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1. Fung MM, Viveros OH, O'Connor DT: Diseases of the adrenal medulla. Acta Physiol (Oxf); 2008 Feb;192(2):325-35
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  • [Title] Diseases of the adrenal medulla.
  • The adrenal glands are vital in the organism's response to environmental stress.
  • The medulla is different developmentally, functionally and structurally.
  • Pathology within the adrenal medulla and the autonomic nervous system is primarily because of neoplasms.
  • The most common tumour, called phaeochromocytoma when located in the adrenal medulla, originates from chromaffin cells and excretes catecholamines, but may be referred to as secreting paragangliomas when found in extra-adrenal chromaffin cells.

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  • (PMID = 18021328.001).
  • [ISSN] 1748-1716
  • [Journal-full-title] Acta physiologica (Oxford, England)
  • [ISO-abbreviation] Acta Physiol (Oxf)
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL058120-090004; United States / NIDDK NIH HHS / DK / DK060702-05; United States / NHLBI NIH HHS / HL / HL058120-099006; United States / NIDDK NIH HHS / DK / R01 DK060702-05; United States / NHLBI NIH HHS / HL / HL058120-09; United States / NHLBI NIH HHS / HL / P01 HL058120-09; United States / NHLBI NIH HHS / HL / P01 HL058120-099006; United States / NIDDK NIH HHS / DK / R01 DK060702; United States / NHLBI NIH HHS / HL / P01 HL058120; United States / NHLBI NIH HHS / HL / P01 HL058120-090004
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Catecholamines
  • [Number-of-references] 33
  • [Other-IDs] NLM/ NIHMS57919; NLM/ PMC2576282
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2. Tonks ID, Mould AW, Schroder WA, Cotterill A, Hayward NK, Walker GJ, Kay GF: Dual loss of rb1 and Trp53 in the adrenal medulla leads to spontaneous pheochromocytoma. Neoplasia; 2010 Mar;12(3):235-43
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  • [Title] Dual loss of rb1 and Trp53 in the adrenal medulla leads to spontaneous pheochromocytoma.
  • Using a Cre/loxP system, we have determined the phenotypic consequences attributable to in vivo deletion of both Rb1 and Trp53 in the mouse adrenal medulla.
  • The coablation of these two tumor suppressor genes during embryogenesis did not disrupt adrenal gland development but resulted in the neoplastic transformation of the neural crest-derived adrenal medulla, yielding pheochromocytomas (PCCs) that developed with complete penetrance and were inevitably bilateral.
  • The structural remodeling of the heart in mice harboring Rb1(-/-):Trp53(-/-) PCCs suggests that the mortality of these mice may be attributable to the inappropriate release of catecholamines from the mutated adrenal chromaffin cells.
  • On the basis of the collective data from Rb1 and Trp53 knockout mouse models, it seems that the conversion of Rb1 loss-driven adrenal medulla hyperplasia to PCC can be greatly enhanced by the compound loss of Trp53, whereas the loss of Trp53 alone is generally ineffectual on adrenal chromaffin cell homeostasis.
  • Consequently, the Trp53 tumor suppressor gene is an efficient genetic modifier of Rb1 loss in the development of PCC, and their compound loss in the adrenal medulla has a profound impact on both cellular homeostasis and animal vitality.
  • [MeSH-major] Adrenal Gland Neoplasms / pathology. Genes, p53 / physiology. Pheochromocytoma / pathology. Retinoblastoma Protein / physiology

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  • (PMID = 20234817.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Catecholamines; 0 / Retinoblastoma Protein; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases
  • [Other-IDs] NLM/ PMC2838441
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3. Fliedner SM, Breza J, Kvetnansky R, Powers JF, Tischler AS, Wesley R, Merino M, Lehnert H, Pacak K: Tyrosine hydroxylase, chromogranin A, and steroidogenic acute regulator as markers for successful separation of human adrenal medulla. Cell Tissue Res; 2010 Jun;340(3):607-12
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  • [Title] Tyrosine hydroxylase, chromogranin A, and steroidogenic acute regulator as markers for successful separation of human adrenal medulla.
  • Progress in high throughput "-omic" techniques now allows the simultaneous measurement of expression levels of thousands of genes and promises the improved understanding of the molecular biology of diseases such as cancer.
  • This is difficult to obtain from pheochromocytomas (PHEOs), rare chromaffin tumors derived from adrenal medulla.
  • The two options for obtaining adrenal tissue are:.
  • Access to high quality normal adrenal tissue is limited.
  • Adjacent normal adrenal tissue can almost never be obtained from resected PHEOs, because they often replace the entire medulla or are well-encapsulated.
  • If a margin of normal adrenal is attached to a resected PHEO, it seldom contains any medulla.
  • The clean separation of medulla and cortex is further complicated, because their border is convoluted, and because adult adrenal consists of approximately 90% cortex.
  • [MeSH-major] Adrenal Medulla / enzymology. Chromogranin A / metabolism. Phosphoproteins / metabolism. Tissue Culture Techniques / methods. Tyrosine 3-Monooxygenase / metabolism
  • [MeSH-minor] Adrenal Cortex / pathology. Aged. Biomarkers / metabolism. Female. Humans. Male. Middle Aged. RNA, Messenger / genetics. RNA, Messenger / metabolism

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  • (PMID = 20440513.001).
  • [ISSN] 1432-0878
  • [Journal-full-title] Cell and tissue research
  • [ISO-abbreviation] Cell Tissue Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 HD008735-08
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Chromogranin A; 0 / Phosphoproteins; 0 / RNA, Messenger; 0 / steroidogenic acute regulatory protein; EC 1.14.16.2 / Tyrosine 3-Monooxygenase
  • [Other-IDs] NLM/ NIHMS750167; NLM/ PMC4714581
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4. Cardoso CC, Bornstein SR, Hornsby PJ: Optimizing orthotopic cell transplantation in the mouse adrenal gland. Cell Transplant; 2010;19(5):565-72
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  • [Title] Optimizing orthotopic cell transplantation in the mouse adrenal gland.
  • Orthotopic cell transplantation models are important for a complete understanding of cell-cell interactions as well as tumor biology.
  • In published studies of orthotopic transplantation in the mouse adrenal gland, human neuroblastoma cells have been shown to invade and occupy the adrenal, but in these investigations a true orthotopic model was not established.
  • Here we show an orthotopic model in which transplanted cells are retained within the adrenal gland by formation of a fibrin clot.
  • To establish an appropriate technique, we used brightly fluorescent 10 microm polystyrene microspheres injected into the mouse adrenal gland.
  • When the microspheres were injected in a fibrinogen/thrombin mixture, fluorescence was confined to the adrenal gland.
  • When 3 x 10(5) cells were implanted orthotopically, by 16 days the cell mass had expanded and had invaded the cortex, whereas when 1 x 10(5) cells were used, tumor masses were much smaller.
  • When mice were sacrificed at different time points, we found that tumor growth resulting was progressive and that by 26 days cells there was extensive invasion into the cortex or almost complete replacement of the cortex with tumor cells.
  • In summary, the present orthotopic model for intra-adrenal cell transplantation is valuable for investigation of growth of neoplastic cells of both cortical and medullary origin and should be useful for future studies of cortex-medulla interactions.

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  • (PMID = 20525431.001).
  • [ISSN] 1555-3892
  • [Journal-full-title] Cell transplantation
  • [ISO-abbreviation] Cell Transplant
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / AG012287-14; United States / NIA NIH HHS / AG / P01 AG020752-020006; United States / NIA NIH HHS / AG / AG020752-020006; United States / NIA NIH HHS / AG / P01 AG020752; United States / NIA NIH HHS / AG / R37 AG012287-14; United States / NIA NIH HHS / AG / R37 AG012287
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 9001-31-4 / Fibrin; 9001-32-5 / Fibrinogen; EC 3.4.21.5 / Thrombin
  • [Other-IDs] NLM/ NIHMS246503; NLM/ PMC3735364
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5. Berthon A, Sahut-Barnola I, Lambert-Langlais S, de Joussineau C, Damon-Soubeyrand C, Louiset E, Taketo MM, Tissier F, Bertherat J, Lefrançois-Martinez AM, Martinez A, Val P: Constitutive beta-catenin activation induces adrenal hyperplasia and promotes adrenal cancer development. Hum Mol Genet; 2010 Apr 15;19(8):1561-76
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  • [Title] Constitutive beta-catenin activation induces adrenal hyperplasia and promotes adrenal cancer development.
  • Adrenocortical carcinoma is a rare but aggressive cancer with unknown aetiology.
  • Here, we show that constitutive activation of beta-catenin in the adrenal cortex of transgenic mice resulted in progressive steroidogenic and undifferentiated spindle-shaped cells hyperplasia as well as dysplasia of the cortex and medulla.
  • Altogether these observations demonstrate that constitutively active beta-catenin is an adrenal oncogene which triggers benign aldosterone-secreting tumour development and promotes malignancy.
  • [MeSH-major] Adrenal Cortex / pathology. Adrenal Gland Neoplasms / metabolism. Adrenal Gland Neoplasms / pathology. beta Catenin / metabolism
  • [MeSH-minor] Aldosterone / metabolism. Animals. Cell Proliferation. Disease Models, Animal. Humans. Hyperplasia. Mice. Mice, Inbred C57BL. Mice, Transgenic. Neoplasm Metastasis


6. Kamensky Y, Liu W, Tsai AL, Kulmacz RJ, Palmer G: Axial ligation and stoichiometry of heme centers in adrenal cytochrome b561. Biochemistry; 2007 Jul 24;46(29):8647-58
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  • [Title] Axial ligation and stoichiometry of heme centers in adrenal cytochrome b561.
  • Cytochrome (cyt) b561 transports electrons across the membrane of chromaffin granules (CG) present in the adrenal medulla, supporting the biosynthesis of norepinephrine in the CG matrix.

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  • (PMID = 17602662.001).
  • [ISSN] 0006-2960
  • [Journal-full-title] Biochemistry
  • [ISO-abbreviation] Biochemistry
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / GM080575-01; United States / NIGMS NIH HHS / GM / R01 GM044911; United States / NIGMS NIH HHS / GM / R01 GM044911-13; United States / NIGMS NIH HHS / GM / GM44911; United States / NIGMS NIH HHS / GM / GM044911-13; United States / NIGMS NIH HHS / GM / R01 GM080575; United States / NIGMS NIH HHS / GM / R01 GM080575-01
  • [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 / Cytochrome b Group; 0 / Ligands; 0 / Recombinant Proteins; 11130-51-1 / cytochrome b561; 42VZT0U6YR / Heme; 4QD397987E / Histidine
  • [Other-IDs] NLM/ NIHMS62555; NLM/ PMC2551744
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7. Ohno N, Terada N, Komada M, Saitoh S, Costantini F, Pace V, Germann PG, Weber K, Yamakawa H, Ohara O, Ohno S: Dispensable role of protein 4.1B/DAL-1 in rodent adrenal medulla regarding generation of pheochromocytoma and plasmalemmal localization of TSLC1. Biochim Biophys Acta; 2009 Mar;1793(3):506-15
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  • [Title] Dispensable role of protein 4.1B/DAL-1 in rodent adrenal medulla regarding generation of pheochromocytoma and plasmalemmal localization of TSLC1.
  • Protein 4.1B is a membrane skeletal protein expressed in various organs, and is associated with tumor suppressor in lung cancer-1 (TSLC1) in vitro.
  • Although involvement of 4.1B in the intercellular junctions and tumor-suppression was suggested, some controversial results posed questions to the general tumor-suppressive function of 4.1B and its relation to TSLC1 in vivo.
  • In this study, the expression of 4.1B and its interaction with TSLC1 were examined in rodent adrenal gland, and the involvement of 4.1B in tumorigenesis and the effect of 4.1B deficiency on TSLC1 distribution were also investigated using rodent pheochromocytoma and 4.1B-knockout mice.
  • Although plasmalemmal immunolocalization of 4.1B was shown in chromaffin cells of rodent adrenal medulla, expression of 4.1B was maintained in developed pheochromocytoma, and morphological abnormality or pheochromocytoma generation could not be found in 4.1B-deficient mice.
  • Furthermore, molecular interaction and colocalization of 4.1B and TSLC1 were observed in mouse adrenal gland, but the immunolocalization of TSLC1 along chromaffin cell membranes was not affected in the 4.1B-deficient mice.
  • These results suggest that the function of 4.1B as tumor suppressor might significantly differ among organs and species, and that plasmalemmal retention of TSLC1 would be maintained by molecules other than 4.1B interacting in rodent chromaffin cells.
  • [MeSH-major] Adrenal Gland Neoplasms / metabolism. Adrenal Medulla / metabolism. Immunoglobulins / metabolism. Membrane Proteins / metabolism. Pheochromocytoma / metabolism. Tumor Suppressor Proteins / metabolism

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  • (PMID = 19321127.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5P01CA023767
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Epb4.1l3 protein, mouse; 0 / Immunoglobulins; 0 / Membrane Proteins; 0 / Microfilament Proteins; 0 / Tumor Suppressor Proteins; 0 / cell adhesion molecule 1, mouse
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8. Colomer C, Desarménien MG, Guérineau NC: Revisiting the stimulus-secretion coupling in the adrenal medulla: role of gap junction-mediated intercellular communication. Mol Neurobiol; 2009 Aug;40(1):87-100
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Revisiting the stimulus-secretion coupling in the adrenal medulla: role of gap junction-mediated intercellular communication.
  • The current view of stimulation-secretion coupling in adrenal neuroendocrine chromaffin cells holds that catecholamines are released upon transsynaptic sympathetic stimulation mediated by acetylcholine released from the splanchnic nerve terminals.
  • The experimental clues supporting this hypothesis are presented and discussed with regards to both interaction with the excitatory cholinergic synaptic transmission and physiopathology of the adrenal medulla.
  • [MeSH-major] Adrenal Medulla / metabolism. Cell Communication. Gap Junctions / physiology

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  • (PMID = 19444654.001).
  • [ISSN] 0893-7648
  • [Journal-full-title] Molecular neurobiology
  • [ISO-abbreviation] Mol. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Catecholamines
  • [Number-of-references] 147
  • [Other-IDs] NLM/ HALMS398108; NLM/ PMC2879034
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9. Opocher G, Schiavi F, Cicala MV, Patalano A, Mariniello B, Boaretto F, Zovato S, Pignataro V, Macino B, Negro I, Mantero F: Genetics of adrenal tumors. Minerva Endocrinol; 2009 Jun;34(2):107-21
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] Genetics of adrenal tumors.
  • Endocrinology pioneered the development of molecular medicine, but also the study of adrenal tumors had a great impact in this field.
  • Particularly important was the detection of genetics of tumors derived from the adrenal medulla, as well as that of those derived from the sympathetic and parasympathetic paraganglia.
  • Less well understood is the genetics of adrenal cortex tumors, in particular adrenocortical carcinoma, a rare and particularly aggressive disease.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Biomarkers, Tumor / genetics. Mutation. Pheochromocytoma / genetics
  • [MeSH-minor] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Genetic Predisposition to Disease. Genomics. Humans. Neoplasm Proteins / genetics. Paraganglioma / genetics

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  • (PMID = 19471236.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
  • [Number-of-references] 81
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10. Lai EW, Rodriguez OC, Aventian M, Cromelin C, Fricke ST, Martiniova L, Lubensky IA, Lisanti MP, Picard KL, Powers JF, Tischler AS, Pacak K, Albanese C: ErbB-2 induces bilateral adrenal pheochromocytoma formation in mice. Cell Cycle; 2007 Aug 01;6(15):1946-50
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  • [Title] ErbB-2 induces bilateral adrenal pheochromocytoma formation in mice.
  • Pheochromocytoma (PCC) is a rare catecholamine-producing tumor that arises from the adrenal medulla and is often familial.
  • In the present study, ectopic expression of an activated ErbB-2 transgene resulted in bilateral adrenal PCC.
  • Analyses of tumor samples and normal adrenal tissue revealed that levels of the Pten tumor suppressor protein were greatly reduced in PCCs, while levels of the cell cycle regulatory protein cyclin D1 were usually increased.
  • In addition, levels of phospo-AKT were increased in PCCs versus normal adrenal tissue.
  • These data establish that increased ErbB-2 growth factor receptor signaling in the adrenal medulla can lead to PCC through combined influences on Pten, AKT andcyclin D1.
  • [MeSH-major] Adrenal Gland Neoplasms / metabolism. Adrenal Gland Neoplasms / pathology. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Pheochromocytoma / metabolism. Pheochromocytoma / pathology. Receptor, ErbB-2 / metabolism


11. Korpershoek E, Petri BJ, van Nederveen FH, Dinjens WN, Verhofstad AA, de Herder WW, Schmid S, Perren A, Komminoth P, de Krijger RR: Candidate gene mutation analysis in bilateral adrenal pheochromocytoma and sympathetic paraganglioma. Endocr Relat Cancer; 2007 Jun;14(2):453-62
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  • [Title] Candidate gene mutation analysis in bilateral adrenal pheochromocytoma and sympathetic paraganglioma.
  • Pheochromocytomas (PCCs) are rare tumors that arise from chromaffin tissue in the adrenal medulla, but can also occur in the abdomen outside the adrenals and are then called sympathetic paragangliomas (sPGLs).
  • According to the literature, between 15 and 25% of apparently sporadic adrenal PCC and sPGL are caused by germline mutations in RET, von Hippel-Lindau disease (VHL), succinate dehydrogenase subunit B (SDHB), or subunit D SDHD.
  • However, few studies have addressed the mutationfrequency of these candidate genes in selected subgroups of PCC andsPGL, such as bilateral adrenal PCC or extra-adrenal sPGL, and none have looked at somatic mutations by analyzing tumor tissue.
  • Therefore, we have investigated the occurrence of germline and somatic mutations in RET, VHL, SDHB, and SDHD in comparatively large series of bilateral adrenal PCC (n = 33 patients) and sPGL (n = 26 patients), with the aim of determining the mutation frequency of each of these genes and to establish a genetic testing algorithm.
  • Twenty-one RET, two VHL germline, and one SDHD mutations were found in the patients with bilateral adrenal PCC.
  • We suggest that sequential mutation analysis should be directed first at RET, followed by VHL and SDHD for patients with bilateral adrenal PCC at diagnosis, and at SDHB and SDHD for patients with sPGL.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Genes, Neoplasm. Paraganglioma / genetics. Pheochromocytoma / genetics
  • [MeSH-minor] Adult. Aged. Amino Acid Sequence. Animals. Cattle. DNA Mutational Analysis. Female. Germ-Line Mutation. Humans. Iron-Sulfur Proteins / genetics. Male. Mice. Middle Aged. Molecular Sequence Data. Mutation. Proto-Oncogene Proteins c-ret / genetics. Rats. Succinate Dehydrogenase / genetics. Von Hippel-Lindau Tumor Suppressor Protein / genetics

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  • (PMID = 17639058.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Iron-Sulfur Proteins; 0 / SDHD protein, human; EC 1.3.5.1 / SDHB protein, human; EC 1.3.99.1 / Succinate Dehydrogenase; EC 2.7.10.1 / Proto-Oncogene Proteins c-ret; EC 2.7.10.1 / RET protein, human; EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
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12. Ilias I, Sahdev A, Reznek RH, Grossman AB, Pacak K: The optimal imaging of adrenal tumours: a comparison of different methods. Endocr Relat Cancer; 2007 Sep;14(3):587-99
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  • [Title] The optimal imaging of adrenal tumours: a comparison of different methods.
  • Computed tomography (CT; unenhanced, followed by contrast-enhanced examinations) is the cornerstone of imaging of adrenal tumours.
  • Functional nuclear medicine imaging is useful for adrenal lesions that are not adequately characterised with CT and MRI.
  • Scintigraphy with [(131)I]-6-iodomethyl norcholesterol (a labelled cholesterol analogue) can differentiate adrenal cortical adenomas from carcinomas.
  • The specific and useful roles of adrenal imaging include the characterisation of tumours, assessment of true tumour size, differentiation of adenomas from carcinomas and metastases, and differentiation of hyperfunctioning from non-functioning lesions.
  • Adrenal imaging complements and assists the clinical and hormonal evaluation of adrenal tumours.
  • [MeSH-major] Adenoma / diagnosis. Adrenal Gland Neoplasms / diagnosis. Diagnostic Imaging / methods
  • [MeSH-minor] Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / pathology. Adrenal Medulla / pathology. Adrenocortical Hyperfunction / diagnosis. Diagnosis, Differential. Ganglioneuroma / diagnosis. Ganglioneuroma / pathology. Hemangioma / diagnosis. Hemangioma / pathology. Hemangiosarcoma / diagnosis. Hemangiosarcoma / pathology. Humans. Leiomyosarcoma / diagnosis. Leiomyosarcoma / pathology. Lymphoma / diagnosis. Lymphoma / pathology. Magnetic Resonance Imaging. Myelolipoma / diagnosis. Myelolipoma / pathology. Neoplasm Metastasis. Neuroblastoma / diagnosis. Neuroblastoma / pathology. Pheochromocytoma / diagnosis. Pheochromocytoma / pathology. Tomography, X-Ray Computed. Whole Body Imaging

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  • (PMID = 17914090.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 61
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13. Hattori Y, Kanamoto N, Kawano K, Iwakura H, Sone M, Miura M, Yasoda A, Tamura N, Arai H, Akamizu T, Nakao K, Maitani Y: Molecular characterization of tumors from a transgenic mouse adrenal tumor model: comparison with human pheochromocytoma. Int J Oncol; 2010 Sep;37(3):695-705
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  • [Title] Molecular characterization of tumors from a transgenic mouse adrenal tumor model: comparison with human pheochromocytoma.
  • Adrenal neuroblastoma and pheochromocytoma have the same embryonic origin from neural crest cells and mainly arise from the adrenal medulla.
  • Recently, transgenic mice exhibiting tumors in the bilateral adrenal medulla by the expression of SV40 T-antigen were developed.
  • In this study, we investigated mRNA expression in adrenal tumors of transgenic mice and compared them with human pheochromocytoma by DNA microarray analysis.
  • To compare mouse adrenal tumors and human pheochromacytoma, we found that the expressions of noradrenergic neuron-related genes, including dopa decarboxylase, phenylethanolamine-N-methyltransferase and chromogranin B, were up-regulated in humans but not in mice; however, the expression of neuroblastoma-related genes, including Mycn, paired-like homeobox 2b, gamma-aminobutyric acid A receptor beta3 subunit, islet 1 and kinesin family member 1A, was up-regulated in both species.
  • From the gene expression profiles, the characterization of mouse adrenal tumor, may be similar to that of human adrenal neuroblastoma rather than pheochromacytomas.
  • This mouse model would be a useful tool for the development of anti-cancer drugs and for understanding the etiology of adrenal neuroblastoma.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Pheochromocytoma / genetics


14. Shi G, Ma K, Pappas GD, Qu T: Phenotypic characteristics of hybrid cells produced by cell fusion of porcine adrenal chromaffin cells with human mesenchymal stem cells: a preliminary study. Neurol Res; 2008 Apr;30(3):217-22
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  • [Title] Phenotypic characteristics of hybrid cells produced by cell fusion of porcine adrenal chromaffin cells with human mesenchymal stem cells: a preliminary study.
  • BACKGROUND AND PURPOSE: Transplantation of adrenal chromaffin cells (CCs) that release endogenous opioid peptides and catecholamines produces significant antinociceptive effects in patients with terminal cancer pain.
  • In clinical practice, however, obtaining a sufficient number of chromaffin cells may not be possible because of the limited availability of human adrenal tissue.
  • [MeSH-major] Adrenal Medulla / cytology. Chromaffin Cells / physiology. Hybrid Cells / physiology. Mesenchymal Stromal Cells / physiology. Phenotype

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  • (PMID = 18252039.001).
  • [ISSN] 0161-6412
  • [Journal-full-title] Neurological research
  • [ISO-abbreviation] Neurol. Res.
  • [Language] eng
  • [Grant] United States / NIDA NIH HHS / DA / R01DA015511
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Fluorescent Dyes; 0 / Surface-Active Agents; 30IQX730WE / Polyethylene Glycols; EC 1.14.16.2 / Tyrosine 3-Monooxygenase; G34N38R2N1 / Bromodeoxyuridine
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15. Berber E, Siperstein A: Laparoscopic radiofrequency thermal ablation of adrenal tumors: technical details. Surg Laparosc Endosc Percutan Tech; 2010 Feb;20(1):58-62
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  • [Title] Laparoscopic radiofrequency thermal ablation of adrenal tumors: technical details.
  • BACKGROUND: Despite reports of percutaneous radiofrequency ablation (RFA), laparoscopic ablative techniques have not been described to treat adrenal tumors.
  • The aim of this study is to describe patient selection criteria and the technique for laparoscopic adrenal RFA.
  • METHODS: Four patients underwent laparoscopic RFA of adrenal tumors under general anesthesia for adrenal tumors.
  • RESULTS: Pathology included lung metastasis in 2 patients, and renal cell cancer metastasis and cortical adenoma in 1 patient each.
  • Despite normal catecholamine levels preoperatively, 2 patients had a transient hypertensive period during the ablation possibly owing to the release of catecholamines from the normal adrenal medulla.
  • CONCLUSIONS: To our knowledge, this is the first report of laparoscopic adrenal RFA.
  • Laparoscopic RFA is an option for patients with unresectable adrenal tumors owing to the extent of disease or comorbidities.
  • [MeSH-major] Adrenal Gland Neoplasms / therapy. Adrenalectomy / methods. Catheter Ablation / methods. Hot Temperature / therapeutic use. Laparoscopy

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  • (PMID = 20173624.001).
  • [ISSN] 1534-4908
  • [Journal-full-title] Surgical laparoscopy, endoscopy & percutaneous techniques
  • [ISO-abbreviation] Surg Laparosc Endosc Percutan Tech
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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16. Namour F, Ayav A, Lu X, Klein M, Muresan M, Bresler L, Tramoy D, Guéant JL, Brunaud L: Lack of association between microsatellite instability and benign adrenal tumors. World J Surg; 2006 Jul;30(7):1240-6
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  • [Title] Lack of association between microsatellite instability and benign adrenal tumors.
  • BACKGROUND: The adrenal gland may give rise to pheochromocytomas, which are catecholamine-producing tumors originating from the adrenal medulla, or to adrenocortical tumors, which derive from the adrenocortical cortex and may be secreting or not.
  • AIM: The aim of this study was to investigate a third genetic mechanism by evaluating microsatellite instability using the reference markers (Bat25, Bat26, D2S123, D5S346, D17S250) validated by the National Cancer Institute.
  • No microsatellite instability was detected in any tumor.
  • A second patient with a MEN-2A syndrome and a two-sided pheochromocytoma exhibited a loss of heterozygosity for D2S123 in the right tumor only and a retention of heterozygosity for all markers in the left tumor.
  • CONCLUSIONS: These results suggest that microsatellite instability, evaluated by the five reference markers of the National Cancer Institute, is not a feature of benign adrenal tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Microsatellite Repeats / genetics. Pheochromocytoma / genetics
  • [MeSH-minor] Adult. Aged. Alleles. DNA, Neoplasm / analysis. Female. Humans. Loss of Heterozygosity. Male. Middle Aged. Polymerase Chain Reaction. Proto-Oncogene Proteins / genetics

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  • (PMID = 16715450.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Proto-Oncogene Proteins
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17. Murray SA, Nickel BM, Gay VL: Gap junctions as modulators of adrenal cortical cell proliferation and steroidogenesis. Mol Cell Endocrinol; 2009 Mar 5;300(1-2):51-6
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  • [Title] Gap junctions as modulators of adrenal cortical cell proliferation and steroidogenesis.
  • In the adrenal gland, as in most other tissues, intercellular communication provides the potential for regulation of a number of complex interactive cell processes including differentiation, steroidogenesis, migration, and proliferation.
  • This review is concerned with the regulation of gap junctions and cell function in cortical cells of the adrenal gland and in pathological disorders such as adrenal cancer.
  • [MeSH-major] Adrenal Cortex. Cell Proliferation. Gap Junctions / metabolism. Steroids / biosynthesis
  • [MeSH-minor] Adrenal Cortex Neoplasms / metabolism. Adrenal Cortex Neoplasms / physiopathology. Adrenal Medulla / cytology. Adrenal Medulla / physiology. Animals. Cell Movement / physiology. Connexins / metabolism

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  • (PMID = 18973789.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Connexins; 0 / Steroids
  • [Number-of-references] 55
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18. Nomikos IN, Zizi-Serbetzoglou A, Matsakis G, Elemenoglou J, Vamvakopoulos NC: Association of an oversized adrenal cortical adenoma with expression of pheochromocytoma-like neurosecretory features. J BUON; 2008 Jul-Sep;13(3):425-8
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  • [Title] Association of an oversized adrenal cortical adenoma with expression of pheochromocytoma-like neurosecretory features.
  • Abnormal stimulation of adrenal function may be either direct, affecting similarly cortical and medullary secretion, or indirect affecting primarily the medulla.
  • Indirect activation of clinically detectable adrenomedullary function may develop as a physical consequence of a non-functional adrenal tumor exerting pressure on the medulla by its size, location and direction of growth.
  • Our case of an oversized and overweight adrenal tumor associated with expression of late-onset pheochromocytoma-like clinical symptoms may be explained by the physical indirect rather than the biological direct activation of adrenomedullary function like hyperplasia or cancer.
  • [MeSH-major] Adenoma / pathology. Adrenal Cortex Neoplasms / pathology. Adrenal Medulla / pathology. Pheochromocytoma / pathology

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  • (PMID = 18979561.001).
  • [ISSN] 1107-0625
  • [Journal-full-title] Journal of B.U.ON. : official journal of the Balkan Union of Oncology
  • [ISO-abbreviation] J BUON
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 57285-09-3 / Inhibins
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19. Yoshikawa N, Nemoto T, Satoh S, Maruta T, Yanagita T, Chosa E, Wada A: Distinct regulation of insulin receptor substrate-1 and -2 by 90-kDa heat-shock protein in adrenal chromaffin cells. Neurochem Int; 2010 Jan;56(1):42-50
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  • [Title] Distinct regulation of insulin receptor substrate-1 and -2 by 90-kDa heat-shock protein in adrenal chromaffin cells.
  • The 90-kDa heat-shock protein (Hsp90) is an emerging target molecule of therapeutics, Hsp90 inhibitors being promising against various diseases (e.g., cancer, brain and cardiac ischemia, and neurodegenerative diseases).
  • In cultured bovine adrenal chromaffin cells, we observed that 24-h treatment with 1 microM geldanamycin (an inhibitor of Hsp90) decreased insulin receptor substrate-1 level, while increasing insulin receptor substrate-2 level; besides, geldanamycin lowered phosphoinositide 3-kinase, phosphoinositide-dependent kinase-1, Akt, glycogen synthase kinase-3beta, and Raf-1 levels, without changing extracellular signal-regulated kinase and its upstream kinase levels.
  • [MeSH-major] Adrenal Medulla / metabolism. Chromaffin Cells / metabolism. HSP90 Heat-Shock Proteins / metabolism. Insulin Receptor Substrate Proteins / metabolism. Signal Transduction / physiology

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  • [Copyright] 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19737590.001).
  • [ISSN] 1872-9754
  • [Journal-full-title] Neurochemistry international
  • [ISO-abbreviation] Neurochem. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzoquinones; 0 / Enzyme Inhibitors; 0 / HSP90 Heat-Shock Proteins; 0 / Insulin Receptor Substrate Proteins; 0 / Lactams, Macrocyclic; 0 / Protein Synthesis Inhibitors; 0 / RNA, Messenger; EC 2.7.- / Phosphotransferases; EC 3.4.25.1 / Proteasome Endopeptidase Complex; Z3K3VJ16KU / geldanamycin
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20. Macova M, Armando I, Zhou J, Baiardi G, Tyurmin D, Larrayoz-Roldan IM, Saavedra JM: Estrogen reduces aldosterone, upregulates adrenal angiotensin II AT2 receptors and normalizes adrenomedullary Fra-2 in ovariectomized rats. Neuroendocrinology; 2008;88(4):276-86
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  • [Title] Estrogen reduces aldosterone, upregulates adrenal angiotensin II AT2 receptors and normalizes adrenomedullary Fra-2 in ovariectomized rats.
  • We studied the effect of ovariectomy and estrogen replacement on expression of adrenal angiotensin II AT1 and AT2 receptors, aldosterone content, catecholamine synthesis, and the transcription factor Fos-related antigen 2 (Fra-2).
  • Ovariectomy increased AT1 receptor expression in the adrenal zona glomerulosa and medulla, and decreased adrenomedullary catecholamine content and Fra-2 expression when compared to intact female rats.
  • Estrogen treatment decreased adrenal aldosterone content.
  • In the adrenal medulla, the effects of estrogen replacement were: normalized AT1 receptor expression, increased AT2 receptor expression, AT2 receptor mRNA, and tyrosine hydroxylase mRNA, and normalized Fra-2 expression and catecholamine content.
  • We demonstrate that the constitutive adrenal expression of AT1 receptors, catecholamine synthesis and Fra-2 expression are partially under the control of reproductive hormones.
  • [MeSH-major] Adrenal Medulla / metabolism. Aldosterone / metabolism. Estrogens / pharmacology. Fos-Related Antigen-2 / metabolism. Ovariectomy. Receptor, Angiotensin, Type 2 / metabolism. Zona Glomerulosa / metabolism

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  • [Copyright] Copyright 2008 S. Karger AG, Basel.
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  • (PMID = 18679017.001).
  • [ISSN] 1423-0194
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 MH002762-11; United States / Intramural NIH HHS / / Z99 MH999999
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Catecholamines; 0 / Estrogens; 0 / Fos-Related Antigen-2; 0 / Fosl2 protein, rat; 0 / RNA, Messenger; 0 / Receptor, Angiotensin, Type 1; 0 / Receptor, Angiotensin, Type 2; 4964P6T9RB / Aldosterone; EC 1.14.16.2 / Tyrosine 3-Monooxygenase
  • [Other-IDs] NLM/ NIHMS104518; NLM/ PMC2677380
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21. Molatore S, Liyanarachchi S, Irmler M, Perren A, Mannelli M, Ercolino T, Beuschlein F, Jarzab B, Wloch J, Ziaja J, Zoubaa S, Neff F, Beckers J, Höfler H, Atkinson MJ, Pellegata NS: Pheochromocytoma in rats with multiple endocrine neoplasia (MENX) shares gene expression patterns with human pheochromocytoma. Proc Natl Acad Sci U S A; 2010 Oct 26;107(43):18493-8
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  • [Title] Pheochromocytoma in rats with multiple endocrine neoplasia (MENX) shares gene expression patterns with human pheochromocytoma.
  • Pheochromocytomas are rare neoplasias of neural crest origin arising from chromaffin cells of the adrenal medulla and sympathetic ganglia (extra-adrenal pheochromocytoma).
  • Pheochromocytoma that develop in rats homozygous for a loss-of-function mutation in p27Kip1 (MENX syndrome) show a clear progression from hyperplasia to tumor, offering the possibility to gain insight into tumor pathobiology.
  • We compared the gene-expression signatures of both adrenomedullary hyperplasia and pheochromocytoma with normal rat adrenal medulla.
  • Hyperplasia and tumor show very similar transcriptome profiles, indicating early determination of the tumorigenic signature.
  • Overexpression of these genes precedes histological changes in affected adrenal glands.
  • Adrenal and extra-adrenal pheochromocytoma development clearly follows diverged molecular pathways in MENX rats.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Multiple Endocrine Neoplasia / genetics. Pheochromocytoma / genetics
  • [MeSH-minor] Adrenal Medulla / metabolism. Adrenal Medulla / pathology. Animals. Base Sequence. Biomarkers, Tumor / genetics. Cyclin-Dependent Kinase Inhibitor p27 / genetics. DNA Primers / genetics. Disease Models, Animal. Gene Expression Profiling. Homeodomain Proteins / genetics. Humans. Hyperplasia. Neural Cell Adhesion Molecule L1 / genetics. PC12 Cells. Paraganglioma / genetics. Rats. Rats, Mutant Strains. Species Specificity

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  • (PMID = 20937862.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE21006
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cdkn1b protein, rat; 0 / DNA Primers; 0 / Homeodomain Proteins; 0 / Neural Cell Adhesion Molecule L1; 0 / PHOX2A protein, human; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27
  • [Other-IDs] NLM/ PMC2972990
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22. van Nederveen FH, Korpershoek E, deLeeuw RJ, Verhofstad AA, Lenders JW, Dinjens WN, Lam WL, de Krijger RR: Array-comparative genomic hybridization in sporadic benign pheochromocytomas. Endocr Relat Cancer; 2009 Jun;16(2):505-13
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  • Pheochromocytomas (PCC) are catecholamine-producing tumors arising from the adrenal medulla that occur either sporadically or in the context of hereditary cancer syndromes, such as multiple endocrine neoplasia type 2 (MEN2), von Hippel-Lindau disease (VHL), neurofibromatosis type 1, and the PCC-paraganglioma syndrome.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Chromosome Aberrations. Comparative Genomic Hybridization. Oligonucleotide Array Sequence Analysis. Pheochromocytoma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 22 / genetics. Chromosomes, Human, Pair 3 / genetics. Female. Humans. Loss of Heterozygosity. Male. Middle Aged. Multiple Endocrine Neoplasia Type 2a / genetics. Mutation / genetics. Von Hippel-Lindau Tumor Suppressor Protein / genetics. Young Adult

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  • (PMID = 19153209.001).
  • [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] EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
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23. Korpershoek E, Van Nederveen FH, Dannenberg H, Petri BJ, Komminoth P, Perren A, Lenders JW, Verhofstad AA, De Herder WW, De Krijger RR, Dinjens WN: Genetic analyses of apparently sporadic pheochromocytomas: the Rotterdam experience. Ann N Y Acad Sci; 2006 Aug;1073:138-48
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  • They are usually located in the adrenal medulla, although in about 10% the tumors arise from extra-adrenal chromaffin tissue.
  • The majority of PCCs arise sporadically, but PCCs occur also in the context of hereditary cancer syndromes.
  • Familial PCC is inherited as an autosomal dominant trait alone or as a component of the multiple endocrine neoplasia Type 2 (MEN2) syndrome (RET gene), Von Hippel-Lindau (VHL) disease (VHL gene), neurofibromatosis Type 1 (NF1 gene), or familial pheochromocytoma-paraganglioma (PCC-PGL) syndrome (SDHD/B and C genes).
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Pheochromocytoma / genetics
  • [MeSH-minor] Genetic Predisposition to Disease. Germ-Line Mutation. Humans. Polymerase Chain Reaction. Proto-Oncogene Proteins c-ret / genetics. Succinate Dehydrogenase / genetics. Von Hippel-Lindau Tumor Suppressor Protein / genetics

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  • (PMID = 17102080.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.3.99.1 / Succinate Dehydrogenase; EC 2.7.10.1 / Proto-Oncogene Proteins c-ret; EC 2.7.10.1 / RET protein, human; EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
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24. Nakamura M, Han B, Nunobiki O, Kakudo K: Adrenomedullin: a tumor progression factor via angiogenic control. Curr Cancer Drug Targets; 2006 Nov;6(7):635-43
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  • [Title] Adrenomedullin: a tumor progression factor via angiogenic control.
  • ADM is synthesized and is secreted from many mammalian tissues, including the adrenal medulla, endothelial and vascular smooth muscle cells, as well as the myocardium and central nervous system.
  • ADM has been implicated as a mediator of several diseases such as cardiovascular and renal disorders, sepsis, inflammation, diabetes and cancer.
  • ADM is also expressed in a variety of tumors, including breast, endometrial and prostate cancer.
  • ADM has been shown to be a mitogenic factor capable of stimulating growth of several cancer cell types.
  • In addition, ADM is a survival factor for certain cancer cells and an indirect suppressor of the immune response.
  • The major focus of this review will be on the role of ADM in cancer, with emphasis on its utility in diagnostic and prognostic terms, along with its relevance as a therapeutic target.

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  • (PMID = 17100569.001).
  • [ISSN] 1873-5576
  • [Journal-full-title] Current cancer drug targets
  • [ISO-abbreviation] Curr Cancer Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Receptors, Adrenomedullin; 0 / Receptors, Peptide; 148498-78-6 / Adrenomedullin
  • [Number-of-references] 111
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25. Boren J, Ramos-Montoya A, Bosch KS, Vreeling H, Jonker A, Centelles JJ, Cascante M, Frederiks WM: In situ localization of transketolase activity in epithelial cells of different rat tissues and subcellularly in liver parenchymal cells. J Histochem Cytochem; 2006 Feb;54(2):191-9
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  • In situ detection of transketolase is important because this multifunctional enzyme has been related with diseases such as cancer, diabetes, Alzheimer's disease, and Wernicke-Korsakoff's syndrome.
  • Transketolase activity was studied in liver, small intestine, trachea, tongue, kidney, adrenal gland, and eye.
  • Activity was found in liver parenchyma, epithelium of small intestine, trachea, tongue, proximal tubules of kidney and cornea, and ganglion cells in medulla of adrenal gland.
  • It is concluded that the method developed for in situ localization of transketolase activity for light and electron microscopy is specific and allows further investigation of the role of transketolase in (proliferation of) cancer cells and other pathophysiological processes.

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  • (PMID = 16116031.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.2.1.1 / Transketolase
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26. Plouin PF, Gimenez-Roqueplo AP: Pheochromocytomas and secreting paragangliomas. Orphanet J Rare Dis; 2006;1:49
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  • Catecholamine-producing tumors may arise in the adrenal medulla (pheochromocytomas) or in extraadrenal chromaffin cells (secreting paragangliomas).
  • Their prevalence is about 0.1% in patients with hypertension and 4% in patients with a fortuitously discovered adrenal mass.
  • These tumors may be sporadic or part of any of several genetic diseases: familial pheochromocytoma-paraganglioma syndromes, multiple endocrine neoplasia type 2, neurofibromatosis 1 and von Hippel-Lindau disease.
  • The most specific and sensitive diagnostic test for the tumor is the determination of plasma or urinary metanephrines.
  • The tumor can be located by computed tomography, magnetic resonance imaging and metaiodobenzylguanidine scintigraphy.
  • Treatment requires resection of the tumor, generally by laparoscopic surgery.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis. Adrenal Gland Neoplasms / therapy. Paraganglioma, Extra-Adrenal / diagnosis. Paraganglioma, Extra-Adrenal / secretion. Pheochromocytoma / diagnosis. Pheochromocytoma / therapy
  • [MeSH-minor] Adrenal Gland Diseases / diagnosis. Catecholamines / biosynthesis. Catecholamines / secretion. Diagnosis, Differential. Genetic Testing / methods. Humans. Hypertension / etiology. Prognosis. Proto-Oncogene Proteins c-ret / genetics

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  • (PMID = 17156452.001).
  • [ISSN] 1750-1172
  • [Journal-full-title] Orphanet journal of rare diseases
  • [ISO-abbreviation] Orphanet J Rare Dis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Catecholamines; EC 2.7.10.1 / Proto-Oncogene Proteins c-ret; EC 2.7.10.1 / RET protein, human
  • [Number-of-references] 29
  • [Other-IDs] NLM/ PMC1702343
  • [General-notes] NLM/ Original DateCompleted: 20070718
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27. Parlato R, Otto C, Tuckermann J, Stotz S, Kaden S, Gröne HJ, Unsicker K, Schütz G: Conditional inactivation of glucocorticoid receptor gene in dopamine-beta-hydroxylase cells impairs chromaffin cell survival. Endocrinology; 2009 Apr;150(4):1775-81
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  • The analysis of mice carrying a germ line deletion of the glucocorticoid receptor (GR) gene has challenged these previous results because the embryonic development of adrenal chromaffin cells is largely unaltered.
  • In the present study, we have analyzed the role of GC-dependent signaling in the postnatal development of adrenal chromaffin cells by conditional inactivation of the GR gene in cells expressing dopamine-beta-hydroxylase, an enzyme required for the synthesis of noradrenaline and adrenaline.
  • These mutant mice are viable, allowing to study whether in the absence of GC signaling further development of the adrenal medulla is affected.
  • Our analysis shows that the loss of GR leads not only to the loss of phenylethanolamine-N-methyl-transferase expression and, therefore, to inhibition of adrenaline synthesis, but also to a dramatic reduction in the number of adrenal chromaffin cells.
  • [MeSH-minor] Adrenal Glands / cytology. Adrenal Glands / metabolism. Adrenal Medulla / metabolism. Adrenal Medulla / pathology. Animals. Cells, Cultured. Immunohistochemistry. In Situ Nick-End Labeling. Mice. Phenylethanolamine N-Methyltransferase / metabolism

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  • (PMID = 19036879.001).
  • [ISSN] 1945-7170
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Glucocorticoid; EC 1.14.17.1 / Dopamine beta-Hydroxylase; EC 2.1.1.28 / Phenylethanolamine N-Methyltransferase
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28. Zhou M, Shen D, Head JE, Chew EY, Chévez-Barrios P, Green WR, Chan CC: Ocular clusterin expression in von Hippel-Lindau disease. Mol Vis; 2007;13:2129-36
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  • Its mRNA is ubiquitously expressed, with high levels in von Hippel-Lindau (VHL) target organs such as the brain, liver, kidney, and adrenal medulla.
  • RESULTS: All retinal hemangioblastoma were composed of typical VHL tumor cells admixed with small vascular channels as well as glial cells.
  • CONCLUSIONS: Clusterin shows possible important functions in tumor suppression by the VHL gene product (pVHL) and the potential to be a novel biomarker in retinal hemangioblastoma associated VHL disease.

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  • (PMID = 18079682.001).
  • [ISSN] 1090-0535
  • [Journal-full-title] Molecular vision
  • [ISO-abbreviation] Mol. Vis.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 EY000222-22; United States / Intramural NIH HHS / / Z99 EY999999
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Clusterin; 0 / RNA, Messenger
  • [Other-IDs] NLM/ NIHMS36212; NLM/ PMC2173882
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29. Nofech-Mozes S, Mackenzie R, Kahn HJ, Ehrlich L, Raphael SJ: Breast metastasis by medullary thyroid carcinoma detected by FDG positron emission tomography. Ann Diagn Pathol; 2008 Feb;12(1):67-71
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  • Medullary thyroid carcinoma (MTC) is an uncommon thyroid cancer comprising 5% to 8% of thyroid neoplasms.
  • In contrast to common thyroid tumors, this tumor originates from the calcitonin-producing C cells.
  • Common metastatic sites include the liver, bone, brain, and adrenal medulla.
  • (1) metastasis to the breast is an extremely rare occurrence and could be easily confused clinically and pathologically with a primary breast neoplasm and (2) this is the first reported case of detection of breast metastasis by an MTC using FDG ((18)F-fluoro-2-deoxy-D-glucose) positron emission tomography with an accompanying histologic description.
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Cisplatin / therapeutic use. Combined Modality Therapy. Doxorubicin / therapeutic use. Female. Humans. Immunohistochemistry. Middle Aged. Palliative Care

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  • (PMID = 18164420.001).
  • [ISSN] 1092-9134
  • [Journal-full-title] Annals of diagnostic pathology
  • [ISO-abbreviation] Ann Diagn Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18; 80168379AG / Doxorubicin; Q20Q21Q62J / Cisplatin
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30. Kupka S, Haack B, Zdichavsky M, Mlinar T, Kienzle C, Bock T, Kandolf R, Kroeber SM, Königsrainer A: Large proportion of low frequency microsatellite-instability and loss of heterozygosity in pheochromocytoma and endocrine tumors detected with an extended marker panel. J Cancer Res Clin Oncol; 2008 Apr;134(4):463-71
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  • PURPOSE: Pheochromocytoma (PCC) is a usually benign tumor originated in the majority of patients from the adrenal medulla.
  • Among the 23 patients with endocrine tumors, only three (one pancreatic endocrine tumor, one duodenal neuro-endocrine tumor, one hepatic metastasis of a primary tumor with unknown origin) demonstrated MSI.

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  • (PMID = 17828419.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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31. Niederhuber JE, Fojo T: Treatment of metastatic disease in patients with neuroendocrine tumors. Surg Oncol Clin N Am; 2006 Jul;15(3):511-33, viii
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  • Their predominant site of origin is the gastrointestinal tract, where most involve the small intestine and appendix, but are also found in the adrenal medulla, bronchopulmonary system, pancreas, thyroid, parathyroid, and paraganglia cells.
  • [MeSH-minor] Algorithms. Antibiotics, Antineoplastic / administration & dosage. Antineoplastic Agents / administration & dosage. Chemoembolization, Therapeutic. Diagnostic Imaging. Hepatic Artery. Humans. Neoplasm Staging. Positron-Emission Tomography. Prognosis. Receptors, Somatostatin. Sensitivity and Specificity. Somatostatin / analogs & derivatives. Streptozocin / administration & dosage

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  • (PMID = 16882495.001).
  • [ISSN] 1055-3207
  • [Journal-full-title] Surgical oncology clinics of North America
  • [ISO-abbreviation] Surg. Oncol. Clin. N. Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents; 0 / Receptors, Somatostatin; 51110-01-1 / Somatostatin; 5W494URQ81 / Streptozocin
  • [Number-of-references] 87
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32. National Toxicology Program: NTP toxicology and carcinogenesis studies of decalin (CAS No. 91-17-8) in F344/N rats and B6C3F(1) mice and a toxicology study of decalin in male NBR rats (inhalation studies). Natl Toxicol Program Tech Rep Ser; 2005 Jan;(513):1-316
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  • Decalin was nominated for study by the National Cancer Institute because of its chemical structure, its potential for consumer exposure, and a lack of adequate testing of the chemical.
  • Incidences of renal tubule regeneration and granular casts in the medulla of the kidney in exposed male rats were increased, and the severities of hyaline droplets generally increased with increasing exposure concentration.
  • Incidences of renal tubule adenoma and adenoma or carcinoma (combined) and of benign or malignant pheochromocytoma (combined) of the adrenal medulla in 100 and 400 ppm males were significantly increased.
  • There was a significant association between nephropathy severity and adrenal pheochromocytoma incidence.
  • The increased incidences of benign or malignant pheochromocytoma (combined) of the adrenal medulla in male rats were also considered to be exposure related.

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  • (PMID = 15891779.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Mutagens; 0 / Naphthalenes; 88451Q4XYF / decalin
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33. Puc J, Placha G, Wocial B, Podsypanina K, Parsons R, Gaciong Z: Analysis of PTEN mutation in non-familial pheochromocytoma. Ann N Y Acad Sci; 2006 Aug;1073:317-31
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  • PTEN, a tumor suppressor gene, is frequently mutated in a variety of human tumors.
  • In mice, monoallelic inactivation of this gene predisposes animals to neoplasia of multiple organs.
  • Interestingly, Pten heterozygous mice develop bilateral hyperplasia of the adrenal medulla.
  • Examination of protein expression by immunohistochemistry using 8 normal adrenals and 11 sporadic pheochromocytomas showed no decrease in the PTEN protein expression in the tumor tissue, but upregulation of insulin-like growth factor II, a peptide implicated in growth of adrenal tissue, was observed in four cases (36%).
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Mutation. PTEN Phosphohydrolase / genetics. Pheochromocytoma / genetics

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  • (PMID = 17102102.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase
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34. Lai EW, Joshi BH, Martiniova L, Dogra R, Fujisawa T, Leland P, de Krijger RR, Lubensky IA, Elkahloun AG, Morris JC, Puri RK, Pacak K: Overexpression of interleukin-13 receptor-alpha2 in neuroendocrine malignant pheochromocytoma: a novel target for receptor directed anti-cancer therapy. J Clin Endocrinol Metab; 2009 Aug;94(8):2952-7
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  • [Title] Overexpression of interleukin-13 receptor-alpha2 in neuroendocrine malignant pheochromocytoma: a novel target for receptor directed anti-cancer therapy.
  • CONTEXT: Pheochromocytomas and paragangliomas are rare catecholamine-secreting neuroendocrine tumors arising from the adrenal medulla and sympathetic tissues.
  • OBJECTIVE: The objective of the study was to identify and characterize overexpression of IL-13 receptor-alpha2 (IL-13Ralpha2) gene expression in human and murine tumors and verify xenograft mouse pheochromocytoma cell (MPC)-derived tumor's response to a selective cytotoxin.
  • INTERVENTION: The function of IL-13Ralpha2 in these tumor cells was examined by evaluating tumor sensitivity to a recombinant IL-13-Pseudomonas exotoxin (IL-13PE).
  • MAIN OUTCOME MEASURES: IC(50) and tumor size were measured.
  • Our results showed a statistically significant decrease in tumor size as early as 3 d after initial treatment and further suppressed growth of MPC tumors.

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  • (PMID = 19491224.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bacterial Proteins; 0 / Immunotoxins; 0 / Interleukin-13 Receptor alpha2 Subunit; 0 / pseudomonas exoprotein A protein, Pseudomonas aeruginosa
  • [Other-IDs] NLM/ PMC2730867
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35. Crivellato E, Finato N, Ribatti D, Beltrami CA: Piecemeal degranulation in human tumour pheochromocytes. J Anat; 2005 Jan;206(1):47-53
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  • [Title] Piecemeal degranulation in human tumour pheochromocytes.
  • Piecemeal degranulation (PMD) has been recognized in two cases of human pheochromocytoma from the adrenal medulla, which were studied by transmission electron microscopy.
  • Tumour pheochromocytes presented a highly characteristic cytoplasmic admixture of normal resting granules, swollen granules with eroded matrices and enlarged empty containers.
  • This is the first description of PMD in human adrenal chromaffin cells and, in addition, is the first report of PMD in tumour secretory cells.
  • [MeSH-major] Adrenal Gland Neoplasms / secretion. Cell Degranulation. Pheochromocytoma / secretion

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  • (PMID = 15679870.001).
  • [ISSN] 0021-8782
  • [Journal-full-title] Journal of anatomy
  • [ISO-abbreviation] J. Anat.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1571454
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36. Chen ML, Xu PZ, Peng XD, Chen WS, Guzman G, Yang X, Di Cristofano A, Pandolfi PP, Hay N: The deficiency of Akt1 is sufficient to suppress tumor development in Pten+/- mice. Genes Dev; 2006 Jun 15;20(12):1569-74
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  • [Title] The deficiency of Akt1 is sufficient to suppress tumor development in Pten+/- mice.
  • The tumor suppressor PTEN is frequently inactivated in human cancers.
  • Here we showed that the deficiency of Akt1 is sufficient to dramatically inhibit tumor development in Pten+/- mice.
  • Akt1 deficiency had a profound effect on endometrium and prostate neoplasia, two types of human cancer, in which PTEN is frequently mutated, and also affected thyroid and adrenal medulla tumors and intestinal polyps.
  • Even haplodeficiency of Akt1 was sufficient to markedly attenuate the development of high-grade prostate intraepithelial neoplasia (PIN) and endometrial carcinoma.
  • These results have significant implications for cancer therapy.


37. Sandgren J, Andersson R, Rada-Iglesias A, Enroth S, Akerstrom G, Dumanski JP, Komorowski J, Westin G, Wadelius C: Integrative epigenomic and genomic analysis of malignant pheochromocytoma. Exp Mol Med; 2010 Jul 31;42(7):484-502
Hazardous Substances Data Bank. L-Lysine .

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  • Epigenomic and genomic changes affect gene expression and contribute to tumor development.
  • The histone modifications trimethylated histone H3 lysine 4 (H3K4me3) and lysine 27 (H3K27me3) are epigenetic regulators associated to active and silenced genes, respectively and alterations of these modifications have been observed in cancer.
  • Pheochromocytoma is a rare endocrine tumor of the adrenal gland that mostly occurs sporadic with unknown epigenetic/genetic cause.
  • The integrated analysis of the tumor expression levels, in relation to normal adrenal medulla, indicated that either histone modifications or chromosomal alterations, or both, have great impact on the expression of a substantial fraction of the genes in the investigated sample.
  • Candidate tumor suppressor genes identified with decreased expression, a H3K27me3 mark and/or in regions of deletion were for instance TGIF1, DSC3, TNFRSF10B, RASSF2, HOXA9, PTPRE and CDH11.
  • Our approach to associate histone methylations and DNA copy number changes to gene expression revealed apparent impact on global gene transcription, and enabled the identification of candidate tumor genes for further exploration.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Adrenal Gland Neoplasms / pathology. Epigenesis, Genetic. Genome, Human / genetics. Genomics. Pheochromocytoma / genetics. Pheochromocytoma / pathology
  • [MeSH-minor] Female. Gene Dosage / genetics. Gene Expression Regulation, Neoplastic. Gene Regulatory Networks / genetics. Histones / metabolism. Humans. Lysine / metabolism. Methylation. Protein Processing, Post-Translational. Tumor Suppressor Proteins / genetics. Tumor Suppressor Proteins / metabolism

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  • (PMID = 20534969.001).
  • [ISSN] 2092-6413
  • [Journal-full-title] Experimental & molecular medicine
  • [ISO-abbreviation] Exp. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Histones; 0 / Tumor Suppressor Proteins; K3Z4F929H6 / Lysine
  • [Other-IDs] NLM/ PMC2912476
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38. Shyla A, Hölzlwimmer G, Calzada-Wack J, Bink K, Tischenko O, Guilly MN, Chevillard S, Samson E, Graw J, Atkinson MJ, Pellegata NS: Allelic loss of chromosomes 8 and 19 in MENX-associated rat pheochromocytoma. Int J Cancer; 2010 May 15;126(10):2362-72
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

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  • Pheochromocytomas are neoplasias of neural crest origin that arise from the chromaffin cells of the adrenal medulla.
  • We also analyzed additional candidate genes, that is, rat homologues of genes predisposing to human pheochromocytoma and known tumor-suppressor genes, but we found no AI.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Chromosomes, Human, Pair 19. Chromosomes, Human, Pair 8. Cyclin-Dependent Kinase Inhibitor p27 / genetics. Frameshift Mutation. Loss of Heterozygosity. Pheochromocytoma / genetics

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  • (PMID = 19876893.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cdkn1b protein, rat; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27
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39. Corti A: Chromogranin A and the tumor microenvironment. Cell Mol Neurobiol; 2010 Nov;30(8):1163-70
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  • [Title] Chromogranin A and the tumor microenvironment.
  • Chromogranin A (CgA) is an acidic glycoprotein belonging to a family of regulated secretory proteins stored in the dense core granules of the adrenal medulla and of many other neuroendocrine cells and neurons.
  • A growing body of evidence suggests that CgA is more than a diagnostic/prognostic marker for cancer patients.
  • Indeed, results of in vitro experiments and in vivo studies in animal models suggest that this protein and its fragments can affect several elements of the tumor microenvironment, including fibroblasts and endothelial cells.
  • In this article, recent findings implicating CgA as a modulator of the tumor microenvironment and suggesting that abnormal secretion of CgA could play important roles in tumor progression and response to therapy in cancer patients are reviewed and discussed.
  • [MeSH-major] Chromogranin A / metabolism. Neoplasms / metabolism. Tumor Microenvironment

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  • (PMID = 21080056.001).
  • [ISSN] 1573-6830
  • [Journal-full-title] Cellular and molecular neurobiology
  • [ISO-abbreviation] Cell. Mol. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromogranin A; 0 / Peptide Fragments; 126729-24-6 / vasostatin I
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40. Guillemot J, Compagnon P, Cartier D, Thouennon E, Bastard C, Lihrmann I, Pichon P, Thuillez C, Plouin PF, Bertherat J, Anouar Y, Kuhn JM, Yon L, Lefebvre H: Metoclopramide stimulates catecholamine- and granin-derived peptide secretion from pheochromocytoma cells through activation of serotonin type 4 (5-HT4) receptors. Endocr Relat Cancer; 2009 Mar;16(1):281-90
Hazardous Substances Data Bank. CISAPRIDE .

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  • Tissue explants, obtained from 18 pheochromocytomas including the tumor removed from a 46-year-old female patient who experienced life-threatening hypertension crisis after metoclopramide administration and 17 additional pheochromocytomas (9 benign and 8 malignant) were studied.
  • RESULTS: Metoclopramide and the 5-HT(4) receptor agonist cisapride were found to activate catecholamine- and granin-derived peptide secretions by cultured tumor cells.
  • 5-HT(4) receptor mRNAs were detected in the patient's tumor and the series of 17 additional pheochromocytomas.
  • [MeSH-major] Adrenal Gland Neoplasms / drug therapy. Dopamine Antagonists / pharmacology. Metoclopramide / pharmacology. Pheochromocytoma / drug therapy. Receptors, Serotonin, 5-HT4 / genetics
  • [MeSH-minor] Adrenal Medulla / cytology. Adrenal Medulla / drug effects. Catecholamines / secretion. Chromogranins / secretion. Cisapride / pharmacology. Domperidone / pharmacology. Female. Humans. Middle Aged. RNA, Messenger / metabolism. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction. Serotonin Receptor Agonists / pharmacology. Tumor Cells, Cultured

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  • (PMID = 18948374.001).
  • [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 / Catecholamines; 0 / Chromogranins; 0 / Dopamine Antagonists; 0 / RNA, Messenger; 0 / Serotonin Receptor Agonists; 158165-40-3 / Receptors, Serotonin, 5-HT4; 5587267Z69 / Domperidone; L4YEB44I46 / Metoclopramide; UVL329170W / Cisapride
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41. Cascón A, Montero-Conde C, Ruiz-Llorente S, Mercadillo F, Letón R, Rodríguez-Antona C, Martínez-Delgado B, Delgado M, Díez A, Rovira A, Díaz JA, Robledo M: Gross SDHB deletions in patients with paraganglioma detected by multiplex PCR: a possible hot spot? Genes Chromosomes Cancer; 2006 Mar;45(3):213-9
SciCrunch. OMIM: Data: Gene Annotation .

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  • Pheochromocytoma and paraganglioma are rare neuroendocrine tumors that arise in the adrenal medulla and the extra-adrenal paraganglia, respectively.
  • Although this is the first report describing the presence of gross deletions in patients with apparently sporadic paragangliomas, the extra-adrenal location of the tumor seems to constitute a determining factor for whether to include these patients in genetic testing for gross deletions in the SDHB gene.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Gene Deletion. Iron-Sulfur Proteins / genetics. Paraganglioma / genetics. Pheochromocytoma / genetics. Protein Subunits / genetics. Succinate Dehydrogenase / genetics


42. Sveinbjörnsson B, Rasmuson A, Baryawno N, Wan M, Pettersen I, Ponthan F, Orrego A, Haeggström JZ, Johnsen JI, Kogner P: Expression of enzymes and receptors of the leukotriene pathway in human neuroblastoma promotes tumor survival and provides a target for therapy. FASEB J; 2008 Oct;22(10):3525-36
COS Scholar Universe. author profiles.

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  • [Title] Expression of enzymes and receptors of the leukotriene pathway in human neuroblastoma promotes tumor survival and provides a target for therapy.
  • The metabolism of arachidonic acid by the cyclooxygenase (COX) or lipoxygenase (LO) pathways generates eicosanoids that have been implicated in the pathogenesis of a variety of human diseases, including cancer.
  • In this study, we examined the expression and significance of components within the 5-LO pathway in human neuroblastoma, an embryonal tumor of the sympathetic nervous system.
  • Expression of 5-LO and FLAP was evident in tumor cells but not in nonmalignant adrenal medulla where neuroblastomas typically arise.
  • [MeSH-minor] 5-Lipoxygenase-Activating Proteins. Apoptosis. Arachidonate 5-Lipoxygenase / biosynthesis. Carrier Proteins / antagonists & inhibitors. Carrier Proteins / biosynthesis. Cell Cycle. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Enzyme Inhibitors / pharmacology. Epoxide Hydrolases / biosynthesis. Glutathione Transferase / biosynthesis. Humans. Leukotriene Antagonists / pharmacology. Lipoxygenase Inhibitors. Membrane Proteins / antagonists & inhibitors. Membrane Proteins / biosynthesis. Receptors, Leukotriene / biosynthesis. Receptors, Leukotriene / drug effects

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  • (PMID = 18591367.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 5-Lipoxygenase-Activating Proteins; 0 / ALOX5AP protein, human; 0 / Carrier Proteins; 0 / Enzyme Inhibitors; 0 / Leukotriene Antagonists; 0 / Leukotrienes; 0 / Lipoxygenase Inhibitors; 0 / Membrane Proteins; 0 / Receptors, Leukotriene; EC 1.13.11.34 / Arachidonate 5-Lipoxygenase; EC 2.5.1.18 / Glutathione Transferase; EC 3.3.2.- / Epoxide Hydrolases; EC 3.3.2.- / leukotriene A4 hydrolase; EC 4.4.1.20 / leukotriene-C4 synthase
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43. Bach U, Hailey JR, Hill GD, Kaufmann W, Latimer KS, Malarkey DE, Maronpot RM, Miller RA, Moore RR, Morrison JP, Nolte T, Rinke M, Rittinghausen S, Suttie AW, Travlos GS, Vahle JL, Willson GA, Elmore SA: Proceedings of the 2009 National Toxicology Program Satellite Symposium. Toxicol Pathol; 2010 Jan;38(1):9-36
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

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  • The topic of the 2009 Symposium was "Tumor Pathology and INHAND (International Harmonization of Nomenclature and Diagnostic Criteria for Lesions in Rats and Mice) Nomenclature."
  • [MeSH-minor] Adrenal Medulla / pathology. Animals. Cell Proliferation. Cholangiocarcinoma / pathology. Immunohistochemistry. Liver Neoplasms / pathology. Meningioma / pathology. Mice. Rats. Terminology as Topic

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  • (PMID = 20008954.001).
  • [ISSN] 1533-1601
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 ES999999
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS623985; NLM/ PMC4195590
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44. Karagiannis A, Mikhailidis DP, Athyros VG, Harsoulis F: Pheochromocytoma: an update on genetics and management. Endocr Relat Cancer; 2007 Dec;14(4):935-56
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  • Pheochromocytomas (PHEOs) are rare neoplasms that produce catecholamines and usually arise from the adrenal medulla and are considered to be an adrenal paraganglioma (PGL).
  • Most PHEOs are sporadic, but a significant percentage (approximately 25%) may be found in patients with germline mutations of genes predisposing to the development of von Hippel-Lindau disease, neurofibromatosis 1, multiple endocrine neoplasia type 1 (MEN1) and 2 (MEN2), and the PGL/PHEOs syndrome, based on the described mutations of the genes for succinate dehydrogenase subunit D (SDHD), B (SDHB), and C (SDHC).
  • This review discusses the genetics, the pathophysiology of hypertension, the clinical picture, the biochemical and imaging diagnosis, and the preferred therapeutic approach for PGLs/PHEOs.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Adrenal Gland Neoplasms / therapy. Pheochromocytoma / genetics. Pheochromocytoma / therapy
  • [MeSH-minor] Adrenal Medulla / pathology. Adult. Age of Onset. Aged. Child. Chromogranin A / blood. Chromogranin A / genetics. Genetic Predisposition to Disease. Humans. Multiple Endocrine Neoplasia Type 2a / genetics. Paraganglioma / genetics. Prevalence

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  • (PMID = 18045948.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chromogranin A
  • [Number-of-references] 194
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45. Minor RK, Smith DL Jr, Sossong AM, Kaushik S, Poosala S, Spangler EL, Roth GS, Lane M, Allison DB, de Cabo R, Ingram DK, Mattison JA: Chronic ingestion of 2-deoxy-D-glucose induces cardiac vacuolization and increases mortality in rats. Toxicol Appl Pharmacol; 2010 Mar 15;243(3):332-9
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  • 2DG treatment has been shown to have potential therapeutic benefits for treating cancer and seizures.
  • Increased incidence of pheochromocytoma in the adrenal medulla was also noted in the 2DG treated rats.
  • [MeSH-minor] Adrenal Glands / drug effects. Adrenal Glands / pathology. Animals. Autophagy / drug effects. Blotting, Western. Body Temperature / drug effects. Body Weight / drug effects. Glucose / metabolism. Glycogen / metabolism. Insulin / metabolism. Lipid Metabolism / drug effects. Male. Rats. Rats, Inbred BN. Rats, Inbred F344. Survival Analysis

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  • [Copyright] Published by Elsevier Inc.
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  • (PMID = 20026095.001).
  • [ISSN] 1096-0333
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 AG000371-03
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Insulin; 9005-79-2 / Glycogen; 9G2MP84A8W / Deoxyglucose; IY9XDZ35W2 / Glucose
  • [Other-IDs] NLM/ NIHMS163022; NLM/ PMC2830378
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46. Khorram-Manesh A, Ahlman H, Nilsson O, Friberg P, Odén A, Stenström G, Hansson G, Stenquist O, Wängberg B, Tisell LE, Jansson S: Long-term outcome of a large series of patients surgically treated for pheochromocytoma. J Intern Med; 2005 Jul;258(1):55-66
MedlinePlus Health Information. consumer health - Pheochromocytoma.

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  • DESIGN: Retrospective review of patients with PC/PG regarding presenting symptoms, tumour characteristics, clinical management and long-term outcome after treatment.
  • At diagnosis 85% of the patients were hypertensive; one year after surgery more than half were still hypertensive.
  • We recommend life-long follow-up of patients treated for PC/PG with screening for recurrent tumour in sporadic cases and for associated tumours in hereditary cases.
  • [MeSH-major] Adrenal Gland Neoplasms / surgery. Pheochromocytoma / surgery
  • [MeSH-minor] Adrenal Medulla / pathology. Adult. Aged. Blood Pressure / physiology. Female. Humans. Hyperplasia. Hypertension / complications. Male. Middle Aged. Neoplasm Invasiveness. Paraganglioma / mortality. Paraganglioma / pathology. Paraganglioma / surgery. Postoperative Period. Preoperative Care / methods. Receptors, Adrenergic, alpha / administration & dosage. Retrospective Studies. Survival Analysis. Treatment Outcome

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  • (PMID = 15953133.001).
  • [ISSN] 0954-6820
  • [Journal-full-title] Journal of internal medicine
  • [ISO-abbreviation] J. Intern. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Adrenergic, alpha
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47. Bayley JP, van Minderhout I, Hogendoorn PC, Cornelisse CJ, van der Wal A, Prins FA, Teppema L, Dahan A, Devilee P, Taschner PE: Sdhd and SDHD/H19 knockout mice do not develop paraganglioma or pheochromocytoma. PLoS One; 2009;4(11):e7987
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  • SDHD is remarkable in showing an 'imprinted' tumor suppressor phenotype.
  • We also crossed this mouse with a knockout of H19, a postulated imprinted modifier gene of Sdhd tumorigenesis, to evaluate if loss of these genes together would lead to the initiation or enhancement of tumor development.
  • No paraganglioma or other tumor development was seen in Sdhd KO mice followed for their entire lifespan, in sharp contrast to the highly penetrant phenotype in humans.
  • Heterozygous Sdhd KO mice did not show hyperplasia of paraganglioma-related tissues such as the carotid body or of the adrenal medulla, or any genotype-related pathology, with similar body and organ weights to wildtype mice.
  • [MeSH-minor] Animals. Female. Gene Expression Regulation, Neoplastic. Genes, Tumor Suppressor. Genotype. Heterozygote. Male. Mice. Mice, Knockout. Phenotype. RNA, Long Noncoding

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  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
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  • (PMID = 19956719.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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48. Tsai CJ, Del Sol A, Nussinov R: Protein allostery, signal transmission and dynamics: a classification scheme of allosteric mechanisms. Mol Biosyst; 2009 Mar;5(3):207-16
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  • Other schemes would account for epinephrine when secreted by the adrenal medulla to be hormone-like.


49. Pollard PJ, El-Bahrawy M, Poulsom R, Elia G, Killick P, Kelly G, Hunt T, Jeffery R, Seedhar P, Barwell J, Latif F, Gleeson MJ, Hodgson SV, Stamp GW, Tomlinson IP, Maher ER: Expression of HIF-1alpha, HIF-2alpha (EPAS1), and their target genes in paraganglioma and pheochromocytoma with VHL and SDH mutations. J Clin Endocrinol Metab; 2006 Nov;91(11):4593-8
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  • These similarities between the downstream consequences of VHL inactivation and HIF dysregulation in renal cell carcinoma and PCC may explain how inactivation of the ubiquitously expressed VHL protein results in susceptibility to specific tumor types.
  • [MeSH-major] Adrenal Gland Neoplasms / metabolism. Head and Neck Neoplasms / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Paraganglioma / metabolism. Pheochromocytoma / metabolism. Succinate Dehydrogenase / genetics. Transcription Factors / metabolism. Von Hippel-Lindau Tumor Suppressor Protein / genetics
  • [MeSH-minor] Adrenal Medulla / metabolism. Basic Helix-Loop-Helix Transcription Factors. Gene Expression Regulation, Neoplastic. Germ-Line Mutation. Humans. Immunohistochemistry


50. Minn AJ, Kang Y, Serganova I, Gupta GP, Giri DD, Doubrovin M, Ponomarev V, Gerald WL, Blasberg R, Massagué J: Distinct organ-specific metastatic potential of individual breast cancer cells and primary tumors. J Clin Invest; 2005 Jan;115(1):44-55
The Lens. Cited by Patents in .

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  • [Title] Distinct organ-specific metastatic potential of individual breast cancer cells and primary tumors.
  • We used bioluminescence imaging to reveal patterns of metastasis formation by human breast cancer cells in immunodeficient mice.
  • Individual cells from a population established in culture from the pleural effusion of a breast cancer patient showed distinct patterns of organ-specific metastasis.
  • Single-cell progenies derived from this population exhibited markedly different abilities to metastasize to the bone, lung, or adrenal medulla, which suggests that metastases to different organs have different requirements.
  • Unsupervised classification using the transcriptomic data set supported the hypothesis that organ-specific metastasis by breast cancer cells is controlled by metastasis-specific genes that are separate from a general poor-prognosis gene expression signature.

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  • (PMID = 15630443.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA094060; United States / NIGMS NIH HHS / GM / T32 GM007739; United States / NIGMS NIH HHS / GM / GM07739; United States / NCI NIH HHS / CA / P01-CA94060
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC539194
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51. Kanamori M, Suzuki H, Sato I, Ohyama K, Tezuka F, Katakura R: A case of idiopathic hypereosinophilic syndrome with leptomeningeal dissemination and intraventricular mass lesion: an autopsy report. Clin Neuropathol; 2009 May-Jun;28(3):197-202
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  • She had no history of either malignancy or allergic disorder.
  • Autopsy demonstrated significant infiltration by eosinophils and lymphocytes into the mass lesion in the ventricle, subarachnoid space, perivascular space and parenchyma of the medulla oblongata.
  • The final diagnosis was idiopathic HES.
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Adult. Autopsy. Fatal Outcome. Female. Humans. Immunohistochemistry. Otitis Media / drug therapy. Otitis Media / etiology. Radiotherapy


52. Longo L, Borghini S, Schena F, Parodi S, Albino D, Bachetti T, Da Prato L, Truini M, Gambini C, Tonini GP, Ceccherini I, Perri P: PHOX2A and PHOX2B genes are highly co-expressed in human neuroblastoma. Int J Oncol; 2008 Nov;33(5):985-91
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  • In this light, we have carried out a quantitative expression analysis of PHOX2B and its paralogue PHOX2A on a panel of NB cell lines and NB tumour samples to identify a possible differential expression between NB cells and their normal counterpart (adrenal medulla cells).
  • Our results revealed that both PHOX2A and PHOX2B are over-expressed in tumour samples and NB cell lines.
  • [MeSH-minor] Adrenal Medulla / metabolism. Cell Line, Tumor. DNA Mutational Analysis. Humans. Pedigree. Up-Regulation

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  • (PMID = 18949361.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / NBPhox protein; 0 / PHOX2A protein, human; 0 / Transcription Factors
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53. Kremens B: [Systemic therapy in children and adolescents]. Urologe A; 2007 Oct;46(10):1404-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • National and supranational treatment studies are the standard of care for pediatric cancer in Germany; they yield 5-year survival rates of almost 90% for nephroblastoma and germ cell tumors and 60% for neuroblastoma (all stages) and rhabdomyosarcoma.
  • The principles of antineoplastic therapy are the same as in adult cancer medicine; the drugs used depend upon the disease.
  • [MeSH-minor] Adolescent. Adrenal Gland Neoplasms / drug therapy. Adrenal Gland Neoplasms / mortality. Adrenal Gland Neoplasms / pathology. Adrenal Gland Neoplasms / surgery. Adrenal Medulla. Chemotherapy, Adjuvant. Child. Child, Preschool. Combined Modality Therapy. Humans. Infant. Kidney Neoplasms / drug therapy. Kidney Neoplasms / mortality. Kidney Neoplasms / pathology. Kidney Neoplasms / surgery. Neoplasm Staging. Neoplasms, Germ Cell and Embryonal / drug therapy. Neoplasms, Germ Cell and Embryonal / mortality. Neoplasms, Germ Cell and Embryonal / pathology. Neoplasms, Germ Cell and Embryonal / surgery. Neuroblastoma / drug therapy. Neuroblastoma / mortality. Neuroblastoma / pathology. Neuroblastoma / surgery. Prognosis. Radiotherapy, Adjuvant. Rhabdomyosarcoma / drug therapy. Rhabdomyosarcoma / mortality. Rhabdomyosarcoma / pathology. Rhabdomyosarcoma / surgery. Survival Rate. Wilms Tumor / drug therapy. Wilms Tumor / mortality. Wilms Tumor / pathology. Wilms Tumor / surgery

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  • (PMID = 17823786.001).
  • [ISSN] 0340-2592
  • [Journal-full-title] Der Urologe. Ausg. A
  • [ISO-abbreviation] Urologe A
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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54. Hazell GG, Yao ST, Roper JA, Prossnitz ER, O'Carroll AM, Lolait SJ: Localisation of GPR30, a novel G protein-coupled oestrogen receptor, suggests multiple functions in rodent brain and peripheral tissues. J Endocrinol; 2009 Aug;202(2):223-36
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  • In the rat and mouse periphery, GPR30-ir was detected in the anterior, intermediate and neural lobe of the pituitary, adrenal medulla, renal pelvis and ovary.
  • In situ hybridisation histochemistry using GPR30 riboprobes, revealed intense hybridisation signal for GPR30 in the paraventricular nucleus and supraoptic nucleus (SON) of the hypothalamus, anterior and intermediate lobe of the pituitary, adrenal medulla, renal pelvis and ovary of both rat and mouse.
  • [MeSH-minor] Adrenal Medulla / metabolism. Animals. Arginine Vasopressin / metabolism. Female. Fluorescent Antibody Technique. Immunohistochemistry. In Situ Hybridization. Kidney Pelvis / metabolism. Male. Mice. Mice, Knockout. Neurons / metabolism. Ovary / metabolism. Oxytocin / metabolism. Pituitary Gland, Posterior / metabolism. RNA, Messenger / metabolism. Rats. Rats, Sprague-Dawley. Receptors, Estrogen. Tissue Distribution

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  • (PMID = 19420011.001).
  • [ISSN] 1479-6805
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / / BB/D00196X/1; United Kingdom / Biotechnology and Biological Sciences Research Council / / ; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / GPR30 protein, mouse; 0 / GPR30 protein, rat; 0 / RNA, Messenger; 0 / Receptors, Estrogen; 0 / Receptors, G-Protein-Coupled; 113-79-1 / Arginine Vasopressin; 50-56-6 / Oxytocin
  • [Other-IDs] NLM/ PMC2710976
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55. Waldmann J, Fendrich V, Holler J, Buchholz M, Heinmöller E, Langer P, Ramaswamy A, Samans B, Walz MK, Rothmund M, Bartsch DK, Slater EP: Microarray analysis reveals differential expression of benign and malignant pheochromocytoma. Endocr Relat Cancer; 2010 Sep;17(3):743-56
The Lens. Cited by Patents in .

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  • The diagnosis of a malignant pheochromocytoma (PC) can only be established by the presence of distant metastases, but a subset of apparently benign PCs develop metastases.
  • The reference consisted of laser microdissected tissue from normal adrenal medulla.
  • Comparative analysis by microarray of all ten PCs (benign/malignant) versus normal adrenal medulla revealed a more than twofold expression difference in 455/539 and 491/671 genes respectively.
  • Several of these genes are known to participate on adrenal tumorigenesis, potential tumor suppressor genes, and oncogenes.
  • [MeSH-major] Adrenal Gland Neoplasms / metabolism. Adrenal Medulla / metabolism. Biomarkers, Tumor / metabolism. Gene Expression Profiling. Pheochromocytoma / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Case-Control Studies. Humans. Immunoenzyme Techniques. Middle Aged. Neoplasm Metastasis. Oligonucleotide Array Sequence Analysis. Prognosis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Young Adult


56. Zhang FR, Tao LH, Shen ZY, Lv Z, Xu LY, Li EM: Fascin expression in human embryonic, fetal, and normal adult tissue. J Histochem Cytochem; 2008 Feb;56(2):193-9
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  • Fascin was expressed in the cortex and medulla of the adrenal gland at 8-12 weeks of gestation, whereas immunoreactivity decreased from the zona glomerulosa through the zona reticularis and was essentially negative in the adrenal medulla of adults.

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  • (PMID = 17998567.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Microfilament Proteins; 146808-54-0 / fascin
  • [Other-IDs] NLM/ PMC2324166
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57. Kinoshita Y, Kuratsukuri K, Landas S, Imaida K, Rovito PM Jr, Wang CY, Haas GP: Expression of prostate-specific membrane antigen in normal and malignant human tissues. World J Surg; 2006 Apr;30(4):628-36
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  • BACKGROUND: Prostate-specific membrane antigen (PSMA) is upregulated in androgen-dependent prostate carcinoma and it has been targeted for immunotherapy and diagnosis of this cancer.
  • RESULTS: Prostate-specific membrane antigen was detected in the epithelium of prostate, urinary bladder, proximal tubules of kidney, liver, esophagus, stomach, small intestine, colon, breast, fallopian tubes and testicular seminiferous tubules, hippocampal neurons and astrocytes, ependyma, cortex and medulla of the adrenal gland, and ovary stroma.
  • It was also detected in neoplasms of the prostate, kidney, urinary bladder, stomach, small intestine, colon, lung, adrenal gland, and testis.
  • The broad distribution of PSMA may make it suitable for the diagnosis and therapy of a wide variety of tumors.
  • [MeSH-major] Antigens, Surface / analysis. Biomarkers, Tumor / analysis. Glutamate Carboxypeptidase II / analysis. Neoplasms / pathology. Prostate / pathology. Prostatic Neoplasms / pathology. Tumor Cells, Cultured / pathology

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  • (PMID = 16555021.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / 1R01AG21389-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Surface; 0 / Biomarkers, Tumor; EC 3.4.17.21 / Glutamate Carboxypeptidase II; EC 3.4.17.21 / glutamate carboxypeptidase II, human
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58. Jarbo C, Buckley PG, Piotrowski A, Mantripragada KK, Benetkiewicz M, Diaz de Ståhl T, Langford CF, Gregory SG, Dralle H, Gimm O, Bäckdahl M, Geli J, Larsson C, Westin G, Akerström G, Dumanski JP: Detailed assessment of chromosome 22 aberrations in sporadic pheochromocytoma using array-CGH. Int J Cancer; 2006 Mar 1;118(5):1159-64
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  • Pheochromocytoma is a predominantly sporadic neuroendocrine tumor derived from the adrenal medulla.
  • Future analysis of this tumor type should preferably be performed in the context of the entire human genome using genome-wide array-CGH, which is a superior methodological approach.
  • Supplemental material for this article can be found on the International Journal of Cancer website at http://www.interscience.wiley.com/jpages/0020-7136/suppmat/index.html.

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16161042.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
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59. Yang JY, Yang MQ, Luo Z, Ma Y, Li J, Deng Y, Huang X: A hybrid machine learning-based method for classifying the Cushing's Syndrome with comorbid adrenocortical lesions. BMC Genomics; 2008;9 Suppl 1:S23
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  • It follows from a comprehensive statistical analysis that a number of antigens such as hTERT, PCNA and Ki-67 can be considered as cancer markers, while another set of antigens such as P27KIP1 and FHIT are possible markers for normal tissue.
  • Because more than one marker must be considered to obtain a classification of cancer or no cancer, and if cancer, to classify it as malignant, borderline, or benign, we must develop an intelligent decision system that can fullfill such an unmet medical need.
  • While no significant difference was found between cell-arrest antigens such as P27KIP1 for malignant, borderline, and benign tumors, there was a significant difference between expression levels of such antigens in normal adrenal medulla samples and in adrenomedullary tumors.
  • This research has many potential applications; it might provide an alternative diagnostic tool and a better understanding of the mechanisms involved in malignant transformation as well as information that is useful for treatment planning and cancer prevention.
  • [MeSH-major] Adrenal Cortex Neoplasms / classification. Algorithms. Artificial Intelligence. Biomarkers, Tumor / metabolism. Cushing Syndrome / classification

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  • (PMID = 18366613.001).
  • [ISSN] 1471-2164
  • [Journal-full-title] BMC genomics
  • [ISO-abbreviation] BMC Genomics
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Proliferating Cell Nuclear Antigen
  • [Other-IDs] NLM/ PMC2386065
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60. Ait-Ali D, Turquier V, Tanguy Y, Thouënnon E, Ghzili H, Mounien L, Derambure C, Jégou S, Salier JP, Vaudry H, Eiden LE, Anouar Y: Tumor necrosis factor (TNF)-alpha persistently activates nuclear factor-kappaB signaling through the type 2 TNF receptor in chromaffin cells: implications for long-term regulation of neuropeptide gene expression in inflammation. Endocrinology; 2008 Jun;149(6):2840-52
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  • [Title] Tumor necrosis factor (TNF)-alpha persistently activates nuclear factor-kappaB signaling through the type 2 TNF receptor in chromaffin cells: implications for long-term regulation of neuropeptide gene expression in inflammation.
  • Chromaffin cells of the adrenal medulla elaborate and secrete catecholamines and neuropeptides for hormonal and paracrine signaling in stress and during inflammation.
  • TNF-alpha-dependent signaling in neuroendocrine cells thus leads to a unique, persistent mode of NF-kappaB activation that features long-lasting transcription of both IkappaB and MIG-6, which may play a role in the long-lasting effects of TNF-alpha in regulating neuropeptide output from the adrenal, a potentially important feedback station for modulating long-term cytokine effects in inflammation.

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  • (PMID = 18292192.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] ENG
  • [Grant] United States / NIMH NIH HHS / MH / Z01 MH002386
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Neuropeptides; 0 / Recombinant Proteins; 0 / TNF Receptor-Associated Factor 2; 0 / Tumor Necrosis Factor-alpha; 63231-63-0 / RNA
  • [Other-IDs] NLM/ PMC2408812
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61. Nevo I, Sagi-Assif O, Edry Botzer L, Amar D, Maman S, Kariv N, Leider-Trejo LE, Savelyeva L, Schwab M, Yron I, Witz IP: Generation and characterization of novel local and metastatic human neuroblastoma variants. Neoplasia; 2008 Aug;10(8):816-27
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  • Neuroblastoma (NB) is the most commonly occurring solid tumor in children.
  • The disease usually arises in the adrenal medulla, and it is characterized by a remarkable heterogeneity in its progression.
  • Most NB patients with an advanced disease have massive bone marrow infiltration at diagnosis.
  • Currently, models consisting of metastatic and nonmetastatic cell variants of the same genetic background exist for several types of cancer; however, none exists for NB.
  • SH-SY5Y and MHH-NB-11 NB cells were inoculated orthotopically into the adrenal glands of athymic nude mice.
  • Neuroblastoma cells metastasizing to the lungs were isolated from mice bearing adrenal tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / pathology. Disease Models, Animal. Lung Neoplasms / secondary. Neoplasms, Experimental / secondary. Neuroblastoma / secondary
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Deferoxamine / pharmacology. Doxorubicin / therapeutic use. Drug Screening Assays, Antitumor. Flow Cytometry. Humans. Immunophenotyping. Karyotyping. Male. Matrix Metalloproteinase 2 / secretion. Matrix Metalloproteinase 9 / secretion. Mice. Mice, Inbred BALB C. Mice, Nude. Survival Rate. Xenograft Model Antitumor Assays

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  • (PMID = 18683320.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 80168379AG / Doxorubicin; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9; J06Y7MXW4D / Deferoxamine
  • [Other-IDs] NLM/ PMC2504768
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62. Machens A, Dralle H: Multiple endocrine neoplasia type 2 and the RET protooncogene: from bedside to bench to bedside. Mol Cell Endocrinol; 2006 Mar 9;247(1-2):34-40
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  • [Title] Multiple endocrine neoplasia type 2 and the RET protooncogene: from bedside to bench to bedside.
  • Although the initial characterization of the various MEN-2 associated phenotypes (familial medullary thyroid cancer, multiple endocrine neoplasia 2A and 2B) evolved at the bedside, it was at the bench where the underlying RET (REarranged during Transfection) germline mutations were identified.
  • Molecular information has revolutionized our understanding and continues to transform the clinical management of this fascinating endocrine tumor syndrome of neural crest derivation, which consists of medullary thyroid cancer, pheochromocytoma, and parathyroid hyperplasia/adenoma.
  • With the continuing expansion of our knowledge about the underlying molecular mechanisms and our growing therapeutic abilities, multiple endocrine neoplasia type 2 is gradually returning home to the bedside, closing the loop from bedside to bench to bedside.
  • [MeSH-major] Multiple Endocrine Neoplasia Type 2a / genetics. Proto-Oncogene Proteins c-ret / genetics
  • [MeSH-minor] Adenoma / genetics. Adenoma / pathology. Adrenal Gland Neoplasms / genetics. Adrenal Gland Neoplasms / pathology. Adrenal Medulla / pathology. Age Factors. Animals. Carcinoma, Medullary / genetics. Carcinoma, Medullary / pathology. Genotype. Germ-Line Mutation. Humans. Hyperplasia. Multiple Endocrine Neoplasia Type 2b / genetics. Multiple Endocrine Neoplasia Type 2b / pathology. Neural Crest / pathology. Parathyroid Neoplasms / genetics. Parathyroid Neoplasms / pathology. Phenotype. Pheochromocytoma / genetics. Pheochromocytoma / pathology. Syndrome. Thyroid Neoplasms / genetics. Thyroid Neoplasms / pathology

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  • (PMID = 16343738.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] EC 2.7.10.1 / Proto-Oncogene Proteins c-ret
  • [Number-of-references] 58
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63. Aarts M, Dannenberg H, deLeeuw RJ, van Nederveen FH, Verhofstad AA, Lenders JW, Dinjens WN, Speel EJ, Lam WL, de Krijger RR: Microarray-based CGH of sporadic and syndrome-related pheochromocytomas using a 0.1-0.2 Mb bacterial artificial chromosome array spanning chromosome arm 1p. Genes Chromosomes Cancer; 2006 Jan;45(1):83-93
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  • Pheochromocytomas (PCC) are relatively rare neuroendocrine tumors, mainly of the adrenal medulla.
  • They arise sporadically or occur secondary to inherited cancer syndromes, such as multiple endocrine neoplasia type II (MEN2), von Hippel-Lindau disease (VHL), or neurofibromatosis type I (NF1).
  • In conclusion, these data strongly suggest that chromosome arm 1p is the site for multiple tumor suppressor genes, although the potential candidate genes CDKN2C and PTPRF/LAR are not included in these regions.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Chromosome Deletion. Chromosomes, Artificial, Bacterial. Chromosomes, Human, Pair 1 / genetics. Pheochromocytoma / genetics

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc
  • (PMID = 16215979.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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64. Cayo MA, Cayo AK, Jarjour SM, Chen H: Sodium butyrate activates Notch1 signaling, reduces tumor markers, and induces cell cycle arrest and apoptosis in pheochromocytoma. Am J Transl Res; 2009 Jan 31;1(2):178-83
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  • [Title] Sodium butyrate activates Notch1 signaling, reduces tumor markers, and induces cell cycle arrest and apoptosis in pheochromocytoma.
  • BACKGROUND: Pheochromocytoma is a neuroendocrine (NE) tumor of the adrenal medulla for which surgical resection is the only therapy.
  • Our lab has demonstrated the importance of the Notch1 signaling pathway in NE neoplasia, indicating that this pathway could be a target for emergent treatments in pheochromocytoma.
  • We hypothesized that the HDAC inhibitor Sodium Butyrate (NaB) might activate Notch1 in pheochromocytoma resulting in altered tumor cell proliferation.

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  • (PMID = 19956429.001).
  • [ISSN] 1943-8141
  • [Journal-full-title] American journal of translational research
  • [ISO-abbreviation] Am J Transl Res
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA109053; United States / NCI NIH HHS / CA / R21 CA117117; United States / NIDDK NIH HHS / DK / T35 DK062709
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2776315
  • [Keywords] NOTNLM ; Butyrate / HDAC inhibitor / Notch1 / PC-12 / neuroendocrine / pheochromocytoma
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65. Opocher G, Schiavi F: Genetics of pheochromocytomas and paragangliomas. Best Pract Res Clin Endocrinol Metab; 2010 Dec;24(6):943-56
MedlinePlus Health Information. consumer health - Pheochromocytoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Pheochromocytoma is the tumor of the main sympathetic paraganglia, which is the adrenal medulla.
  • Both of them originate from neural crest cells and share similar mechanisms of tumor development.
  • The best known hereditary forms of pheochromocytoma and paraganglioma are the von Hippel-Lindau disease, in which pheochromocytoma may be associated with CNS hemangioblastoma, retinal angioma, pancreatic endocrine tumor/cysts and renal clear cell carcinoma/cysts; the multiple endocrine neoplasia type 2, in which pheochromocytoma is associated with medullary thyroid carcinoma and primary hyperparathyroidism, Type 1 neurofibromatosis, the most frequent hereditary cancer syndrome.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Paraganglioma / genetics. Pheochromocytoma / genetics


66. Krawczyk A, Hasse-Lazar K, Pawlaczek A, Szpak-Ulczok S, Krajewska J, Paliczka-Cieślak E, Jurecka-Lubieniecka B, Roskosz J, Chmielik E, Ziaja J, Cierpka L, Peczkowska M, Preibisz A, Januszewicz A, Otto M, Jarzab B: Germinal mutations of RET, SDHB, SDHD, and VHL genes in patients with apparently sporadic pheochromocytomas and paragangliomas. Endokrynol Pol; 2010 Jan-Feb;61(1):43-8
MedlinePlus Health Information. consumer health - Pheochromocytoma.

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  • INTRODUCTION: Pheochromocytomas and paragangliomas are derived from neural crest cells and are localized mainly in adrenal medulla and sympathetic or parasympathetic ganglia.
  • Clinical presentation can sometimes be atypical and does not always allow proper diagnosis.
  • MATERIAL AND METHODS: We analyzed DNA from 60 patients diagnosed and treated in the Centre of Oncology with a diagnosis of pheochromocytoma or paraganglioma.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Germ-Line Mutation. Paraganglioma / genetics. Pheochromocytoma / genetics. Proto-Oncogene Proteins c-ret / genetics. Succinate Dehydrogenase / genetics. Von Hippel-Lindau Tumor Suppressor Protein / genetics

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  • (PMID = 20205103.001).
  • [ISSN] 0423-104X
  • [Journal-full-title] Endokrynologia Polska
  • [ISO-abbreviation] Endokrynol Pol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / SDHD protein, human; EC 1.3.5.1 / SDHB protein, human; EC 1.3.99.1 / Succinate Dehydrogenase; EC 2.3.2.27 / Von Hippel-Lindau Tumor Suppressor Protein; EC 2.7.10.1 / Proto-Oncogene Proteins c-ret; EC 2.7.10.1 / RET protein, human; EC 6.3.2.- / VHL protein, human
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67. National Toxicology Program: Toxicology and carcinogenesis studies of methyl isobutyl ketone (Cas No. 108-10-1) in F344/N rats and B6C3F1 mice (inhalation studies). Natl Toxicol Program Tech Rep Ser; 2007 Feb;(538):1-236
Hazardous Substances Data Bank. 2-HEXANONE .

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  • Methyl isobutyl ketone was nominated for study by the National Cancer Institute and the United States Environmental Protection Agency because of its widespread use, the high potential for worker exposure due to its many industrial applications, and its high production volume.
  • The incidence of adrenal medulla hyperplasia in the 1,800 ppm males was significantly increased.
  • [MeSH-minor] Administration, Oral. Adrenal Glands / drug effects. Animals. Body Weight / drug effects. Female. Kidney / drug effects. Kidney / pathology. Kidney Neoplasms / chemically induced. Kidney Neoplasms / pathology. Leukemia, Myeloid / chemically induced. Leukemia, Myeloid / pathology. Liver / drug effects. Liver / pathology. Liver Neoplasms / chemically induced. Liver Neoplasms / pathology. Lung Neoplasms / chemically induced. Lung Neoplasms / pathology. Male. Mice. Mice, Inbred Strains. Occupational Exposure. Rats. Rats, Inbred F344. Water Supply

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  • (PMID = 17557116.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Environmental Pollutants; 0 / Solvents; 6QDY60NH6N / Methyl n-Butyl Ketone; U5T7B88CNP / methyl isobutyl ketone
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68. Lau SK, Romansky SG, Weiss LM: Sustentaculoma: report of a case of a distinctive neoplasm of the adrenal medulla. Am J Surg Pathol; 2006 Feb;30(2):268-73
MedlinePlus Health Information. consumer health - Adrenal Gland Disorders.

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  • [Title] Sustentaculoma: report of a case of a distinctive neoplasm of the adrenal medulla.
  • A case of a morphologically distinctive tumor of the adrenal medulla occurring in a 54-year-old woman is described.
  • On microscopic examination, the tumor was well circumscribed and characterized by the presence of ill-defined, irregular nests of spindle cells with oval to elongated nuclei, tiny nucleoli, and abundant eosinophilic cytoplasm.
  • The tumor was associated with a moderate infiltrate of lymphocytes and plasma cells with occasional lymphoid follicles.
  • Immunohistochemical studies demonstrated the tumor cells to be strongly reactive for vimentin, S-100 protein, and CD56, and nonreactive for glial fibrillary acidic protein, chromogranin, synaptophysin, melanoma-associated antigens, and dendritic cell markers.
  • The morphology, immunophenotype, and ultrastructure of this unique neoplasm suggest derivation from sustentacular cells of the adrenal medulla.
  • We propose the designation "sustentaculoma" for this hitherto undescribed neoplasm of the adrenal gland.
  • [MeSH-major] Adrenal Gland Diseases / metabolism. Adrenal Gland Diseases / pathology. Adrenal Medulla / metabolism. Adrenal Medulla / pathology. Biomarkers, Tumor / analysis

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  • (PMID = 16434904.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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69. Mobine HR, Baker AB, Wang L, Wakimoto H, Jacobsen KC, Seidman CE, Seidman JG, Edelman ER: Pheochromocytoma-induced cardiomyopathy is modulated by the synergistic effects of cell-secreted factors. Circ Heart Fail; 2009 Mar;2(2):121-8
The Lens. Cited by Patents in .

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  • BACKGROUND: Pheochromocytomas are rare tumors derived from the chromaffin cells of the adrenal medulla.

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  • (PMID = 19808327.001).
  • [ISSN] 1941-3297
  • [Journal-full-title] Circulation. Heart failure
  • [ISO-abbreviation] Circ Heart Fail
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL083935-01A1; United States / NHLBI NIH HHS / HL / R01 HL084553; United States / NHLBI NIH HHS / HL / F31 HL083935-01A1; United States / PHS HHS / / R01 49039
  • [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 / Catecholamines; X4W3ENH1CV / Norepinephrine
  • [Other-IDs] NLM/ NIHMS129904; NLM/ PMC2769512
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70. Torii S, Kobayashi K, Takahashi M, Katahira K, Goryo K, Matsushita N, Yasumoto K, Fujii-Kuriyama Y, Sogawa K: Magnesium deficiency causes loss of response to intermittent hypoxia in paraganglion cells. J Biol Chem; 2009 Jul 10;284(28):19077-89
Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .

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  • Here we show that hypomagnesemia suppresses reactive oxygen species (ROS)-induced HIF-1alpha activity in paraganglion cells of the adrenal medulla and carotid body.
  • Induction of tyrosine hydroxylase, a target of HIF-1, by CoCl(2) injection was suppressed in the adrenal medulla of magnesium-deficient mice because of up-regulation of IPAS.

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  • (PMID = 19433582.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Small Interfering; 0 / Reactive Oxygen Species; EC 1.14.16.2 / Tyrosine 3-Monooxygenase; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ PMC2707206
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71. Huebener N, Fest S, Strandsby A, Michalsky E, Preissner R, Zeng Y, Gaedicke G, Lode HN: A rationally designed tyrosine hydroxylase DNA vaccine induces specific antineuroblastoma immunity. Mol Cancer Ther; 2008 Jul;7(7):2241-51
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  • Therapeutic vaccination against tumor antigens without induction of autoimmunity remains a major challenge in cancer immunotherapy.
  • Importantly, no cell infiltration was detectable in TH-expressing adrenal medulla, indicating the absence of autoimmunity.
  • [MeSH-minor] Amino Acid Sequence. Animals. Antibody Specificity / immunology. COS Cells. Cercopithecus aethiops. Cytotoxicity, Immunologic. Histocompatibility Antigens Class I / immunology. Lymphocyte Activation. Lymphocytes, Tumor-Infiltrating / immunology. Mice. Models, Molecular. Molecular Sequence Data. Peptides / chemistry. T-Lymphocytes / immunology. Ubiquitin / metabolism. Vaccination

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  • (PMID = 18645033.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histocompatibility Antigens Class I; 0 / Peptides; 0 / Ubiquitin; 0 / Vaccines, DNA; EC 1.14.16.2 / Tyrosine 3-Monooxygenase
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72. Tofighi R, Joseph B, Xia S, Xu ZQ, Hamberger B, Hökfelt T, Ceccatelli S: Galanin decreases proliferation of PC12 cells and induces apoptosis via its subtype 2 receptor (GalR2). Proc Natl Acad Sci U S A; 2008 Feb 19;105(7):2717-22
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  • Finally, as shown with real-time PCR, galanin and its receptors were expressed at very high levels in human pheochromocytoma tissues as compared with normal adrenal medulla.

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  • (PMID = 18272487.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptor, Galanin, Type 1; 0 / Receptor, Galanin, Type 2; 88813-36-9 / Galanin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ PMC2268202
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73. Bishop T, Gallagher D, Pascual A, Lygate CA, de Bono JP, Nicholls LG, Ortega-Saenz P, Oster H, Wijeyekoon B, Sutherland AI, Grosfeld A, Aragones J, Schneider M, van Geyte K, Teixeira D, Diez-Juan A, Lopez-Barneo J, Channon KM, Maxwell PH, Pugh CW, Davies AM, Carmeliet P, Ratcliffe PJ: Abnormal sympathoadrenal development and systemic hypotension in PHD3-/- mice. Mol Cell Biol; 2008 May;28(10):3386-400
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  • Reduced apoptosis in superior cervical ganglion (SCG) neurons cultured from PHD3(-/-) mice is associated with an increase in the number of cells in the SCG, as well as in the adrenal medulla and carotid body.
  • Despite the increased number of cells, the sympathoadrenal system appeared hypofunctional in PHD3(-/-) mice, with reduced target tissue innervation, adrenal medullary secretory capacity, sympathoadrenal responses, and systemic blood pressure.
  • [MeSH-major] Adrenal Glands / abnormalities. Hypotension / etiology. Procollagen-Proline Dioxygenase / deficiency. Sympathetic Nervous System / abnormalities

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  • (PMID = 18332118.001).
  • [ISSN] 1098-5549
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / / 071251; United Kingdom / Medical Research Council / / G0200482; United Kingdom / British Heart Foundation / / ; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA Primers; 0 / Hif1a protein, mouse; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / endothelial PAS domain-containing protein 1; EC 1.14.11.2 / PHD3 protein, mouse; EC 1.14.11.2 / Procollagen-Proline Dioxygenase
  • [Other-IDs] NLM/ PMC2423159
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74. Geli J, Kiss N, Lanner F, Foukakis T, Natalishvili N, Larsson O, Kogner P, Höög A, Clark GJ, Ekström TJ, Bäckdahl M, Farnebo F, Larsson C: The Ras effectors NORE1A and RASSF1A are frequently inactivated in pheochromocytoma and abdominal paraganglioma. Endocr Relat Cancer; 2007 Mar;14(1):125-34
MedlinePlus Health Information. consumer health - Pheochromocytoma.

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  • NORE1A (RASSF5) and RASSF1A are newly described Ras effectors with tumour suppressor functions.
  • Significantly suppressed NORE1A and RASSF1A mRNA levels were detected in primary tumours compared with normal adrenal medulla (P<0.001).
  • [MeSH-major] Abdominal Neoplasms / genetics. Monomeric GTP-Binding Proteins / genetics. Paraganglioma / genetics. Pheochromocytoma / genetics. Tumor Suppressor Proteins / genetics

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  • (PMID = 17395981.001).
  • [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 / RASSF1 protein, human; 0 / RASSF5 protein, human; 0 / RNA, Messenger; 0 / Sulfites; 0 / Tumor Suppressor Proteins; EC 3.6.5.2 / Monomeric GTP-Binding Proteins; OJ9787WBLU / hydrogen sulfite
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