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1. 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.
  • Attenuation values of <10 Hounsfield units on an unenhanced CT are practically diagnostic for adenomas.
  • 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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2. Willenberg HS, Päth G, Vögeli TA, Scherbaum WA, Bornstein SR: Role of interleukin-6 in stress response in normal and tumorous adrenal cells and during chronic inflammation. Ann N Y Acad Sci; 2002 Jun;966:304-14
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  • [Title] Role of interleukin-6 in stress response in normal and tumorous adrenal cells and during chronic inflammation.
  • Interleukin-6 (IL-6) is the end-product of a cytokine signaling cascade and is secreted by specialized immune cells during inflammation.
  • Thus, IL-6 serves as a key messenger in its communication with the neuroendocrine system, and serves as a potent activator of the hypothalamic-pituitary-adrenal axis at all levels.
  • Therefore, we studied the effect of IL-6 on normal and adenomatous human adrenal cells in vitro.
  • IL-6 potently stimulated cortisol secretion from dispersed normal human adrenal cells.
  • We found immunoreactivity for the IL-6 receptor on cultured cells and paraffin-embedded sections of adrenal tissues.
  • Further, there was a more pronounced expression of IL-6 mRNA in adrenal adenomas of patients with Cushing's syndrome, compared to normal human adrenals.
  • Despite this fact, the sensitivity of cells of adenomatous adrenal glands to IL-6 was significantly decreased relative to cells from normal controls.
  • These results were confirmed employing the permanent adrenocortical cancer cell line model NCI-H295.
  • We infer that the loss of responsivity of tumorous adrenal cells to IL-6, and in part corticotropin, is an important step in the process of adrenal tumorigenesis by which regulation by differentiating proteins is bypassed.
  • [MeSH-major] Adenoma / physiopathology. Adrenal Cortex / physiology. Adrenal Cortex Neoplasms / physiopathology. Adrenal Medulla / physiology. Inflammation / physiopathology. Interleukin-6 / physiology. Neoplasm Proteins / physiology. Stress, Physiological / physiopathology
  • [MeSH-minor] Cell Differentiation. Chromaffin Cells / drug effects. Cushing Syndrome / etiology. Cushing Syndrome / pathology. Drug Resistance, Neoplasm. Gene Expression Regulation / drug effects. Humans. Hydrocortisone / biosynthesis. Hydrocortisone / genetics. Neuroimmunomodulation. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. RNA, Neoplasm / biosynthesis. RNA, Neoplasm / genetics. Receptors, Interleukin-6 / biosynthesis. Receptors, Interleukin-6 / genetics. Tumor Cells, Cultured / drug effects

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  • (PMID = 12114287.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Interleukin-6; WI4X0X7BPJ / Hydrocortisone
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3. Opocher G, Schiavi F, Cicala MV, Patalano A, Mariniello B, Boaretto F, Zovato S, Pignataro V, Macino B, Negro I, Mantero F: Genetics of adrenal tumors. Minerva Endocrinol; 2009 Jun;34(2):107-21
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  • [Title] Genetics of adrenal tumors.
  • The impact of genetics and genomics on clinical medicine is becoming more and more important.
  • 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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4. Kvacheniuk AM: [The surgical treatment of malignant adrenal chromaphinomas]. Lik Sprava; 2004 Oct-Nov;(7):52-4
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  • [Title] [The surgical treatment of malignant adrenal chromaphinomas].
  • Pheochromoblastoma (PHB) is a tumor developing from adrenal medulla and characterized by severe course and high mortality level (15%).
  • The eradication of malignant growth requires not only complete tumor removal in single capsule with the adrenal gland but also thorough revision of paranephric, paracaval and paraaortal lymphnodes.
  • The disease persists in two patients though it is better controlled after the operation than earlier with medicine.

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  • (PMID = 15724615.001).
  • [ISSN] 1019-5297
  • [Journal-full-title] Likars'ka sprava
  • [ISO-abbreviation] Lik. Sprava
  • [Language] UKR
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Catecholamines
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5. Lafferty JS, Kamendulis LM, Kaster J, Jiang J, Klaunig JE: Subchronic acrylamide treatment induces a tissue-specific increase in DNA synthesis in the rat. Toxicol Lett; 2004 Dec 1;154(1-2):95-103
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  • Chronic treatment with acrylamide results in increased incidence of adrenal (pheochromocytoma), testicular (mesotheliomas) and thyroid (adenoma) neoplasia in male rats.
  • While acrylamide has been demonstrated to be DNA reactive, the tissue pattern of neoplasm induction by acrylamide suggests other mechanisms in addition to DNA reactivity may be involved in the carcinogenesis of this compound.
  • Acrylamide increased DNA synthesis in the target tissues for tumor development (thyroid, testicular mesothelium, adrenal medulla) in both rat species.
  • In contrast, cell growth was not altered in the liver and adrenal cortex (non-target tissues for acrylamide carcinogenesis).
  • Inhibition of oxidative metabolism of acrylamide using 1-aminobenzotriazole reduced acrylamide-induced DNA synthesis only in the adrenal medulla, having no apparent effect in the testicular mesolthelium or thyroid.
  • In summary, acrylamide produced a selective increase in DNA synthesis that correlates with the previously reported tumor target tissues.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Bromodeoxyuridine / metabolism. Cell Division / drug effects. Dose-Response Relationship, Drug. Drug Therapy, Combination. Male. Mitosis / drug effects. Rats. Rats, Inbred F344. Rats, Sprague-Dawley. Triazoles / pharmacology

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  • (PMID = 15475183.001).
  • [ISSN] 0378-4274
  • [Journal-full-title] Toxicology letters
  • [ISO-abbreviation] Toxicol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Environmental Pollutants; 0 / Triazoles; 1614-12-6 / 1-aminobenzotriazole; 20R035KLCI / Acrylamide; 9007-49-2 / DNA; G34N38R2N1 / Bromodeoxyuridine
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6. Reubi JC: In vitro evaluation of VIP/PACAP receptors in healthy and diseased human tissues. Clinical implications. Ann N Y Acad Sci; 2000;921:1-25
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  • The evaluation of peptide receptors in man is relevant to identifying the physiological target tissues of a given peptide and to selecting diseases with a sufficient receptor overexpression for diagnostic or therapeutic intervention.
  • VPAC2 receptors are predominantly found in vessels and smooth muscles, whereas PAC1 receptors are present in the adrenal medulla.
  • Moreover, the receptor expression in tumors is the molecular basis for clinical applications of VIP/PACAP such as in vivo scintigraphy and radiotherapy of tumors as well as VIP/PACAP analog treatment for tumor growth inhibition.
  • [MeSH-minor] Autoradiography. Epithelium / metabolism. Female. Humans. In Vitro Techniques. Male. Neoplasm Metastasis. Neoplasms / drug therapy. Neoplasms / metabolism. Neoplasms / radiotherapy. Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide. Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type I. Receptors, Vasoactive Intestinal Peptide, Type II. Receptors, Vasoactive Intestinal Polypeptide, Type I. Tissue Distribution


7. 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
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  • BACKGROUND: Pheochromocytomas are rare tumors derived from the chromaffin cells of the adrenal medulla.
  • PC12 cell implantation increased left ventricular dilation by 35+/-6% and 9.6+/-1.4% and reduced left ventricular fractional shortening by 20+/-3% and 28+/-4% in rats and mice compared with animals dosed only with NE, respectively.

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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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8. Kremens B: [Systemic therapy in children and adolescents]. Urologe A; 2007 Oct;46(10):1404-6
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  • 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-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Neoadjuvant Therapy. Urogenital Neoplasms / drug therapy
  • [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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9. Palaoğlu S, Sungur A, Cila A, Ozdemir N, Ruacan S: Diethylstilbestrol-induced prolactinoma: dose-related tumor growth and effect of catecholaminergic cells on prolactin tumor cells. Surg Neurol; 2005;64 Suppl 2:S42-7
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  • [Title] Diethylstilbestrol-induced prolactinoma: dose-related tumor growth and effect of catecholaminergic cells on prolactin tumor cells.
  • Unfortunately, there appears to be a relatively high recurrence rate despite all pharmacological, radiological, and surgical therapeutic interventions.
  • We transplanted, in rats, DES-induced prolactinoma cells into the adrenal medulla or under the renal capsule, two tissues rich and poor in catecholaminergic innervation, respectively.
  • METHODS: Prolactinoma was dose-dependently induced in ovariectomized female rats implanted with 10 and 20 mg DES, and tumor cells taken from prolactinoma induced by 20 mg DES were either transplanted under the renal capsule or into the adrenal medulla.
  • RESULTS: Although the adrenal medulla, with its high dopamine content to inhibit prolactin secretion, was devoid of any tumoral development, a significant tumoral development was evident under the renal capsule, seemingly because of no inhibitory control over prolactin secretion coexisting with the dopamine deficiency of the tissue.
  • [MeSH-major] Adrenal Medulla / pathology. Catecholamines / physiology. Kidney Cortex / pathology. Pituitary Neoplasms / pathology. Prolactinoma / pathology
  • [MeSH-minor] Animals. Carcinogens / administration & dosage. Diethylstilbestrol / administration & dosage. Dose-Response Relationship, Drug. Female. Neoplasm Transplantation. Rats

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  • (PMID = 16256840.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Catecholamines; 731DCA35BT / Diethylstilbestrol
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10. Klaunig JE, Kamendulis LM: Mechanisms of acrylamide induced rodent carcinogenesis. Adv Exp Med Biol; 2005;561:49-62
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  • It has been established that following chronic exposure, rats exhibited an increase in the incidence of adrenal pheochromocytomas, testicular mesotheliomas, thyroid adenomas and mammary neoplasms in F344 rats.
  • Acrylamide increased DNA synthesis in the target tissues (thyroid, testicular mesothelium, adrenal medulla) at all doses and time points examined.
  • In summary, acrylamide caused both an increase in DNA synthesis and DNA damage in mammalian tissues and cells suggesting that DNA reactivity and cell proliferation, in concert, may contribute to the observed acrylamide-induced carcinogenicity in the rat and has implication on the possible risk for human neoplasm development.
  • [MeSH-minor] Animals. Bromodeoxyuridine / pharmacology. Cell Line. Cell Proliferation. Cell Transformation, Neoplastic. Comet Assay. Cricetinae. DNA / metabolism. DNA Adducts. DNA Damage. Dose-Response Relationship, Drug. Fluorescent Dyes / pharmacology. Food Handling. Glutathione / metabolism. Mesocricetus. Rats. Rats, Inbred F344. Time Factors

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  • (PMID = 16438288.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / DNA Adducts; 0 / Fluorescent Dyes; 20R035KLCI / Acrylamide; 9007-49-2 / DNA; G34N38R2N1 / Bromodeoxyuridine; GAN16C9B8O / Glutathione
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