-91 [8507129.001]
  • (PMID = 17848847.001).
  • [ISSN] 1720-8386
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Glucocorticoids; 68-96-2 / 17-alpha-Hydroxyprogesterone; EC 1.14.14.16 / Steroid 21-Hydroxylase
  • [Number-of-references] 64
  •  go-up   go-down


37. West AN, Neale GA, Pounds S, Figueredo BC, Rodriguez Galindo C, Pianovski MA, Oliveira Filho AG, Malkin D, Lalli E, Ribeiro R, Zambetti GP: Gene expression profiling of childhood adrenocortical tumors. Cancer Res; 2007 Jan 15;67(2):600-8
SciCrunch. ArrayExpress: Data: Microarray .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression profiling of childhood adrenocortical tumors.
  • Pediatric adrenocortical tumors (ACT) are rare and often fatal malignancies; little is known regarding their etiology and biology.
  • To provide additional insight into the nature of ACT, we determined the gene expression profiles of 24 pediatric tumors (five adenomas, 18 carcinomas, and one undetermined) and seven normal adrenal glands.
  • Distinct patterns of gene expression, validated by quantitative real-time PCR and Western blot analysis, were identified that distinguish normal adrenal cortex from tumor.
  • Differences in gene expression were also identified between adrenocortical adenomas and carcinomas.
  • In addition, pediatric adrenocortical carcinomas were found to share similar patterns of gene expression when compared with those published for adult ACT.
  • Our findings lay the groundwork for establishing gene expression profiles that may aid in the diagnosis and prognosis of pediatric ACT, and in the identification of signaling pathways that contribute to this disease.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics. Adrenocortical Carcinoma / genetics

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17234769.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / CA63230; United States / NCI NIH HHS / CA / CA71907
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


38. Barczyński M, Konturek A, Gołkowski F, Cichoń S, Huszno B, Peitgen K, Walz MK: Posterior retroperitoneoscopic adrenalectomy: a comparison between the initial experience in the invention phase and introductory phase of the new surgical technique. World J Surg; 2007 Jan;31(1):65-71
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Today, the posterior retroperitoneoscopic technique has become a standard procedure in adrenal surgery.
  • The procedure allows direct access to the adrenal glands, but it seems to be difficult because of the uncommon anatomic view.
  • Group A consisted of 44 patients (14 males, 30 females; age: 48.7 +/- 14.5 years) undergoing surgery between 07/1994 and 8/1996 (24 right, 26 left; 8 Cushing adenomas, 14 Conn adenomas, 11 pheochromocytomas, 7 nonfunctioning adrenocortical adenomas, 10 ACTH-dependent adrenal hyperplasias).
  • Group B consisted of 50 patients (12 males, 38 females; mean age 59.3 +/- 10.7 years) operated between 01/2004 and 01/2006 (28 right, 22 left tumors; 5 Cushing adenomas, 12 Conn adenomas, 4 pheochromocytomas, 29 nonfunctioning adrenocortical adenomas).
  • After comprehensive training, the operative time and conversion rate are dramatically reduced, allowing for a short learning period.
  • [MeSH-minor] Adrenal Cortex Neoplasms / surgery. Adrenal Glands / pathology. Adrenocortical Adenoma / surgery. Adult. Clinical Competence. Feasibility Studies. Female. Humans. Hyperplasia. Male. Middle Aged. Pheochromocytoma / surgery. Pituitary ACTH Hypersecretion / surgery. Retroperitoneal Space

  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Urol. 2005 Aug;174(2):442-5; discussion 445 [16006861.001]
  • [Cites] Urology. 1997 Jul;50(1):19-24 [9218013.001]
  • [Cites] World J Surg. 2000 Nov;24(11):1342-6 [11038204.001]
  • [Cites] World J Surg. 2004 Dec;28(12):1323-9 [15517476.001]
  • [Cites] J Endourol. 2004 Sep;18(7):661-4 [15597657.001]
  • [Cites] Aust N Z J Surg. 1994 May;64(5):375-6 [8179535.001]
  • [Cites] World J Surg. 1996 Sep;20(7):769-74 [8678949.001]
  • [Cites] World J Surg. 2001 Jun;25(6):728-34 [11376407.001]
  • [Cites] Nihon Hinyokika Gakkai Zasshi. 1992 Jul;83(7):1130-3 [1387181.001]
  • [Cites] Am J Surg. 1982 Sep;144(3):322-4 [7114370.001]
  • [Cites] J Laparoendosc Adv Surg Tech A. 2001 Dec;11(6):409-13 [11814133.001]
  • [Cites] Zentralbl Chir. 1995;120(1):53-8 [7887040.001]
  • [Cites] Surg Endosc. 1999 Jan;13(1):86-90 [9869699.001]
  • [Cites] Arch Surg. 1995 May;130(5):489-92; discussion 492-4 [7748086.001]
  • [Cites] Surg Endosc. 1994 Feb;8(2):135-8 [8165486.001]
  • [Cites] J Urol. 2005 Aug;174(2):446-50 [16006862.001]
  • [Cites] Surg Endosc. 2002 Sep;16(9):1274-9 [11988798.001]
  • [Cites] N Engl J Med. 1992 Oct 1;327(14):1033 [1387700.001]
  • [Cites] Surg Endosc. 2002 Jan;16(1):96-9 [11961614.001]
  • [Cites] Surgery. 1993 Dec;114(6):1120-4; discussion 1124-5 [8256217.001]
  • [Cites] Arch Surg. 2004 Nov;139(11):1243-7 [15545573.001]
  • [Cites] Br J Surg. 2005 Jun;92(6):719-23 [15856491.001]
  • [Cites] J Urol. 2001 Aug;166(2):437-43 [11458043.001]
  • [Cites] World J Surg. 1998 Dec;22(12):1246-9 [9841752.001]
  • [Cites] Eur J Surg Oncol. 2003 Apr;29(3):272-7 [12657239.001]
  • [Cites] Surg Endosc. 2004 May;18(5):771-3 [15216859.001]
  • (PMID = 17180554.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study
  • [Publication-country] United States
  •  go-up   go-down


39. Mete O, Kapran Y, Güllüoğlu MG, Kiliçaslan I, Erbil Y, Senyürek YG, Dizdaroğlu F: Anti-CD10 (56C6) is expressed variably in adrenocortical tumors and cannot be used to discriminate clear cell renal cell carcinomas. Virchows Arch; 2010 May;456(5):515-21
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anti-CD10 (56C6) is expressed variably in adrenocortical tumors and cannot be used to discriminate clear cell renal cell carcinomas.
  • In the evaluation of retroperitoneal masses, the practicing pathologist faces a dilemma when making a diagnosis based on histology given the often overlapping morphologic appearances of the adrenocortical carcinoma, renal cell carcinoma (RCC), and hepatocellular carcinoma (HCC).
  • CD10 is expressed in a membranous fashion in the vast majority of clear cell RCCs; therefore, it is widely used for distinction from its mimics.
  • However, its expression is not well-investigated in adrenal cortical tumors.
  • We examined CD10 expression in 47 surgically resected adrenocortical tumors (26 adenomas and 21 carcinomas) and compared with 20 clear cell RCCs and 25 HCCs.
  • Twenty HCCs (80%), 18 RCCs (90%), 11 adrenocortical carcinomas (52%), and 18 adrenocortical adenomas (69%) were positive for CD10.
  • HCCs were characterized by a canalicular staining, and clear cell RCCs exhibited membranous or mixed membranous-cytoplasmic staining.
  • Adrenocortical tumors displayed mainly cytoplasmic staining.
  • Four adrenocortical carcinomas and one adenoma also displayed the membranous staining pattern.
  • Despite the relatively small number of samples, our preliminary results revealed that adrenocortical tumors may express CD10 (Clone: 56C6).
  • The most important point from this paper is the fact that anti-CD10 expression has not been previously reported in adrenocortical carcinomas.
  • This suggests that CD10 does not seem to be a useful marker for discriminating clear cell RCCs from adrenocortical tumors since CD10 expression does not rule out the possibility of adrenocortical tumors.
  • This feature should be kept in mind when constructing an antibody panel for an epithelial tumor that involves the adrenal gland and kidney, especially in small biopsy specimens.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Carcinoma, Renal Cell / diagnosis. Kidney Neoplasms / diagnosis. Neprilysin / biosynthesis
  • [MeSH-minor] Adult. Antigens, Neoplasm / analysis. Carcinoma, Hepatocellular / diagnosis. Carcinoma, Hepatocellular / immunology. Female. Humans. Liver Neoplasms / diagnosis. Liver Neoplasms / immunology. Male. Middle Aged

  • MedlinePlus Health Information. consumer health - Kidney Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Histopathology. 2008 Jan;52(2):119-29 [17825057.001]
  • [Cites] Am J Pathol. 1999 Jan;154(1):77-82 [9916921.001]
  • [Cites] Mod Pathol. 2003 Dec;16(12):1205-9 [14681320.001]
  • [Cites] J Clin Endocrinol Metab. 2009 Jun;94(6):2178-83 [19318454.001]
  • [Cites] Horm Res. 2008;70(5):294-9 [18824868.001]
  • [Cites] Histopathology. 2004 Nov;45(5):452-9 [15500648.001]
  • [Cites] J Clin Pathol. 2000 Mar;53(3):206-11 [10823140.001]
  • [Cites] Pathol Int. 2009 Jan;59(1):38-43 [19121090.001]
  • [Cites] Am J Clin Pathol. 2000 Mar;113(3):374-82 [10705818.001]
  • [Cites] J Pediatr Hematol Oncol. 2010 Jan;32(1):2-3 [20051779.001]
  • [Cites] Am J Surg Pathol. 2003 Mar;27(3):413-4 [12604902.001]
  • [Cites] Am J Surg Pathol. 2000 Feb;24(2):203-10 [10680888.001]
  • [Cites] Histopathology. 2004 Nov;45(5):460-7 [15500649.001]
  • [Cites] Mol Cell Endocrinol. 2001 Jan 22;171(1-2):5-7 [11165004.001]
  • [Cites] Appl Immunohistochem Mol Morphol. 2005 Dec;13(4):347-52 [16280664.001]
  • [Cites] Am J Surg Pathol. 2009 Feb;33(2):289-97 [18852677.001]
  • [Cites] Pathology. 2009 Feb;41(2):191-3 [19152193.001]
  • (PMID = 20390424.001).
  • [ISSN] 1432-2307
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; EC 3.4.24.11 / Neprilysin
  •  go-up   go-down


40. Fukuda T, Takahashi K, Suzuki T, Saruta M, Watanabe M, Nakata T, Sasano H: Urocortin 1, urocortin 3/stresscopin, and corticotropin-releasing factor receptors in human adrenal and its disorders. J Clin Endocrinol Metab; 2005 Aug;90(8):4671-8
MedlinePlus Health Information. consumer health - Pheochromocytoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Urocortin 1, urocortin 3/stresscopin, and corticotropin-releasing factor receptors in human adrenal and its disorders.
  • Recently, direct involvement of the locally synthesized CRF family in adrenocortical function has been proposed.
  • OBJECTIVE, DESIGN, AND SETTING: We examined in situ expression of Ucn and CRF receptors in nonpathological human adrenal gland and its disorders using immunohistochemistry and mRNA in situ hybridization.
  • RESULTS: Ucn immunoreactivity was localized in the cortex and medulla of nonpathological adrenal glands.
  • Ucn1 immunoreactivity was marked in the medulla, whereas Ucn3 was immunostained mostly in the cortex.
  • Both CRF type 1 and CRF2 were expressed in the cortex, particularly in the zonae fasciculata and reticularis but very weakly or undetectably in the medulla.
  • Immunohistochemistry in serial tissue sections with mirror images revealed that both Ucn3 and CRF2 were colocalized in more than 85% of the adrenocortical cells. mRNA in situ hybridization confirmed these findings above.
  • In fetal adrenals, Ucn and CRF receptors were expressed in both fetal and definitive zones of the cortex.
  • Ucn and CRF receptors were all expressed in the tumor cells of pheochromocytomas, adrenocortical adenomas, and carcinomas, but its positivity was less than that in nonpathological adrenal glands, suggesting that Ucn1, Ucn3, and CRF receptors were down-regulated in these adrenal neoplasms.
  • CONCLUSIONS: Ucn1, Ucn3, and CRF receptors are all expressed in human adrenal cortex and medulla and may play important roles in physiological adrenal functions.
  • [MeSH-major] Adrenal Cortex / physiology. Adrenal Cortex Neoplasms / physiopathology. Corticotropin-Releasing Hormone / genetics. Pheochromocytoma / physiopathology. Receptors, Corticotropin-Releasing Hormone / genetics
  • [MeSH-minor] Adenoma / metabolism. Adenoma / physiopathology. Adolescent. Adult. Aged. Child. Child, Preschool. Humans. Immunohistochemistry. In Situ Hybridization. Infant. Infant, Newborn. Middle Aged. RNA, Messenger / analysis. Urocortins

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15914529.001).
  • [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 / CRF receptor type 1; 0 / CRF receptor type 2; 0 / RNA, Messenger; 0 / Receptors, Corticotropin-Releasing Hormone; 0 / UCN3 protein, human; 0 / Urocortins; 9015-71-8 / Corticotropin-Releasing Hormone
  •  go-up   go-down


41. Bertherat J, Groussin L, Bertagna X: Mechanisms of disease: adrenocortical tumors--molecular advances and clinical perspectives. Nat Clin Pract Endocrinol Metab; 2006 Nov;2(11):632-41
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mechanisms of disease: adrenocortical tumors--molecular advances and clinical perspectives.
  • Most adrenocortical tumors are benign, unilateral, adrenocortical adenomas that are often discovered incidentally.
  • Adrenocortical cancer is rare.
  • Exceptionally, adrenocortical tumors can be bilateral.
  • Although most adrenocortical tumors occur sporadically, they may also feature in congenital and/or familial disease.
  • The identification of germline genetic defects in familial diseases associated with adrenocortical tumors helped to define the somatic alterations in sporadic disease: for example, overexpression of insulin-like growth factor 2 and alterations at the 11p15 locus (observed in Beckwith-Wiedemann syndrome) are also found in most adrenocortical cancers.
  • Similarly, inactivating mutations of the TP53 gene, located at 17p13 (observed in Li-Fraumeni syndrome), can also be found at the somatic level in sporadic adrenocortical cancers, as can 17p13 allelic losses.
  • Components of the cyclic AMP signaling pathway--for example, adrenocorticotropic hormone receptors and other membrane receptors, Gs proteins and protein kinase A--can be altered to various degrees in adrenocortical tumors.
  • More recently, gene profiling and genetic studies have shown that the Wnt-beta-catenin signaling pathway is frequently activated in adrenocortical tumors.
  • These research findings already have profound implications for clinical management of patients with adrenocortical tumors, for example in unraveling the genetic origin of the disease in some patients, and in the development of molecular markers for diagnosis and prognosis.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17082810.001).
  • [ISSN] 1745-8366
  • [Journal-full-title] Nature clinical practice. Endocrinology & metabolism
  • [ISO-abbreviation] Nat Clin Pract Endocrinol Metab
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 54
  •  go-up   go-down


42. Barzon L, Pacenti M, Masi G, Stefani AL, Fincati K, Palù G: Loss of growth hormone secretagogue receptor 1a and overexpression of type 1b receptor transcripts in human adrenocortical tumors. Oncology; 2005;68(4-6):414-21
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Loss of growth hormone secretagogue receptor 1a and overexpression of type 1b receptor transcripts in human adrenocortical tumors.
  • OBJECTIVE AND METHODS: Quantitative analysis of mRNA expression of ghrelin and its receptors GHS-R1a and -R1b in a large series of normal and neoplastic human adrenocortical tissues.
  • Evaluation of the effects of ghrelin on GHS-R expression and proliferation of human adrenocortical carcinoma (ACC) cell lines.
  • RESULTS: Ghrelin and GHS-R transcripts are expressed in normal adrenal cortex, with GHS-R1b mRNA levels being 5- to 10-fold higher than GHS-R1amRNA.
  • A significant increase in ghrelin expression was observed in adrenocortical adenomas, but not in carcinomas.
  • GHS-R1a was undetectable in about 60% of both benign and malignant tumor samples, except for cortisol-producing adenomas, which showed increased receptor expression.
  • At variance, GHS-R1b was overexpressed in both benign and malignant adrenocortical tumors.
  • In vitro studies in human ACC cell lines demonstrated that GHS-R1a is downregulated and GHS-R1bmRNA expression is upregulated by ghrelin, while inhibiting cell proliferation.
  • CONCLUSION: Downregulation ofGHS-R1a in adrenal tumors and the presence of high levels of GHS-R1b transcripts in adrenocortical tissue suggest a role for these receptors in adrenal function and growth.
  • In this regard, ghrelin inhibits cell proliferation and modulates GHS-R expression in ACC cells in vitro.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenocortical Adenoma / metabolism. Adrenocortical Carcinoma / metabolism. Gene Expression Regulation, Neoplastic. Receptors, G-Protein-Coupled / metabolism
  • [MeSH-minor] Adrenal Cortex / metabolism. Cell Proliferation. Ghrelin. Growth Hormone / pharmacology. Humans. Peptide Hormones / pharmacology. Peptides / genetics. Peptides / metabolism. RNA, Messenger. Receptors, Ghrelin. Tumor Cells, Cultured

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2005 S. Karger AG, Basel
  • (PMID = 16020971.001).
  • [ISSN] 0030-2414
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Ghrelin; 0 / Peptide Hormones; 0 / Peptides; 0 / RNA, Messenger; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Ghrelin; 9002-72-6 / Growth Hormone
  •  go-up   go-down


43. Soon PS, Gill AJ, Benn DE, Clarkson A, Robinson BG, McDonald KL, Sidhu SB: Microarray gene expression and immunohistochemistry analyses of adrenocortical tumors identify IGF2 and Ki-67 as useful in differentiating carcinomas from adenomas. Endocr Relat Cancer; 2009 Jun;16(2):573-83
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Microarray gene expression and immunohistochemistry analyses of adrenocortical tumors identify IGF2 and Ki-67 as useful in differentiating carcinomas from adenomas.
  • The management of adrenocortical tumors (ACTs) is complex.
  • The Weiss score is the present most widely used system for ACT diagnosis.
  • However, ACTs with a score of 3 can be phenotypically benign or malignant.
  • Our objective is to use microarray profiling of a cohort of adrenocortical carcinomas (ACCs) and adrenocortical adenomas (ACAs) to identify discriminatory genes that could be used as an adjunct to the Weiss score.
  • [MeSH-major] Adrenocortical Adenoma / genetics. Adrenocortical Carcinoma / genetics. Biomarkers, Tumor / genetics. Gene Expression Profiling. Insulin-Like Growth Factor II / genetics. Ki-67 Antigen / genetics
  • [MeSH-minor] Adolescent. Adrenal Cortex / metabolism. Adrenal Cortex / pathology. Adult. Aged. Female. Humans. Immunoenzyme Techniques. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Sensitivity and Specificity. Young Adult

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19218281.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / IGF2 protein, human; 0 / Ki-67 Antigen; 0 / RNA, Messenger; 67763-97-7 / Insulin-Like Growth Factor II
  •  go-up   go-down


44. de Cremoux P, Rosenberg D, Goussard J, Brémont-Weil C, Tissier F, Tran-Perennou C, Groussin L, Bertagna X, Bertherat J, Raffin-Sanson ML: Expression of progesterone and estradiol receptors in normal adrenal cortex, adrenocortical tumors, and primary pigmented nodular adrenocortical disease. Endocr Relat Cancer; 2008 Jun;15(2):465-74

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of progesterone and estradiol receptors in normal adrenal cortex, adrenocortical tumors, and primary pigmented nodular adrenocortical disease.
  • Adrenal tumors occur more frequently in women and are the leading cause of Cushing's syndrome during pregnancy.
  • We aimed to evaluate the potential role of sex steroids in the susceptibility of women to adrenocortical tumors.
  • We evaluated the presence of the progesterone receptor (PR), estradiol receptors (ERs), and aromatase in 5 patients with primary pigmented nodular adrenal disease (PPNAD), 15 adrenocortical adenomas (ACAs) and adjacent normal tissues, 12 adrenocortical carcinomas (ACCs), and 3 normal adrenal glands (NA).
  • ERalpha concentrations were low in NA, in adrenal tissues adjacent to ACA (51+/-33), in ACC (53+/-78), and lower in ACA (11+/-11 fmol/mg DNA).
  • Conversely, PR concentrations were high in NA and adrenal tissues adjacent to ACA, at 307+/-216 fmol/mg DNA, and were even higher in tumors - 726+/-706 fmol/mg DNA in ACA and 1154+/-1586 fmol/mg DNA in ACC - and in isolated PPNAD nodules.
  • PR and ERbeta are clearly present in normal adrenal glands and adrenal tumors.
  • Further studies may shed light on the possible pathogenic role of these receptors in adrenal proliferation.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics. Estrogen Receptor alpha / genetics. Estrogen Receptor beta / genetics. Receptors, Progesterone / genetics
  • [MeSH-minor] Adolescent. Adrenal Cortex / pathology. Adrenal Cortex / physiology. Adrenal Cortex Diseases / genetics. Adrenal Cortex Diseases / metabolism. Adrenal Cortex Diseases / pathology. Adult. Aged. Aged, 80 and over. Aromatase / metabolism. Child. Cytosol / metabolism. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. RNA, Messenger / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18508999.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / RNA, Messenger; 0 / Receptors, Progesterone; EC 1.14.14.1 / Aromatase
  •  go-up   go-down


45. Onoda N, Ishikawa T, Nishio K, Tahara H, Inaba M, Wakasa K, Sumi T, Yamazaki T, Shigematsu K, Hirakawa K: Cushing's syndrome by left adrenocortical adenoma synchronously associated with primary aldosteronism by right adrenocortical adenoma: report of a case. Endocr J; 2009;56(3):495-502
MedlinePlus Health Information. consumer health - Cushing's Syndrome.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cushing's syndrome by left adrenocortical adenoma synchronously associated with primary aldosteronism by right adrenocortical adenoma: report of a case.
  • Synchronous associations of Cushing's syndrome (CS) and primary aldosteronism (PA) with multiple adrenocortical adenomas secreting each hormone independently have rarely been reported.
  • Bilateral adrenal masses with clinical symptoms of CS and PA were found in a 43-year-old woman.
  • The right adrenal tumor (3 cm) was yellow in color with abundant lipofuscin granules, and was composed of both eosinophilic compact cells and clear cells.
  • Left adrenal tumor (2.4 cm) was golden-yellow in color, and composed of clear cells only.
  • Furthermore, minute nodules were found at the surface of normal-appearing cortex on both sides of the adrenal glands, and the expression of HSD3B2 and CYP11B mRNAs was clearly demonstrated within the nodules, indicating aldosterone synthesis.
  • We diagnosed that the present case had 1) cortisol-producing right adrenocortical adenoma, 2) aldosterone producing left adrenocortical adenoma, and 3) cortical minute nodules with aldosterone production in both adrenal glands compatible with idiopathic adrenal hyperplasia.
  • We reviewed the cases reported, and discussed the significance of the minute nodules in the adrenal cortex, often found in association with the adrenocortical adenoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications. Cushing Syndrome / etiology. Hyperaldosteronism / etiology

  • Genetic Alliance. consumer health - Cushing's Syndrome.
  • Genetic Alliance. consumer health - Primary aldosteronism.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19270420.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] EC 1.1.1.145 / 3 beta-hydroxysteroid dehydrogenase type II; EC 1.1.1.145 / Progesterone Reductase; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase
  •  go-up   go-down


46. Waldmann J, Feldmann G, Slater EP, Langer P, Buchholz M, Ramaswamy A, Saeger W, Rothmund M, Fendrich V: Expression of the zinc-finger transcription factor Snail in adrenocortical carcinoma is associated with decreased survival. Br J Cancer; 2008 Dec 2;99(11):1900-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of the zinc-finger transcription factor Snail in adrenocortical carcinoma is associated with decreased survival.
  • In this study, we evaluate whether Snail is expressed in adrenocortical cancer (ACC) and if its expression is related to patient outcome.
  • Snail expression was neither detected in normal adrenocortical tissue, nor in benign adrenocortical adenomas.
  • Survival rates were significantly decreased in Snail-positive tumours compared to Snail-negative tumours: 10 out of 16 vs one out of eight patients succumbed to disease after a median follow up of 14.5 and 28.5 months, respectively (P=0.03).
  • Patients with Snail-expressing ACCs presented in advanced disease (11 out of 12 vs 6 out of 14, P=0.01) and tend to develop distant metastases more frequently than patients with negative staining (7 out of 11 vs two out of eight, P=0.19).
  • Furthermore, Snail expression is associated with decreased survival, advanced disease and higher risk of developing distant metastases.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenocortical Carcinoma / metabolism. Biomarkers, Tumor / analysis. Transcription Factors / biosynthesis

  • Genetic Alliance. consumer health - Adrenocortical Carcinoma.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nature. 1998 Mar 12;392(6672):190-3 [9515965.001]
  • [Cites] Horm Res. 1997;47(4-6):279-83 [9167965.001]
  • [Cites] Physiol Rev. 1959 Jan;39(1):162-82 [13623432.001]
  • [Cites] Br J Cancer. 2005 Jan 31;92(2):252-8 [15668718.001]
  • [Cites] Dig Dis Sci. 2005 Jan;50(1):42-6 [15712635.001]
  • [Cites] Cancer. 2005 Apr 15;103(8):1631-43 [15742334.001]
  • [Cites] Cell Cycle. 2005 Jun;4(6):772-6 [15917668.001]
  • [Cites] Cancer Res. 2005 Sep 1;65(17):7622-7 [16140927.001]
  • [Cites] Curr Opin Cell Biol. 2005 Oct;17(5):548-58 [16098727.001]
  • [Cites] Cancer Cell. 2005 Sep;8(3):197-209 [16169465.001]
  • [Cites] Nat Rev Mol Cell Biol. 2006 Feb;7(2):131-42 [16493418.001]
  • [Cites] Eur J Endocrinol. 2006 Apr;154(4):587-98 [16556722.001]
  • [Cites] Oncol Rep. 2006 Jul;16(1):65-71 [16786124.001]
  • [Cites] Jpn J Clin Oncol. 2006 Jun;36(6):357-63 [16766568.001]
  • [Cites] Clin Cancer Res. 2006 Sep 15;12(18):5395-402 [17000672.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Jan;92(1):148-54 [17062775.001]
  • [Cites] Breast Cancer Res. 2006;8(4):105 [16834762.001]
  • [Cites] Endocr Pathol. 2006 Winter;17(4):345-54 [17525483.001]
  • [Cites] Histopathology. 2007 Aug;51(2):239-45 [17593212.001]
  • [Cites] Endocr Relat Cancer. 2007 Sep;14(3):865-74 [17914115.001]
  • [Cites] Nat Cell Biol. 2000 Feb;2(2):76-83 [10655586.001]
  • [Cites] Cancer. 2000 Feb 15;88(4):711-36 [10679640.001]
  • [Cites] Mol Cell. 2001 Jun;7(6):1267-78 [11430829.001]
  • [Cites] Eur J Endocrinol. 2001 Sep;145(3):335-41 [11517015.001]
  • [Cites] Cancer. 2001 Sep 1;92(5):1113-21 [11571723.001]
  • [Cites] World J Surg. 2001 Jul;25(7):891-7 [11572030.001]
  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
  • [Cites] Cancer Res. 2002 Mar 15;62(6):1613-8 [11912130.001]
  • [Cites] Am J Pathol. 2003 Feb;162(2):521-31 [12547710.001]
  • [Cites] Am J Clin Pathol. 2004 Jul;122(1):78-84 [15272533.001]
  • [Cites] Development. 2004 Sep;131(17):4213-24 [15280211.001]
  • [Cites] Nat Cell Biol. 2004 Oct;6(10):931-40 [15448698.001]
  • [Cites] Am J Clin Pathol. 1979 Sep;72(3):390-9 [474519.001]
  • [Cites] Cancer. 1985 Feb 15;55(4):766-73 [3967172.001]
  • [Cites] Am J Surg Pathol. 1989 Mar;13(3):202-6 [2919718.001]
  • [Cites] Endocrinology. 1990 Jun;126(6):3251-62 [2161753.001]
  • [Cites] Anticancer Res. 1997 Mar-Apr;17(2B):1303-9 [9137490.001]
  • [Cites] Horm Metab Res. 1998 Jun-Jul;30(6-7):421-5 [9694573.001]
  • (PMID = 19018264.001).
  • [ISSN] 1532-1827
  • [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] 0 / Biomarkers, Tumor; 0 / Cadherins; 0 / Ki-67 Antigen; 0 / RNA, Messenger; 0 / Transcription Factors; 0 / snail family transcription factors
  • [Other-IDs] NLM/ PMC2600683
  •  go-up   go-down


47. Chen G, Yao J, Mou L, Fang X, Huang H, Liang J, Li L, Ye L, Lin L, Wen J: Clinical analysis of 249 cases of adrenal tumors in a Chinese hospital. Urol Int; 2010;85(3):270-5
MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical analysis of 249 cases of adrenal tumors in a Chinese hospital.
  • OBJECTIVE: This study was designed to evaluate the clinical and pathological characteristics of adrenal masses.
  • METHODS: The clinical data of 249 cases of adrenal masses which were confirmed at operation and by pathology were analyzed.
  • Overall, females were more commonly represented than males, especially with Cushing's syndrome and typical pheochromocytoma (female:male ratio 3.3:1.9), however the prevalence of adrenal incidentalomas (AIs) in males and females was similar.
  • Of 109 adrenocortical adenomas, 47 were primary aldosteronism, 31 were Cushing's syndrome, 30 were AIs, and 1 was adrenal virilization.
  • Of 72 benign pheochromocytomas, 51 were typical pheochromocytomas and 21 were AIs.
  • Of 14 adrenal nodular hyperplasias, 6 were Cushing's syndrome and 8 were primary aldosteronism.
  • Of the remaining 30 benign tumors, all presented as AIs.
  • The diameter of malignant tumors (10.9 ± 5.6 cm) was significantly larger than that of benign tumors (4.5 ± 3.7 cm) (p < 0.001).
  • CONCLUSION: This study shows a high rate of AIs in patients with adrenal masses selected for surgery.
  • Hormone levels should be determined in symptomatic or incidental patients with adrenal masses.
  • Imaging examination (CT and MRI) is the first method used to detect and localize adrenal masses.
  • Tumor size is an important parameter of diagnosis and management of patients with adrenal masses, especially AIs.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. China. Cushing Syndrome / diagnosis. Female. Hospitals. Humans. Magnetic Resonance Imaging / methods. Male. Middle Aged. Pheochromocytoma / diagnosis. Retrospective Studies. Tomography, X-Ray Computed / methods

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 S. Karger AG, Basel.
  • (PMID = 20606391.001).
  • [ISSN] 1423-0399
  • [Journal-full-title] Urologia internationalis
  • [ISO-abbreviation] Urol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  •  go-up   go-down


48. Hofland J, Timmerman MA, de Herder WW, van Schaik RH, de Krijger RR, de Jong FH: Expression of activin and inhibin subunits, receptors and binding proteins in human adrenocortical neoplasms. Clin Endocrinol (Oxf); 2006 Dec;65(6):792-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of activin and inhibin subunits, receptors and binding proteins in human adrenocortical neoplasms.
  • OBJECTIVE: The growth and differentiation factors activin and inhibin can affect tumour formation and steroid production in the adrenal cortex.
  • Expression of these activin-related mRNAs was measured in different types of adrenocortical tissues and tumours to study the relationship with tumorigenesis.
  • DESIGN: Quantitative expression of activin-related mRNAs was investigated in patient adrenocortical samples.
  • PATIENTS: Twenty-eight human adrenocortical samples from normal and hyperplastic adrenals and from adrenocortical adenomas and carcinomas were collected after surgery for study purposes.
  • MEASUREMENTS: Using quantitative reverse transcription polymerase chain reaction (RT-PCR), we investigated the expression of inhibin alpha-, betaA- and betaB-subunits, follistatin, betaglycan, ActRIIA, ActRIIB and Alk-4 in the adrenocortical tissues.
  • RESULTS: All genes studied were expressed in all tissues, with the exception of the inhibin alpha-subunit in one hyperplastic adrenal and three adrenocortical carcinomas.
  • We conclude that the expression of activin and inhibin subunits, receptors and binding proteins is affected by tumour formation in the adrenal gland and may play a role in tumorigenesis.
  • [MeSH-major] Activins / metabolism. Adrenal Cortex Neoplasms / metabolism. Adrenocortical Adenoma / metabolism. Adrenocortical Carcinoma / metabolism. Inhibins / metabolism
  • [MeSH-minor] Activin Receptors, Type II / genetics. Activin Receptors, Type II / metabolism. Adrenal Cortex / metabolism. Adrenal Cortex / pathology. Adult. Carrier Proteins / genetics. Carrier Proteins / metabolism. Female. Follistatin / genetics. Follistatin / metabolism. Gene Expression. Humans. Hyperplasia. Inhibin-beta Subunits / genetics. Inhibin-beta Subunits / metabolism. Male. Middle Aged. Proteoglycans / genetics. Proteoglycans / metabolism. Receptors, Transforming Growth Factor beta / genetics. Receptors, Transforming Growth Factor beta / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Statistics, Nonparametric. Steroid 17-alpha-Hydroxylase / genetics. Steroid 17-alpha-Hydroxylase / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17121532.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Follistatin; 0 / Proteoglycans; 0 / Receptors, Transforming Growth Factor beta; 0 / inhibin beta A subunit; 0 / inhibin-alpha subunit; 104625-48-1 / Activins; 145170-29-2 / betaglycan; 57285-09-3 / Inhibins; 93443-12-0 / Inhibin-beta Subunits; EC 1.14.99.9 / Steroid 17-alpha-Hydroxylase; EC 2.7.11.30 / Activin Receptors, Type II
  •  go-up   go-down


49. Willenberg HS, Haase M, Papewalis C, Schott M, Scherbaum WA, Bornstein SR: Corticotropin-releasing hormone receptor expression on normal and tumorous human adrenocortical cells. Neuroendocrinology; 2005;82(5-6):274-81
MedlinePlus Health Information. consumer health - Pheochromocytoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Corticotropin-releasing hormone receptor expression on normal and tumorous human adrenocortical cells.
  • Corticotropin-releasing hormone (CRH) is not only the principal regulator of the central hypothalamic-pituitary-adrenal (HPA) axis but also exerts direct actions on peripheral tissues.
  • We analyzed the expression of CRH receptors in microdissected preparations of normal human adrenal glands and in adrenocortical and adrenomedullary tumors, employing immunohistochemistry, quantitative RT-PCR of microdissected adrenal tissues, and in situ hybridization.
  • The effect of CRH on adrenal steroidogenesis was tested in adrenal cells.
  • In addition, we found a higher expression of CRH type-1 and 2 receptors mRNAs in preparations of adrenal cortices as compared to pheochromocytomas, a 6-fold increase in preparations of clinically unapparent adrenocortical adenomas, and a 10- to 60-fold increase in cortisol-producing adrenal adenomas.
  • Stimulation of the adrenal tumor cell line NCI-H295R with CRH elicited a 1.4-fold increase in DHEA secretion.
  • This result could be reproduced in a culture of primary human adrenocortical cells.
  • We conclude that adrenocortical cells exhibit a higher expression of functional CRH receptors than chromaffin cells and that CRH acts on adrenal DHEA production.
  • The data support the assertion of a direct action of CRH on human adrenocortical cells in addition to an intra-adrenal CRH receptor/adrenocorticotropin system.
  • Enhanced CRH1R expression may be involved in adrenocortical tumorigenesis.
  • [MeSH-major] Adrenal Cortex / chemistry. Adrenal Cortex Neoplasms / chemistry. Adrenocortical Adenoma / chemistry. Adrenocortical Carcinoma / chemistry. Pheochromocytoma / chemistry. Receptors, Corticotropin-Releasing Hormone / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16721033.001).
  • [ISSN] 0028-3835
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / CRF receptor type 1; 0 / CRF receptor type 2; 0 / RNA, Messenger; 0 / Receptors, Corticotropin-Releasing Hormone; 9015-71-8 / Corticotropin-Releasing Hormone
  •  go-up   go-down


50. Hosogi H, Nagayama S, Kanamoto N, Yoshizawa A, Suzuki T, Nakao K, Sakai Y: Biallelic APC inactivation was responsible for functional adrenocortical adenoma in familial adenomatous polyposis with novel germline mutation of the APC gene: report of a case. Jpn J Clin Oncol; 2009 Dec;39(12):837-46
Genetic Alliance. consumer health - Familial Polyposis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Biallelic APC inactivation was responsible for functional adrenocortical adenoma in familial adenomatous polyposis with novel germline mutation of the APC gene: report of a case.
  • Familial adenomatous polyposis (FAP) patients develop various extracolonic lesions, among which functional adrenocortical neoplasms are infrequent.
  • Furthermore, bilateral adrenocortical adenomas were detected, and functional analyses showed a hormonal secretion pattern consistent with Cushing's syndrome.
  • At 10 months post-operative with no detectable metastatic lesions, the residual colorectum and the larger, left adrenal gland were resected, and the hormonal hypersecretion was normalized.
  • Biallelic APC inactivation due to loss of the normal allele was evident in the adrenocortical adenoma.
  • Immunostaining for beta-catenin revealed diffuse cytoplasmic expression in resected tissues including adrenocortical adenoma.
  • Biallelic APC inactivation may play a role in developing cortisol-secreting adrenocortical adenoma in FAP patients.
  • [MeSH-major] Adenomatous Polyposis Coli / metabolism. Adenomatous Polyposis Coli Protein / genetics. Adrenocortical Adenoma / metabolism. Genes, APC / physiology

  • Genetic Alliance. consumer health - Familial Adenomatous Polyposis (FAP).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19684041.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein
  •  go-up   go-down


51. Joubert M, Louiset E, Rego JL, Contesse V, Kong LC, Benhaim A, Mittre H, Lefebvre H, Reznik Y, REHOS Study Group: Aberrant adrenal sensitivity to vasopressin in adrenal tumours associated with subclinical or overt autonomous hypercortisolism: is this explained by an overexpression of vasopressin receptors? Clin Endocrinol (Oxf); 2008 May;68(5):692-9
Hazardous Substances Data Bank. HYDROCORTISONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant adrenal sensitivity to vasopressin in adrenal tumours associated with subclinical or overt autonomous hypercortisolism: is this explained by an overexpression of vasopressin receptors?
  • OBJECTIVE: Abnormal responsiveness to arginine vasopressin (AVP) was previously observed in cortisol-producing adrenocortical tumours but the mechanism remains unclear.
  • The aim of this study was to characterize the effect of AVP on cortisol secretion from adrenocortical tumours compared to normal human adrenal gland.
  • DESIGN: A multicentre study based on pharmacological, molecular and immunohistochemical experiments performed in adenomatous and normal adrenal tissues.
  • PATIENTS: Twenty patients with adrenocortical adenomas and subclinical Cushing's syndrome (SCCS) or Cushing's syndrome (CS) were compared to six control normal subjects.
  • MEASUREMENTS: In vivo and in vitro cortisol response to vasopressin, vasopressin receptor subtype mRNA measurement by real-time polymerase chain reaction (RT-PCR), immunohistochemical localization of AVP and its V1a receptor in tumour and normal adrenal tissues.
  • AVP receptor subtype mRNA levels were similar in SCCS, CS cells and normal adrenal cells.
  • CONCLUSIONS: SCCS and CS adrenocortical tumours often exhibit in vivo and in vitro hyper-responsiveness to AVP, which is not related to vasopressin receptor overexpression, but may be explained by more efficient coupling pathways or by the indirect action of AVP through an autocrine/paracrine mechanism.
  • [MeSH-major] Adenoma / drug therapy. Adrenal Gland Neoplasms / drug therapy. Cushing Syndrome / drug therapy. Receptors, Vasopressin / biosynthesis. Vasoconstrictor Agents / pharmacology


52. Giordano TJ, Kuick R, Else T, Gauger PG, Vinco M, Bauersfeld J, Sanders D, Thomas DG, Doherty G, Hammer G: Molecular classification and prognostication of adrenocortical tumors by transcriptome profiling. Clin Cancer Res; 2009 Jan 15;15(2):668-76
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular classification and prognostication of adrenocortical tumors by transcriptome profiling.
  • PURPOSE: Our understanding of adrenocortical carcinoma (ACC) has improved considerably, yet many unanswered questions remain.
  • EXPERIMENTAL DESIGN: We did a whole genome gene expression study of a large cohort of adrenocortical tissues annotated with clinicopathologic data.
  • Using Affymetrix Human Genome U133 Plus 2.0 oligonucleotide arrays, transcriptional profiles were generated for 10 normal adrenal cortices (NC), 22 adrenocortical adenomas (ACA), and 33 ACCs.
  • RESULTS: The overall classification of adrenocortical tumors was recapitulated using principal component analysis of the entire data set.
  • Cluster analysis of the ACCs revealed two subtypes that reflected tumor proliferation, as measured by mitotic counts and cell cycle genes.
  • CONCLUSIONS: This study lays the foundation for the molecular classification and prognostication of adrenocortical tumors and also provides a rich source of potential diagnostic and prognostic markers.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Science. 1999 Oct 15;286(5439):531-7 [10521349.001]
  • [Cites] Am J Pathol. 1999 Oct;155(4):1039-45 [10514385.001]
  • [Cites] World J Surg. 2004 Sep;28(9):896-903 [15593464.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Mar;90(3):1819-29 [15613424.001]
  • [Cites] Nat Genet. 2005 Jun;37(6):579-83 [15920519.001]
  • [Cites] Eur J Endocrinol. 2005 Oct;153(4):477-87 [16189167.001]
  • [Cites] Oncogene. 2005 Oct 6;24(44):6646-56 [16007166.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517.001]
  • [Cites] Surgery. 2005 Dec;138(6):1087-94 [16360395.001]
  • [Cites] Eur J Endocrinol. 2006 Apr;154(4):587-98 [16556722.001]
  • [Cites] Nat Genet. 2006 Sep;38(9):1043-8 [16921376.001]
  • [Cites] J Clin Oncol. 2006 Nov 1;24(31):5079-90 [17075127.001]
  • [Cites] Nat Clin Pract Endocrinol Metab. 2006 Nov;2(11):632-41 [17082810.001]
  • [Cites] Nucleic Acids Res. 2007 Jan;35(Database issue):D760-5 [17099226.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Jan;92(1):148-54 [17062775.001]
  • [Cites] Cancer Res. 2007 Jan 15;67(2):600-8 [17234769.001]
  • [Cites] Mol Cancer Ther. 2007 Jan;6(1):1-12 [17237261.001]
  • [Cites] Endocr Rev. 2007 Feb;28(1):20-47 [16931767.001]
  • [Cites] Endocr Relat Cancer. 2007 Mar;14(1):13-28 [17395972.001]
  • [Cites] Exp Clin Endocrinol Diabetes. 2007 Mar;115(3):175-8 [17427106.001]
  • [Cites] APMIS. 2007 Apr;115(4):381-4 [17504308.001]
  • [Cites] Endocr Pathol. 2006 Winter;17(4):345-54 [17525483.001]
  • [Cites] Endocr Pathol. 2006 Winter;17(4):355-63 [17525484.001]
  • [Cites] N Engl J Med. 2007 Jun 7;356(23):2372-80 [17554118.001]
  • [Cites] Nat Clin Pract Oncol. 2007 Oct;4(10):591-602 [17898809.001]
  • [Cites] Mol Cancer Ther. 2008 Feb;7(2):425-31 [18281524.001]
  • [Cites] Endocr J. 2008 Mar;55(1):49-55 [18187873.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Apr;93(4):1442-9 [18198226.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10869-74 [11553815.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Genes Chromosomes Cancer. 2000 Jun;28(2):145-52 [10824999.001]
  • [Cites] Am J Pathol. 2001 Oct;159(4):1231-8 [11583950.001]
  • [Cites] Nature. 2002 Jan 31;415(6871):530-6 [11823860.001]
  • [Cites] J Clin Oncol. 2002 Feb 15;20(4):941-50 [11844815.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Mar;87(3):1170-6 [11889182.001]
  • [Cites] Endocr Pathol. 2001 Winter;12(4):397-406 [11914473.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Jul;87(7):3467-74 [12107267.001]
  • [Cites] Nat Med. 2002 Aug;8(8):816-24 [12118244.001]
  • [Cites] Am J Surg Pathol. 2002 Dec;26(12):1612-9 [12459628.001]
  • [Cites] Am J Pathol. 2003 Feb;162(2):521-31 [12547710.001]
  • [Cites] Oncogene. 2003 Oct 2;22(43):6810-8 [14555994.001]
  • [Cites] Am J Pathol. 2003 Nov;163(5):1985-95 [14578198.001]
  • [Cites] Eur J Endocrinol. 2004 Jun;150(6):809-17 [15191351.001]
  • [Cites] Horm Metab Res. 2004 Jun;36(6):397-405 [15241731.001]
  • [Cites] Am J Surg Pathol. 1984 Mar;8(3):163-9 [6703192.001]
  • [Cites] Am J Surg Pathol. 1989 Mar;13(3):202-6 [2919718.001]
  • [Cites] Cancer Res. 1996 Sep 15;56(18):4219-23 [8797595.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14863-8 [9843981.001]
  • [Cites] J Mol Endocrinol. 1999 Aug;23(1):23-32 [10425444.001]
  • [Cites] Bioinformatics. 2004 Nov 22;20(17):3246-8 [15180930.001]
  • (PMID = 19147773.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA046592-209023; United States / NCI NIH HHS / CA / CA046592-219023; United States / NCI NIH HHS / CA / P30 CA046592; United States / NCI NIH HHS / CA / 5 P30 CA46592; United States / NCI NIH HHS / CA / CA046592-199023; United States / NCI NIH HHS / CA / P30 CA046592-219023; United States / NCI NIH HHS / CA / P30 CA046592-199023; United States / NCI NIH HHS / CA / P30 CA046592-209023
  • [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 / Cyclin E
  • [Other-IDs] NLM/ NIHMS78831; NLM/ PMC2629378
  •  go-up   go-down


53. Bielinska M, Kiiveri S, Parviainen H, Mannisto S, Heikinheimo M, Wilson DB: Gonadectomy-induced adrenocortical neoplasia in the domestic ferret (Mustela putorius furo) and laboratory mouse. Vet Pathol; 2006 Mar;43(2):97-117
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • 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.
  • [MeSH-major] Adrenal Cortex Neoplasms / veterinary. Castration / veterinary. Ferrets

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


54. Szabó PM, Wiener Z, Tömböl Z, Kovács A, Pócza P, Horányi J, Kulka J, Riesz P, Tóth M, Patócs A, Gaillard RC, Falus A, Rácz K, Igaz P: Differences in the expression of histamine-related genes and proteins in normal human adrenal cortex and adrenocortical tumors. Virchows Arch; 2009 Aug;455(2):133-42
Hazardous Substances Data Bank. HISTAMINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differences in the expression of histamine-related genes and proteins in normal human adrenal cortex and adrenocortical tumors.
  • Histamine is involved in the pathogenesis of several tumors; however, there are no data on its possible involvement in human adrenocortical tumorigenesis.
  • The expression of genes and proteins involved in the biosynthesis (histidine decarboxylase, HDC), action (histamine receptors: HRH1-HRH4), and metabolism of histamine is largely unknown both in the normal human adrenal cortex and in adrenocortical tumors.
  • In this study, we examined the expression of histamine-related genes and proteins and histamine content in normal adrenal cortex, benign adrenocortical adenomas, and malignant adrenocortical cancer (ACC).
  • We found that all proteins involved in histamine biosynthesis and action are present both in the normal adrenal cortex and in the tumors studied.
  • HDC expression and histamine content was highest in the normal tissues and lower in benign tumors, whereas it was significantly less in ACCs.
  • Adrenocortical tumorigenesis might, thus, be characterized by reduced histamine biosynthesis; furthermore, different adrenocortical tumor subtypes may show unique histamine receptor expression profiles.
  • [MeSH-major] Adrenal Cortex / metabolism. Adrenal Cortex Neoplasms / metabolism. Adrenocortical Adenoma / metabolism. Histamine / metabolism. Histidine Decarboxylase / metabolism. Receptors, Histamine / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Brain Res. 1985 Jul 29;339(2):393-6 [3896403.001]
  • [Cites] Am J Pathol. 1993 Apr;142(4):965-74 [7682764.001]
  • [Cites] Cancer Lett. 1995 Feb 10;89(1):23-8 [7882298.001]
  • [Cites] Histol Histopathol. 1997 Oct;12(4):1081-9 [9302569.001]
  • [Cites] Endocr Relat Cancer. 2007 Mar;14(1):13-28 [17395972.001]
  • [Cites] Digestion. 1999 Nov-Dec;60(6):522-7 [10545721.001]
  • [Cites] Arch Pathol Lab Med. 1985 Apr;109(4):357-60 [3157360.001]
  • [Cites] Br J Pharmacol. 1991 Dec;104(4):839-46 [1725765.001]
  • [Cites] J Steroid Biochem Mol Biol. 1991;40(1-3):381-9 [1659878.001]
  • [Cites] Trends Pharmacol Sci. 2005 Sep;26(9):462-9 [16054239.001]
  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
  • [Cites] Br J Clin Pharmacol. 1992 Oct;34(4):322-7 [1457266.001]
  • [Cites] Oncologist. 2008 May;13(5):548-61 [18515740.001]
  • [Cites] Cancer Biol Ther. 2008 Jan;7(1):28-35 [17932461.001]
  • [Cites] Eur J Endocrinol. 2005 Aug;153(2):307-15 [16061838.001]
  • [Cites] J Pharmacol Sci. 2005 Jan;97(1):116-23 [15655289.001]
  • [Cites] J Physiol. 1922 Dec 22;57(1-2):82-99 [16993603.001]
  • [Cites] Biochem Biophys Res Commun. 1995 Jun 15;211(2):570-7 [7794271.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Mar;87(3):1211-6 [11889190.001]
  • [Cites] Eur J Cell Biol. 2008 Apr;87(4):227-36 [18258331.001]
  • [Cites] Jpn J Pharmacol. 1997 Oct;75(2):115-21 [9414025.001]
  • [Cites] Am J Physiol Endocrinol Metab. 2005 Dec;289(6):E1058-63 [16076876.001]
  • [Cites] Int Immunol. 2007 Jan;19(1):51-8 [17118966.001]
  • [Cites] Inflamm Res. 1995 Apr;44 Suppl 1:S48-9 [8520996.001]
  • [Cites] Methods Mol Biol. 2006;315:13-34 [16110146.001]
  • [Cites] Neuroscience. 1992;47(4):999-1007 [1374544.001]
  • [Cites] Inflammopharmacology. 2005;13(1-3):281-9 [16259747.001]
  • [Cites] Eur J Pharmacol. 2006 Mar 8;533(1-3):69-76 [16448645.001]
  • [Cites] Horm Res. 2009 Jan;71 Suppl 1:99-104 [19153517.001]
  • [Cites] Pathol Int. 2004 Jun;54(6):408-12 [15144399.001]
  • [Cites] J Steroid Biochem Mol Biol. 2006 Oct;101(2-3):87-96 [16891114.001]
  • [Cites] Methods Mol Biol. 2006;315:63-76 [16110149.001]
  • [Cites] Pharmacol Ther. 2003 Apr;98(1):1-34 [12667886.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Dec;87(12):5367-84 [12466322.001]
  • [Cites] Mod Pathol. 2003 Jun;16(6):591-7 [12808065.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Jan;92(1):148-54 [17062775.001]
  • [Cites] Cancer Res. 2008 Mar 15;68(6):1997-2005 [18339882.001]
  • [Cites] Rheumatol Int. 2005 Dec;26(2):173-8 [15986084.001]
  • [Cites] Inflamm Res. 1997 Mar;46 Suppl 1:S57-8 [9098764.001]
  • [Cites] J Clin Endocrinol Metab. 2006 May;91(5):1943-9 [16464939.001]
  • [Cites] Mod Pathol. 2003 Jan;16(1):72-8 [12527716.001]
  • [Cites] Nat Med. 1995 Dec;1(12):1243-4 [7489398.001]
  • [Cites] J Pharmacol Sci. 2003 Nov;93(3):321-30 [14646250.001]
  • [Cites] Curr Allergy Asthma Rep. 2008 Mar;8(1):21-7 [18377770.001]
  • [Cites] Trends Immunol. 2001 Dec;22(12):648-52 [11738976.001]
  • (PMID = 19568768.001).
  • [ISSN] 1432-2307
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / HRH4 protein, human; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Histamine; 0 / Receptors, Histamine H1; 0 / Receptors, Histamine H2; 0 / Receptors, Histamine H3; 820484N8I3 / Histamine; EC 4.1.1.22 / Histidine Decarboxylase
  •  go-up   go-down


55. Blanes A, Diaz-Cano SJ: DNA and kinetic heterogeneity during the clonal evolution of adrenocortical proliferative lesions. Hum Pathol; 2006 Oct;37(10):1295-303

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DNA and kinetic heterogeneity during the clonal evolution of adrenocortical proliferative lesions.
  • Monoclonal adrenocortical lesions show inverse correlation between proliferation and apoptosis, with proliferation being the single most important criterion of malignancy in adrenal lesions.
  • No study yet has evaluated the variability of proliferation regarding the clonal pattern and diagnosis in adrenocortical nodular hyperplasias (ACNHs), adrenocortical adenomas (ACAs), and adrenocortical carcinomas (ACCs).
  • Statistics included analysis of variance/Student t tests regarding the clonal patterns and diagnosis.
  • Only tetraploid percentage (P = .0496) and 5cER (P = .0352) distinguished polyclonal (3.64 +/- 2.20 and 0.14 +/- 0.15) from monoclonal (7.25 +/- 7.52 and 1.00 +/- 1.74) benign lesions.
  • Cell kinetic heterogeneity is the hallmark of adrenocortical neoplasms: tetraploid/hypertetraploid cell accumulation characterizes monoclonal lesions (suggesting nondisjunctional mitoses), whereas heterogeneously distributed mitotic figures and decreased diploid percentage define ACCs.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics. Adrenocortical Carcinoma / genetics. DNA, Neoplasm / analysis
  • [MeSH-minor] Apoptosis. Cell Nucleus / genetics. Cell Nucleus / pathology. Cell Proliferation. Clone Cells. Disease Progression. Flow Cytometry. Humans. Hyperplasia. Image Cytometry. Ki-67 Antigen / metabolism. Kinetics. Mitotic Index. Polyploidy. X Chromosome Inactivation / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16949934.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Ki-67 Antigen
  •  go-up   go-down


56. Alevizaki M, Stratakis CA: Multiple endocrine neoplasias: advances and challenges for the future. J Intern Med; 2009 Jul;266(1):1-4
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Several important advances have been made over the last 2 years, since the last international workshop on multiple endocrine neoplasias (MENs) that was held in Marseilles, France (MEN2006).
  • The series of articles that are included in this issue summarize the most important of these advances as they were presented in Delphi, Greece, during the 11th International Workshop on MENs, September 25-27, 2008 (MEN2008).
  • This editorial summarizes some of these advances: the identification of the AIP, and the PDE11A and PDE8B genes by genome-wide association (GWA) studies as predisposing genes for pituitary and adrenal tumours, respectively, the discovery of p27 mutations in a new form of MEN similar to MEN type 1 (MEN 1) that is now known as MEN 4, the molecular investigations of Carney triad (CT), a disorder that associates paragangliomas (PGLs), gastrointestinal stromal tumour (GISTs), and pulmonary chondromas (PCH) with pheochromocytomas and adrenocortical adenomas and other lesions, and the molecular elucidation of the association of GISTs with paragangliomas (Carney-Stratakis syndrome) that is now known to be because of SDHB, SDHC, and SDHD mutations.
  • Indeed, new advances in the preventive diagnosis and molecular treatment of MEN 1 and MEN 2, respectively, continued unabated, and an update on this front was also presented at MEN2008 and is included in this issue.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Ann Oncol. 2001;12 Suppl 2:S3-11 [11762348.001]
  • [Cites] J Intern Med. 2009 Jul;266(1):126-40 [19522831.001]
  • [Cites] N Engl J Med. 2002 May 9;346(19):1459-66 [12000816.001]
  • [Cites] J Intern Med. 2005 Jan;257(1):2-5 [15606371.001]
  • [Cites] Horm Metab Res. 2005 Jun;37(6):343-6 [16001325.001]
  • [Cites] Endocr Rev. 2005 Aug;26(5):615-61 [15632315.001]
  • [Cites] Science. 2006 May 26;312(5777):1228-30 [16728643.001]
  • [Cites] Nat Genet. 2006 Jul;38(7):794-800 [16767104.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Oct 17;103(42):15558-63 [17030811.001]
  • [Cites] Cancer Res. 2006 Dec 15;66(24):11571-5 [17178847.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Aug;92(8):2938-43 [17535989.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Aug;92(8):3321-5 [17519308.001]
  • [Cites] N Engl J Med. 2007 Sep 6;357(10):1054-6 [17804857.001]
  • [Cites] Eur J Hum Genet. 2008 Jan;16(1):79-88 [17667967.001]
  • [Cites] N Engl J Med. 2008 Feb 14;358(7):750-2 [18272904.001]
  • [Cites] J Intern Med. 2009 Jul;266(1):5-18 [19522822.001]
  • [Cites] J Intern Med. 2009 Jul;266(1):19-42 [19522823.001]
  • [Cites] J Intern Med. 2009 Jul;266(1):43-52 [19522824.001]
  • [Cites] J Intern Med. 2009 Jul;266(1):53-9 [19522825.001]
  • [Cites] J Intern Med. 2009 Jul;266(1):60-8 [19522826.001]
  • [Cites] J Intern Med. 2009 Jul;266(1):69-83 [19522827.001]
  • [Cites] J Intern Med. 2009 Jul;266(1):84-98 [19522828.001]
  • [Cites] J Intern Med. 2009 Jul;266(1):99-113 [19522829.001]
  • [Cites] J Intern Med. 2009 Jul;266(1):114-25 [19522830.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Dec;86(12):5658-71 [11739416.001]
  • (PMID = 19522821.001).
  • [ISSN] 1365-2796
  • [Journal-full-title] Journal of internal medicine
  • [ISO-abbreviation] J. Intern. Med.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / Z01 HD000642; United States / Intramural NIH HHS / / Z01 HD000642-10; United States / NICHD NIH HHS / HD / Z01-HD-000642-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Other-IDs] NLM/ NIHMS307447; NLM/ PMC3138202
  •  go-up   go-down


57. Pawlikowski M, Winczyk K, Sledź B: Immunohistochemical detection of angiotensin receptors AT1 and AT2 in adrenal tumors. Folia Histochem Cytobiol; 2008;46(1):51-5
Hazardous Substances Data Bank. HYDROCORTISONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical detection of angiotensin receptors AT1 and AT2 in adrenal tumors.
  • Angiotensin II is well known to affect the adrenal cell growth and function.
  • Angiotensin receptors AT1 and AT2 were found to be present in the normal adrenal gland.
  • However, the data on the expression of the angiotensin receptors in the adrenal tumors are very scarce.
  • To overcome this gap, the paraffin sections of the adrenal cortical tumors and of pheochromocytomas from the archival material were immunostained with antibodies raised against AT1 (sc-1173) and AT2 (sc-9040) receptor proteins.
  • In hyperplasia of the adrenal cortex and in benign adrenocortical adenomas, both functioning and non-functioning, the AT1 immunostaining was present mainly in the cell membranes.
  • A positive immunoreaction was also found in the subpopulation of cell nuclei and within the cytoplasm.
  • In the adrenal cancer, as well as in pheochromocytomas, neither cell membranes nor cell nuclei were immunostained with anti-AT1 antibody.
  • Our data indicates that the expression of AT1 receptors is altered in adrenal cancer and in pheochromocytomas.

  • MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18296263.001).
  • [ISSN] 1897-5631
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Receptor, Angiotensin, Type 1; 0 / Receptor, Angiotensin, Type 2; 4964P6T9RB / Aldosterone; WI4X0X7BPJ / Hydrocortisone
  •  go-up   go-down


58. Soon PS, Libe R, Benn DE, Gill A, Shaw J, Sywak MS, Groussin L, Bertagna X, Gicquel C, Bertherat J, McDonald KL, Sidhu SB, Robinson BG: Loss of heterozygosity of 17p13, with possible involvement of ACADVL and ALOX15B, in the pathogenesis of adrenocortical tumors. Ann Surg; 2008 Jan;247(1):157-64
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


59. Slater EP, Diehl SM, Langer P, Samans B, Ramaswamy A, Zielke A, Bartsch DK: Analysis by cDNA microarrays of gene expression patterns of human adrenocortical tumors. Eur J Endocrinol; 2006 Apr;154(4):587-98
Hazardous Substances Data Bank. HYDROCORTISONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis by cDNA microarrays of gene expression patterns of human adrenocortical tumors.
  • OBJECTIVES: Adrenocortical carcinoma (ACC) is a rare malignant neoplasm with extremely poor prognosis.
  • The molecular mechanisms of adrenocortical tumorigenesis are still not well understood.
  • The comparative analysis by cDNA microarrays of gene-expression patterns of benign and malignant adrenocortical tumors allows us to identify new tumor-suppressor genes and proto-oncogenes underlying adrenocortical tumorigenesis.
  • DESIGN AND METHODS: Total RNA from fresh-frozen tissue of 10 ACC and 10 benign adrenocortical adenomas was isolated after histologic confirmation of neoplastic cellularity of at least 85%.
  • The reference consisted of pooled RNA of 10 normal adrenal cortex samples.
  • RESULTS: The comparative analysis of gene expression revealed many genes with more than fourfold expression difference between ACC and normal tissue (42 genes), cortical adenoma and normal tissue (11 genes), and ACC and cortical adenoma (21 genes) respectively.
  • As confirmed by real-time PCR, the IGF2 gene was significantly upregulated in ACCs versus cortical adenomas and normal cortical tissue.
  • Genes that were downregulated in adrenocortical tumors included chromogranin B and early growth response factor 1.
  • CONCLUSIONS: Comprehensive expression profiling of adrenocortical tumors by the cDNA microarray technique is a very powerful tool to elucidate the molecular steps associated with the tumorigenesis of these ill-defined neoplasms.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16556722.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 4964P6T9RB / Aldosterone; WI4X0X7BPJ / Hydrocortisone
  •  go-up   go-down


60. Gaujoux S, Tissier F, Groussin L, Libé R, Ragazzon B, Launay P, Audebourg A, Dousset B, Bertagna X, Bertherat J: Wnt/beta-catenin and 3',5'-cyclic adenosine 5'-monophosphate/protein kinase A signaling pathways alterations and somatic beta-catenin gene mutations in the progression of adrenocortical tumors. J Clin Endocrinol Metab; 2008 Oct;93(10):4135-40

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Wnt/beta-catenin and 3',5'-cyclic adenosine 5'-monophosphate/protein kinase A signaling pathways alterations and somatic beta-catenin gene mutations in the progression of adrenocortical tumors.
  • BACKGROUND: The Wnt/beta-catenin and cAMP signaling pathways play an important role in adrenal cortex tumorigenesis.
  • Somatic activating mutations of the beta-catenin gene (CTNNB1) are the most frequent genetic defects identified both in adrenocortical adenomas (ACAs) and adrenocortical cancers (ACCs).
  • PRKAR1A mutations leading to cAMP pathway dysregulation are observed in primary pigmented nodular adrenocortical diseases (PPNADs) and some sporadic ACAs.
  • OBJECTIVE: The objective of the investigation was to study Wnt/beta-catenin dysregulation in adrenocortical tumors (ACTs) with cAMP pathway genetic alteration and search for secondary CTNNB1 somatic mutations in heterogeneous tumors.
  • In addition, the occurrence as an additional hit of a CTNNB1 somatic mutation is associated with larger or more aggressive ACTs.
  • This underlines the importance of the Wnt/beta-catenin pathway in adrenal cortex tumorigenesis and the importance of genetic accumulation in the progression of ACTs.
  • [MeSH-major] Adenoma / genetics. Adrenal Cortex Neoplasms / genetics. Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / genetics. Mutation. Signal Transduction / genetics. Wnt Proteins / genetics. beta Catenin / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Cyclic AMP / metabolism. DNA Mutational Analysis. Disease Progression. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Neoplasm Invasiveness. Tumor Burden / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18647815.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human; 0 / Wnt Proteins; 0 / beta Catenin; E0399OZS9N / Cyclic AMP
  •  go-up   go-down


61. Iwase K, Nagasaka A, Kato K, Itoh A, Jimbo S, Hibi Y, Kobayashi N, Yamamoto H, Seko T, Miura K: Cu/Zn- and Mn-superoxide dismutase distribution and concentration in adrenal tumors. J Surg Res; 2006 Sep;135(1):150-5
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cu/Zn- and Mn-superoxide dismutase distribution and concentration in adrenal tumors.
  • The tissue distribution of Cu/Zn- and Mn-superoxide dismutases (SOD) in adrenal tumors was studied by an immunohistochemical technique, and the concentrations of both SODs were measured by a sensitive sandwich enzyme immunoassay technique.
  • In the normal adrenal gland, both Cu/Zn- and Mn-SODs were localized predominantly in the reticular zone of the cortex.
  • Cu/Zn-SOD was stained clearly in the inner fascicular zone of the cortex, but not in the medulla, whereas Mn-SOD was stained weakly in the medulla.
  • In different adrenal tumors, the localization of both stained SODs reflected the origin of the tumor cell.
  • Thus, in one section of a pheochromocytoma only Mn-SOD was stained clearly.
  • The concentrations of both SODs in the tissues of medullary tumors were lower than those in the normal adrenal gland and adrenocortical adenomas.
  • The concentration of Cu/Zn-SOD in the tumor tissue of Cushing's syndrome adenoma was higher, and that of Mn-SOD was lower than the concentrations in the normal adrenal gland.
  • The ratio of the tissue concentrations of Mn-SOD to Cu/Zn-SOD was lower in adrenal medullary tumors and Cushing's syndrome adenomas than in the normal adrenal gland and primary aldosteronism adenomas, indicating the predominance of Cu/Zn-SOD in the former, and Mn-SOD in the latter.
  • These data suggest that the localization of Cu/Zn- and Mn-SODs in adrenal tissues reflects the specificity of the adrenal cells that produce the tissue-specific hormones.
  • An investigation of changes in these enzymes in adrenal tumors may also provide useful information on adrenal tumor cell differentiation.
  • [MeSH-major] Adrenal Cortex / enzymology. Adrenal Cortex Neoplasms / metabolism. Adrenocortical Adenoma / metabolism. Superoxide Dismutase / metabolism
  • [MeSH-minor] Cell Differentiation. Ganglioneuroma / metabolism. Ganglioneuroma / pathology. Humans. Immunoenzyme Techniques. Immunohistochemistry. Neuroblastoma / metabolism. Neuroblastoma / pathology. Pheochromocytoma / metabolism. Pheochromocytoma / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16780879.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.15.1.1 / Superoxide Dismutase
  •  go-up   go-down


62. Fassnacht M, Weismann D, Ebert S, Adam P, Zink M, Beuschlein F, Hahner S, Allolio B: AKT is highly phosphorylated in pheochromocytomas but not in benign adrenocortical tumors. J Clin Endocrinol Metab; 2005 Jul;90(7):4366-70
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] AKT is highly phosphorylated in pheochromocytomas but not in benign adrenocortical tumors.
  • OBJECTIVE: The objective of this study was the investigation of the role of AKT in the pathogenesis of pheochromocytomas and adrenocortical tumors.
  • DESIGN, SETTING, AND PARTICIPANTS: Total AKT and phosphorylated AKT (pAKT) in 15 pheochromocytomas, nine aldosterone-producing adenomas, nine cortisol-producing adenomas, eight adrenocortical carcinomas (ACC), and 15 normal adrenals were investigated by Western blot analysis.
  • Immunohistochemistry for total AKT and pAKT was performed in pheochromocytomas (n = 8), ACC (n = 4), and normal adrenal glands (n = 2).
  • MAIN OUTCOME MEASURES: Determination of pAKT/total AKT ratio in adrenal tissues was the main outcome.
  • The pAKT/AKT ratio was significantly increased in pheochromocytomas (338 +/- 49% vs. 100 +/- 11%) but not in ACC, aldosterone-producing adenomas, and cortisol-producing adenomas.
  • CONCLUSION: Our findings provide evidence for increased activation of AKT in pheochromocytomas but not in adrenocortical adenomas.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenal Gland Neoplasms / metabolism. Pheochromocytoma / metabolism. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins / metabolism

  • MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.
  • MedlinePlus Health Information. consumer health - Pheochromocytoma.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15855265.001).
  • [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 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Proteins; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
  •  go-up   go-down


63. Nishimoto K, Nakagawa K, Li D, Kosaka T, Oya M, Mikami S, Shibata H, Itoh H, Mitani F, Yamazaki T, Ogishima T, Suematsu M, Mukai K: Adrenocortical zonation in humans under normal and pathological conditions. J Clin Endocrinol Metab; 2010 May;95(5):2296-305
Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenocortical zonation in humans under normal and pathological conditions.
  • CONTEXT: Aldosterone synthase (CYP11B2) and steroid 11 beta-hydroxylase (CYP11B1) catalyze the terminal steps for aldosterone and cortisol syntheses, respectively, thereby determining the functional differentiation of human adrenocortical cells.
  • OBJECTIVE: The objective of the study was to determine the localization of CYP11B2 and -B1 in human adrenal specimens by using developed antibodies capable of distinguishing the two enzymes from each other.
  • Adrenocortical cells lacking both enzymes were observed in the outer cortical regions.
  • In addition to conventional zonation, we found a variegated zonation consisting of a subcapsular cell cluster expressing CYP11B2, which we termed aldosterone-producing cell cluster, and a CYP11B1-expressing area.
  • Aldosterone-producing adenomas differed in cell populations expressing CYP11B2 from one another, whereas CYP11B1-expressing and double-negative cells were also intermingled.
  • Adenomas from patients with Cushing's syndrome expressed CYP11B1 entirely but not CYP11B2, resulting in atrophic nontumor glands.
  • The nontumor portions of both types of adenomas bore frequently one or more aldosterone-producing cell clusters, which sustained CYP11B2 expression markedly under the conditions of the suppressed renin-angiotensin system.
  • CONCLUSION: Immunohistochemistry of the human normal adrenal cortex for CYP11B2 and CYP11B1 revealed a variegated zonation with cell clusters constitutively expressing CYP11B2.
  • This technique may provide a pathological confirmatory diagnosis of adrenocortical adenomas.
  • [MeSH-major] Adrenal Cortex / pathology. Adrenal Cortex / physiology
  • [MeSH-minor] Aldosterone / metabolism. Amino Acid Sequence. Animals. Antibodies. Carcinoma, Renal Cell / enzymology. Corticosterone / metabolism. Cushing Syndrome / enzymology. Cytochrome P-450 CYP11B2 / deficiency. Cytochrome P-450 CYP11B2 / metabolism. Humans. Kidney Neoplasms / enzymology. Mammals. Peptide Fragments / chemistry. Rabbits. Reference Values. Rodentia. Steroid 11-beta-Hydroxylase / metabolism. Zona Fasciculata / enzymology. Zona Glomerulosa / enzymology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20200334.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Peptide Fragments; 4964P6T9RB / Aldosterone; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase; W980KJ009P / Corticosterone
  •  go-up   go-down


64. Groussin L, Cazabat L, René-Corail F, Jullian E, Bertherat J: Adrenal pathophysiology: lessons from the Carney complex. Horm Res; 2005;64(3):132-9
Genetic Alliance. consumer health - Carney Complex.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenal pathophysiology: lessons from the Carney complex.
  • Adrenocorticotropic hormone independent Cushing's syndrome due to primary pigmented nodular adrenocortical disease (PPNAD) is a main characteristic of CNC.
  • PPNAD is a very rare cause of Cushing's syndrome due to a primary bilateral adrenal defect that can be also observed in some patients without other CNC manifestations nor familial history.
  • Interestingly, patients with isolated PPNAD and no familial history of CNC can also present a germline de novo mutation of PRKAR1A.
  • Somatic mutations of PRKAR1A have been found in PPNAD as a mechanism of inactivation of the wild-type allele, in a patient already presenting a germline mutation, and in a subset of sporadic secreting adrenocortical adenomas with clinical, hormonal, and pathological features quite similar to PPNAD.
  • This review will summarize the recent findings on CNC from the perspective of the pathophysiology of adrenal Cushing's syndrome and PPNAD.
  • [MeSH-major] Adrenal Cortex Diseases / physiopathology. Adrenal Glands / physiopathology. Multiple Endocrine Neoplasia / physiopathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2005 S. Karger AG, Basel.
  • (PMID = 16192737.001).
  • [ISSN] 0301-0163
  • [Journal-full-title] Hormone research
  • [ISO-abbreviation] Horm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human; 0 / Proteins; E0399OZS9N / Cyclic AMP; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
  • [Number-of-references] 31
  •  go-up   go-down


65. Kiiveri S, Liu J, Arola J, Heikkilä P, Kuulasmaa T, Lehtonen E, Voutilainen R, Heikinheimo M: Transcription factors GATA-6, SF-1, and cell proliferation in human adrenocortical tumors. Mol Cell Endocrinol; 2005 Apr 15;233(1-2):47-56
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transcription factors GATA-6, SF-1, and cell proliferation in human adrenocortical tumors.
  • Transcription factor GATA-6 is expressed in fetal and adult human adrenal cortex and has been suggested to have a role in adrenal androgen synthesis.
  • In other tissues GATA-6 has been linked to the cell cycle regulation and the dedifferentiation of carcinoma cells.
  • GATA-6 has been shown to be downregulated in mouse adrenocortical tumors, but has not been studied in human adrenocortical tumors in detail.
  • We have now analyzed GATA-6 expression in 20 human adrenocortical adenomas and 16 carcinomas using Northern blot analysis and immunohistochemistry.
  • GATA-6 mRNA and protein expression was remarkably diminished in adrenocortical carcinomas as compared to normal adrenal cortex and adenomas (p<0.05).
  • Steroidogenic factor 1 (SF-1) has been functionally linked to GATA-6, and the expression of these two factors correlated in the adrenal tumors.
  • In contrast to GATA-6, we found upregulated cyclin-dependent kinase inhibitor p21 and proliferation marker Ki67 in adrenocortical carcinomas indicating that GATA-6 is not linked to cell proliferation in human adrenal tumors.
  • Taken together, the present and earlier results link GATA-6 to adrenocortical steroidogenesis and to the benign adrenocortical phenotype.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenocortical Adenoma / metabolism. Adrenocortical Carcinoma / metabolism. DNA-Binding Proteins / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Adrenal Glands / chemistry. Adrenal Glands / cytology. Adult. Aged. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Cell Cycle Proteins / genetics. Cell Cycle Proteins / metabolism. Cell Proliferation. Child. Child, Preschool. Cyclin-Dependent Kinase Inhibitor p21. Female. GATA6 Transcription Factor. Homeodomain Proteins. Humans. Infant. Ki-67 Antigen / genetics. Ki-67 Antigen / metabolism. Male. Middle Aged. RNA, Messenger / analysis. RNA, Messenger / metabolism. Receptors, Cytoplasmic and Nuclear. Steroidogenic Factor 1. Up-Regulation

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15767045.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDKN1A protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / DNA-Binding Proteins; 0 / GATA6 Transcription Factor; 0 / GATA6 protein, human; 0 / Homeodomain Proteins; 0 / Ki-67 Antigen; 0 / NR5A1 protein, human; 0 / RNA, Messenger; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Steroidogenic Factor 1; 0 / Transcription Factors; 0 / steroidogenic factor 1, mouse
  •  go-up   go-down


66. Bertherat J, Gimenez-Roqueplo AP: New insights in the genetics of adrenocortical tumors, pheochromocytomas and paragangliomas. Horm Metab Res; 2005 Jun;37(6):384-90
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New insights in the genetics of adrenocortical tumors, pheochromocytomas and paragangliomas.
  • Recent advances in the molecular genetic of adrenal tumors give new insights in the pathophysiology of these neoplasms in both hereditary and sporadic cases.
  • The practice of genetic counselling in patients with adrenal tumors have been recently changed by the identification and the understanding of new specific hereditary cancer susceptibility syndromes.
  • In the case of sporadic adrenocortical tumors these progress also offer new prognosis predictors.
  • The genetic predisposition to adrenocortical cancer in children has been well established in the Li-Fraumeni and Beckewith-Wiedeman syndromes due to germline p53 mutation located at 17p13 and dysregulation of the imprinted IGF-2 locus at 11p15, respectively.
  • Adrenocortical tumors are also observed in Multiple Endocrine Neoplasia type I syndrome.
  • Cushing's syndrome due to primary pigmented nodular adrenocortical disease have been observed in patients with germline PRKAR1A inactivating mutations.
  • Interestingly allelic loss at 17p13 and 11p15 have been observed in sporadic adrenocortical cancer and somatic PRKAR1A mutations in secreting adrenocortical adenomas.
  • The potential interest of these finding for the diagnosis of these tumors will be discussed.
  • Up to date, four diagnosis of familal disease (multiple endocrine neoplasia type II, von Hippel Lindau disease, neurofibromatosis type 1 and hereditary paraganglioma) should be discussed and causative mutations in six different phaechomocytoma susceptibility genes (RET, VHL, NF1, SDHB, SDHD, SDHC) could be identified.
  • We will suggest guidelines for the practice of the phaeochomocytoma genetic testing in the patients and their families, and for an early detection of tumors in the patients or in individuals determined to be at-risk of disease by the presymptomatic genetic testing.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Gene Expression Regulation, Neoplastic / genetics. Paraganglioma / genetics. Pheochromocytoma / genetics

  • MedlinePlus Health Information. consumer health - Pheochromocytoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16001332.001).
  • [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; Review
  • [Publication-country] Germany
  • [Number-of-references] 53
  •  go-up   go-down


67. Orhan D, Kale G, Cağlar M, Göğüş S, Karaağaoğlu E: Histone mRNA in situ hybridization and Ki 67 immunohistochemistry in pediatric adrenocortical tumors. Virchows Arch; 2006 May;448(5):591-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Histone mRNA in situ hybridization and Ki 67 immunohistochemistry in pediatric adrenocortical tumors.
  • Adrenocortical tumors in the pediatric population are rare.
  • Classification of these tumors as adenomas or carcinomas using histological criteria is often difficult.
  • Immunohistochemical expressions of proliferative markers are currently under investigation for utilization in the differential diagnosis and prediction of clinical outcomes.
  • The value of histone proteins as prognostic markers in adrenocortical tumors has not yet been elucidated.
  • We evaluated the histological features, immunohistochemical staining of Ki 67, and in situ hybridization for histone mRNA in 30 pediatric adrenocortical tumors.
  • Using the classification proposed by Weiss, 19 tumors were classified as carcinomas and 11 as adenomas.
  • Ki 67 and histone mRNA labeling indices (LIs, the percentage of Ki 67-positive and histone mRNA-positive tumor cells, respectively) were significantly higher in carcinomas than in adenomas (Ki 67 LI was 14.62+/-5.79 in adenomas and 20.35+/-6.23 in carcinomas, p=0.02.
  • Histone mRNA LI was 1.73+/-1.71 in adenomas and 6.62+/-2.28 in carcinomas, p=0.00).
  • The cut off point for the diagnosis of malignancy was found to be 14.55 for Ki 67 LI and 5.75 for histone mRNA LI.
  • We concluded that the proliferative activity of the tumor assessed by Ki 67 and histone mRNA may assist in differentiating adrenocortical adenomas and carcinomas.
  • In addition, our results suggest that the most reliable parameter to predict prognosis in pediatric adrenocortical tumors is the histone mRNA LI.
  • [MeSH-major] Adrenocortical Adenoma / diagnosis. Adrenocortical Carcinoma / diagnosis. Biomarkers, Tumor / analysis. Histones / metabolism. Ki-67 Antigen / metabolism. RNA, Messenger / analysis
  • [MeSH-minor] Child. Diagnosis, Differential. Humans. Immunohistochemistry. In Situ Hybridization. Prognosis. ROC Curve

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer. 1986 Jun 1;57(11):2235-7 [3697922.001]
  • [Cites] Anat Rec. 2002 Apr 1;266(4):234-40 [11920386.001]
  • [Cites] Am J Surg Pathol. 2003 Jul;27(7):867-81 [12826878.001]
  • [Cites] Am J Surg Pathol. 1990 Oct;14(10):948-55 [2403197.001]
  • [Cites] Eur J Cancer. 2004 May;40(8):1117-26 [15110875.001]
  • [Cites] Eur J Endocrinol. 2001 Sep;145(3):335-41 [11517015.001]
  • [Cites] Mod Pathol. 1993 Nov;6(6):663-8 [7508113.001]
  • [Cites] Cancer. 1987 Jun 15;59(12):2059-63 [3567866.001]
  • [Cites] Am J Surg Pathol. 1982 Oct;6(7):655-63 [7180965.001]
  • [Cites] Am J Surg Pathol. 2002 Dec;26(12):1612-9 [12459628.001]
  • [Cites] Am J Clin Pathol. 1979 Sep;72(3):390-9 [474519.001]
  • [Cites] Histopathology. 1998 Jan;32(1):43-50 [9522215.001]
  • [Cites] Cancer. 1986 Oct 1;58(7):1499-505 [3742468.001]
  • [Cites] J Urol. 2005 Jun;173(6):2138-42 [15879867.001]
  • [Cites] Am J Surg Pathol. 1989 Mar;13(3):202-6 [2919718.001]
  • [Cites] Semin Pediatr Surg. 1997 Aug;6(3):156-63 [9263338.001]
  • [Cites] Am J Pathol. 1990 Apr;136(4):729-33 [2327469.001]
  • [Cites] Arch Pathol Lab Med. 2005 Sep;129(9):1127-31 [16119984.001]
  • [Cites] Eur J Cancer. 1993;29A(10):1454-61 [8398275.001]
  • [Cites] Am J Clin Pathol. 1992 Jan;97(1):73-83 [1728867.001]
  • [Cites] Urol Clin North Am. 2000 Aug;27(3):403-21 [10985141.001]
  • [Cites] Mod Pathol. 2003 Aug;16(8):742-51 [12920217.001]
  • [Cites] Cell Tissue Res. 1993 Aug;273(2):269-77 [8395985.001]
  • [Cites] Cancer. 1985 Feb 15;55(4):766-73 [3967172.001]
  • [Cites] Am J Surg Pathol. 1997 May;21(5):556-62 [9158680.001]
  • [Cites] Am J Surg Pathol. 1984 Mar;8(3):163-9 [6703192.001]
  • (PMID = 16489441.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Histones; 0 / Ki-67 Antigen; 0 / RNA, Messenger
  •  go-up   go-down


68. 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
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • The TMM classification was: 19 of 24 TA (79%), two of which displayed very long telomeres, one of 24 ALT (4%) and two of 24 (8%) TA and ALT.
  • 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

  • Genetic Alliance. consumer health - Adrenocortical Carcinoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


69. Almeida MQ, Soares IC, Ribeiro TC, Fragoso MC, Marins LV, Wakamatsu A, Ressio RA, Nishi MY, Jorge AA, Lerario AM, Alves VA, Mendonca BB, Latronico AC: Steroidogenic factor 1 overexpression and gene amplification are more frequent in adrenocortical tumors from children than from adults. J Clin Endocrinol Metab; 2010 Mar;95(3):1458-62

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Steroidogenic factor 1 overexpression and gene amplification are more frequent in adrenocortical tumors from children than from adults.
  • BACKGROUND: Steroidogenic factor 1 (SF-1) is a key determinant of endocrine development and function of adrenal cortex.
  • SF-1 overexpression and gene amplification were previously demonstrated in a small group of pediatric adrenocortical tumors.
  • OBJECTIVE: Our objective was to determine the frequency of SF-1 protein expression and gene amplification in a large cohort of pediatric and adult adrenocortical tumors.
  • PATIENTS: SF-1 protein expression was assessed in a cohort of 103 adrenocortical tumors from 36 children and 67 adults, whereas gene amplification was studied in 38 adrenocortical tumors (17 from children).
  • RESULTS: A strong nuclear SF-1 expression was detected by tissue microarray in 56% (20 of 36) and 19% (13 of 67) of the pediatric and adult adrenocortical tumors, respectively (P = 0.0004).
  • Increased SF-1 copy number was identified in 47% (eight of 17) and 10% (two of 21) of the pediatric and adult adrenocortical tumors, respectively (P = 0.02).
  • All adrenocortical tumors with SF-1 gene amplification showed a strong SF-1 staining, whereas most of the tumors (61%) without SF-1 amplification displayed a weak or negative staining (P = 0.0008).
  • Interestingly, a strong SF-1 staining was identified in five (29%) pediatric adrenocortical tumors without SF-1 amplification.
  • The frequency of SF-1 overexpression and gene amplification was similar in adrenocortical adenomas and carcinomas.
  • CONCLUSION: We demonstrated a higher frequency of SF-1 overexpression and gene amplification in pediatric than in adult adrenocortical tumors, suggesting an important role of SF-1 in pediatric adrenocortical tumorigenesis.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics. Adrenocortical Carcinoma / genetics. Gene Amplification / genetics. Steroidogenic Factor 1 / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20080844.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Steroidogenic Factor 1
  •  go-up   go-down


70. Lumachi F, Borsato S, Tregnaghi A, Marino F, Fassina A, Zucchetta P, Marzola MC, Cecchin D, Bui F, Iacobone M, Favia G: High risk of malignancy in patients with incidentally discovered adrenal masses: accuracy of adrenal imaging and image-guided fine-needle aspiration cytology. Tumori; 2007 May-Jun;93(3):269-74
Hazardous Substances Data Bank. EPINEPHRINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High risk of malignancy in patients with incidentally discovered adrenal masses: accuracy of adrenal imaging and image-guided fine-needle aspiration cytology.
  • AIMS AND BACKGROUND: The incidental finding of nonfunctioning adrenal masses (incidentalomas) is common, but no reliable criteria in differentiating between benign and malignant adrenal masses have been defined.
  • The aim of this preliminary study was to assess the usefulness of adrenal imaging and image-guided fine-needle aspiration cytology in patients with nonfunctioning adrenal incidentalomas with the aim of excluding or confirming malignancy before surgery.
  • METHODS: Forty-two consecutive patients (18 men and 24 women; median age, 54 years; range, 25-75 years) with incidentally discovered adrenal masses of 3 cm or more in the greatest diameter were prospectively enrolled in the study.
  • RESULTS: The revised final pathology showed 30 (71.4%) benign (26 adrenocortical adenomas, of which 3 were atypical, 2 ganglioneuromas, and 2 nonfunctioning benign pheochromocytomas) and 12 (28.6%, 95% CI = 15-42) adrenal malignancies (8 adrenocortical carcinomas and 4 unsuspected adrenal metastases).
  • The definitive diagnosis of adrenocortical carcinoma was made according to Weiss criteria and confirmed on the basis of local invasion at surgery or metastases.
  • CONCLUSIONS: With the aim of selecting for surgery patients with a non-functioning adrenal incidentaloma of 3 cm or more in diameter, the combination of magnetic resonance imaging and fine-needle aspiration cytology should be considered the strategy of choice.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis. Biopsy, Fine-Needle. Incidental Findings. Magnetic Resonance Imaging
  • [MeSH-minor] 19-Iodocholesterol / analogs & derivatives. Adrenal Gland Diseases / diagnosis. Adrenal Gland Diseases / metabolism. Adrenal Gland Diseases / pathology. Adrenal Gland Diseases / radiography. Adrenal Gland Diseases / surgery. Adrenalectomy. Adrenocortical Adenoma / diagnosis. Adrenocortical Adenoma / metabolism. Adrenocortical Adenoma / pathology. Adrenocortical Adenoma / radiography. Adrenocortical Adenoma / surgery. Adrenocortical Carcinoma / diagnosis. Adrenocortical Carcinoma / metabolism. Adrenocortical Carcinoma / pathology. Adrenocortical Carcinoma / radiography. Adrenocortical Carcinoma / surgery. Adult. Aged. Aldosterone / blood. Epinephrine / urine. Female. Ganglioneuroma / diagnosis. Ganglioneuroma / metabolism. Ganglioneuroma / pathology. Ganglioneuroma / radiography. Ganglioneuroma / surgery. Humans. Hydrocortisone / blood. Iodine Radioisotopes. Laparoscopy. Male. Middle Aged. Norepinephrine / urine. Pheochromocytoma / diagnosis. Pheochromocytoma / metabolism. Pheochromocytoma / pathology. Pheochromocytoma / radiography. Pheochromocytoma / surgery. Predictive Value of Tests. Prospective Studies. Radiography, Abdominal. Renin / blood. Sensitivity and Specificity. Tomography, X-Ray Computed

  • MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.
  • MedlinePlus Health Information. consumer health - MRI Scans.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. HYDROCORTISONE .
  • Hazardous Substances Data Bank. Norepinephrine .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17679462.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Iodine Radioisotopes; 30461-91-7 / 19-Iodocholesterol; 4964P6T9RB / Aldosterone; 68232-36-0 / 6-iodomethylcholesterol; EC 3.4.23.15 / Renin; WI4X0X7BPJ / Hydrocortisone; X4W3ENH1CV / Norepinephrine; YKH834O4BH / Epinephrine
  •  go-up   go-down


71. Porterfield JR, Thompson GB, Young WF Jr, Chow JT, Fryrear RS, van Heerden JA, Farley DR, Atkinson JL, Meyer FB, Abboud CF, Nippoldt TB, Natt N, Erickson D, Vella A, Carpenter PC, Richards M, Carney JA, Larson D, Schleck C, Churchward M, Grant CS: Surgery for Cushing's syndrome: an historical review and recent ten-year experience. World J Surg; 2008 May;32(5):659-77
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Cushing's syndrome (CS), due to multiple etiologies, is a disorder associated with the ravages of cortisol excess.
  • The purpose of this review article is to provide a historical synopsis of surgery for CS, review a recent 10-year period of operative management at a tertiary care facility, and to outline a practical approach to diagnosis and management.
  • Fifty-four patients (18%) had cortisol-secreting adenomas, 10 patients (3%) had cortisol-producing adrenocortical carcinomas, and 1% had other causes.
  • Most benign adrenal processes could be managed laparoscopically.
  • Five-year survival rates (all causes) were 90%, 51%, and 23% for adrenocortical adenomas, ectopic ACTH syndrome, and adrenocortical carcinomas, respectively.
  • CONCLUSIONS: Surgery for CS is highly successful for pituitary-dependent CS and most ACTH-independent adrenal causes.
  • Unfortunately, to date, adrenocortical carcinomas are rarely cured.
  • Future successes with this disease will likely depend on a better understanding of tumor biology, more effective adjuvant therapies and earlier detection.

  • Genetic Alliance. consumer health - Cushing's Syndrome.
  • Genetic Alliance. consumer health - TEN.
  • MedlinePlus Health Information. consumer health - Cushing's Syndrome.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Arch Surg. 2001 May;136(5):543-9 [11343545.001]
  • [Cites] N Engl J Med. 1967 Nov 16;277(20):1050-6 [6059584.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Jun;82(6):1776-9 [9177381.001]
  • [Cites] Medicina (B Aires). 2000;60(3):326-30 [11050809.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Aug;83(8):2681-6 [9709931.001]
  • [Cites] Trends Endocrinol Metab. 2004 Oct;15(8):375-82 [15380809.001]
  • [Cites] N Engl J Med. 1991 Sep 26;325(13):897-905 [1652686.001]
  • [Cites] Neurosurg Focus. 2004 Apr 15;16(4):E5 [15191334.001]
  • [Cites] Endocrinol Metab Clin North Am. 2005 Jun;34(2):459-78, xi [15850853.001]
  • [Cites] Ann Surg. 1909 Dec;50(6):1002-17 [17862444.001]
  • [Cites] Acta Med Scand. 1980;208(1-2):101-9 [7192045.001]
  • [Cites] Endocr Relat Cancer. 2005 Sep;12(3):667-80 [16172199.001]
  • [Cites] Pituitary. 2004;7(4):209-15 [16132203.001]
  • [Cites] J Neurosurg. 2005 Sep;103(3):570-4 [16235694.001]
  • [Cites] Horm Res. 2005;64(3):140-3 [16192738.001]
  • [Cites] Clin Endocrinol (Oxf). 2001 Jun;54(6):797-804 [11422115.001]
  • [Cites] Int J Urol. 2006 Jun;13(6):677-81 [16834641.001]
  • [Cites] Arch Surg. 1998 May;133(5):541-5; discussion 545-6 [9605918.001]
  • [Cites] Radiology. 1992 Oct;185(1):143-7 [1523298.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Sep;84(9):3401-2 [10487721.001]
  • [Cites] Ann Surg. 1934 Oct;100(4):670-88 [17856387.001]
  • [Cites] J Clin Endocrinol Metab. 1991 Aug;73(2):408-13 [1649842.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Aug;80(8):2475-9 [7629245.001]
  • [Cites] Eur J Endocrinol. 2006 Apr;154(4):519-24 [16556713.001]
  • [Cites] Am J Surg. 1982 Sep;144(3):322-4 [7114370.001]
  • [Cites] J Clin Endocrinol Metab. 1988 May;66(5):1056-64 [3360898.001]
  • [Cites] Surg Clin North Am. 2004 Jun;84(3):875-85 [15145240.001]
  • [Cites] Acta Endocrinol (Copenh). 1990 Oct;123(4):423-30 [2173325.001]
  • [Cites] Arch Med Res. 2006 Nov;37(8):976-80 [17045113.001]
  • [Cites] World J Surg. 2004 Nov;28(11):1169-75 [15490057.001]
  • [Cites] Ann Surg. 1993 Jun;217(6):595-601; discussion 601-3 [8099474.001]
  • [Cites] Surgery. 1997 Dec;122(6):1132-6 [9426429.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Dec;88(12):5593-602 [14671138.001]
  • [Cites] Cancer. 2006 Sep 15;107(6):1355-64 [16894526.001]
  • [Cites] Surgery. 2006 Dec;140(6):943-8; discussion 948-50 [17188142.001]
  • [Cites] Endocrinol Metab Clin North Am. 2005 Jun;34(2):385-402, ix-x [15850849.001]
  • [Cites] Ann Surg Oncol. 1999 Dec;6(8):719-26 [10622498.001]
  • [Cites] AJR Am J Roentgenol. 1976 Jul;127(1):23-51 [180837.001]
  • [Cites] Cancer. 2000 Feb 15;88(4):711-36 [10679640.001]
  • [Cites] Best Pract Res Clin Endocrinol Metab. 2006 Sep;20(3):483-99 [16980207.001]
  • [Cites] Surg Oncol. 2003 Aug;12(2):105-23 [12946482.001]
  • [Cites] J Endocrinol Invest. 2006 May;29(5):471-82 [16794373.001]
  • [Cites] World J Surg. 2007 Jan;31(1):65-71 [17180554.001]
  • [Cites] Endocr Rev. 2005 Oct;26(6):775-99 [15827110.001]
  • [Cites] Semin Nucl Med. 1978 Jan;8(1):23-41 [345445.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Jul;89(7):3173-82 [15240590.001]
  • [Cites] J Endocrinol Invest. 2004 Jul-Aug;27(7):654-8 [15505989.001]
  • [Cites] Neurochirurgie. 2002 May;48(2-3 Pt 2):294-9 [12058134.001]
  • [Cites] Am J Rhinol. 2001 Jul-Aug;15(4):281-7 [11554662.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Apr;84(4):1193-202 [10199752.001]
  • [Cites] Surg Today. 2006;36(1):94-7 [16378204.001]
  • [Cites] Surg Clin North Am. 2004 Jun;84(3):755-74 [15145233.001]
  • [Cites] Urology. 2005 Sep;66(3):476-83 [16140061.001]
  • [Cites] J Clin Endocrinol Metab. 1962 Jul;22:693-703 [14471915.001]
  • [Cites] Radiographics. 2004 Mar-Apr;24(2):435-52 [15026592.001]
  • [Cites] Ann Clin Biochem. 2000 Jan;37 ( Pt 1):85-9 [10672380.001]
  • [Cites] Ann Oncol. 2000 Oct;11(10):1281-7 [11106117.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Mar;84(3):1116-21 [10084604.001]
  • [Cites] World J Surg. 1998 Jun;22(6):613-9; discussion 619-20 [9597937.001]
  • [Cites] Endocrinol Metab Clin North Am. 2005 Jun;34(2):489-99, xi [15850855.001]
  • [Cites] World J Surg. 2006 May;30(5):909-16 [16467980.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Feb;84(2):487-92 [10022405.001]
  • [Cites] J Urol. 1987 Nov;138(5):1134-6 [3669155.001]
  • [Cites] Clin Endocrinol (Oxf). 1984 Dec;21(6):621-9 [6509784.001]
  • [Cites] Clin Endocrinol (Oxf). 2003 Dec;59(6):793-9 [14974924.001]
  • [Cites] Endocrinol Metab Clin North Am. 2005 Jun;34(2):293-313, viii [15850843.001]
  • [Cites] Cancer. 1998 Nov 15;83(10):2194-200 [9827725.001]
  • [Cites] Am J Med. 2005 Dec;118(12):1340-6 [16378774.001]
  • [Cites] Cancer. 2000 Mar 1;88(5):1159-65 [10699907.001]
  • [Cites] Endocrinol Metab Clin North Am. 2005 Jun;34(2):441-58, x [15850852.001]
  • [Cites] Surg Clin North Am. 2004 Jun;84(3):743-53 [15145232.001]
  • [Cites] World J Surg. 2001 Jul;25(7):934-40 [11572035.001]
  • [Cites] J Endocrinol Invest. 2000 Sep;23(8):542-4 [11021772.001]
  • [Cites] N Engl J Med. 1992 Oct 1;327(14):1033 [1387700.001]
  • [Cites] N Engl J Med. 1989 Dec 14;321(24):1659-64 [2586567.001]
  • [Cites] Surgery. 1995 Dec;118(6):1071-5; discussion 1075-6 [7491525.001]
  • [Cites] Clin Endocrinol (Oxf). 2004 Nov;61(5):553-9 [15521956.001]
  • [Cites] Lancet. 2006 May 13;367(9522):1605-17 [16698415.001]
  • [Cites] N Engl J Med. 2007 Feb 8;356(6):601-10 [17287480.001]
  • [Cites] Int J Urol. 2005 Feb;12(2):134-9 [15733106.001]
  • [Cites] Surgery. 2007 Feb;141(2):147-51; discussion 151-2 [17263968.001]
  • [Cites] Lancet. 1952 Aug 2;2(6727):226-8 [14939896.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Feb;84(2):533-40 [10022412.001]
  • [Cites] N Engl J Med. 2007 Jun 7;356(23):2372-80 [17554118.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 1997 May;62(5):527-8 [9153615.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Dec;86(12 ):5711-4 [11739426.001]
  • [Cites] Ann Intern Med. 2003 Jun 17;138(12):980-91 [12809455.001]
  • [Cites] J Endourol. 2005 Apr;19(3):272-8 [15865511.001]
  • [Cites] AJR Am J Roentgenol. 1996 Mar;166(3):531-6 [8623622.001]
  • [Cites] J Surg Oncol. 2005 Mar 1;89(3):186-92 [15719374.001]
  • [Cites] Eur J Endocrinol. 2003 Oct;149(4):273-85 [14514341.001]
  • [Cites] J Clin Endocrinol Metab. 1989 Dec;69(6):1122-6 [2555381.001]
  • [Cites] Pituitary. 2004;7(4):265-9 [16416039.001]
  • [Cites] Am J Surg. 2005 May;189(5):581-5; discussion 585-6 [15862500.001]
  • [Cites] Microsc Res Tech. 2003 Jun 15;61(3):308-14 [12768546.001]
  • [Cites] Pituitary. 1999;1(2):125-32 [11081191.001]
  • [Cites] Endocrinol Metab Clin North Am. 2005 Jun;34(2):271-92, vii [15850842.001]
  • [Cites] JAMA. 1993 May 5;269(17):2232-8 [8386285.001]
  • [Cites] J Neurosurg. 1989 Oct;71(4):520-7 [2552045.001]
  • [Cites] Endocrinol Metab Clin North Am. 2005 Jun;34(2):403-21, x [15850850.001]
  • [Cites] Eur J Endocrinol. 2005 Apr;152(4):521-5 [15817906.001]
  • [Cites] Surgery. 1992 Dec;112(6):972-9; discussion 979-80 [1455322.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Dec;88(12):5808-13 [14671173.001]
  • [Cites] Ann Surg. 1951 Sep;134(3):464-75 [14869034.001]
  • [Cites] Endocrinol Metab Clin North Am. 2005 Jun;34(2):423-39, x [15850851.001]
  • [Cites] Clin Endocrinol (Oxf). 1999 Sep;51(3):265-71 [10469003.001]
  • [Cites] AJNR Am J Neuroradiol. 2000 Apr;21(4):690-6 [10782779.001]
  • (PMID = 18196319.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 139
  •  go-up   go-down


72. Razifar P, Hennings J, Monazzam A, Hellman P, Långström B, Sundin A: Masked volume wise Principal Component Analysis of small adrenocortical tumours in dynamic [11C]-metomidate Positron Emission Tomography. BMC Med Imaging; 2009;9:6
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Masked volume wise Principal Component Analysis of small adrenocortical tumours in dynamic [11C]-metomidate Positron Emission Tomography.
  • METHODS: In this study, MVW-PCA was applied to 14 dynamic 11C-metomidate-PET (MTO-PET) examinations of 7 patients with small adrenocortical tumours.
  • Time activity curves derived from "50% cut-off" ROIs based on an isocontour function whereby the pixels with SUVs between 50 to 100% of the highest radioactivity concentration were delineated, showed a significant decrease of the SUVs in normal adrenal glands and in adrenocortical adenomas after cortisone treatment.
  • [MeSH-major] Adrenal Cortex Neoplasms / radionuclide imaging. Algorithms. Etomidate / analogs & derivatives. Image Interpretation, Computer-Assisted / methods. Imaging, Three-Dimensional / methods. Pattern Recognition, Automated / methods. Positron-Emission Tomography / methods

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] NIH Consens State Sci Statements. 2002 Feb 4-6;19(2):1-25 [14768652.001]
  • [Cites] Ann Intern Med. 2003 Mar 4;138(5):424-9 [12614096.001]
  • [Cites] Endocr Rev. 2004 Apr;25(2):309-40 [15082524.001]
  • [Cites] J Nucl Med. 2004 Jun;45(6):972-9 [15181132.001]
  • [Cites] Eur J Nucl Med Mol Imaging. 2004 Sep;31(9):1224-30 [15197504.001]
  • [Cites] J Nucl Med. 2004 Sep;45(9):1519-27 [15347719.001]
  • [Cites] J Nucl Med. 1996 Nov;37(11):1766-70 [8917171.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Apr;91(4):1410-4 [16403816.001]
  • [Cites] Neuroimage. 2006 Nov 1;33(2):588-98 [16934493.001]
  • [Cites] Neuroimage. 2007 Jan 15;34(2):518-41 [17113312.001]
  • [Cites] Biomed Eng Online. 2007;6:36 [17915012.001]
  • [Cites] Eur J Radiol. 2009 Feb;69(2):314-23 [18082990.001]
  • [Cites] Endocr Rev. 1995 Aug;16(4):460-84 [8521790.001]
  • [Cites] J Nucl Med. 2000 Feb;41(2):275-82 [10688111.001]
  • [Cites] J Intern Med. 2002 Sep;252(3):239-46 [12270004.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Mar;89(3):1045-50 [15001583.001]
  • (PMID = 19386097.001).
  • [ISSN] 1471-2342
  • [Journal-full-title] BMC medical imaging
  • [ISO-abbreviation] BMC Med Imaging
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 5377-20-8 / metomidate; Z22628B598 / Etomidate
  • [Other-IDs] NLM/ PMC2680831
  •  go-up   go-down


73. Saito T, Ikoma A, Saito T, Tamemoto H, Suminaga Y, Yamada S, Kawakami M, Suzuki T, Sasano H, Ishikawa SE: Possibly simultaneous primary aldosteronism and preclinical Cushing's syndrome in a patient with double adenomas of right adrenal gland. Endocr J; 2007 Apr;54(2):287-93
Hazardous Substances Data Bank. HYDROCORTISONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Possibly simultaneous primary aldosteronism and preclinical Cushing's syndrome in a patient with double adenomas of right adrenal gland.
  • We reported a rare case of simultaneous primary aldosteronism and preclinical Cushing's syndrome due to unilateral double adrenocortical adenomas in a 57 year-old woman who had had hypertension for the last 10 years.
  • Abdominal computed tomography showed double tumors in her right adrenal gland.
  • They were macroscopically composed of a golden-yellow portion admixed with a brown portion, which corresponded to clear cells and compact cells, respectively.
  • Immunohistochemical staining for steroidogenic enzymes demonstrated the presence of all the enzymes involved in corticosteroidogenesis in these two adenomas, indicating that the two adenomas produced both cortisol and mineralocorticoid.
  • Specifically, one adenoma mainly caused excessive production of cortisol as compared to the other one.
  • These findings indicate that overproduction of both cortisol and mineralocorticoid was evident in the two adenomas of the right adrenal gland in immunohistochemical study for steroidogenic enzymes, whereas there was less clinical manifestation of primary aldosteronism and Cushing's syndrome in the present patient.
  • [MeSH-major] Adenoma / complications. Adrenal Gland Neoplasms / complications. Cushing Syndrome / etiology. Hyperaldosteronism / etiology


74. Okura T, Miyoshi K, Watanabe S, Kurata M, Irita J, Manabe S, Fukuoka T, Higaki J, Sasano H: Coexistence of three distinct adrenal tumors in the same adrenal gland in a patient with primary aldosteronism and preclinical Cushing's syndrome. Clin Exp Nephrol; 2006 Jun;10(2):127-30
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Coexistence of three distinct adrenal tumors in the same adrenal gland in a patient with primary aldosteronism and preclinical Cushing's syndrome.
  • Physical examination revealed no signs of excessive adrenocortical steroid production, as are found in Cushing's syndrome.
  • Magnetic resonance image revealed three sequential nodular masses (each 15 mm x 15 mm) in the right adrenal gland.
  • Microscopic examination revealed that the upper and lower tumors were adrenocortical adenomas, and the middle tumor was a black adenoma.
  • Surprisingly, at 33 years of age, she had been diagnosed with Cushing's syndrome, due to a cortisol-producing adrenocortical adenoma, and she had received a left adrenalectomy.
  • [MeSH-major] Adenoma / physiopathology. Adrenal Gland Neoplasms / physiopathology. Adrenocortical Adenoma / physiopathology. Hyperaldosteronism / etiology. Neoplasms, Multiple Primary
  • [MeSH-minor] Adrenalectomy. Cushing Syndrome / diagnosis. Female. Humans. Hydrocortisone / secretion. Immunohistochemistry. Incidental Findings. Magnetic Resonance Imaging. Middle Aged


75. Rizk-Rabin M, Assie G, Rene-Corail F, Perlemoine K, Hamzaoui H, Tissier F, Lieberherr M, Bertagna X, Bertherat J, Bouizar Z: Differential expression of parathyroid hormone-related protein in adrenocortical tumors: autocrine/paracrine effects on the growth and signaling pathways in H295R cells. Cancer Epidemiol Biomarkers Prev; 2008 Sep;17(9):2275-85
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential expression of parathyroid hormone-related protein in adrenocortical tumors: autocrine/paracrine effects on the growth and signaling pathways in H295R cells.
  • Adrenocortical tumors (ACT) are rare and heterogeneous, but their pathogenesis is unclear.
  • We monitored the synthesis of PTHrP and PTH-R1 in a series of 25 ACT: 12 adrenocortical carcinomas (ACC) and 13 adrenocortical adenomas (ACA), and investigated the effects of PTHrP(1-34) on H295R cells derived from an ACC.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Parathyroid Hormone-Related Protein / metabolism. Receptor, Parathyroid Hormone, Type 1 / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Apoptosis. Blotting, Western. Calcium / metabolism. Cell Cycle. Cell Line, Tumor. Cyclic AMP-Dependent Protein Kinases / metabolism. Female. Humans. Male. Middle Aged. Prognosis. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction

  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18768493.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Parathyroid Hormone-Related Protein; 0 / RNA, Messenger; 0 / Receptor, Parathyroid Hormone, Type 1; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; SY7Q814VUP / Calcium
  •  go-up   go-down


76. Hennings J, Hellman P, Ahlström H, Sundin A: Computed tomography, magnetic resonance imaging and 11C-metomidate positron emission tomography for evaluation of adrenal incidentalomas. Eur J Radiol; 2009 Feb;69(2):314-23
MedlinePlus Health Information. consumer health - MRI Scans.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Computed tomography, magnetic resonance imaging and 11C-metomidate positron emission tomography for evaluation of adrenal incidentalomas.
  • BACKGROUND: Given the higher sensitivity of modern computed tomography (CT) scanners, adrenal incidentalomas are being discovered increasingly often.
  • Recently, positron emission tomography (PET) using the tracer (11)C-metomidate (MTO) has been established as an alternative diagnostic method with high sensitivity for identifying adrenocortical lesions.
  • The aim of this study was to evaluate the clinical use and value of MTO-PET compared to CT and MRI in the characterisation and work-up of adrenal incidentalomas.
  • METHODS: Initially, we retrospectively evaluated 20 adrenal incidentalomas in patients who had undergone CT, MRI and MTO-PET and from whom we had either histopathological diagnosis or clinical follow-up data.
  • In the latter study, 24 incidentalomas were imaged by CT, MRI and MTO-PET and the results were correlated to those from histopathology (n=8) and clinical diagnosis after follow-up (n=16).
  • RESULTS: In the retrospective analysis, MRI and especially MTO-PET, correlated well to histopathology and clinical diagnosis after follow-up, whereas specificity with CT was low.
  • This was possibly due to the presence of several haematomas/fibrosis which were misdiagnosed as adrenocortical adenomas.
  • CONCLUSION: The diagnosis of an adrenocortical adenoma may be established by CT in most patients and by MRI in an additional number.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis. Etomidate / analogs & derivatives. Magnetic Resonance Imaging / methods. Positron-Emission Tomography / methods. Tomography, X-Ray Computed / methods

  • MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.
  • MedlinePlus Health Information. consumer health - CT Scans.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18082990.001).
  • [ISSN] 1872-7727
  • [Journal-full-title] European journal of radiology
  • [ISO-abbreviation] Eur J Radiol
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 5377-20-8 / metomidate; Z22628B598 / Etomidate
  •  go-up   go-down


77. Libé R, Bertherat J: Molecular genetics of adrenocortical tumours, from familial to sporadic diseases. Eur J Endocrinol; 2005 Oct;153(4):477-87
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular genetics of adrenocortical tumours, from familial to sporadic diseases.
  • Adrenal masses can be detected in up to 4% of the population, and are mostly of adrenocortical origin.
  • Adrenocortical tumours (ACTs) may be responsible for excess steroid production and, in the case of adrenocortical cancers, for morbidity or mortality due to tumour growth.
  • The familial diseases concerned are Li-Fraumeni syndrome, which may be due to germline mutation of the tumour-suppressor gene TP53 and Beckwith-Wiedemann syndrome, which is caused by dys-regulation of the imprinted IGF-II locus at 11p15.
  • Cushing's syndrome due to primary pigmented nodular adrenocortical disease (PPNAD) has been observed in Carney complex patients presenting inactivating germline PRKAR1A mutations.
  • Interestingly, allelic losses at 17p13 and 11p15 have been demonstrated in sporadic adrenocortical cancer and somatic PRKAR1A mutations have been found in secreting adrenocortical adenomas.
  • The genetics of another group of adrenal diseases that can lead to adrenal nodular hyperplasia -- congenital adrenal hyperplasia (CAH) and glucocorticoid-remediable aldosteronism (GRA) -- have also been studied extensively.
  • This review summarizes recent advances in the genetics of ACTs, highlighting both improvements in our understanding of the pathophysiology and the diagnosis of these tumours.

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16189167.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 97
  •  go-up   go-down


78. Kim HY, Kim SG, Lee KW, Seo JA, Kim NH, Choi KM, Baik SH, Choi DS: Clinical study of adrenal incidentaloma in Korea. Korean J Intern Med; 2005 Dec;20(4):303-9
MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical study of adrenal incidentaloma in Korea.
  • BACKGROUND: This study was designed to evaluate the clinical, endocrinological and histological characteristics of adrenal incidentalomas.
  • METHODS: Eighty patients (41, males; 38, females; age range 17-80 years) who were diagnosed with adrenal incidentaloma at Korea University Hospital from 1992 to 2003 were studied retrospectively.
  • Pathologic examination revealed 16 adrenocortical adenomas (20%), five carcinomas (6%), 13 pheochromocytomas (16%), three metastatic cancers (4%), and other tumors (10%).
  • The diameter of the carcinomas (mean: 10.8 cm, range: 5-19 cm) were significantly larger than the diameter of benign adenomas (mean: 2.84 cm, range: 1-6 cm) (p=0.002).
  • Twenty-four patients with non-functioning tumors were followed up for a period of 3 to 72 months.
  • Changes in mass size and function were observed only between 10 and 26 months after the initial diagnosis.
  • CONCLUSIONS: These data show that an endocrine evaluation should be performed in all adrenal incidentalomas, and an adrenalectomy is recommended for tumors 5 cm or greater or tumors with adrenocortical hyperfunction.
  • In addition, these tumors should be monitored for changes in mass size and function for a follow up period of approximately 26 months.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis. Incidental Findings
  • [MeSH-minor] Adolescent. Adrenocortical Adenoma / diagnosis. Adult. Aged. Aged, 80 and over. Carcinoma / diagnosis. Female. Humans. Korea. Male. Middle Aged. Pheochromocytoma / diagnosis. Retrospective Studies

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] N Engl J Med. 1995 Mar 23;332(12):791-803 [7862184.001]
  • [Cites] Eur J Endocrinol. 1995 Apr;132(4):422-8 [7711879.001]
  • [Cites] Endocr Rev. 1995 Aug;16(4):460-84 [8521790.001]
  • [Cites] Clin Endocrinol (Oxf). 1998 Jan;48(1):89-97 [9509073.001]
  • [Cites] Clin Endocrinol (Oxf). 1998 Apr;48(4):379-88 [9640401.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Aug;83(8):2681-6 [9709931.001]
  • [Cites] Clin Radiol. 1998 Nov;53(11):796-804 [9833781.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Feb;84(2):520-6 [10022410.001]
  • [Cites] J Urol. 2000 Feb;163(2):398-407 [10647642.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Feb;85(2):637-44 [10690869.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Apr;85(4):1440-8 [10770179.001]
  • [Cites] Eur J Endocrinol. 2000 Jul;143(1):111-7 [10870039.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Mar;87(3):998-1003 [11889151.001]
  • [Cites] J Intern Med. 2002 Sep;252(3):239-46 [12270004.001]
  • [Cites] Eur J Endocrinol. 2002 Oct;147(4):489-94 [12370111.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Nov;87(11):4872-8 [12414841.001]
  • [Cites] Ann Intern Med. 2003 Mar 4;138(5):424-9 [12614096.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Sep;88(9):4153-7 [12970280.001]
  • [Cites] NIH Consens State Sci Statements. 2002 Feb 4-6;19(2):1-25 [14768652.001]
  • [Cites] Lancet. 1967 Mar 4;1(7488):468-70 [4164067.001]
  • [Cites] Acta Med Scand. 1968 Sep;184(3):211-4 [5703975.001]
  • [Cites] AJR Am J Roentgenol. 1982 Jul;139(1):81-5 [6979870.001]
  • [Cites] Ann Intern Med. 1983 Jun;98(6):940-5 [6344711.001]
  • [Cites] Am J Surg. 1985 Jun;149(6):783-8 [4014556.001]
  • [Cites] Surgery. 1991 Dec;110(6):1014-21 [1745970.001]
  • [Cites] J Clin Endocrinol Metab. 1992 Sep;75(3):826-32 [1517373.001]
  • [Cites] J Clin Endocrinol Metab. 1993 Oct;77(4):885-8 [8408461.001]
  • [Cites] World J Surg. 1993 Sep-Oct;17(5):634-9 [8273385.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Dec;79(6):1532-9 [7989452.001]
  • (PMID = 16491828.001).
  • [ISSN] 1226-3303
  • [Journal-full-title] The Korean journal of internal medicine
  • [ISO-abbreviation] Korean J. Intern. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC3891076
  •  go-up   go-down


79. Groussin L, Bonardel G, Silvéra S, Tissier F, Coste J, Abiven G, Libé R, Bienvenu M, Alberini JL, Salenave S, Bouchard P, Bertherat J, Dousset B, Legmann P, Richard B, Foehrenbach H, Bertagna X, Tenenbaum F: 18F-Fluorodeoxyglucose positron emission tomography for the diagnosis of adrenocortical tumors: a prospective study in 77 operated patients. J Clin Endocrinol Metab; 2009 May;94(5):1713-22
Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 18F-Fluorodeoxyglucose positron emission tomography for the diagnosis of adrenocortical tumors: a prospective study in 77 operated patients.
  • CONTEXT: Most adrenal incidentalomas are nonfunctioning adrenocortical adenomas (ACAs).
  • Adrenocortical carcinomas (ACCs) are rare but should be recognized at an early stage.
  • All underwent surgery because of hypersecretory and/or growing benign lesions (n = 18), obvious ACCs (n = 21), or radiologically indeterminate lesions (n = 38).
  • Using a cutoff value above 1.45 for adrenal to liver maxSUV ratio, the sensitivity and specificity to distinguish ACAs from ACCs were, respectively, 1.00 (95% confidence interval 0.85-1.00) and 0.88 (95% confidence interval 0.75-0.96).
  • Among the 38 indeterminate lesions at CT scan, we could analyze a subgroup of 16 adrenocortical tumors with high unenhanced density (>10 HU) and an inappropriate washout: (18)F-FDG PET correctly predicted the benignity in 13 of 15 ACAs.
  • An adrenal to liver maxSUV ratio less than 1.45 is highly predictive of a benign lesion.
  • [MeSH-major] Adrenal Cortex Neoplasms / radionuclide imaging. Adrenal Cortex Neoplasms / surgery. Fluorodeoxyglucose F18

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19190108.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Hormones; 0Z5B2CJX4D / Fluorodeoxyglucose F18
  •  go-up   go-down


80. Sbiera S, Schmull S, Assie G, Voelker HU, Kraus L, Beyer M, Ragazzon B, Beuschlein F, Willenberg HS, Hahner S, Saeger W, Bertherat J, Allolio B, Fassnacht M: High diagnostic and prognostic value of steroidogenic factor-1 expression in adrenal tumors. J Clin Endocrinol Metab; 2010 Oct;95(10):E161-71

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High diagnostic and prognostic value of steroidogenic factor-1 expression in adrenal tumors.
  • CONTEXT: No immunohistochemical marker has been established to reliably differentiate adrenocortical tumors from other adrenal masses.
  • We hypothesized that expression of steroidogenic factor-1 (SF-1), a transcription factor involved in adrenal development, is of value for the differential diagnosis of adrenal masses and predicts prognosis in adrenocortical carcinoma (ACC).
  • PATIENTS AND METHODS: SF-1 protein expression was assessed by immunohistochemistry on tissue samples from 167 ACC, 52 adrenocortical adenomas (ACA), six normal adrenal glands, six normal ovaries and 73 neoplastic nonsteroidogenic tissues.
  • RESULTS: SF-1 protein staining was detectable in 158 of 161 (98%) evaluable ACC samples including 49 (30%) with strong SF-1 staining and in all normal and benign steroidogenic tissues.
  • In addition, SF-1 mRNA expression was present in all 91 analyzed adrenocortical tumors.
  • CONCLUSION: SF-1 is a highly valuable immunohistochemical marker to determine the adrenocortical origin of an adrenal mass with high sensitivity and specificity.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenocortical Adenoma / diagnosis. Adrenocortical Carcinoma / diagnosis. Steroidogenic Factor 1 / genetics
  • [MeSH-minor] Adult. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Cohort Studies. Diagnosis, Differential. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Metastasis. Neoplasm Staging. Predictive Value of Tests. Prognosis. Sensitivity and Specificity

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20660055.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / NR5A1 protein, human; 0 / Steroidogenic Factor 1
  •  go-up   go-down


81. Fagour C, Bardet S, Rohmer V, Arimone Y, Lecomte P, Valli N, Tabarin A: Usefulness of adrenal scintigraphy in the follow-up of adrenocortical incidentalomas: a prospective multicenter study. Eur J Endocrinol; 2009 Feb;160(2):257-64
MedlinePlus Health Information. consumer health - Nuclear Scans.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Usefulness of adrenal scintigraphy in the follow-up of adrenocortical incidentalomas: a prospective multicenter study.
  • OBJECTIVES: Prognostic factors for progression of benign adrenocortical adenomas (AI) remain poorly known.
  • We assessed the usefulness of (131)I-6-beta-iodomethylnorcholesterol scintigraphy (IMS) to predict the occurrence of adrenal hyperfunction or mass enlargement.
  • DESIGN: Fifty-one consecutive inpatients with unilateral AI and normal 24-h urinary free cortisol (UFC) were enrolled in a multicenter observational prospective study to investigate the relationship between the scintigraphic pattern and the progression of biological abnormalities of the hypothalamo-pituitary-adrenal axis or tumor size.

  • MedlinePlus Health Information. consumer health - Benign Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18974229.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Iodine Radioisotopes
  •  go-up   go-down


82. Szücs N, Gláz E, Varga I, Tóth M, Kiss R, Patócs A, Jakab C, Perner F, Járay J, Horányi J, Dabasi G, Molnár F, Major L, Füto L, Rácz K, Tulassay Z: [Diagnosis and treatment outcome in primary aldosteronism based on a retrospective analysis of 187 cases]. Orv Hetil; 2006 Jan 15;147(2):51-9
Genetic Alliance. consumer health - Primary aldosteronism.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Diagnosis and treatment outcome in primary aldosteronism based on a retrospective analysis of 187 cases].
  • The disease has been described by Jerome W.
  • Conn in 1955; since that time there has been a great progress in the knowledge concerning the prevalence, diagnostics and treatment of the disease.
  • METHODS: The efficacy of different methods used for the diagnosis, the frequency of the different subtypes of primary aldosteronism, as well as the surgical outcomes in patients with surgically treated subtypes of primary aldosteronism were studied.
  • RESULTS: Aldosterone-producing adenoma was detected in more than two thirds of patients (n = 135), whereas idiopathic hyperaldosteronism was found in 46 patients.
  • Other subtypes of primary hyperaldosteronism occurred less frequently (unilateral primary adrenocortical hyperplasia in 5 patients and adrenocortical carcinoma in one patient).
  • For the diagnosis of familial hyperaldosteronism type I, molecular biological studies of the aldosterone-synthase/11beta-hydroxylase gene chimera were carried out in 30 patients but none of them showed the presence of the chimeric gene.
  • When comparing the clinical parameters of patients with aldosterone-producing adenoma and idiopathic hyperaldosteronism, no significant differences were found in the time period between the diagnosis of hypertension and the diagnosis of primary aldosteronism, or in the systolic and diastolic blood pressure values.
  • The mean of the lowest documented serum potassium concentration was slightly lower in patients with aldosterone-producing adenoma (2.8 +/- 0.1 mmol/l) compared to those with idiopathic hyperaldosteronism (3.1 +/- 0.2 mmol/l), but the difference was not significant.
  • The ratio of plasma aldosterone concentration (ng/dl) to plasma renin activity (ng/ml/h) was above 20 in all patients with aldosterone-producing adenoma and in all but 5 cases with idiopathic hyperaldosteronism.
  • To confirm the diagnosis and to differentiate the subtypes of primary aldosteronism, the postural test combined with furosemide administration was performed in the majority of patients.
  • When cases showing an elevation of plasma cortisol level during the test were excluded, this test differentiated patients with aldosterone-producing adenoma from those with idiopathic hyperaldosteronism with a sensitivity of 69% and a specificity of 92%.
  • In cases of adrenocortical adenomas not or not clearly detectable by radiological imaging techniques, as well as in cases with bilateral adrenocortical adenomas, selective adrenal vein sampling was performed (n = 55).
  • All but 4 patients with aldosterone-producing adenoma underwent adrenalectomy.
  • Histology and postoperative hormone results confirmed the preoperative diagnosis in all operated patients.
  • CONCLUSIONS: These observations are in contrast with the results of international studies which showed a high frequency of normokalemic primary aldosteronism and a more frequent occurrence of idiopathic hyperaldosteronism well treatable with aldosterone-antagonists.
  • [MeSH-major] Adenoma / surgery. Adrenal Cortex Neoplasms / surgery. Aldosterone / secretion. Hyperaldosteronism / diagnosis. Hyperaldosteronism / therapy. Mineralocorticoid Receptor Antagonists / therapeutic use

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16509213.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Mineralocorticoid Receptor Antagonists; 0 / Mutant Chimeric Proteins; 4964P6T9RB / Aldosterone; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase
  •  go-up   go-down


83. Hahner S, Fassnacht M, Hammer F, Schammann M, Weismann D, Hansen IA, Allolio B: Evidence against a role of human airway trypsin-like protease--the human analogue of the growth-promoting rat adrenal secretory protease--in adrenal tumourigenesis. Eur J Endocrinol; 2005 Jan;152(1):143-53

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evidence against a role of human airway trypsin-like protease--the human analogue of the growth-promoting rat adrenal secretory protease--in adrenal tumourigenesis.
  • OBJECTIVE: A serine protease from rat adrenal cortex was recently characterized and named adrenal secretory protease (AsP).
  • AsP is expressed in the adrenal cortex and is capable of cleaving pro-gamma-melanocyte-stimulating hormone (1-76 N-terminus of pro-opiomelanocortin) into fragments that act as adrenal mitogens.
  • AsP may therefore play a crucial role in adrenal growth and tumourigenesis.
  • The aim of this study was to further characterize the human homologue of AsP and its possible role in adrenal tumourigenesis.
  • Further analysis revealed that the HAT gene is the human homologue of a long splice variant of AsP, which we recently described as rat airway trypsin-like serine protease 1.
  • In contrast to rodents, no short isoform of HAT was found in humans due to a stop codon in exon 6 which prevents the expression of a short isoform.
  • While high expression of HAT mRNA was found in the trachea and in the gastrointestinal tract, expression in the adrenal was only very weak.
  • We further investigated HAT expression in five normal adrenal glands, 15 adrenocortical adenomas (five hormonally inactive adenomas, five aldosterone-producing adenomas and five cortisol-producing adenomas), nine adrenocortical carcinomas, five phaeochromocytomas and two adrenal hyperplasias.
  • Weak HAT expression was detectable in only two out of five normal adrenal glands, in one out of twenty-four adrenocortical tumours and four out of five phaeochromocytomas.
  • However, the expression in the adrenal tissue was several orders of magnitude lower than in the trachea.
  • In addition, we could not detect any HAT transcripts in a sample of fetal adrenal.
  • CONCLUSION: Gene structure and tissue distribution of HAT, the human homologue of the rat adrenal secretory protease AsP, reveal major interspecies differences.
  • The observation of very low expression levels in normal adrenal tissue and adrenocortical tumours casts doubt about a role for HAT in the physiological and pathological growth of adrenocortical cells.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15762198.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / RNA, Neoplasm; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / human airway trypsin-like protease
  •  go-up   go-down


84. Vincent-Dejean C, Cazabat L, Groussin L, Perlemoine K, Fumey G, Tissier F, Bertagna X, Bertherat J: Identification of a clinically homogenous subgroup of benign cortisol-secreting adrenocortical tumors characterized by alterations of the protein kinase A (PKA) subunits and high PKA activity. Eur J Endocrinol; 2008 Jun;158(6):829-39
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of a clinically homogenous subgroup of benign cortisol-secreting adrenocortical tumors characterized by alterations of the protein kinase A (PKA) subunits and high PKA activity.
  • Inactivating PRKAR1A mutations have been observed in Carney complex and a subset of adrenocortical tumors (ACT).
  • METHODS: In this study, 35 ACT (10 non-secreting adrenocortical adenomas (ACA-NS), 13 cortisol-secreting adenomas (ACA-S), and 12 malignant s (ACC)) were studied.
  • RESULTS: A subgroup of ACA-S with a 96% R2B protein decrease by comparison with normal adrenal (4.1%+/-4 vs 100%+/-19, P<0.001) was identified, ACA-S2 (6/13).
  • The ACA-S2 tumors with the loss of the R2B protein presented a homogenous phenotype and were all small benign cortisol-secreting tumors.
  • CONCLUSION: This loss of PRKAR2B protein due to a post-transcriptional mechanism in ACA-S is a new mechanism of cAMP pathway dysregulation in adrenocortical tumorigenesis.
  • It defines a new subtype of secreting adenomas with high basal PKA activity presenting a homogenous clinical phenotype.

  • Hazardous Substances Data Bank. HYDROCORTISONE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18505904.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIIbeta Subunit; 0 / PRKAR2B protein, human; E0399OZS9N / Cyclic AMP; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; WI4X0X7BPJ / Hydrocortisone
  •  go-up   go-down


85. Stratakis CA, Carney JA: The triad of paragangliomas, gastric stromal tumours and pulmonary chondromas (Carney triad), and the dyad of paragangliomas and gastric stromal sarcomas (Carney-Stratakis syndrome): molecular genetics and clinical implications. J Intern Med; 2009 Jul;266(1):43-52
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A number of other lesions have been described in the condition including pheochromocytomas, oesophageal leiomyomas and adrenocortical adenomas; CT is a novel form of multiple endocrine neoplasia (MEN), a genetic condition with a female predilection.
  • We recently reported an international series of patients with CT, 34 females and three males (median age of presentation 21 years) who did not carry SDHA, SDHB, SDHC, SDHD, KIT or PDGFRA gene mutations.
  • The above have clinical implications (i) for patients with GISTs that are cKIT- and PDGFRA-mutation negative: these tumours are usually resistant to treatment with currently available tyrosine kinase inhibitors and may be part of a syndrome such as CT or CSS; and (ii) for patients with an inherited PGL syndrome, family history should be explored to identify any other tumours in the family, and in particular other endocrine lesions and GISTs.

  • Genetics Home Reference. consumer health - SDHB gene.
  • Genetics Home Reference. consumer health - SDHC gene.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Rofo. 2000 Mar;172(3):287-94 [10778462.001]
  • [Cites] J Intern Med. 2009 Jul;266(1):19-42 [19522823.001]
  • [Cites] Am J Med Genet. 2002 Mar 1;108(2):132-9 [11857563.001]
  • [Cites] Hum Pathol. 2002 May;33(5):459-65 [12094370.001]
  • [Cites] Hum Pathol. 2002 May;33(5):478-83 [12094372.001]
  • [Cites] Eur J Hum Genet. 2002 Dec;10(12):790-800 [12461685.001]
  • [Cites] J Clin Oncol. 2004 May 15;22(10):2029-31 [15143098.001]
  • [Cites] N Engl J Med. 1977 Jun 30;296(26):1517-8 [865533.001]
  • [Cites] Am J Med. 1981 Jun;70(6):1288-92 [6263093.001]
  • [Cites] Medicine (Baltimore). 1983 May;62(3):159-69 [6843355.001]
  • [Cites] Aust N Z J Surg. 1988 Aug;58(8):679-81 [2845908.001]
  • [Cites] Am J Pathol. 1998 May;152(5):1259-69 [9588894.001]
  • [Cites] Eur Respir J. 1998 Jun;11(6):1409-11 [9657587.001]
  • [Cites] Mayo Clin Proc. 1999 Jun;74(6):543-52 [10377927.001]
  • [Cites] Cancer Detect Prev. 1999;23(5):435-43 [10468897.001]
  • [Cites] Hum Pathol. 2005 Jan;36(1):112-6 [15712189.001]
  • [Cites] Pediatr Blood Cancer. 2005 Jul;45(1):20-4 [15795882.001]
  • [Cites] Transplantation. 2005 Jul 27;80(2):283-4 [16041278.001]
  • [Cites] Am J Surg Pathol. 2006 Jan;30(1):42-9 [16330941.001]
  • [Cites] Semin Diagn Pathol. 2006 May;23(2):63-9 [17193819.001]
  • [Cites] J Pathol. 2007 Mar;211(4):463-70 [17226762.001]
  • [Cites] Oncol Rep. 2007 Jul;18(1):9-15 [17549339.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Aug;92(8):2938-43 [17535989.001]
  • [Cites] N Engl J Med. 2007 Sep 6;357(10):1054-6 [17804857.001]
  • [Cites] Eur J Hum Genet. 2008 Jan;16(1):79-88 [17667967.001]
  • [Cites] Am J Surg Pathol. 2008 May;32(5):738-43 [18360281.001]
  • [Cites] J Intern Med. 2009 Jul;266(1):1-4 [19522821.001]
  • [Cites] J Thorac Cardiovasc Surg. 2001 May;121(5):1011-2 [11326257.001]
  • (PMID = 19522824.001).
  • [ISSN] 1365-2796
  • [Journal-full-title] Journal of internal medicine
  • [ISO-abbreviation] J. Intern. Med.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / Z01 HD000642; United States / Intramural NIH HHS / / ZIA HD000642-13
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 32
  • [Other-IDs] NLM/ NIHMS307247; NLM/ PMC3129547
  •  go-up   go-down


86. Kamenicky P, Houdoin L, Ferlicot S, Salenave S, Brailly S, Droupy S, Meduri G, Sasano H, Suzuki T, Young J, Chanson P: Benign cortisol-secreting adrenocortical adenomas produce small amounts of androgens. Clin Endocrinol (Oxf); 2007 Jun;66(6):778-88
Hazardous Substances Data Bank. Corticotropin .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Benign cortisol-secreting adrenocortical adenomas produce small amounts of androgens.
  • BACKGROUND: Serum androgen levels are below normal in patients with benign cortisol-secreting adrenocortical adenomas, owing to ACTH suppression.
  • The objective of the study was to analyse the androgen-producing ability of cortisol-secreting adrenocortical adenomas.
  • METHODS: Dehydroepiandrosterone sulfate (DHEAS), Delta4androstenedione and testosterone concentrations were measured before and after adrenalectomy and then at 6-month intervals in 20 women (eight cortisol-secreting adrenocortical adenomas, six subclinical cortisol-secreting adrenocortical adenomas, and six nonfunctional adenomas).
  • RESULTS: Before adrenalectomy, serum androgen concentrations were measurable in all women with clinically apparent and subclinical cortisol-secreting adrenocortical adenomas.
  • Postoperatively, during adrenocortical insufficiency, DHEAS, Delta4androstenedione and testosterone concentrations fell to near the detection limit in all patients with cortisol-secreting adrenocortical adenomas (P = 0.008 for each marker) and showed a similar tendency to fall in all patients with subclinical cortisol-secreting adrenocortical adenomas.
  • Pre- and post-treatment androgen concentrations did not differ in patients with nonfunctional adenomas.
  • The intensity of CYP17 and SULT2A1 expression was stronger in cortisol-secreting adenomas than in their adjacent normal adrenal tissue.
  • CONCLUSION: Both clinically apparent and subclinical cortisol-secreting adrenocortical adenomas appear to show moderate autonomous androgen production.
  • Thus, weak androgen secretion in patients with adrenocortical tumours should not necessarily be considered as a sign of malignancy.
  • [MeSH-major] Adenoma / secretion. Adrenal Cortex Neoplasms / secretion. Androgens / secretion. Hydrocortisone / secretion

  • Hazardous Substances Data Bank. HYDROCORTISONE .
  • Hazardous Substances Data Bank. TESTOSTERONE .
  • Hazardous Substances Data Bank. ANDROSTENEDIONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17408424.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / Estrogens; 0 / Gonadotropins, Pituitary; 3XMK78S47O / Testosterone; 409J2J96VR / Androstenedione; 57B09Q7FJR / Dehydroepiandrosterone Sulfate; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
  •  go-up   go-down


87. Shigematsu K, Nishida N, Sakai H, Igawa T, Toriyama K, Nakatani A, Takahara O, Kawai K: Synaptophysin immunoreactivity in adrenocortical adenomas: a correlation between synaptophysin and CYP17A1 expression. Eur J Endocrinol; 2009 Dec;161(6):939-45
MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Synaptophysin immunoreactivity in adrenocortical adenomas: a correlation between synaptophysin and CYP17A1 expression.
  • DESIGN AND METHODS: The adrenal cortex is not considered to be an intrinsic part of the diffuse neuroendocrine system, but adrenocortical neoplasms possess neuroendocrine properties.
  • In this study, we examined synaptophysin (SYP) and neural cell adhesion molecule (NCAM) expression in adrenocortical adenomas in relation to adrenal function.
  • RESULTS: Immunohistochemical analysis showed that 50.7 and 98.6% of the cortical adenomas showed SYP and NCAM immunoreactivities respectively.
  • There was no apparent difference in NCAM immunoreactivity among the adenomas.
  • However, the immunostaining for SYP was significantly stronger in cortisol-producing adenomas (CPA) than in aldosterone-producing adenomas (APA), nonfunctioning adenomas (NFA), showing no clinical or endocrinological abnormality, or adenomas associated with preclinical Cushing's syndrome (preCS).
  • CONCLUSIONS: We propose that SYP expression in adrenocortical cells may be involved in some aspect of adrenal function such as transport or secretion of glucocorticoids.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19755404.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neural Cell Adhesion Molecules; 0 / RNA, Messenger; 0 / Synaptophysin; EC 1.14.99.9 / CYP17A1 protein, human; EC 1.14.99.9 / Steroid 17-alpha-Hydroxylase
  •  go-up   go-down


88. Hennings J, Sundin A, Hägg A, Hellman P: 11C-metomidate positron emission tomography after dexamethasone suppression for detection of small adrenocortical adenomas in primary aldosteronism. Langenbecks Arch Surg; 2010 Sep;395(7):963-7
Hazardous Substances Data Bank. DEXAMETHASONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 11C-metomidate positron emission tomography after dexamethasone suppression for detection of small adrenocortical adenomas in primary aldosteronism.
  • PURPOSE: To evaluate whether dexamethasone suppression treatment can improve (11) C-metomidate positron emission tomography (MTO-PET) detection of small adrenocortical adenomas in primary aldosteronism (PA).
  • MATERIALS AND METHODS: Eleven patients with proven PA and two patients with non-hyperfunctioning adrenocortical incidentalomas and small adrenocortical tumours observed on CT underwent MTO-PET before and 3 days after administration of oral dexamethasone suppression treatment.
  • RESULTS: All tumours were detected and categorised as adrenocortical by MTO-PET.
  • SUVhs as well as SUVmax were higher in PA compared to nonfunctional adenomas.
  • Normal adrenal cortex was suppressed after dexamethasone (p < 0.05), but tumour SUV was not significantly decreased after suppression in either PA or nonfunctional tumours (p > 0.05).
  • However, these changes caused no significant increase in the tumour-to-normal adrenal ratio (p > 0.05).
  • CONCLUSION: MTO-PET is a highly sensitive method for detecting and categorising even small adrenocortical tumours in PA.
  • In this series, dexamethasone-suppressed MTO-PET was unable to increase the tumour-to-normal adrenal ratio to further facilitate detection of small adenomas in PA as an alternative to adrenal venous sampling.
  • [MeSH-major] Adrenocortical Adenoma / diagnostic imaging. Adrenocortical Adenoma / drug therapy. Dexamethasone / therapeutic use. Hyperaldosteronism / diagnostic imaging. Hyperaldosteronism / drug therapy. Positron-Emission Tomography / methods

  • Genetic Alliance. consumer health - Primary aldosteronism.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Am J Med. 1984 Nov;77(5):839-44 [6496538.001]
  • [Cites] Am Surg. 2007 Feb;73(2):174-80 [17305298.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Mar;89(3):1045-50 [15001583.001]
  • [Cites] Eur J Nucl Med Mol Imaging. 2004 Sep;31(9):1224-30 [15197504.001]
  • [Cites] J Hypertens. 2003 Nov;21(11):2149-57 [14597859.001]
  • [Cites] Langenbecks Arch Surg. 2007 Sep;392(5):623-8 [17242897.001]
  • [Cites] Surgery. 2008 Dec;144(6):926-33; discussion 933 [19040999.001]
  • [Cites] ANZ J Surg. 2007 Sep;77(9):768-73 [17685956.001]
  • [Cites] Arch Intern Med. 2008 Jan 14;168(1):80-5 [18195199.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Apr;91(4):1410-4 [16403816.001]
  • [Cites] Scand J Surg. 2008;97(3):248-53 [18812275.001]
  • [Cites] World J Surg. 2008 May;32(5):847-53 [18343972.001]
  • [Cites] Eur J Radiol. 2009 Feb;69(2):314-23 [18082990.001]
  • [Cites] Semin Nucl Med. 1989 Apr;19(2):122-43 [2652311.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Sep;93(9):3266-81 [18552288.001]
  • [Cites] Nat Clin Pract Nephrol. 2006 Apr;2(4):198-208; quiz, 1 p following 230 [16932426.001]
  • [Cites] Eur J Endocrinol. 2004 Jul;151(1):73-85 [15248825.001]
  • [Cites] J Hypertens. 2008 Sep;26(9):1816-23 [18698217.001]
  • [Cites] J Nucl Med. 2004 Jun;45(6):972-9 [15181132.001]
  • [Cites] Eur J Nucl Med. 1999 Oct;26(10 ):1326-32 [10541832.001]
  • [Cites] J Nucl Med. 2000 Feb;41(2):275-82 [10688111.001]
  • [Cites] J Vasc Interv Radiol. 2008 Jan;19(1):66-71 [18192469.001]
  • (PMID = 20644954.001).
  • [ISSN] 1435-2451
  • [Journal-full-title] Langenbeck's archives of surgery
  • [ISO-abbreviation] Langenbecks Arch Surg
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 5377-20-8 / metomidate; 7S5I7G3JQL / Dexamethasone; Z22628B598 / Etomidate
  •  go-up   go-down


89. Oki K, Yamane K, Sakashita Y, Kamei N, Watanabe H, Toyota N, Shigeta M, Sasano H, Kohno N: Primary aldosteronism and hypercortisolism due to bilateral functioning adrenocortical adenomas. Clin Exp Nephrol; 2008 Oct;12(5):382-7
Hazardous Substances Data Bank. HYDROCORTISONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary aldosteronism and hypercortisolism due to bilateral functioning adrenocortical adenomas.
  • A 50-year-old male patient with a 15-year history of hypertension was referred to our hospital for evaluation of bilateral adrenal tumors.
  • Computed tomographic scan showed 10-mm masses in each adrenal gland.
  • The results of a subsequent adrenal venous catheterization study were consistent with the presence of a left cortisol-producing tumor and a right aldosterone-producing tumor.
  • Pathological examination of the resected specimens, including immunohistochemical analysis, demonstrated that both adenomas possibly produced cortisol and aldosterone.
  • This is an extremely rare case of bilateral adrenal tumors, in which the left adrenocortical tumor produced and secreted cortisol or both cortisol and aldosterone and the right one produced and secreted both aldosterone and cortisol, as confirmed by clinical findings and pathological studies using immunohistochemical analysis.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications. Cushing Syndrome / etiology. Hyperaldosteronism / etiology
  • [MeSH-minor] Aldosterone / metabolism. Diagnosis, Differential. Humans. Hydrocortisone / metabolism. Male. Middle Aged

  • Genetic Alliance. consumer health - Primary aldosteronism.
  • MedlinePlus Health Information. consumer health - Cushing's Syndrome.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Vasc Interv Radiol. 2004 Nov;15(11):1245-50 [15525743.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Oct;91(10):3746-53 [16868050.001]
  • [Cites] Acta Clin Belg. 1995;50(5):310-3 [8533534.001]
  • [Cites] Clin Exp Nephrol. 2006 Jun;10(2):127-30 [16791399.001]
  • [Cites] Intern Med. 2003 Aug;42(8):714-8 [12924498.001]
  • [Cites] Am J Hypertens. 2006 Apr;19(4):373-9; discussion 380 [16580572.001]
  • [Cites] Klin Wochenschr. 1990 Oct 3;68(19):981-3 [2232630.001]
  • [Cites] J Hypertens. 2006 Feb;24(2):371-9 [16508586.001]
  • [Cites] Radiographics. 2007 Jul-Aug;27(4):1145-57 [17620472.001]
  • [Cites] Surgery. 2006 Dec;140(6):847-53; discussion 853-5 [17188130.001]
  • [Cites] Hypertens Res. 2006 Nov;29(11):883-9 [17345788.001]
  • [Cites] Horm Res. 1997;47(4-6):279-83 [9167965.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Mar;86(3):1083-90 [11238490.001]
  • [Cites] Metabolism. 2006 Aug;55(8):1135-40 [16839852.001]
  • [Cites] Lancet. 1994 Jul 23;344(8917):240-3 [7913162.001]
  • [Cites] Cancer Treat Res. 1997;89:263-92 [9204197.001]
  • [Cites] Hum Pathol. 1989 Feb;20(2):113-7 [2914700.001]
  • [Cites] World J Surg. 2006 May;30(5):879-85; discussion 886-7 [16680603.001]
  • [Cites] Jpn J Med. 1991 Jan-Feb;30(1):26-31 [1865573.001]
  • [Cites] JAMA. 2006 Jun 14;295(22):2638-45 [16772627.001]
  • [Cites] Hypertens Res. 2001 Nov;24(6):723-6 [11768734.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Dec;88(12):5808-13 [14671173.001]
  • (PMID = 18543063.001).
  • [ISSN] 1342-1751
  • [Journal-full-title] Clinical and experimental nephrology
  • [ISO-abbreviation] Clin. Exp. Nephrol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone; WI4X0X7BPJ / Hydrocortisone
  •  go-up   go-down


90. Tan HS, Thai AC, Nga ME, Mukherjee JJ: Development of ipsilateral adrenocortical carcinoma sixteen years after resection of an adrenal tumour causing Cushing's syndrome. Ann Acad Med Singapore; 2005 Apr;34(3):271-4
MedlinePlus Health Information. consumer health - Cushing's Syndrome.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development of ipsilateral adrenocortical carcinoma sixteen years after resection of an adrenal tumour causing Cushing's syndrome.
  • INTRODUCTION: At times, it may be difficult to differentiate early stage, low-grade adrenocortical carcinoma from benign adrenal adenoma.
  • CLINICAL PICTURE: A 53-year-old lady underwent right adrenalectomy for a 4-cm adrenocortical tumour causing Cushing's syndrome.
  • Histology revealed an adrenocortical adenoma.
  • Sixteen years later, she presented with a 14-cm adrenal tumour, again on the right side.
  • Histology confirmed adrenocortical carcinoma.
  • OUTCOME: She died of metastatic disease 17 months later.
  • CONCLUSIONS: This case highlights the importance of long-term, systematic follow-up of patients treated for benign adrenal adenomas, especially if the tumour size exceeds 4 cm.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Cushing Syndrome / etiology. Neoplasm Recurrence, Local / pathology
  • [MeSH-minor] Adrenocortical Adenoma / pathology. Diagnosis, Differential. Fatal Outcome. Female. Humans. Middle Aged

  • Genetic Alliance. consumer health - Cushing's Syndrome.
  • Genetic Alliance. consumer health - Adrenocortical Carcinoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15902349.001).
  • [ISSN] 0304-4602
  • [Journal-full-title] Annals of the Academy of Medicine, Singapore
  • [ISO-abbreviation] Ann. Acad. Med. Singap.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Singapore
  •  go-up   go-down


91. Schittenhelm J, Ebner FH, Harter P, Bornemann A: Symptomatic intraspinal oncocytic adrenocortical adenoma. Endocr Pathol; 2009;20(1):73-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Symptomatic intraspinal oncocytic adrenocortical adenoma.
  • Benign epithelial tumors are rarely found at this site.
  • We here present the case of a 44-year-old woman with a lesion in the cauda equina that fulfilled the radiologic criteria of schwannoma and caused clinical symptoms for 3 years.
  • This immunoprofile indicated adrenocortical origin.
  • The diagnosis of an oncocytic adrenal cortical adenoma was made.
  • These extraadrenal tumors are thought to arise from heterotopic adrenocortical tissue in the spinal cavity.
  • Oncocytic tumors are rare neoplasms and they comprise non-functioning variants of adrenal cortical adenomas.
  • Immunohistochemistry excluded oncocytic paraganglioma, oncocytic meningioma, renal cell carcinoma, alveolar soft part sarcoma, and granular cell tumor.
  • [MeSH-major] Adenoma, Oxyphilic / pathology. Adrenocortical Adenoma / pathology. Spinal Cord Neoplasms / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Clin Radiol. 2005 Sep;60(9):953-9 [16124976.001]
  • [Cites] Pediatr Neurosurg. 2002 May;36(5):260-5 [12053045.001]
  • [Cites] Spinal Cord. 2007 Feb;45(2):183-6 [16505829.001]
  • [Cites] Am J Surg Pathol. 1998 Jan;22(1):57-63 [9422316.001]
  • [Cites] Int J Surg Pathol. 2004 Jul;12(3):259-64 [15306940.001]
  • [Cites] J Neurosurg. 2001 Apr;94(2 Suppl):310-2 [11302638.001]
  • [Cites] J Pediatr Surg. 1980 Jun;15(3):289-92 [6103925.001]
  • [Cites] Neurosurgery. 2006 Nov;59(5):E1144; discussion E1144 [17143207.001]
  • [Cites] Am J Surg Pathol. 1991 Oct;15(10 ):949-56 [1928551.001]
  • [Cites] Neurosurgery. 1993 Apr;32(4):658-61; discussion 661-2 [8474656.001]
  • [Cites] Histopathology. 1997 Aug;31(2):167-73 [9279569.001]
  • [Cites] Mol Cell Endocrinol. 2005 Apr 15;233(1-2):47-56 [15767045.001]
  • [Cites] Am J Surg Pathol. 1997 Apr;21(4):375-82 [9130983.001]
  • [Cites] J Med Case Rep. 2008 Jul 13;2:228 [18620603.001]
  • [Cites] Am J Surg Pathol. 1990 May;14(5):481-4 [2327553.001]
  • [Cites] Histopathology. 1986 Mar;10(3):311-9 [2422107.001]
  • [Cites] Fetal Pediatr Pathol. 2006 Jul-Aug;25(4):191-7 [17162526.001]
  • [Cites] J Clin Pathol. 1998 Feb;51(2):114-6 [9602683.001]
  • [Cites] AMA Arch Pathol. 1959 Feb;67(2):228-33 [13616833.001]
  • [Cites] Neurosurgery. 2000 Sep;47(3):756-9 [10981764.001]
  • [Cites] Int J Surg Pathol. 2004 Jul;12(3):231-43 [15306935.001]
  • (PMID = 19039533.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


92. Ouzounian S, Tissier F, Gouya H, Kujas M, Louvel A, Legmann P, Bertagna X: [Cushing's syndrome and adrenal adenoma. Two surprising associations]. Presse Med; 2005 Apr 09;34(7):511-5
MedlinePlus Health Information. consumer health - Cushing's Syndrome.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Cushing's syndrome and adrenal adenoma. Two surprising associations].
  • [Transliterated title] Maladie de Cushing et adénome cortico-surrénalien. Deux associations étonnantes.
  • CASES: In the first case, we describe the case of a patient with an adrenal adenoma 20 years before the occurrence of Cushing's disease related to the pineal gland.
  • In the second case, two members of the same family were diagnosed almost simultaneously with adrenal cortical adenoma (mother) and Cushing's disease (daughter).
  • [MeSH-major] Adenoma / complications. Adrenal Gland Neoplasms / complications. Cushing Syndrome / etiology

  • Genetic Alliance. consumer health - Cushing's Syndrome.
  • MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15903005.001).
  • [ISSN] 0755-4982
  • [Journal-full-title] Presse medicale (Paris, France : 1983)
  • [ISO-abbreviation] Presse Med
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  •  go-up   go-down


93. Szolar DH, Korobkin M, Reittner P, Berghold A, Bauernhofer T, Trummer H, Schoellnast H, Preidler KW, Samonigg H: Adrenocortical carcinomas and adrenal pheochromocytomas: mass and enhancement loss evaluation at delayed contrast-enhanced CT. Radiology; 2005 Feb;234(2):479-85
MedlinePlus Health Information. consumer health - Pheochromocytoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenocortical carcinomas and adrenal pheochromocytomas: mass and enhancement loss evaluation at delayed contrast-enhanced CT.
  • PURPOSE: To retrospectively measure the adrenal gland attenuation and the percentage loss of adrenal gland enhancement at delayed contrast medium-enhanced computed tomography (CT) in patients with adrenocortical carcinomas and pheochromocytomas and to compare these data with those in patients with adenomas and metastases.
  • Eleven patients with proved adrenocortical carcinoma, 17 with proved pheochromocytoma, 23 with adrenal adenoma, and 16 with metastasis to the adrenal gland underwent helical CT.
  • RESULTS: The mean attenuation of adenomas (8 HU +/- 18 [standard deviation]) was significantly lower than those of adrenocortical carcinomas (39 HU +/- 14), pheochromocytomas (44 HU +/- 11), and metastases (34 HU +/- 11) on nonenhanced CT scans (P < .001).
  • Although the mean attenuation values for nonadenomas (ie, adrenocortical carcinomas, pheochromocytomas, and metastases) were significantly higher than the value for adenomas on the 1-minute contrast-enhanced CT scans (P < .001), there was more overlap in attenuation between adenomas and nonadenomas on contrast-enhanced scans than on nonenhanced scans.
  • On the 10-minute delayed contrast-enhanced scans, the mean attenuation of adenomas (32 HU +/- 17) was significantly lower than the mean attenuations of carcinomas (72 HU +/- 15), pheochromocytomas (83 HU +/- 14), and metastases (66 HU +/- 13) (P < .001).
  • At optimal threshold values of 50% for absolute percentage of enhancement loss and 40% for relative percentage of enhancement loss at 10 minutes, both the sensitivity and the specificity for the diagnosis of adenoma were 100% when adenomas were compared with carcinomas, pheochromocytomas, and metastases.
  • CONCLUSION: The enhancement loss in adrenocortical carcinomas and pheochromocytomas is similar to that in adrenal metastases but significantly less than that in adrenal adenomas.
  • The percentage change in contrast material washout is a useful adjunct to absolute CT attenuation values in differentiating adrenal adenomas from adrenocortical carcinomas and pheochromocytomas.
  • [MeSH-major] Adrenal Cortex Neoplasms / radiography. Adrenal Gland Neoplasms / radiography. Adrenocortical Carcinoma / radiography. Pheochromocytoma / radiography. Tomography, X-Ray Computed / methods
  • [MeSH-minor] Adenoma / radiography. Adolescent. Adult. Aged. Female. Humans. Male. Middle Aged. Sensitivity and Specificity

  • MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.
  • MedlinePlus Health Information. consumer health - CT Scans.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) RSNA, 2005.
  • [CommentIn] Radiology. 2005 Sep;236(3):1112-3 [16118181.001]
  • [CommentIn] Radiology. 2006 Jan;238(1):373; author reply 373-4 [16373781.001]
  • (PMID = 15671003.001).
  • [ISSN] 0033-8419
  • [Journal-full-title] Radiology
  • [ISO-abbreviation] Radiology
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


94. Wu Z, Ni D, Yan Y, Li J, Wang B, Ouyang J, Zhang G, Ma X, Li H, Zhang X: Expression of angiotensin II receptors in aldosterone-producing adenoma of the adrenal gland and their clinical significance. J Huazhong Univ Sci Technolog Med Sci; 2010 Aug;30(4):486-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of angiotensin II receptors in aldosterone-producing adenoma of the adrenal gland and their clinical significance.
  • The expression of angiotensin II type 1 receptor (AT1R) and angiotensin II type 2 receptor (AT2R) in aldosterone-producing adenoma (APA) of the adrenal gland was detected, and their relationship with clinical indexes of APA was analyzed.
  • The mRNA expression of AT1R and AT2R in 50 cases of APA and tissues adjacent to tumors and 12 cases of normal adrenal tissues was detected by using reverse transcriptase polymerase chain reaction (RT-PCR).
  • The expression of AT1R in adenoma, tissues adjacent to tumor, and normal tissues of the adrenal gland showed no significant differences.
  • The expression of AT2R in APA tissue was lower than that in normal adrenal gland tissues (P<0.05).
  • [MeSH-major] Adenoma / metabolism. Adrenal Gland Neoplasms / metabolism. Aldosterone / blood. Receptor, Angiotensin, Type 1 / metabolism. Receptor, Angiotensin, Type 2 / metabolism

  • MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Steroids. 1995 Jan;60(1):28-34 [7792812.001]
  • [Cites] Lab Invest. 2002 Oct;82(10):1305-17 [12379765.001]
  • [Cites] J Steroid Biochem. 1979 Jul;11(1C):1043-50 [491637.001]
  • [Cites] Endocr Rev. 1998 Apr;19(2):101-43 [9570034.001]
  • [Cites] Clin Endocrinol (Oxf). 2001 May;54(5):627-32 [11380493.001]
  • [Cites] J Am Coll Cardiol. 2005 Apr 19;45(8):1243-8 [15837256.001]
  • [Cites] J Clin Invest. 1991 Sep;88(3):921-33 [1885777.001]
  • [Cites] Lancet. 1999 Apr 17;353(9161):1341-7 [10218547.001]
  • [Cites] Folia Histochem Cytobiol. 2008;46(1):51-5 [18296263.001]
  • [Cites] Pharmacol Rev. 2000 Sep;52(3):415-72 [10977869.001]
  • [Cites] J Am Soc Nephrol. 1999 Jan;10 Suppl 11:S57-61 [9892141.001]
  • [Cites] Am J Physiol. 1999 Feb;276(2 Pt 1):E303-9 [9950790.001]
  • [Cites] Cytogenet Cell Genet. 1995;71(1):77-80 [7606933.001]
  • [Cites] Brain Res Bull. 1995;38(5):441-6 [8665267.001]
  • [Cites] J Biol Chem. 1997 Jul 25;272(30):19022-6 [9228085.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Nov 7;92(23):10663-7 [7479861.001]
  • [Cites] Acta Endocrinol (Copenh). 1991 Sep;125(3):319-30 [1950344.001]
  • [Cites] Hypertension. 2000 Jan;35(1 Pt 2):155-63 [10642292.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Mar;82(3):865-9 [9062498.001]
  • (PMID = 20714875.001).
  • [ISSN] 1672-0733
  • [Journal-full-title] Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban
  • [ISO-abbreviation] J. Huazhong Univ. Sci. Technol. Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / AGTR1 protein, human; 0 / RNA, Messenger; 0 / Receptor, Angiotensin, Type 1; 0 / Receptor, Angiotensin, Type 2; 4964P6T9RB / Aldosterone
  •  go-up   go-down


95. Farkas A, Horányi J, Gláz E, Kulka J: [Oncocytic tumor of the adrenal gland]. Orv Hetil; 2005 Jul 3;146(27):1453-8
MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Oncocytic tumor of the adrenal gland].
  • [Transliterated title] Oncocytás mellékvese-adenoma.
  • Oncocytic tumor of the adrenal gland.
  • The authors describe a case of a rare tumor arising in the adrenal gland.
  • The tumor 6 cm in diameter, connected to the right adrenal gland, was found incidentally in a healthy young man of 34 years of age, who suffered an accident and had a rib fracture.
  • The right adrenal gland with the tumor was removed by laparoscopic surgery.
  • Histopathological examination revealed an oncocytic adenoma of the adrenal cortex.
  • The authors describe the morphology and the differential diagnosis of this rare tumor of the adrenal gland.
  • [MeSH-major] Adenoma, Oxyphilic / diagnosis. Adrenal Gland Neoplasms / diagnosis
  • [MeSH-minor] Adult. Diagnosis, Differential. Humans. Incidental Findings. Male

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16089107.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Number-of-references] 12
  •  go-up   go-down


96. Schittenhelm J, Jacob SN, Rutczynska J, Tsiflikas I, Meyermann R, Beschorner R: Extra-adrenal paravertebral myelolipoma mimicking a thoracic schwannoma. BMJ Case Rep; 2009;2009

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extra-adrenal paravertebral myelolipoma mimicking a thoracic schwannoma.
  • Myelolipoma of the adrenal gland is composed of both adipose tissue and normal haematopoietic elements.
  • Extra-adrenal myelolipomas are rare.
  • We present the case of a 63-year-old female patient with adenoma of the adrenal gland and an additional paravertebral lesion in the thoracic spine.
  • Post-mortem histopathology showed the incidental finding of a paravertebral myelolipoma.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Radiographics. 2005 Jan-Feb;25(1):69-85 [15653588.001]
  • [Cites] Am J Surg Pathol. 1982 Jun;6(4):363-74 [7051876.001]
  • [Cites] Arch Pathol Lab Med. 1994 Sep;118(9):895-6 [8080359.001]
  • [Cites] Radiographics. 1997 Nov-Dec;17(6):1373-85 [9397452.001]
  • (PMID = 21686745.001).
  • [ISSN] 1757-790X
  • [Journal-full-title] BMJ case reports
  • [ISO-abbreviation] BMJ Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC3027965
  •  go-up   go-down


97. Araki A, Shinohara M, Yamakawa J, Tanaka M, Natsui S, Izumi Y: Gastric diverticulum preoperatively diagnosed as one of two left adrenal adenomas. Int J Urol; 2006 Jan;13(1):64-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gastric diverticulum preoperatively diagnosed as one of two left adrenal adenomas.
  • A 47-year-old man was diagnosed with primary aldosteronism due to two left adrenal adenomas, suggested on computed tomography (CT) to be located at the upper and lower adrenal portion.
  • However, adosterol scintigraphy revealed negligible uptake at the upper portion of the left adrenal.
  • Laparoscopic left adrenalectomy was performed, but macroscopic examination of the specimen revealed only one adrenal tumor.
  • Postoperatively, aldosteronism resolved and repeat CT revealed staining of the adrenal pseudotumor when oral contrast was administered.
  • Since organs located near the adrenals can simulate adrenal tumors, caution must be exercised in interpreting suprarenal masses on CT.
  • To our knowledge, this is the first reported case of concurrent pseudotumor and true tumor of the ipsilateral adrenal.
  • [MeSH-major] Adrenocortical Adenoma / diagnosis. Diverticulum, Stomach / diagnosis. Preoperative Care
  • [MeSH-minor] Adrenalectomy / methods. Diagnosis, Differential. Humans. Hyperaldosteronism / diagnosis. Hyperaldosteronism / etiology. Laparoscopy. Male. Middle Aged. Tomography, X-Ray Computed

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16448434.001).
  • [ISSN] 0919-8172
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  •  go-up   go-down


98. Park BK, Kim B, Ko K, Jeong SY, Kwon GY: Adrenal masses falsely diagnosed as adenomas on unenhanced and delayed contrast-enhanced computed tomography: pathological correlation. Eur Radiol; 2006 Mar;16(3):642-7
MedlinePlus Health Information. consumer health - CT Scans.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenal masses falsely diagnosed as adenomas on unenhanced and delayed contrast-enhanced computed tomography: pathological correlation.
  • OBJECTIVES: To assess the accuracy of CT for the diagnosis of histologically confirmed adrenal adenoma and nonadenoma using CT numbers.
  • MATERIALS AND METHODS: Our study included 91 adrenal masses in 83 patients; histopathological diagnoses were 45 adenomas, 31 pheochromocytomas, 6 hyperplasias, 4 metastasis, and 5 miscellaneous lesions.
  • RESULTS: Sensitivity, specificity, and accuracy for adenoma were 40% (18/45), 91% (42/46), and 66% (60/91) with unenhanced CT, and 96% (24/25), 61% (11/18), and 81% (35/43) with DCE CT.
  • Adrenal masses falsely diagnosed as adenoma on unenhanced CT included three hyperplasias and one endothelial cyst, and those falsely diagnosed as adenoma on DCE CT were five pheochromocytomas, one oncocytic cortical tumor, and one primary pigmented nodular adrenocortical dysplasia.
  • Twenty-five lipid-poor adenomas were falsely diagnosed as nonadenomas on unenhanced CT and one degenerated adenoma both on unenhanced CT and on DCE CT.
  • CONCLUSION: Diagnosing adenoma merely on CT numbers can lead to misdiagnosis.
  • [MeSH-major] Adenoma / diagnostic imaging. Adrenal Gland Neoplasms / diagnostic imaging. Tomography, X-Ray Computed / methods
  • [MeSH-minor] Adult. Analysis of Variance. Contrast Media. Diagnosis, Differential. Diagnostic Errors. Female. Humans. Hyperplasia. Male. Middle Aged. Neoplasm Metastasis. Pheochromocytoma / diagnostic imaging. Pheochromocytoma / pathology. Sensitivity and Specificity

  • MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Eur Radiol. 2006 Mar;16(3):768
  • [Cites] AJR Am J Roentgenol. 2003 Sep;181(3):843-9 [12933492.001]
  • [Cites] Endocr J. 2004 Feb;51(1):89-95 [15004414.001]
  • [Cites] Radiology. 2005 Feb;234(2):479-85 [15671003.001]
  • [Cites] Radiology. 1998 May;207 (2):369-75 [9577483.001]
  • [Cites] Am J Med. 1996 Jul;101(1):88-94 [8686720.001]
  • [Cites] Radiology. 1996 Sep;200(3):743-7 [8756925.001]
  • [Cites] AJR Am J Roentgenol. 1999 Apr;172(4):997-1002 [10587135.001]
  • [Cites] Eur Radiol. 2004 Oct;14(10):1787-92 [15241622.001]
  • [Cites] AJR Am J Roentgenol. 1998 Jul;171(1):201-4 [9648789.001]
  • [Cites] Radiology. 1997 Mar;202(3):693-6 [9051018.001]
  • [Cites] Radiology. 2000 Dec;217(3):798-802 [11110946.001]
  • [Cites] J Comput Assist Tomogr. 1994 May-Jun;18(3):432-8 [8188912.001]
  • [Cites] Radiology. 2002 Mar;222(3):629-33 [11867777.001]
  • [Cites] AJR Am J Roentgenol. 1995 Dec;165(6):1453-9 [7484585.001]
  • [Cites] AJR Am J Roentgenol. 2000 Nov;175(5):1411-5 [11044054.001]
  • [Cites] AJR Am J Roentgenol. 1998 Mar;170(3):747-52 [9490968.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Feb;84(2):520-6 [10022410.001]
  • (PMID = 16215735.001).
  • [ISSN] 0938-7994
  • [Journal-full-title] European radiology
  • [ISO-abbreviation] Eur Radiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Contrast Media
  •  go-up   go-down


99. Mete O, Asa SL: Aldosterone-producing adrenal cortical adenoma with oncocytic change and cytoplasmic eosinophilic globular inclusions. Endocr Pathol; 2009;20(3):182-5
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aldosterone-producing adrenal cortical adenoma with oncocytic change and cytoplasmic eosinophilic globular inclusions.
  • We report an interesting morphological alteration in the adrenal of a 72-year-old woman suffering from severe hypertension due to primary hyperaldosteronism.
  • The laparoscopic left adrenalectomy specimen revealed an adrenal cortical adenoma composed of varying proportions of oncocytic and clear cells, predominantly showing central oncocytic change.
  • Oncocytes also exhibited numerous eosinophilic intracytoplasmic globular inclusions, which are not commonly observed in aldosterone-producing adrenal cortical adenomas.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / pathology. Aldosterone / secretion. Inclusion Bodies / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Virchows Arch. 1998 Jul;433(1):5-12 [9692819.001]
  • [Cites] Virchows Arch. 2008 Sep;453(3):301-6 [18688642.001]
  • [Cites] Virchows Arch. 2005 Dec;447(6):938-46 [16133362.001]
  • [Cites] Semin Diagn Pathol. 1999 May;16(2):82-90 [10452573.001]
  • [Cites] Ultrastruct Pathol. 2002 Jul-Aug;26(4):229-35 [12227948.001]
  • [Cites] Hepatogastroenterology. 2008 May-Jun;55(84):900-2 [18705293.001]
  • [Cites] Br J Cancer. 2005 May 23;92(10):1817-8 [15900303.001]
  • [Cites] Mod Pathol. 2002 Sep;15(9):973-8 [12218215.001]
  • [Cites] Rhinology. 2007 Mar;45(1):89-92 [17432078.001]
  • [Cites] Cancer. 1970 Dec;26(6):1300-10 [5483659.001]
  • [Cites] J Clin Pathol. 2004 Mar;57(3):225-32 [14990587.001]
  • [Cites] Hum Pathol. 2009 Apr;40(4):478-83 [19144383.001]
  • [Cites] Arch Pathol Lab Med. 1983 Apr;107(4):178-82 [6299227.001]
  • [Cites] Pathol Annu. 1992;27 Pt 1:263-304 [1736246.001]
  • [Cites] Pathol Int. 1996 Apr;46(4):286-91 [8726853.001]
  • [Cites] Br J Cancer. 2005 May 23;92(10):1892-8 [15841082.001]
  • (PMID = 19462261.001).
  • [ISSN] 1559-0097
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antihypertensive Agents; 4964P6T9RB / Aldosterone
  •  go-up   go-down


100. Walz MK, Gwosdz R, Levin SL, Alesina PF, Suttorp AC, Metz KA, Wenger FA, Petersenn S, Mann K, Schmid KW: Retroperitoneoscopic adrenalectomy in Conn's syndrome caused by adrenal adenomas or nodular hyperplasia. World J Surg; 2008 May;32(5):847-53
MedlinePlus Health Information. consumer health - Endoscopy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Retroperitoneoscopic adrenalectomy in Conn's syndrome caused by adrenal adenomas or nodular hyperplasia.
  • BACKGROUND: In patients with primary hyperaldosteronism, solitary adrenal adenomas are an indication for surgical intervention.
  • In contrast, adrenal hyperplasia is almost exclusively treated by drugs.
  • PATIENTS AND METHODS: In a prospective clinical study 183 patients (81 men, 102 women; age 49.6+/-12.8 years) with Conn's syndrome were operated on using the posterior retroperitoneoscopic approach.
  • Final histology described a solitary adenoma in 127 patients and adrenal hyperplasia in 56 patients.
  • CONCLUSIONS: Retroperitoneoscopic removal of adrenal glands in patients with Conn's syndrome is a safe, rapidly performed surgical procedure and can thus be considered as first choice option for treatment of both solitary adrenal adenomas and hyperplasia presenting with a clinically predominating nodule.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenal Glands / pathology. Adrenalectomy / methods. Adrenocortical Adenoma / surgery. Endoscopy. Hyperaldosteronism / surgery

  • Genetic Alliance. consumer health - Conn's Syndrome.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] World J Surg. 2008 May;32(5):854-5 [18246389.001]
  • [Cites] World J Surg. 2007 Jan;31(1):72-9 [17180480.001]
  • [Cites] Zhonghua Wai Ke Za Zhi. 2004 Sep 22;42(18):1093-5 [15498293.001]
  • [Cites] Am Surg. 2007 Feb;73(2):174-80 [17305298.001]
  • [Cites] Eur Urol. 2003 Apr;43(4):381-5 [12667719.001]
  • [Cites] Eur J Endocrinol. 2004 Apr;150(4):517-23 [15080782.001]
  • [Cites] World J Surg. 2004 Dec;28(12):1323-9 [15517476.001]
  • [Cites] World J Surg. 1996 Sep;20(7):769-74 [8678949.001]
  • [Cites] World J Surg. 1998 Jun;22(6):621-6; discussion 626-7 [9597938.001]
  • [Cites] World J Surg. 2001 Jun;25(6):728-34 [11376407.001]
  • [Cites] Arch Surg. 1999 Jun;134(6):628-31; discussion 631-2 [10367872.001]
  • [Cites] Surgery. 1998 Dec;124(6):1128-33 [9854594.001]
  • [Cites] Surgery. 2001 Oct;130(4):629-34; discussion 634-5 [11602893.001]
  • [Cites] Anesth Analg. 1996 Apr;82(4):827-31 [8615505.001]
  • [Cites] J Urol. 2003 Jan;169(1):32-5 [12478096.001]
  • [Cites] Arch Surg. 2006 May;141(5):497-502; discussion 502-3 [16702522.001]
  • [Cites] Clin Exp Pharmacol Physiol. 1994 Apr;21(4):319-22 [7923899.001]
  • [Cites] Surgery. 2006 Dec;140(6):943-8; discussion 948-50 [17188142.001]
  • [Cites] Urology. 2003 Jan;61(1):69-72; discussion 72 [12559268.001]
  • [Cites] Surg Endosc. 2002 Jan;16(1):108-11 [11961617.001]
  • [Cites] Ann Surg. 1997 Sep;226(3):238-46; discussion 246-7 [9339930.001]
  • [Cites] Arch Surg. 1996 Jun;131(6):646-50 [8645073.001]
  • [Cites] World J Surg. 1992 Jul-Aug;16(4):680-3; discussion 683-4 [1413836.001]
  • [Cites] Ann Surg. 1996 Dec;224(6):727-34; discussion 734-6 [8968227.001]
  • [Cites] Am Surg. 2002 Mar;68(3):253-6; discussion 256-7 [11893103.001]
  • [Cites] Ann Surg. 2000 Dec;232(6):796-803 [11088074.001]
  • [Cites] J Urol. 2007 Apr;177(4):1254-7 [17382700.001]
  • [Cites] Ann Surg. 1996 Aug;224(2):125-30 [8757374.001]
  • [Cites] Surg Endosc. 1999 Apr;13(4):343-5 [10094744.001]
  • [Cites] Clin Endocrinol (Oxf). 2007 May;66(5):607-18 [17492946.001]
  • [Cites] Ann Intern Med. 2001 Aug 21;135(4):258-61 [11511140.001]
  • [Cites] J Urol. 2005 Jul;174(1):40-3 [15947573.001]
  • [Cites] Surgery. 1992 Dec;112(6):987-93 [1455323.001]
  • [Cites] JSLS. 2004 Oct-Dec;8(4):320-5 [15554273.001]
  • [Cites] Ann Chir. 2002 Sep;127(7):512-9 [12404845.001]
  • (PMID = 18343972.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  •  go-up   go-down






Advertisement