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1. Ignaszak-Szczepaniak M, Horst-Sikorska W, Sawicka J, Kaczmarek M, Slomski R: The TP53 codon 72 polymorphism and predisposition to adrenocortical cancer in Polish patients. Oncol Rep; 2006 Jul;16(1):65-71
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  • [Title] The TP53 codon 72 polymorphism and predisposition to adrenocortical cancer in Polish patients.
  • The association between this common polymorphism and risk of different cancers has been extensive studied, however various reports are controversial.
  • We have analyzed the 72Pro polymorphic variant in patients with adrenocortical tumors to evaluate whether 72G--> C substitution at codon 72 of TP53 gene may be associated with increased risk for malignancy in adrenal cortex in comparison to the control group.
  • DNA extracted from peripheral leucocytes of 46 Polish patients with adrenocortical tumors (17 malignant and 29 benign) and 50 controls was examined by PCR-HD method followed by direct sequencing.
  • The genotype Arg/Arg, Arg/Pro and Pro/Pro distribution was respectively 53%/35%/12% for cancers, 72%/28%/0% for benign tumors and 76%/24%/0% for controls.
  • High frequency of 72Pro allele in patients with carcinoma (29%) in comparison to the benign tumors (14%) and controls (12%) was statistically analyzed.
  • Our results suggest that the TP53 codon 72 polymorphism could be associated with susceptibility for adrenocortical cancer in the examined Polish patients.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Genetic Predisposition to Disease. Polymorphism, Genetic. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 16786124.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Codon; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53
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2. Veytsman I, Nieman L, Fojo T: Management of endocrine manifestations and the use of mitotane as a chemotherapeutic agent for adrenocortical carcinoma. J Clin Oncol; 2009 Sep 20;27(27):4619-29
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  • [Title] Management of endocrine manifestations and the use of mitotane as a chemotherapeutic agent for adrenocortical carcinoma.
  • Adrenal cortical carcinoma (ACC) is a rare malignancy in which patients have poor overall 5-year survival.
  • Physicians who treat patients with ACC and severe hypercortisolism should recognize that uncontrolled hormone production is a malignant disease, which has severe consequences that require aggressive management.
  • Despite difficulty administering effective doses, most clinicians agree that mitotane should be used if the tumor cannot be removed surgically or should be used as adjuvant therapy if there is a high likelihood of recurrence.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Adrenal Cortex Neoplasms / physiopathology. Adrenocortical Carcinoma / drug therapy. Adrenocortical Carcinoma / physiopathology. Antineoplastic Agents, Hormonal / therapeutic use. Mitotane / therapeutic use
  • [MeSH-minor] Adrenocortical Hyperfunction / drug therapy. Adrenocortical Hyperfunction / etiology. Female. Humans. Male

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  • (PMID = 19667279.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / ZIE HD008832-03
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 78E4J5IB5J / Mitotane
  • [Number-of-references] 120
  • [Other-IDs] NLM/ PMC2754909
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3. Karim RZ, Wills EJ, McCarthy SW, Scolyer RA: Myxoid variant of adrenocortical carcinoma: report of a unique case. Pathol Int; 2006 Feb;56(2):89-94
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  • [Title] Myxoid variant of adrenocortical carcinoma: report of a unique case.
  • Myxoid variant of adrenocortical carcinomas (ACC) are rare, there being only 11 cases in the literature to date.
  • The patient was a 61-year-old man in whom a left adrenal mass was detected during investigation of Cushing's syndrome.
  • The adrenal was replaced by malignant cells and expanses of myxoid material.
  • The ultrastructural features of the cells were typical of adrenal cortical differentiation.
  • The differential diagnosis of myxoid ACC includes extraskeletal myxoid chondrosarcoma, chordoma, myxoid adenocarcinoma, myxoma, lipomatous tumors, nerve sheath tumors, smooth muscle tumors, gastrointestinal stromal tumor and other sarcomas.
  • The presence of myxoid material in a retroperitoneal lesion raises a broad differential diagnosis in which myxoid adrenocortical neoplasms should be included.
  • Clinicoradiological correlation may be helpful, but special stains, immunohistochemistry and ultrastructural examination may be necessary to establish the diagnosis.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenocortical Carcinoma / diagnosis
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Antigens, Neoplasm. Chordoma / diagnosis. Chordoma / pathology. Diagnosis, Differential. Humans. Immunohistochemistry. MART-1 Antigen. Male. Microscopy, Electron. Middle Aged. Myxoma / diagnosis. Myxoma / pathology. Neoplasm Proteins / analysis. Nerve Sheath Neoplasms / diagnosis. Nerve Sheath Neoplasms / pathology. Retroperitoneal Neoplasms / diagnosis. Retroperitoneal Neoplasms / pathology. Synaptophysin / analysis. Vimentin / analysis

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  • (PMID = 16445821.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / MART-1 Antigen; 0 / MLANA protein, human; 0 / Neoplasm Proteins; 0 / Synaptophysin; 0 / Vimentin
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4. Lindhe O, Skogseid B: Mitotane effects in a H295R xenograft model of adjuvant treatment of adrenocortical cancer. Horm Metab Res; 2010 Sep;42(10):725-30
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  • [Title] Mitotane effects in a H295R xenograft model of adjuvant treatment of adrenocortical cancer.
  • Adrenocortical cancer is one of the most aggressive endocrine malignancies.
  • Growth through the capsule or accidental release of cancer cells during surgery frequently results in metastatic disease.
  • We investigated the antitumoral effect of 2 adrenocorticolytic compounds, O, P'-DDD and MeSO2-DDE, in the adrenocortical cell line H295R both in vitro and as a xenograft model in vivo.
  • Tumor growth was significantly inhibited when O, P'-DDD was given at the same time as injection of tumor cells.
  • We suggest that FLT may be a potential PET biomarker when assessing adrenocortical cancer treatment with O,P'-DDD.
  • [MeSH-major] Adjuvants, Pharmaceutic / therapeutic use. Adrenal Cortex Neoplasms / drug therapy. Mitotane / therapeutic use. Xenograft Model Antitumor Assays
  • [MeSH-minor] Animals. Cell Aggregation / drug effects. Cell Count. Cell Proliferation / drug effects. Female. Humans. Mice. Positron-Emission Tomography. Radioactive Tracers. Spheroids, Cellular / drug effects. Spheroids, Cellular / pathology. Time Factors. Tumor Burden / drug effects. Tumor Cells, Cultured

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  • (PMID = 20665429.001).
  • [ISSN] 1439-4286
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Adjuvants, Pharmaceutic; 0 / Radioactive Tracers; 78E4J5IB5J / Mitotane
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5. Shi Z, Henwood MJ, Bannerman P, Batista D, Horvath A, Guttenberg M, Stratakis CA, Grimberg A: Primary pigmented nodular adrenocortical disease reveals insulin-like growth factor binding protein-2 regulation by protein kinase A. Growth Horm IGF Res; 2007 Apr;17(2):113-21
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  • [Title] Primary pigmented nodular adrenocortical disease reveals insulin-like growth factor binding protein-2 regulation by protein kinase A.
  • OBJECTIVE: Primary pigmented nodular adrenocortical disease (PPNAD) can occur as an isolated trait or part of Carney complex, a familial lentiginosis-multiple endocrine neoplasia syndrome frequently caused by mutations in PRKAR1A, which encodes the 1alpha regulatory subunit of protein kinase A (PKA).
  • Because alterations in the insulin-like growth factor (IGF) axis, particularly IGF-II and IGF binding protein (IGFBP)-2 overexpression, have been implicated in sporadic adrenocortical tumors, we sought to examine the IGF axis in PPNAD.
  • NCI-H295R cells were used to study PKA and IGF axis signaling in adrenocortical cells in vitro.
  • Moreover, PKA inhibitors increased IGFBP-2 expression in NCI-H295R adrenocortical cells, and anti-IGFBP-2 antibody reduced their proliferation.
  • CONCLUSIONS: IGFBP-2 expression is increased in PPNAD caused by PRKAR1A mutations, and in adrenocortical cancer cells.
  • This is the first evidence for PKA-dependent regulation of IGFBP-2 expression in adrenocortical cells.

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  • (PMID = 17280861.001).
  • [ISSN] 1096-6374
  • [Journal-full-title] Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society
  • [ISO-abbreviation] Growth Horm. IGF Res.
  • [Language] ENG
  • [Databank-accession-numbers] OMIM/ 160980
  • [Grant] United States / NIDDK NIH HHS / DK / T32 DK63688; United States / NIDDK NIH HHS / DK / T32 DK063688; United States / NICHD NIH HHS / HD / Z01 HD000642-04; United States / NIDDK NIH HHS / DK / 5 K08 DK64352; United States / NICHD NIH HHS / HD / Z01 HD000642; United States / NIDDK NIH HHS / DK / K08 DK064352
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / Insulin-Like Growth Factor Binding Protein 2; 0 / PRKAR1A protein, human; 0 / Protein Kinase Inhibitors; 0 / RNA, Messenger; 67763-97-7 / Insulin-Like Growth Factor II; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
  • [Other-IDs] NLM/ NIHMS22924; NLM/ PMC2577759
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6. Carmona-Bayonas A, Soler IO, Gómez FI, Billalabeitia EG, Saura HP, Tafalla MS, Díaz MP: Tailored hormonal therapy in secretory adrenocortical cancer. Ann Oncol; 2007 Jul;18(7):1281
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  • [Title] Tailored hormonal therapy in secretory adrenocortical cancer.

  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
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  • Hazardous Substances Data Bank. POTASSIUM, ELEMENTAL .
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  • (PMID = 17675396.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiotensin-Converting Enzyme Inhibitors; 0 / Anti-Inflammatory Agents; 0 / Antifungal Agents; 0 / Antineoplastic Agents, Hormonal; 0 / Mineralocorticoid Receptor Antagonists; 27O7W4T232 / Spironolactone; 4964P6T9RB / Aldosterone; 6PLQ3CP4P3 / Etoposide; 78E4J5IB5J / Mitotane; 80168379AG / Doxorubicin; 9G64RSX1XD / Captopril; Q20Q21Q62J / Cisplatin; R9400W927I / Ketoconazole; RWP5GA015D / Potassium; WI4X0X7BPJ / Hydrocortisone
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7. Igaz P, Tömböl Z, Szabó PM, Likó I, Rácz K: Steroid biosynthesis inhibitors in the therapy of hypercortisolism: theory and practice. Curr Med Chem; 2008;15(26):2734-47
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  • A few drugs inhibiting single or multiple steps in adrenal steroid biosynthesis can be used in clinical practice.
  • Besides blocking multiple steps in adrenal steroid biosynthesis, the DDT (insecticide) analogue mitotane also has adrenolytic properties by inducing mitochondrial degeneration that renders it superior to other drugs in the treatment of adrenocortical cancer.

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  • (PMID = 18991633.001).
  • [ISSN] 0929-8673
  • [Journal-full-title] Current medicinal chemistry
  • [ISO-abbreviation] Curr. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Steroids
  • [Number-of-references] 153
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8. Palazzo FF, Sebag F, Sierra M, Ippolito G, Souteyrand P, Henry JF: Long-term outcome following laparoscopic adrenalectomy for large solid adrenal cortex tumors. World J Surg; 2006 May;30(5):893-8
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  • [Title] Long-term outcome following laparoscopic adrenalectomy for large solid adrenal cortex tumors.
  • INTRODUCTION: Laparoscopic adrenalectomy (LA) is the procedure of choice for small benign adrenal tumors.
  • In the absence of local invasion or metastases, the preoperative diagnosis of an adrenocortical carcinoma (ACC) is difficult, often leaving size as the principal predictor of malignancy.
  • Large tumors are resectable laparoscopically, but the long-term outcome and therefore appropriateness of LA for cortical tumors > 6 cm is not known.
  • METHODS: We reviewed the LA experience in our institution since its introduction in June 1994.
  • Patients who underwent LA for solid cortical tumors > or = 60 mm in diameter without preoperative or intraoperative evidence of malignancy were reviewed.
  • Among them, 19 were solid cortical tumors > or = 60 mm in diameter with no overt malignant preoperative or intraoperative characteristics: 9 nonsecreting tumors, 8 Cushing's syndrome tumors (including 2 virilizing variants), 1 virilizing tumor, and 1 aldosteronoma.
  • The mean age of the patients was 49.9 years (range 22-77 years), and the mean tumor size was 69.0 mm (range 60-80 mm).
  • Histology confirmed a cortical adenoma in eight patients, malignant tumors in three, and indeterminate tumors in eight.
  • CONCLUSIONS: Laparoscopic adrenalectomy for large solid cortical tumors without pre- or intraoperative evidence of malignancy is not contraindicated, and it is unlikely to have a deleterious effect on long-term outcome.
  • We provide an algorithm for the approach to adrenocortical tumors > or = 6 cm.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenalectomy. Adrenocortical Adenoma / surgery. Adrenocortical Carcinoma / surgery
  • [MeSH-minor] Adult. Aged. Algorithms. Humans. Laparoscopy. Middle Aged. Neoplasm Staging. Retrospective Studies. Time Factors. Treatment Outcome

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  • (PMID = 16680605.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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9. Park BK, Kim CK, Jung BC, Suh YL: Cortical adenoma in adrenohepatic fusion tissue: clue to making a correct diagnosis at preoperative computed tomography examination. Eur Urol; 2009 Dec;56(6):1082-5
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  • [Title] Cortical adenoma in adrenohepatic fusion tissue: clue to making a correct diagnosis at preoperative computed tomography examination.
  • A 45-yr-old woman was admitted to excise a solid hepatic tumor which was incidentally detected at ultrasound examination for an unrelated reason.
  • Preoperative differential diagnoses included primary or secondary malignant hepatic tumors or adrenal cortical carcinoma due to aggressive imaging features.
  • The tumor proved to be an adrenal cortical adenoma arising from the adrenohepatic fusion tissue and consisted of adenoma cells with lipid-rich cytoplasm.
  • Retrospective review of preoperative computed tomography (CT) images demonstrated that the tumor measured 6 Hounsfield units in mean CT number and was continuous with a medial limb of the right adrenal gland.
  • [MeSH-major] Adrenal Cortex Neoplasms / radiography. Adrenocortical Adenoma / radiography. Liver Neoplasms / radiography. Tomography, X-Ray Computed
  • [MeSH-minor] Diagnosis, Differential. Female. Humans. Middle Aged. Preoperative Care. Ultrasonography

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  • (PMID = 19447543.001).
  • [ISSN] 1873-7560
  • [Journal-full-title] European urology
  • [ISO-abbreviation] Eur. Urol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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10. Loncarevic IF, Hering A, Posorski N, Linden T, Hoyer H, Bucsky P: Number of genomic imbalances correlates with the overall survival for adrenocortical cancer in childhood. Pediatr Blood Cancer; 2008 Sep;51(3):356-62
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  • [Title] Number of genomic imbalances correlates with the overall survival for adrenocortical cancer in childhood.
  • BACKGROUND: Adrenocortical tumours (ACT) in children are rare and, if malignant, often associated with poor prognosis.
  • PROCEDURES: We analysed 14 adrenocortical cancers (ACC) of children by comparative genomic hybridisation (CGH).
  • RESULTS: The total number of genomic imbalances ranged from 1 to 17 in individual tumour samples.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / mortality. Chromosome Aberrations

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18478573.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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11. Polamaung W, Wisedopas N, Vasinanukorn P, Pak-art P, Snabboon T: Asymptomatic bilateral giant adrenal myelolipomas: case report and review of literature. Endocr Pract; 2007 Oct;13(6):667-71
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  • [Title] Asymptomatic bilateral giant adrenal myelolipomas: case report and review of literature.
  • OBJECTIVE: To describe an unusual case of bilateral giant adrenal masses caused by a primary adrenal myelolipoma.
  • METHODS: We present the clinical, laboratory, and pathologic findings in a 32-year-old man with bilateral adrenal masses.
  • A computed tomographic scan of the abdomen disclosed bilateral adrenal masses; the one on the left was approximately 27 by 24 by 12 cm, and the one on the right side was 9 by 5 by 5 cm.
  • An endocrinologic evaluation revealed no evidence of adrenal cortical or medullary functional abnormalities.
  • Bilateral adrenalectomy was performed because of the large size of the lesions and the inability to rule out malignant involvement.
  • CONCLUSION: Myelolipoma is a relatively rare benign tumor of the adrenal glands composed of adipose cells and mature hematopoietic elements.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis. Myelolipoma / diagnosis

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  • (PMID = 17954426.001).
  • [ISSN] 1934-2403
  • [Journal-full-title] Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
  • [ISO-abbreviation] Endocr Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 31
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12. Willenberg HS, Ansurudeen I, Schebesta K, Haase M, Wess B, Schinner S, Raffel A, Schott M, Scherbaum WA: The endothelium secretes interleukin-6 (IL-6) and induces IL-6 and aldosterone generation by adrenocortical cells. Exp Clin Endocrinol Diabetes; 2008 Sep;116 Suppl 1:S70-4
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  • [Title] The endothelium secretes interleukin-6 (IL-6) and induces IL-6 and aldosterone generation by adrenocortical cells.
  • Endothelial cells have been shown to induce adrenal steroidogenesis and to enhance aldosterone secretion via angiotensin II and endothelin 1-independent mechanisms.
  • It has been demonstrated that endothelial cells and adrenocortical cells are capable of producing interleukin-6 (IL-6) and IL-6 is a factor known to stimulate adrenal cortisol secretion.
  • We therefore asked whether endothelial cells have an effect on adrenal IL-6 generation and whether IL-6 mediates biosynthesis of aldosterone as is observed after exposure of adrenocortical cells to endothelial cell-conditioned medium (ECCM).
  • Cells from the adrenocortical cancer cell line NCI-H295R were incubated with ECCM produced from human umbilical vein endothelial cells at increasing concentrations.
  • As detected by an enzyme-linked immunosorbent assay, pure ECCM significantly increased IL-6 protein secretion by cultured adrenocortical cells in a dose-dependent fashion, to a 18.0+/-2.0 pg/mL (mean+/-SEM).
  • Pure ECCM also induced aldosterone secretion by adrenocortical cells more than three times that of controls with serum-free medium.
  • These data suggest that endothelial cells secrete IL-6 and that endothelial cell-derived factors regulate adrenal IL-6 synthesis which does not alter adrenal aldosterone secretion.
  • Our findings support the hypothesis that the endothelium and the adrenal gland may play a role in the development of some forms of hypertension and - more speculative - inflammation.
  • [MeSH-major] Adrenal Cortex / metabolism. Aldosterone / biosynthesis. Endothelium, Vascular / secretion. Interleukin-6 / biosynthesis. Interleukin-6 / secretion

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  • (PMID = 18777460.001).
  • [ISSN] 0947-7349
  • [Journal-full-title] Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
  • [ISO-abbreviation] Exp. Clin. Endocrinol. Diabetes
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Interleukin-6; 4964P6T9RB / Aldosterone
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13. Misić M, Vidas Z, Skegro D, Kocman B, Jelić-Puskarić B, Kardum-Skelin I: Fine needle aspiration cytology of adrenocortical carcinoma--case report. Coll Antropol; 2010 Jun;34(2):665-9
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  • [Title] Fine needle aspiration cytology of adrenocortical carcinoma--case report.
  • Ultrasonography (US) revealed a solitary tumor mass, eight cm in size, of the right adrenal gland.
  • Laboratory tests showed it to be a hormonally active, androgen secreting tumor (elevated testosterone level), which was consistent with the clinical picture of the disease.
  • After histopathological analysis tumor was signed out as adrenocortical carcinoma, a low risk carcinoma according to Weiss' classification.
  • Cytologic opinion was recidive of primary malignant disease.
  • ACC is a rare malignant epithelial tumor of adrenal cortical cells, with high malignant potential.
  • Morphologically (histopathology and cytology), differential diagnosis includes adenoma on the one hand, and renal cell carcinoma (RCC) and hepatocellular carcinoma (HCC) on the other hand.
  • A combined evaluation of clinical features, size or weight, microscopic appearance, immunohistochemical and molecular genetic data is necessary to ensure a correct diagnosis.
  • The purpose of this case report is to present clinical and cytomorphologic features of our case of adrenocortical carcinoma which is very rare in cytology practice.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Carcinoma / pathology

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  • (PMID = 20698150.001).
  • [ISSN] 0350-6134
  • [Journal-full-title] Collegium antropologicum
  • [ISO-abbreviation] Coll Antropol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Croatia
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14. Hahner S, Stürmer A, Fassnacht M, Hartmann RW, Schewe K, Cochran S, Zink M, Schirbel A, Allolio B: Etomidate unmasks intraadrenal regulation of steroidogenesis and proliferation in adrenal cortical cell lines. Horm Metab Res; 2010 Jun;42(7):528-34
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  • [Title] Etomidate unmasks intraadrenal regulation of steroidogenesis and proliferation in adrenal cortical cell lines.
  • To characterize intraadrenal adaptations for inhibition of cortisol synthesis, we analyzed the effects of etomidate (ETO) on steroid hormone secretion and expression of key regulators of steroidogenesis and proliferation in human NCI-h295 adrenocortical cancer cells.
  • In summary, ETO exhibits pleiotropic effects on adrenal function in vitro.
  • These changes reflect adaptations to maintain steroidogenesis at the cost of adrenal proliferation.
  • [MeSH-major] Adrenal Cortex / cytology. Adrenal Cortex / metabolism. Cell Proliferation / drug effects. Etomidate / pharmacology. Steroids / biosynthesis

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  • [Copyright] Georg Thieme Verlag KG Stuttgart * New York.
  • (PMID = 20352599.001).
  • [ISSN] 1439-4286
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Steroids; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase; EC 1.14.15.6 / Cholesterol Side-Chain Cleavage Enzyme; Z22628B598 / Etomidate
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15. Coulter CL: Fetal adrenal development: insight gained from adrenal tumors. Trends Endocrinol Metab; 2005 Jul;16(5):235-42
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  • [Title] Fetal adrenal development: insight gained from adrenal tumors.
  • Conversely, tumor progression and the development of cancer probably occur through a process of dysregulation and dedifferentiation.
  • Similarities exist between normal human fetal adrenal cortex and adrenal cancers, such as high expression of growth factors, including insulin-like growth factor II.
  • Therefore, we might gain insight into factors involved in adrenocortical development through better understanding the development and progression of adrenocortical tumors.
  • This review is prompted by recent gene profiling studies that have identified genes differentially expressed between normal and abnormal adrenal glands.
  • Several of these genes are specific growth factors or key cell cycle regulators, in addition to genes not previously associated with adrenal growth or function.
  • [MeSH-major] Adrenal Gland Neoplasms / pathology. Adrenal Glands / embryology

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  • (PMID = 15949953.001).
  • [ISSN] 1043-2760
  • [Journal-full-title] Trends in endocrinology and metabolism: TEM
  • [ISO-abbreviation] Trends Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Somatomedins
  • [Number-of-references] 62
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16. Leboulleux S, Dromain C, Bonniaud G, Aupérin A, Caillou B, Lumbroso J, Sigal R, Baudin E, Schlumberger M: Diagnostic and prognostic value of 18-fluorodeoxyglucose positron emission tomography in adrenocortical carcinoma: a prospective comparison with computed tomography. J Clin Endocrinol Metab; 2006 Mar;91(3):920-5
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  • [Title] Diagnostic and prognostic value of 18-fluorodeoxyglucose positron emission tomography in adrenocortical carcinoma: a prospective comparison with computed tomography.
  • OBJECTIVE: Patients with adrenocortical cancer are submitted to multiple imaging procedures for diagnosis of recurrence and staging.
  • METHODS: Twenty-eight consecutive patients with adrenocortical cancer referred from November 2003 to December 2004 to the Institut Gustave Roussy were included.
  • The sensitivities for the detection of distinct lesions and the diagnosis of metastatic organs were 90 and 93% for PET/CT and 88 and 82% for TAP-CT, respectively.
  • Tumor size and mitotic rate were significantly associated with FDG uptake.
  • CONCLUSIONS: We show that FDG-PET/CT is complementary to TAP-CT and of special interest in the diagnosis of local relapses.
  • [MeSH-major] Adrenal Cortex Neoplasms / radiography. Adrenal Cortex Neoplasms / radionuclide imaging. Fluorodeoxyglucose F18
  • [MeSH-minor] Adult. Aged. Female. Humans. Image Processing, Computer-Assisted. Male. Middle Aged. Neoplasm Metastasis. Positron-Emission Tomography. Prognosis. Radiopharmaceuticals. Survival Analysis. Tomography, X-Ray Computed

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  • (PMID = 16368753.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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17. Kanczkowski W, Zacharowski K, Wirth MP, Ehrhart-Bornstein M, Bornstein SR: Differential expression and action of Toll-like receptors in human adrenocortical cells. Mol Cell Endocrinol; 2009 Mar 5;300(1-2):57-65
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential expression and action of Toll-like receptors in human adrenocortical cells.
  • During sepsis, an intact adrenal gland glucocorticoid stress response is critical for survival.
  • However, the exact role which TLRs play in adrenal homeostasis and malfunction is not yet sufficiently known.
  • Using quantitative real-time PCR, confocal microscopy and the NF-kappaB reporter gene assay, we aimed to analyse both, expression and function of all relevant TLRs in the human adrenocortical cell line-NCI-H295R and adrenal cells in primary culture.
  • Our results demonstrate a differential expression pattern of TLR1-9 in human adrenocortical cells as compared to immune cells and adrenocortical cancer cells.
  • Therefore, Toll-like receptors expression and function is a novel feature of the adrenal stress system contributing to adrenal tissue homeostasis, regeneration and tumorigenesis.
  • [MeSH-major] Adrenal Cortex. Gene Expression Regulation. Protein Isoforms / metabolism. Toll-Like Receptors / metabolism
  • [MeSH-minor] Aged. Cells, Cultured. Female. Homeostasis. Humans. Interleukin-8 / metabolism. Male. Middle Aged. NF-kappa B / metabolism. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 19022344.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Interleukin-8; 0 / NF-kappa B; 0 / Protein Isoforms; 0 / Toll-Like Receptors; 0 / Tumor Necrosis Factor-alpha
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18. Geller JL, Azer PC, Weiss LM, Mertens RB: Pigmented adrenocortical carcinoma: case report and review. Endocr Pathol; 2006;17(3):297-304
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  • [Title] Pigmented adrenocortical carcinoma: case report and review.
  • Darkly pigmented adrenocortical neoplasms are rare tumors that are often referred to as "black adenomas," indicative of both their pigmented nature and their invariably benign clinical behavior in previously reported cases.
  • We herein describe an exceptional case of a malignant pigmented adrenocortical neoplasm, with late recurrence and metastasis.
  • At age 53, this female patient was diagnosed with Cushing's syndrome and underwent a laparoscopic right adrenalectomy, revealing a 3 cm well-circumscribed, darkly pigmented adrenocortical tumor.
  • The tumor exhibited several atypical histologic features and was diagnosed as an atypical pigmented adrenal cortical neoplasm of uncertain malignant potential.
  • At subsequent exploratory laparotomy, three separate tumor nodules exhibiting varying degrees of pigmentation and ranging from 2.2 to 3.3 cm maximum dimension were excised.
  • Histologically, the tumor nodules were consistent with local recurrence/metastasis of the patient's previously excised pigmented adrenocortical neoplasm.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / secondary. Pigmentation. Retroperitoneal Neoplasms / secondary
  • [MeSH-minor] Adrenalectomy. Cushing Syndrome / etiology. Female. Humans. Middle Aged. Neoplasm Recurrence, Local / pathology. Neoplasm Recurrence, Local / surgery

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  • (PMID = 17308367.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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19. Libè R, Fratticci A, Bertherat J: Adrenocortical cancer: pathophysiology and clinical management. Endocr Relat Cancer; 2007 Mar;14(1):13-28
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  • [Title] Adrenocortical cancer: pathophysiology and clinical management.
  • Adrenocortical cancer (ACC) is a rare tumor with a poor prognosis.
  • By contrast, benign adrenocortical tumors are frequent, underlying the importance of a correct diagnosis of malignancy of such tumors.
  • ACC can be diagnosed by the investigation of endocrine signs of steroid excess, symptoms due to tumor growth or an adrenal incidentaloma.
  • Imaging by CT-scan or MRI shows a large heterogeneous tumor with a low fat content.
  • Careful pathological investigation with the assessment of the Weiss score is important for the diagnosis of malignancy.
  • Tumors localized to the adrenal gland (McFarlane stages 1 and 2) have a better outcome than invasive and metastatic tumors (stages 3 and 4).
  • Tumor removal by a specialized team is crucial for treatment and should always aim at complete removal.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / therapy
  • [MeSH-minor] Genes, Tumor Suppressor. Humans. Oncogenes / genetics


20. Libè R, Groussin L, Tissier F, Elie C, René-Corail F, Fratticci A, Jullian E, Beck-Peccoz P, Bertagna X, Gicquel C, Bertherat J: Somatic TP53 mutations are relatively rare among adrenocortical cancers with the frequent 17p13 loss of heterozygosity. Clin Cancer Res; 2007 Feb 1;13(3):844-50
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  • [Title] Somatic TP53 mutations are relatively rare among adrenocortical cancers with the frequent 17p13 loss of heterozygosity.
  • PURPOSE: Allelic losses [loss of heterozygosity (LOH)] at the 17p13 locus are frequent (85%) in adrenocortical cancers.
  • The tumor suppressor gene TP53 is located at 17p13.
  • The aim of the study was to determine the frequency of TP53 somatic inactivating mutations in adrenocortical tumors with 17p13 LOH and their clinico-biological correlations.
  • EXPERIMENTAL DESIGN: TP53 somatic mutations, intragenic LOH (VNTR1 marker), and p53 overexpression were studied in 36 adrenocortical tumors with 17p13 LOH determined by Southern blot.
  • TP53-mutant tumors were significantly larger than wild-type TP53 tumors (median tumor weight: 640 versus 185 g; P=0.02), were associated with a more advanced stage of tumor progression (MacFarlane stage IV; P=0.01), and had a shorter disease-free survival (P=0.03).
  • CONCLUSIONS: The finding that only a minority of adrenocortical tumors with 17p13 LOH had either a VNTR1 LOH or a TP53 mutation indicates that TP53 might not be the only or major tumor suppressor gene at 17p13 involved in adrenocortical cancer progression.
  • We suggest that a genetic instability of the 17p13 region, occurring early in adrenocortical cancer development, involves various genes located in this region.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Chromosomes, Human, Pair 17. Genes, p53. Loss of Heterozygosity. Minisatellite Repeats / genetics. Mutation
  • [MeSH-minor] Adult. Alleles. Disease Progression. Female. Humans. Immunohistochemistry. Male. Middle Aged. RNA, Neoplasm / chemistry

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  • (PMID = 17289876.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Neoplasm
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21. Johnsen IK, Kappler R, Auernhammer CJ, Beuschlein F: Bone morphogenetic proteins 2 and 5 are down-regulated in adrenocortical carcinoma and modulate adrenal cell proliferation and steroidogenesis. Cancer Res; 2009 Jul 15;69(14):5784-92
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  • [Title] Bone morphogenetic proteins 2 and 5 are down-regulated in adrenocortical carcinoma and modulate adrenal cell proliferation and steroidogenesis.
  • Quantitative PCR analysis revealed down-regulation of BMP2 and BMP5 in tissue samples from adrenocortical carcinoma and adrenocortical tumor cell lines compared with normal adrenal glands.
  • Taken together, we show that loss of expression of members of the BMP family of ligands is a common finding in adrenocortical tumors and we provide evidence that BMP-dependent pathways are likely to be involved in the modulation of the malignant and functional phenotype of adrenocortical cancer cells.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Bone Morphogenetic Protein 2 / genetics. Bone Morphogenetic Protein 5 / genetics
  • [MeSH-minor] Aldosterone / metabolism. Blotting, Western. Bone Morphogenetic Protein Receptors / genetics. Bone Morphogenetic Protein Receptors / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Colforsin / pharmacology. Dose-Response Relationship, Drug. Down-Regulation / drug effects. GATA6 Transcription Factor / genetics. GATA6 Transcription Factor / metabolism. Humans. Hydrocortisone / metabolism. Insulin-Like Growth Factor I / genetics. Insulin-Like Growth Factor I / pharmacology. Phosphorylation / drug effects. Proto-Oncogene Proteins c-akt / metabolism. Recombinant Proteins / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Steroid 17-alpha-Hydroxylase / genetics. Steroid 17-alpha-Hydroxylase / metabolism. Time Factors. Tretinoin / pharmacology. Tumor Cells, Cultured

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  • (PMID = 19584291.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bone Morphogenetic Protein 2; 0 / Bone Morphogenetic Protein 5; 0 / GATA6 Transcription Factor; 0 / GATA6 protein, human; 0 / Recombinant Proteins; 1F7A44V6OU / Colforsin; 4964P6T9RB / Aldosterone; 5688UTC01R / Tretinoin; 67763-96-6 / Insulin-Like Growth Factor I; EC 1.14.99.9 / Steroid 17-alpha-Hydroxylase; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.30 / Bone Morphogenetic Protein Receptors; WI4X0X7BPJ / Hydrocortisone
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22. Betz MJ, Shapiro I, Fassnacht M, Hahner S, Reincke M, Beuschlein F, German and Austrian Adrenal Network: Peroxisome proliferator-activated receptor-gamma agonists suppress adrenocortical tumor cell proliferation and induce differentiation. J Clin Endocrinol Metab; 2005 Jul;90(7):3886-96
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  • [Title] Peroxisome proliferator-activated receptor-gamma agonists suppress adrenocortical tumor cell proliferation and induce differentiation.
  • Adrenocortical carcinoma (ACC) is a rare tumor entity with poor prognosis due to its highly malignant phenotype and lack of effective treatment options.
  • OBJECTIVE: The purpose of this study was to investigate effects of TZDs on adrenocortical cancer cells.
  • RESULTS: PPARgamma mRNA expression was detectable in all adrenocortical tumors including ACCs at similar levels.
  • Furthermore, incubation of the adrenocortical tumor cell line NCI h295 with the PPARgamma agonist rosiglitazone led to a decrease in cell viability, a decrease of cellular proliferation, and an increase in apoptosis as well as steroidogenesis.
  • On the molecular level, NCI h295 cells expressed higher levels of ACTH receptor (melanocortin receptor-2) mRNA upon treatment, whereas cyclin E mRNA was reduced, thus reflecting a shift toward an expression pattern found in less aggressive adrenocortical tumors in vivo.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. PPAR gamma / agonists. Thiazolidinediones / pharmacology
  • [MeSH-minor] Adult. Aged. Anilides / pharmacology. Apoptosis / drug effects. Cell Differentiation. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin E / genetics. Dose-Response Relationship, Drug. Female. Humans. Insulin-Like Growth Factor II / genetics. Male. Middle Aged. Promoter Regions, Genetic. RNA, Messenger / analysis. Receptor, Melanocortin, Type 2 / genetics

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  • (PMID = 15886257.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-chloro-5-nitrobenzanilide; 0 / Anilides; 0 / Cyclin E; 0 / PPAR gamma; 0 / RNA, Messenger; 0 / Receptor, Melanocortin, Type 2; 0 / Thiazolidinediones; 05V02F2KDG / rosiglitazone; 67763-97-7 / Insulin-Like Growth Factor II
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23. Bertherat J, Groussin L, Bertagna X: Mechanisms of disease: adrenocortical tumors--molecular advances and clinical perspectives. Nat Clin Pract Endocrinol Metab; 2006 Nov;2(11):632-41
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  • [Title] Mechanisms of disease: adrenocortical tumors--molecular advances and clinical perspectives.
  • Most adrenocortical tumors are benign, unilateral, adrenocortical adenomas that are often discovered incidentally.
  • Adrenocortical cancer is rare.
  • Exceptionally, adrenocortical tumors can be bilateral.
  • Although most adrenocortical tumors occur sporadically, they may also feature in congenital and/or familial disease.
  • The identification of germline genetic defects in familial diseases associated with adrenocortical tumors helped to define the somatic alterations in sporadic disease: for example, overexpression of insulin-like growth factor 2 and alterations at the 11p15 locus (observed in Beckwith-Wiedemann syndrome) are also found in most adrenocortical cancers.
  • Similarly, inactivating mutations of the TP53 gene, located at 17p13 (observed in Li-Fraumeni syndrome), can also be found at the somatic level in sporadic adrenocortical cancers, as can 17p13 allelic losses.
  • Components of the cyclic AMP signaling pathway--for example, adrenocorticotropic hormone receptors and other membrane receptors, Gs proteins and protein kinase A--can be altered to various degrees in adrenocortical tumors.
  • More recently, gene profiling and genetic studies have shown that the Wnt-beta-catenin signaling pathway is frequently activated in adrenocortical tumors.
  • These research findings already have profound implications for clinical management of patients with adrenocortical tumors, for example in unraveling the genetic origin of the disease in some patients, and in the development of molecular markers for diagnosis and prognosis.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics

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  • (PMID = 17082810.001).
  • [ISSN] 1745-8366
  • [Journal-full-title] Nature clinical practice. Endocrinology & metabolism
  • [ISO-abbreviation] Nat Clin Pract Endocrinol Metab
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 54
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24. Ziegler CG, Brown JW, Schally AV, Erler A, Gebauer L, Treszl A, Young L, Fishman LM, Engel JB, Willenberg HS, Petersenn S, Eisenhofer G, Ehrhart-Bornstein M, Bornstein SR: Expression of neuropeptide hormone receptors in human adrenal tumors and cell lines: antiproliferative effects of peptide analogues. Proc Natl Acad Sci U S A; 2009 Sep 15;106(37):15879-84
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  • [Title] Expression of neuropeptide hormone receptors in human adrenal tumors and cell lines: antiproliferative effects of peptide analogues.
  • Peptide analogues targeting various neuropeptide receptors have been used effectively in cancer therapy.
  • A hallmark of adrenocortical tumor formation is the aberrant expression of peptide receptors relating to uncontrolled cell proliferation and hormone overproduction.
  • Our microarray results have also demonstrated a differential expression of neuropeptide hormone receptors in tumor subtypes of human pheochromocytoma.
  • In light of these findings, we performed a comprehensive analysis of relevant receptors in both human adrenomedullary and adrenocortical tumors and tested the antiproliferative effects of peptide analogues targeting these receptors.
  • Specifically, we examined the receptor expression of somatostatin-type-2 receptor, growth hormone-releasing hormone (GHRH) receptor or GHRH receptor splice variant-1 (SV-1) and luteinizing hormone-releasing hormone (LHRH) receptor at the mRNA and protein levels in normal human adrenal tissues, adrenocortical and adrenomedullary tumors, and cell lines.
  • Cytotoxic derivatives of somatostatin AN-238 and, to a lesser extent, AN-162, reduced cell numbers of uninduced and NGF-induced adrenomedullary pheochromocytoma cells and adrenocortical cancer cells.
  • Both the splice variant of GHRH receptor SV-1 and the LHRH receptor were also expressed in adrenocortical cancer cell lines but not in the pheochromocytoma cell line.
  • The GHRH receptor antagonist MZ-4-71 and LHRH antagonist Cetrorelix both significantly reduced cell growth in the adrenocortical cancer cell line.
  • In conclusion, the expression of receptors for somatostatin, GHRH, and LHRH in the normal human adrenal and in adrenal tumors, combined with the growth-inhibitory effects of the antitumor peptide analogues, may make possible improved treatment approaches to adrenal tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / drug therapy. Adrenal Gland Neoplasms / metabolism. Neuropeptides / pharmacology. Receptors, Neuropeptide / metabolism
  • [MeSH-minor] 2-Hydroxyphenethylamine / analogs & derivatives. 2-Hydroxyphenethylamine / pharmacology. Adrenal Glands / metabolism. Aniline Compounds / pharmacology. Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Cytostatic Agents / pharmacology. Doxorubicin / analogs & derivatives. Doxorubicin / pharmacology. Gene Expression. Humans. Oligonucleotide Array Sequence Analysis. PC12 Cells. Pyrroles / pharmacology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Receptors, LHRH / genetics. Receptors, LHRH / metabolism. Receptors, Somatostatin / genetics. Receptors, Somatostatin / metabolism. Somatostatin / analogs & derivatives. Somatostatin / pharmacology

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  • (PMID = 19717419.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AN 238; 0 / Aniline Compounds; 0 / Cytostatic Agents; 0 / Neuropeptides; 0 / Pyrroles; 0 / RNA, Messenger; 0 / Receptors, LHRH; 0 / Receptors, Neuropeptide; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 2PK59M9GFF / vapreotide; 33189-65-0 / N-(2-diethylaminoethyl)-N-(2-hydroxy-2-phenylethyl)-2,5-dichloroaniline; 51110-01-1 / Somatostatin; 7568-93-6 / 2-Hydroxyphenethylamine; 80168379AG / Doxorubicin
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25. Lacroix A: Approach to the patient with adrenocortical carcinoma. J Clin Endocrinol Metab; 2010 Nov;95(11):4812-22
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  • [Title] Approach to the patient with adrenocortical carcinoma.
  • Adrenocortical cancer (ACC) is a rare and often aggressive malignancy that requires multidisciplinary expertise for optimal management.
  • Thorough imaging and endocrine evaluations can identify the majority of ACCs amongst adrenal tumors; however, some smaller ACCs are better identified using fluorodeoxyglucose-positron emission tomography/computed tomography scan.
  • Complete resection by an expert surgeon is the only potentially curative treatment for ACC, and tumor spillage should be avoided.
  • Histopathology is important for diagnosis, but immunohistochemistry markers and gene profiling of the resected tumor may become superior to current staging systems to stratify prognosis.
  • Careful replacement of glucocorticoid and mineralocorticoid deficiency after surgery or mitotane therapy is important; steroid excess from remaining tumor burden should also be controlled to avoid its morbidities.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenocortical Carcinoma / surgery

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  • (PMID = 21051577.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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26. Bimpaki EI, Iliopoulos D, Moraitis A, Stratakis CA: MicroRNA signature in massive macronodular adrenocortical disease and implications for adrenocortical tumourigenesis. Clin Endocrinol (Oxf); 2010 Jun;72(6):744-51
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  • [Title] MicroRNA signature in massive macronodular adrenocortical disease and implications for adrenocortical tumourigenesis.
  • PURPOSE: Massive macronodular adrenocortical disease (MMAD) may be caused by aberrant microRNA expression.
  • To determine the microRNA profile in MMAD and identify putative microRNA-gene target pairs involved in adrenal tumourigenesis.
  • EXPERIMENTAL DESIGN: We performed microRNA microarray analysis in 10 patients with ACTH-independent Cushing syndrome caused by MMAD (ages 39-60 years) and four normal adrenal cortex samples were used as controls.
  • Interestingly, we detected miR-200b targeting directly Matrin 3 (MATR3) expression in an adrenocortical cancer cell line (H295R).

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  • (PMID = 19849700.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / Z01 HD000642; United States / Intramural NIH HHS / / Z01 HD000642-11; United States / NICHD NIH HHS / HD / Z01-HD-000642-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Validation Studies
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MicroRNAs
  • [Other-IDs] NLM/ NIHMS154316; NLM/ PMC3003432
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27. Mitra S, Roy SG, Sur PK: Adrenocortical carcinoma with skeletal metastases in a postmenopausal woman. Indian J Med Paediatr Oncol; 2009 Jan;30(1):24-7
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  • [Title] Adrenocortical carcinoma with skeletal metastases in a postmenopausal woman.
  • Adrenocortical cancer is a very rare tumor with a poor prognosis.
  • CT-guided fine-needle aspiration cytology of an abdominal mass revealed the presence of a carcinoma of the left adrenal cortex.

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  • (PMID = 20668603.001).
  • [ISSN] 0975-2129
  • [Journal-full-title] Indian journal of medical and paediatric oncology : official journal of Indian Society of Medical & Paediatric Oncology
  • [ISO-abbreviation] Indian J Med Paediatr Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC2902211
  • [Keywords] NOTNLM ; Adrenocortical carcinoma / androgen secreting tumors / mitotane
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28. Mahe E, El-Shinnawy I: A "tumour trifecta:" myelolipomata arising within an adrenocortical adenoma ipsilateral to a synchronous clear cell renal cell carcinoma. Malays J Pathol; 2010 Dec;32(2):123-8
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  • [Title] A "tumour trifecta:" myelolipomata arising within an adrenocortical adenoma ipsilateral to a synchronous clear cell renal cell carcinoma.
  • We present an intriguing case of adrenal myelolipomata occurring within an adrenocortical adenoma in concert with an ipsilateral clear cell renal cell carcinoma.
  • Computed tomography indicated a 2.5 cm right renal mass as well as a 5 cm right adrenal mass.
  • Histology of the renal mass was consistent with conventional clear cell renal cell carcinoma, Fuhrman grade III.
  • The adrenal mass was a cortical adenoma with solid and nested patterns, with discrete zones consisting of erythroid, myeloid and megakaryocytic cells intermixed with mature adipocytes.
  • The solid tumour component was strongly positive for vimentin, inhibin and CD56, focally positive for low-molecular-weight cytokeratin (Cam 5.2), calretinin and CD10 (chiefly in the myelolipomatous zones), and negative for chromogranin, S100, HMB-45, melan-A (A103), Mart-1, synaptophysin, SMA, CK7, CK20, ER, PR, TTF-1, CD99 and GCDFP (BRST-2).
  • Ki67 (MIB1) staining indicated a low tumour proliferation index.
  • We also present a relevant review of the literature pertaining to adrenal lesions.
  • In particular, we emphasize the epidemiological, histological and immunohistochemical features that are helpful in determining the origin and malignant potential of adrenal lesions.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / pathology. Carcinoma, Renal Cell / pathology. Kidney Neoplasms / pathology. Myelolipoma / pathology. Neoplasms, Multiple Primary / pathology
  • [MeSH-minor] Biomarkers, Tumor / analysis. Female. Humans. Immunohistochemistry. Middle Aged


29. Libé R, Bertherat J: Molecular genetics of adrenocortical tumours, from familial to sporadic diseases. Eur J Endocrinol; 2005 Oct;153(4):477-87
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  • [Title] Molecular genetics of adrenocortical tumours, from familial to sporadic diseases.
  • Adrenal masses can be detected in up to 4% of the population, and are mostly of adrenocortical origin.
  • Adrenocortical tumours (ACTs) may be responsible for excess steroid production and, in the case of adrenocortical cancers, for morbidity or mortality due to tumour growth.
  • The familial diseases concerned are Li-Fraumeni syndrome, which may be due to germline mutation of the tumour-suppressor gene TP53 and Beckwith-Wiedemann syndrome, which is caused by dys-regulation of the imprinted IGF-II locus at 11p15.
  • ACTs also occur in type 1 multiple endocrine neoplasia (MEN 1), which is characterized by a germline mutation of the menin gene.
  • Cushing's syndrome due to primary pigmented nodular adrenocortical disease (PPNAD) has been observed in Carney complex patients presenting inactivating germline PRKAR1A mutations.
  • Interestingly, allelic losses at 17p13 and 11p15 have been demonstrated in sporadic adrenocortical cancer and somatic PRKAR1A mutations have been found in secreting adrenocortical adenomas.
  • The genetics of another group of adrenal diseases that can lead to adrenal nodular hyperplasia -- congenital adrenal hyperplasia (CAH) and glucocorticoid-remediable aldosteronism (GRA) -- have also been studied extensively.
  • This review summarizes recent advances in the genetics of ACTs, highlighting both improvements in our understanding of the pathophysiology and the diagnosis of these tumours.

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  • (PMID = 16189167.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 97
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30. Daffara F, De Francia S, Reimondo G, Zaggia B, Aroasio E, Porpiglia F, Volante M, Termine A, Di Carlo F, Dogliotti L, Angeli A, Berruti A, Terzolo M: Prospective evaluation of mitotane toxicity in adrenocortical cancer patients treated adjuvantly. Endocr Relat Cancer; 2008 Dec;15(4):1043-53
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  • [Title] Prospective evaluation of mitotane toxicity in adrenocortical cancer patients treated adjuvantly.
  • Seventeen consecutive patients who were treated with mitotane after radical resection of adrenocortical cancer (ACC) from 1999 to 2005 underwent physical examination, routine laboratory evaluation, monitoring of mitotane concentrations, and a hormonal work-up at baseline and every 3 months till ACC relapse or study end (December 2007).
  • Mitotane affected adrenal steroidogenesis with a more remarkable inhibition of cortisol and DHEAS than aldosterone.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Mitotane / therapeutic use
  • [MeSH-minor] Adult. Chemotherapy, Adjuvant. Chromatography, High Pressure Liquid. Female. Humans. Hydrocortisone / metabolism. Hypothyroidism / etiology. Male. Middle Aged. Neoplasm Staging. Prospective Studies. Survival Rate. Testosterone / metabolism. Young Adult

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  • (PMID = 18824557.001).
  • [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 / Antineoplastic Agents, Hormonal; 3XMK78S47O / Testosterone; 78E4J5IB5J / Mitotane; WI4X0X7BPJ / Hydrocortisone
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31. Lee JA, Duh QY: Reoperation for adrenocortical neoplasms. Curr Treat Options Oncol; 2006 Jul;7(4):320-5
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  • [Title] Reoperation for adrenocortical neoplasms.
  • Adrenocortical cancer is a highly lethal malignancy.
  • Patients with widely metastatic disease or those with tumors not amenable to re-resection may benefit from tumor debulking to help control symptoms associated with oversecretion syndromes.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery

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  • (PMID = 16916492.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 35
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32. Cerquetti L, Sampaoli C, Amendola D, Bucci B, Misiti S, Raza G, De Paula U, Marchese R, Brunetti E, Toscano V, Stigliano A: Mitotane sensitizes adrenocortical cancer cells to ionizing radiations by involvement of the cyclin B1/CDK complex in G2 arrest and mismatch repair enzymes modulation. Int J Oncol; 2010 Aug;37(2):493-501
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  • [Title] Mitotane sensitizes adrenocortical cancer cells to ionizing radiations by involvement of the cyclin B1/CDK complex in G2 arrest and mismatch repair enzymes modulation.
  • It also has a cytotoxic effect on the adrenocortical cells and represents a primary drug used in the adrenocortical carcinoma (ACC).
  • H295R and SW13 cell lines were treated with mitotane 10(-5) M and ionizing radiations (IR) in combination therapy, inducing an irreversible inhibition of cell growth in both adrenocortical cancer cells.
  • [MeSH-major] Adrenal Cortex Neoplasms / radiotherapy. Adrenocortical Carcinoma / radiotherapy. Cyclin B / metabolism. Cyclin-Dependent Kinases / metabolism. DNA Repair Enzymes / metabolism. Mitotane / pharmacology
  • [MeSH-minor] Cell Proliferation / drug effects. Cell Proliferation / radiation effects. DNA Mismatch Repair / drug effects. DNA Mismatch Repair / physiology. Drug Evaluation, Preclinical. G2 Phase / drug effects. G2 Phase / physiology. Humans. Multiprotein Complexes / metabolism. Protein Kinase Inhibitors / pharmacology. Purines / pharmacology. Radiation, Ionizing. Radiation-Sensitizing Agents / pharmacology. Tumor Cells, Cultured

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  • (PMID = 20596677.001).
  • [ISSN] 1791-2423
  • [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 / 6-((3-chloro)anilino)-2-(isopropyl-2-hydroxyethylamino)-9-isopropylpurine; 0 / Cyclin B; 0 / Multiprotein Complexes; 0 / Protein Kinase Inhibitors; 0 / Purines; 0 / Radiation-Sensitizing Agents; 78E4J5IB5J / Mitotane; EC 2.7.11.22 / Cyclin-Dependent Kinases; EC 6.5.1.- / DNA Repair Enzymes
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33. Bouasker I, Zoghlami A, Farah Klibi F, Smaali I, El Ouaer MA, Zermani R, Dziri C: Adreno-cortical oncocytoma: a case report. Tunis Med; 2010 May;88(5):353-6
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  • [Title] Adreno-cortical oncocytoma: a case report.
  • BACKGROUND: Adrenal oncocytoma is a very rare lesion, non functioning and benignin most cases.
  • AIM: This study aimed to report a new case of adrenal oncocytic tumor with uncertain malignant potential.
  • Ultrasonography and omputed tomography scan revealed a large mass in the right adrenal gland with extension to the right kidney.
  • The diagnosis of adrenal oncocytoma with malignant potential was confirmed by pathology.
  • He was followed up for 8 months, no tumor recurrence detected.
  • CONCLUSION: Adreno cortical oncocytoma is a rare tumor.
  • [MeSH-major] Adenoma, Oxyphilic / pathology. Adrenal Gland Neoplasms / pathology. Kidney Cortex / pathology. Kidney Neoplasms / pathology

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  • (PMID = 20517834.001).
  • [ISSN] 0041-4131
  • [Journal-full-title] La Tunisie médicale
  • [ISO-abbreviation] Tunis Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Tunisia
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34. Gaujoux S, Pinson S, Gimenez-Roqueplo AP, Amar L, Ragazzon B, Launay P, Meatchi T, Libé R, Bertagna X, Audebourg A, Zucman-Rossi J, Tissier F, Bertherat J: Inactivation of the APC gene is constant in adrenocortical tumors from patients with familial adenomatous polyposis but not frequent in sporadic adrenocortical cancers. Clin Cancer Res; 2010 Nov 1;16(21):5133-41
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  • [Title] Inactivation of the APC gene is constant in adrenocortical tumors from patients with familial adenomatous polyposis but not frequent in sporadic adrenocortical cancers.
  • PURPOSE: In adrenocortical tumors (ACT), Wnt/β-catenin pathway activation can be explained by β-catenin somatic mutations only in a subset of tumors.
  • EXPERIMENTAL DESIGN: ACTs from patients with FAP and sporadic adrenocortical carcinomas (ACC) with abnormal β-catenin localization on immunohistochemistry but no somatic β-catenin mutations were studied.
  • RESULTS: Four ACTs were observed in three patients with FAP and were ACC, adrenocortical adenoma, and bilateral macronodular adrenocortical hyperplasia, all with abnormal β-catenin localization.
  • CONCLUSIONS: ACT should be considered a FAP tumor.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Gene Silencing. Genes, APC
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Adenomatous Polyposis Coli Protein / genetics. Adenomatous Polyposis Coli Protein / metabolism. Adult. Aged. DNA Mutational Analysis. Family. Female. Gene Frequency. Humans. Male. Middle Aged. Tumor Suppressor Proteins / genetics. Tumor Suppressor Proteins / metabolism. beta Catenin / genetics. beta Catenin / metabolism

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  • [Copyright] ©2010 AACR.
  • (PMID = 20978149.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AMER1 protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / Adenomatous Polyposis Coli Protein; 0 / Tumor Suppressor Proteins; 0 / beta Catenin
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35. Duenschede F, Bittinger F, Heintz A, Musholt T, Korenkov M, Kann P, Ewald P, Gockel I, Junginger T: Malignant and unclear histological findings in incidentalomas. Eur Surg Res; 2008;40(2):235-8
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  • [Title] Malignant and unclear histological findings in incidentalomas.
  • BACKGROUND: The management of incidentalomas with tumor size 3 cm and larger is still under controversial discussion.
  • Indications for surgery were tumor size equal and larger than 3 cm, recurrent pain, hormone status and patients' fear of malignancy.
  • There were 9 cases of adrenal hyperplasia, and two cysts and two hematomas were found in 4 patients.
  • In 3 patients, a primary adrenocortical carcinoma of 3.4, 4.0, and 5.0 cm in diameter, respectively, was identified.
  • In 1 patient, an adrenal cortical carcinoma of 10.0 cm in diameter was operated.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis. Adrenal Gland Neoplasms / surgery. Adrenalectomy. Incidental Findings
  • [MeSH-minor] Diagnostic Techniques, Endocrine. Female. Hormones / metabolism. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Staging. Tomography, X-Ray Computed. Ultrasonography

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  • [Copyright] Copyright 2008 S. Karger AG, Basel.
  • (PMID = 18032908.001).
  • [ISSN] 1421-9921
  • [Journal-full-title] European surgical research. Europäische chirurgische Forschung. Recherches chirurgicales européennes
  • [ISO-abbreviation] Eur Surg Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Hormones
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36. Montanaro D, Maggiolini M, Recchia AG, Sirianni R, Aquila S, Barzon L, Fallo F, Andò S, Pezzi V: Antiestrogens upregulate estrogen receptor beta expression and inhibit adrenocortical H295R cell proliferation. J Mol Endocrinol; 2005 Oct;35(2):245-56
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  • [Title] Antiestrogens upregulate estrogen receptor beta expression and inhibit adrenocortical H295R cell proliferation.
  • The molecular mechanisms involved in adrenocortical tumorigenesis are still not completely understood.
  • In this study, using the H295R cell line as a model system, we investigated the role of estrogens and estrogen receptor (ER) alpha and ER beta in the growth regulation of adrenocortical tumors.
  • Moreover, this study points towards a role for ER beta as an important mediator of the repressive effects exerted by antiestrogens on H295R cells; however, further studies are needed to clarify its role in the control of adrenocortical cell proliferation and on the potential benefits of antiestrogens for treatment of adrenocortical cancer.
  • [MeSH-major] Adrenal Cortex / cytology. Cell Proliferation. Estrogen Receptor Modulators / metabolism. Estrogen Receptor beta / metabolism
  • [MeSH-minor] Adrenal Cortex Neoplasms / metabolism. Adrenal Cortex Neoplasms / pathology. Androgens / metabolism. Antigens, CD95 / metabolism. Apoptosis. Aromatase / metabolism. Aromatase Inhibitors / metabolism. Autocrine Communication. Caspases / metabolism. Cell Line, Tumor. Colforsin / metabolism. Estradiol / metabolism. Estrogen Receptor alpha / genetics. Estrogen Receptor alpha / metabolism. Fas Ligand Protein. Humans. Membrane Glycoproteins / genetics. Membrane Glycoproteins / metabolism. Nitriles / metabolism. Promoter Regions, Genetic. RNA, Messenger / metabolism. Triazoles / metabolism. Tumor Necrosis Factors / genetics. Tumor Necrosis Factors / metabolism

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  • (PMID = 16216906.001).
  • [ISSN] 0952-5041
  • [Journal-full-title] Journal of molecular endocrinology
  • [ISO-abbreviation] J. Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / Antigens, CD95; 0 / Aromatase Inhibitors; 0 / Estrogen Receptor Modulators; 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Membrane Glycoproteins; 0 / Nitriles; 0 / RNA, Messenger; 0 / Triazoles; 0 / Tumor Necrosis Factors; 1F7A44V6OU / Colforsin; 4TI98Z838E / Estradiol; 7LKK855W8I / letrozole; EC 1.14.14.1 / Aromatase; EC 3.4.22.- / Caspases
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37. Hong DS, Sebti SM, Newman RA, Blaskovich MA, Ye L, Gagel RF, Moulder S, Wheler JJ, Naing A, Tannir NM, Ng CS, Sherman SI, El Naggar AK, Khan R, Trent J, Wright JJ, Kurzrock R: Phase I trial of a combination of the multikinase inhibitor sorafenib and the farnesyltransferase inhibitor tipifarnib in advanced malignancies. Clin Cancer Res; 2009 Nov 15;15(22):7061-8
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  • Interestingly, six of eight patients with medullary thyroid cancer had durable stable disease (n = 3) or partial remissions (n = 3), lasting 12 to 26+ months.
  • Prolonged (> or =6 months) stable disease was also seen in nine patients as follows: papillary thyroid cancer (n = 4; 18+ to 27+ months), adrenocortical cancer (n = 2; 7 and 11 months), and one each of melanoma (platelet-derived growth factor receptor mutation positive; 14 months), renal (6 months), and pancreatic cancer (6 months).
  • Activity was seen, especially in patients with medullary thyroid cancer, a tumor characterized by RET mutations.

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  • (PMID = 19903778.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA062461-10; United States / NCI NIH HHS / CA / U01 CA062461; United States / NCI NIH HHS / CA / 5 U01 CA062461; United States / NCI NIH HHS / CA / U01 CA062461-10
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzenesulfonates; 0 / Phenylurea Compounds; 0 / Pyridines; 0 / Quinolones; 192185-72-1 / tipifarnib; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 2.5.1.29 / Farnesyltranstransferase; EC 2.7.10.1 / Proto-Oncogene Proteins c-ret; EC 2.7.10.1 / RET protein, human
  • [Other-IDs] NLM/ NIHMS140339; NLM/ PMC2784003
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38. Paramonova I, Haase M, Mülders-Opgenoorth B, Ansurudeen-Rafi I, Bornstein SR, Papewalis C, Schinner S, Schott M, Scherbaum WA, Willenberg HS: The effects of the endothelium on adrenal steroidogenesis and growth are mainly mediated by proteins other than endothelin-1. Horm Metab Res; 2010 Nov;42(12):840-5
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  • [Title] The effects of the endothelium on adrenal steroidogenesis and growth are mainly mediated by proteins other than endothelin-1.
  • The endothelium releases factors stimulating the adrenal cortex.
  • It is also known that endothelin-1 (ET-1) promotes generation of cortisol and aldosterone, and proliferation of adrenocortical cells.
  • The aim of the study was to find out whether the effect of the endothelium on adrenocortical cells is dominated by the action of ET-1.
  • The effects of endothelial cell-conditioned medium (ECCM), obtained during growth of human umbilical cord vein endothelial cells, on aldosterone and cortisol release by cells of the adrenocortical cancer cell-line NCI-H295R and the promoter activity of steroidogenic acute-regulatory protein (StAR) were studied.
  • The effect of ECCM on proliferation of human primary normal adrenocortical and NCI-H295R cells was also investigated.
  • In conclusion, the cultured endothelial cells secrete a protein that stimulates steroidogenesis in adrenal cells and their growth.
  • [MeSH-major] Adrenal Cortex / cytology. Aldosterone / metabolism. Cell Proliferation. Endothelial Cells / metabolism. Endothelin-1 / metabolism. Hydrocortisone / metabolism. Proteins / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cells, Cultured. Culture Media, Conditioned / metabolism. Humans. Phosphoproteins / genetics. Phosphoproteins / metabolism. Promoter Regions, Genetic

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  • [Copyright] © Georg Thieme Verlag KG Stuttgart · New York.
  • (PMID = 20839150.001).
  • [ISSN] 1439-4286
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Endothelin-1; 0 / Phosphoproteins; 0 / Proteins; 0 / steroidogenic acute regulatory protein; 4964P6T9RB / Aldosterone; WI4X0X7BPJ / Hydrocortisone
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39. Woo HS, Lee KH, Park SY, Han HS, Yoon CJ, Kim YH: Adrenal cortical adenoma in adrenohepatic fusion tissue: a mimic of malignant hepatic tumor at CT. AJR Am J Roentgenol; 2007 Mar;188(3):W246-8
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  • [Title] Adrenal cortical adenoma in adrenohepatic fusion tissue: a mimic of malignant hepatic tumor at CT.
  • [MeSH-major] Adenoma / radiography. Adrenal Cortex Neoplasms / radiography. Adrenal Glands / abnormalities. Adrenal Glands / radiography. Liver / abnormalities. Liver / radiography. Liver Neoplasms / radiography
  • [MeSH-minor] Aged. Diagnosis, Differential. Female. Humans. Tomography, X-Ray Computed

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  • (PMID = 17312030.001).
  • [ISSN] 1546-3141
  • [Journal-full-title] AJR. American journal of roentgenology
  • [ISO-abbreviation] AJR Am J Roentgenol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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40. Kanczkowski W, Morawietz H, Ziegler CG, Funk RH, Schmitz G, Zacharowski K, Mohn CE, Ehrhart-Bornstein M, Bornstein SR: Pam3CSK4 and LTA-TLRs ligands associated with microdomains induce IL8 production in human adrenocortical cancer cells. Horm Metab Res; 2007 Jun;39(6):457-60
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  • [Title] Pam3CSK4 and LTA-TLRs ligands associated with microdomains induce IL8 production in human adrenocortical cancer cells.
  • Bacterially derived ligands, Pam3CSK4 and LPS, can directly impact adrenal glands steroidogenesis through microdomain-related TLR1/2 and 4, respectively, and indirectly via immune cell-derived cytokines.
  • CXC chemokine-dependent immune cell infiltration into adrenocortical carcinomas (ACC), which correlates with poor prognosis, is a common phenomenon.
  • Recently, IL8 was identified in ACC and NCI-H295R cells, and was found to contribute to ACC tumour growth.
  • This is the first study to demonstrate the expression of several TLRs including TLR1, 3, 6, 7 and 9 in human adrenocortical cells by using the RT-PCR approach.
  • Our data suggest that gram-positive bacteria-related TLR1/2/6 ligands might contribute to adrenal gland tumorigenesis via IL8 production.
  • [MeSH-major] Adrenal Cortex Neoplasms / immunology. Interleukin-8 / biosynthesis. Lipopolysaccharides / pharmacology. Peptides / pharmacology. Teichoic Acids / pharmacology. Toll-Like Receptors / physiology

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  • (PMID = 17578764.001).
  • [ISSN] 0018-5043
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Interleukin-8; 0 / Ligands; 0 / Lipopeptides; 0 / Lipopolysaccharides; 0 / Pam(3)CSK(4) peptide; 0 / Peptides; 0 / Teichoic Acids; 0 / Toll-Like Receptors; 56411-57-5 / lipoteichoic acid
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41. Szabó PM, Wiener Z, Tömböl Z, Kovács A, Pócza P, Horányi J, Kulka J, Riesz P, Tóth M, Patócs A, Gaillard RC, Falus A, Rácz K, Igaz P: Differences in the expression of histamine-related genes and proteins in normal human adrenal cortex and adrenocortical tumors. Virchows Arch; 2009 Aug;455(2):133-42
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  • [Title] Differences in the expression of histamine-related genes and proteins in normal human adrenal cortex and adrenocortical tumors.
  • Histamine is involved in the pathogenesis of several tumors; however, there are no data on its possible involvement in human adrenocortical tumorigenesis.
  • The expression of genes and proteins involved in the biosynthesis (histidine decarboxylase, HDC), action (histamine receptors: HRH1-HRH4), and metabolism of histamine is largely unknown both in the normal human adrenal cortex and in adrenocortical tumors.
  • In this study, we examined the expression of histamine-related genes and proteins and histamine content in normal adrenal cortex, benign adrenocortical adenomas, and malignant adrenocortical cancer (ACC).
  • We found that all proteins involved in histamine biosynthesis and action are present both in the normal adrenal cortex and in the tumors studied.
  • Adrenocortical tumorigenesis might, thus, be characterized by reduced histamine biosynthesis; furthermore, different adrenocortical tumor subtypes may show unique histamine receptor expression profiles.
  • [MeSH-major] Adrenal Cortex / metabolism. Adrenal Cortex Neoplasms / metabolism. Adrenocortical Adenoma / metabolism. Histamine / metabolism. Histidine Decarboxylase / metabolism. Receptors, Histamine / metabolism

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  • (PMID = 19568768.001).
  • [ISSN] 1432-2307
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / HRH4 protein, human; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Histamine; 0 / Receptors, Histamine H1; 0 / Receptors, Histamine H2; 0 / Receptors, Histamine H3; 820484N8I3 / Histamine; EC 4.1.1.22 / Histidine Decarboxylase
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42. Stratakis CA: Cushing syndrome caused by adrenocortical tumors and hyperplasias (corticotropin- independent Cushing syndrome). Endocr Dev; 2008;13:117-32
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  • [Title] Cushing syndrome caused by adrenocortical tumors and hyperplasias (corticotropin- independent Cushing syndrome).
  • Endogenous Cushing syndrome (CS) is caused by excess adrenal glucocorticoid secretion that is adrenocorticotropin (ACTH)-dependent or independent; ACTH-independent adrenocortical causes of CS account for up to 20% of CS in adults, and 15% in children over age 7 years.
  • In both adults and children, adrenocortical lesions causing CS include the common, isolated and sporadic, solitary cortisol-producing adenoma, the rare adrenocortical cancer, and a spectrum of recently recognized, bilateral hyperplasias (bilateral adrenocortical hyperplasias, BAHs): micronodular adrenal disease and its pigmented variant, primary pigmented nodular adrenocortical disease are mostly genetic processes.
  • Macronodular BAHs, ACTH-independent macronodular hyperplasia or massive macronodular adrenocortical disease are less frequently genetic and almost never present in children (except in McCune-Albright syndrome); they present often with atypical CS in middle-aged or elderly adults.
  • The majority of benign adrenocortical tumors associated with CS are associated with defects of the cAMP signaling pathway, whereas adrenal cancer is linked to aberrant expression of growth factors and germline or somatic mutations of tumor suppressor genes such as TP53.
  • Adrenalectomy is the preferred mode of treatment for all adrenocortical causes of CS.
  • [MeSH-major] Adenoma / complications. Adrenal Cortex Neoplasms / complications. Adrenal Glands / pathology. Adrenocorticotropic Hormone / physiology. Cushing Syndrome / etiology
  • [MeSH-minor] Algorithms. Cyclic AMP / physiology. Humans. Hyperplasia / complications. Hyperplasia / diagnosis. Hyperplasia / genetics. Signal Transduction / physiology

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  • (PMID = 18493137.001).
  • [ISSN] 1421-7082
  • [Journal-full-title] Endocrine development
  • [ISO-abbreviation] Endocr Dev
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 HD000642-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; E0399OZS9N / Cyclic AMP
  • [Number-of-references] 33
  • [Other-IDs] NLM/ NIHMS307822; NLM/ PMC3132884
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43. Nieman LK, Ilias I: Evaluation and treatment of Cushing's syndrome. Am J Med; 2005 Dec;118(12):1340-6
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  • Cushing's syndrome results from sustained pathologic hypercortisolism caused by excessive corticotropin (ACTH) secretion by tumors in the pituitary gland (Cushing's disease, 70%) or elsewhere (15%), or by ACTH-independent cortisol secretion from adrenal tumors (15%).
  • The diagnosis of Cushing's syndrome should be followed by the measurement of plasma ACTH concentration to determine whether the hypercortisolism is ACTH-independent.
  • Surgical resection of tumor is the optimal treatment for all forms of Cushing's syndrome; bilateral adrenalectomy, medical treatment, or radiotherapy are sought in inoperable or recurrent cases.
  • The prognosis is better for Cushing's disease and benign adrenal causes of Cushing's syndrome than adrenocortical cancer and malignant ACTH-producing tumors.
  • [MeSH-major] Adrenocorticotropic Hormone / blood. Cushing Syndrome / diagnosis. Cushing Syndrome / drug therapy
  • [MeSH-minor] Adrenalectomy. Adult. Antifungal Agents / therapeutic use. Child. Diagnosis, Differential. Humans. Ketoconazole / therapeutic use. Prognosis. Recurrence. Survival Analysis

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  • (PMID = 16378774.001).
  • [ISSN] 1555-7162
  • [Journal-full-title] The American journal of medicine
  • [ISO-abbreviation] Am. J. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 9002-60-2 / Adrenocorticotropic Hormone; R9400W927I / Ketoconazole
  • [Number-of-references] 100
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44. Balasubramaniam S, Fojo T: Practical considerations in the evaluation and management of adrenocortical cancer. Semin Oncol; 2010 Dec;37(6):619-26
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  • [Title] Practical considerations in the evaluation and management of adrenocortical cancer.
  • Adrenocortical cancer (ACC) is a rare, challenging disease with a broad range of clinical presentations.
  • Often presenting in an advanced stage with a large, locally invasive primary tumor or with Cushing's syndrome, it requires a multidisciplinary approach to treatment.
  • Biopsies should be performed only when metastatic disease is present and a primary tumor has not been clearly established.
  • [MeSH-major] Adrenocortical Carcinoma / pathology. Adrenocortical Carcinoma / therapy

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  • [Copyright] Published by Elsevier Inc.
  • (PMID = 21167380.001).
  • [ISSN] 1532-8708
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 5W494URQ81 / Streptozocin; 78E4J5IB5J / Mitotane
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45. Schteingart DE, Doherty GM, Gauger PG, Giordano TJ, Hammer GD, Korobkin M, Worden FP: Management of patients with adrenal cancer: recommendations of an international consensus conference. Endocr Relat Cancer; 2005 Sep;12(3):667-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Management of patients with adrenal cancer: recommendations of an international consensus conference.
  • Adrenocortical carcinomas are rare, highly malignant tumors that account for only 0.2% of deaths due to cancer.
  • Given the limited number of patients seen in most medical centers with this diagnosis, series usually reported are small and clinical trials not randomized or blinded.
  • In an attempt to answer important questions concerning the management of patients with adrenal cancer, a consensus conference was organized and held at the University of Michigan in Ann Arbor, MI, 11-13 September 2003, with the participation of an international group of physicians who had reported on the largest series of patients with this disease and who had recognized basic and clinical research expertise in adrenal cortical cancer.
  • In addition to setting up guidelines in specific areas of the diagnosis and treatment of adrenal cancer, the conference recommended and initiated the planning of an international prospective trial for treatment of patients with adrenal cancer in stages III and IV.
  • In terms of new therapies, first trials of dendritic cell therapy in human subjects with adrenal cancer have been started, but it is too early to comment on efficacy.
  • There are no clinical gene therapy trials for human adrenal cortical cancer.
  • In addition, there is evidence that histone deacetylase inhibitors can further enhance the rate of adenoviral infectivity in human adrenal cancer cells.
  • The use of these and other agents in the treatment of adrenal cancer should be hypothesis-driven and based on a thorough analysis of tumor biology.
  • [MeSH-major] Adrenal Gland Neoplasms / therapy
  • [MeSH-minor] Humans. Neoplasm Staging

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  • (PMID = 16172199.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / M 01-RR000 42
  • [Publication-type] Consensus Development Conference; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] England
  • [Number-of-references] 75
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46. Nychytaĭlo ME, Diachenko VV, Litvinenko AN, Gul'ko ON, Bulik II, Lukecha II: [Experience of performance of laparoscopic adrenalectomy using lateral transabdominal approach]. Klin Khir; 2008 Sep;(9):41-4
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  • In 2002-2008 yrs. in the Department of Laparoscopic Surgery and Cholelithiasis in 52 patients laparoscopic adrenalectomy (LA) was accomplished, performed for different diseases of suprarenal glands.
  • Incidentaloma was diagnosed in 8, fibroma--in 4, pheokhromocytoma--in 10, aldosteroma--in 11, adrenocortical cancer--in 3, corticosteroma--in 13, suprarenal gland cyst--in 3 patients.
  • The operation time in right-sided and left-sided LA had constituted accordingly 85 and 118 minutes.
  • In 1 (2.4%) observation hemoperitoneum had occurred as a result of traumatic damage of spleen during performance of left-sided LA.

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  • (PMID = 19278040.001).
  • [ISSN] 0023-2130
  • [Journal-full-title] Klinichna khirurhiia
  • [ISO-abbreviation] Klin Khir
  • [Language] RUS
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Ukraine
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47. Bauditz J, Quinkler M, Beyersdorff D, Wermke W: Improved detection of hepatic metastases of adrenocortical cancer by contrast-enhanced ultrasound. Oncol Rep; 2008 May;19(5):1135-9
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  • [Title] Improved detection of hepatic metastases of adrenocortical cancer by contrast-enhanced ultrasound.
  • Adrenocortical carcinoma (ACC) is a rare and heterogeneous malignancy whose pathogenesis and poor prognosis is poorly understood.
  • Computerized tomography (CT) and magnetic resonance imaging (MRI) are routinely performed for the imaging of the adrenal mass and for standard staging of the chest and abdomen as the lung and liver are the primary organs for metastasis in ACC.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Contrast Media / pharmacology. Liver Neoplasms / secondary. Liver Neoplasms / ultrasonography. Ultrasonography / methods
  • [MeSH-minor] Adult. Aged. Female. Humans. Magnetic Resonance Imaging / methods. Male. Middle Aged. Neoplasm Metastasis. Retrospective Studies. Sensitivity and Specificity. Tomography, X-Ray Computed / methods

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  • (PMID = 18425368.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Contrast Media
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48. Tissier F: Classification of adrenal cortical tumors: what limits for the pathological approach? Best Pract Res Clin Endocrinol Metab; 2010 Dec;24(6):877-85
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  • [Title] Classification of adrenal cortical tumors: what limits for the pathological approach?
  • Most adrenocortical tumors are benign; adrenocortical carcinomas are rare but their prognosis is poor and their therapeutics are sparse.
  • In most adrenocortical tumors, the morphological approach in particular by Weiss system, brings sufficient elements to establish the differential diagnosis between a benign and a malignant tumor.
  • But some tumors of Weiss score of 2 or 3 can raise problems: are they benign, malignant or are they of uncertain malignant potential?
  • These genetics findings already have repercussions for the patients in the development of molecular markers for diagnosis and prognosis and in the future they could help in the development of new morphological approaches, in particular immunohistochemical approaches.
  • [MeSH-major] Adrenal Cortex Neoplasms / classification. Adrenal Cortex Neoplasms / pathology
  • [MeSH-minor] Adrenal Cortex / metabolism. Adrenal Cortex / pathology. Animals. Biomarkers, Tumor / metabolism. Diagnosis, Differential. Humans. Neoplasm Staging. Prognosis

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  • [Copyright] 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 21115156.001).
  • [ISSN] 1878-1594
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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49. Sidhu S, Martin E, Gicquel C, Melki J, Clark SJ, Campbell P, Magarey CJ, Schulte KM, Röher HD, Delbridge L, Robinson BG: Mutation and methylation analysis of TP53 in adrenal carcinogenesis. Eur J Surg Oncol; 2005 Jun;31(5):549-54
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  • [Title] Mutation and methylation analysis of TP53 in adrenal carcinogenesis.
  • AIM: To investigate the role of coding region mutation and promoter hypermethylation of TP53 in adrenocortical cancer formation.
  • METHODS: Twenty sporadic adrenocortical cancers (ACCs) and five normal adrenal tissue samples were available for analysis.
  • In 10 ACCs and five normal adrenal tissue specimens, methylation of the 16 CpG sites within the TP53 promoter was examined using bisulphite methylation sequencing.
  • Four of 5 patients with a TP53 mutation had metastases at diagnosis or detected soon thereafter and 3 of 4 died of disease within 12 months of surgical resection.
  • No methylation was seen in the TP53 promoter in 10 ACC and the five normal adrenal tissues examined.
  • Promoter methylation of TP53 is not present in ACC as a mechanism for tumour suppressor gene (TSG) inactivation and, therefore, other genes in the 17p13 region are implicated in adrenal carcinogenesis.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Adrenal Gland Neoplasms / metabolism. DNA Methylation. Genes, p53. Mutation. Promoter Regions, Genetic

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  • (PMID = 15922892.001).
  • [ISSN] 0748-7983
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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51. Mannelli M, Cantini G, Poli G, Mangoni M, Nesi G, Canu L, Rapizzi E, Borgogni E, Ercolino T, Piccini V, Luconi M: Role of the PPAR-γ system in normal and tumoral pituitary corticotropic cells and adrenal cells. Neuroendocrinology; 2010;92 Suppl 1:23-7
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  • [Title] Role of the PPAR-γ system in normal and tumoral pituitary corticotropic cells and adrenal cells.
  • In this minireview, we summarize the current knowledge on PPAR-γ in normal and tumoral corticotropic pituitary and adrenal cells.
  • The receptor expression has been shown in ACTH-secreting cells in both normal and adenomal pituitary as well as in normal and tumor adrenal cortex.
  • Preclinical studies conducted both in vitro on tumor cells and in vivo on xenograft tumor models obtained by subcutaneous injection of cancer cells have evidenced the anticancer properties of TZD, in particular rosiglitazone (RGZ) and pioglitazone (PIO).
  • In both pituitary and adrenocortical cancer, RGZ treatment results in inhibition of cell proliferation, through G0/G1 cell-cycle arrest and induction of cell apoptosis, leading to significant inhibition of tumor growth in the xenograft tumor models.
  • [MeSH-major] Adrenal Cortex / metabolism. Corticotrophs / metabolism. PPAR gamma / metabolism. Pituitary ACTH Hypersecretion / metabolism. Pituitary Gland / metabolism
  • [MeSH-minor] Adrenal Cortex Neoplasms / drug therapy. Adrenal Cortex Neoplasms / metabolism. Humans. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / metabolism. Thiazolidinediones / therapeutic use

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  • [Copyright] Copyright © 2010 S. Karger AG, Basel.
  • (PMID = 20829614.001).
  • [ISSN] 1423-0194
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / PPAR gamma; 0 / Thiazolidinediones; X4OV71U42S / pioglitazone
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52. Patalano A, Brancato V, Mantero F: Adrenocortical cancer treatment. Horm Res; 2009 Jan;71 Suppl 1:99-104
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  • [Title] Adrenocortical cancer treatment.
  • BACKGROUND: With a reported incidence of 1 to 2 cases per million, adrenocortical cancer (ACC) is a rare disease with poor prognosis.
  • In sporadic ACC, some molecular modifications are commonly observed (i.e., overexpression of insulin-like growth factor II or vascular endothelial growth factor and somatic mutations of tumor protein 53).
  • When surgical resection of the tumor is impossible or ineffective, chemotherapy with etoposide, doxorubicin and cisplatin plus mitotane or with streptozotocin plus mitotane is frequently used; however, the overall survival rates are disappointing.
  • New treatments, such as insulin-like growth factor I receptor antibodies, tyrosine kinase inhibitors and other antiangiogenic compounds, are now being intensively investigated to identify better therapies for this extremely severe malignant neoplasia.
  • [MeSH-major] Adrenal Cortex Neoplasms / therapy. Adrenocortical Carcinoma / therapy

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19153517.001).
  • [ISSN] 1423-0046
  • [Journal-full-title] Hormone research
  • [ISO-abbreviation] Horm. Res.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 5W494URQ81 / Streptozocin; 78E4J5IB5J / Mitotane
  • [Number-of-references] 29
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53. Allolio B, Fassnacht M: Clinical review: Adrenocortical carcinoma: clinical update. J Clin Endocrinol Metab; 2006 Jun;91(6):2027-37
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  • [Title] Clinical review: Adrenocortical carcinoma: clinical update.
  • CONTEXT: Adrenocortical carcinoma (ACC) is a rare and heterogeneous malignancy with incompletely understood pathogenesis and poor prognosis.
  • Patients present with hormone excess (e.g. virilization, Cushing's syndrome) or a local mass effect (median tumor size at diagnosis > 10 cm).
  • The following search terms were used in varying combinations: adrenal, adrenocortical, cancer, carcinoma, tumor, diagnosis, imaging, treatment, radiotherapy, mitotane, cytotoxic, surgery.
  • Hormonal analysis reveals evidence of steroid hormone secretion by the tumor in the majority of cases, even in seemingly hormonally inactive lesions.
  • Histopathology is crucial for the diagnosis of malignancy and may also provide important prognostic information.
  • Local recurrence is frequent, particularly after violation of the tumor capsule.
  • Surgery also plays a role in local tumor recurrence and metastatic disease.
  • Adjuvant treatment options after complete tumor removal (e.g. mitotane, radiotherapy) are urgently needed because postoperative disease-free survival at 5 yr is only around 30%, but options have still not been convincingly established.
  • However, future advances in the management of ACC will mainly depend on a better understanding of the molecular pathogenesis facilitating the use of modern cancer treatments (e.g. tyrosine kinase inhibitors).
  • [MeSH-major] Adrenal Cortex Neoplasms / therapy
  • [MeSH-minor] Follow-Up Studies. Humans. Neoplasm Staging. Prognosis

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  • (PMID = 16551738.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 156
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54. Kvacheniuk AN: [Surgical treatment of adrenocortical cancer: significance of systematic lymphodissection]. Klin Khir; 2008 Mar;(3):34-7
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  • [Title] [Surgical treatment of adrenocortical cancer: significance of systematic lymphodissection].
  • Comparative efficacy of radical methods of surgical intervention for adrenocortical cancer (ACC) with lymphodissection (LD) and without it was studied.
  • Adrenalectomy (AE) with en bloc excision of tumor and systematic lymph nodes dissection (paranephral, left-side paraaortal and the right-side paracaval collectors) constitutes the optimal surgical procedure.
  • AE with the tumor en bloc excision without performance of LD may give the same expected efficacy only for I-II stages tumor, when it is impossible to confirm malignancy intraoperatively.

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  • (PMID = 18680995.001).
  • [ISSN] 0023-2130
  • [Journal-full-title] Klinichna khirurhiia
  • [ISO-abbreviation] Klin Khir
  • [Language] RUS
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Ukraine
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55. Gil J, Kalembkiewicz M, Polak E, Kostecka-Matyja M: [Disseminated adrenocortical carcinoma: case report]. Pol Arch Med Wewn; 2007 Jul;117(7):317-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Disseminated adrenocortical carcinoma: case report].
  • Adrenocortical carcinoma is a rare neoplasm occurring with a frequency of 1-2 cases per million.
  • This type of a tumor is slightly more frequent in women (58.6%) than in men (41.4%).
  • Etiology of adrenocortical carcinoma is still unclear, but a role of genetic and environmental factors has been largely considered.
  • The tumor size is still the best single predictor of prognosis.
  • Histopathology specimen from biopsy or obtained during operation should be stained for Melan A, which can confirm the adrenal origin of the tumor.
  • The only method of treatment is a complete surgical excision of the carcinoma.
  • We presented the case of functioning adrenocortical cancer in 37-year-old patient who at time of diagnosis had 12 cm in diameter tumor of the left adrenal gland and metastases to the liver and lung.
  • In the article the symptoms associated with hormones produced by the carcinoma, diagnostics and treatment with regard to the progression of the disease have also been discussed.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Liver Neoplasms / secondary. Lung Neoplasms / secondary

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  • (PMID = 17966598.001).
  • [Journal-full-title] Polskie Archiwum Medycyny Wewnetrznej
  • [ISO-abbreviation] Pol. Arch. Med. Wewn.
  • [Language] pol
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Poland
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61. Luconi M, Mangoni M, Gelmini S, Poli G, Nesi G, Francalanci M, Pratesi N, Cantini G, Lombardi A, Pepi M, Ercolino T, Serio M, Orlando C, Mannelli M: Rosiglitazone impairs proliferation of human adrenocortical cancer: preclinical study in a xenograft mouse model. Endocr Relat Cancer; 2010 Mar;17(1):169-77
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rosiglitazone impairs proliferation of human adrenocortical cancer: preclinical study in a xenograft mouse model.
  • Adrenocortical carcinoma (ACC) is a rare aggressive tumor with a poor prognosis.
  • The lack of a specific and effective medical treatment is due to the poor knowledge of the mechanisms underlying tumor growth.
  • Research on potential drugs able to specifically interfere with tumor proliferation is essential to develop more efficacious therapies.
  • We evaluated for the first time the in vivo effect of rosiglitazone (RGZ), an anti-diabetic drug with in vitro anti-tumor properties, on ACC proliferation in a xenograft model obtained by s.c. injection of human ACC H295R cells in athymic mice.
  • When the tumor size reached 5 mm, animals were allocated to 5 mg/kg RGZ- or water-treated groups.
  • Tumor volume was measured twice a week.
  • A significant reduction of tumor growth in RGZ versus control (control) group was observed and was already maximal following 17 day treatment (1-T/C=75.4% (43.7-93.8%)).
  • After 31 days of treatment, mice were killed and tumor analyzed.
  • Tumor histological evaluation revealed characteristics of invasiveness, richness in small vessels and mitotic figures in control group, while RGZ group tumors presented non infiltrating borders, few vessels, and many apoptotic bodies.
  • Tumor immunohistochemistry showed that Ki-67 was reduced in RGZ versus control group.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Carcinoma / pathology. Cell Proliferation / drug effects. Thiazolidinediones / pharmacology
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Cell Line, Tumor. Female. Gene Expression Regulation, Neoplastic / drug effects. Humans. Hypoglycemic Agents / pharmacology. Hypoglycemic Agents / therapeutic use. Mice. Mice, Nude. Tumor Burden / drug effects. Xenograft Model Antitumor Assays

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  • (PMID = 19955217.001).
  • [ISSN] 1479-6821
  • [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 / Antineoplastic Agents; 0 / Hypoglycemic Agents; 0 / Thiazolidinediones; 05V02F2KDG / rosiglitazone
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62. Boudou-Rouquette P, Alexandre J, Soubrane O, Bertagna X, Goldwasser F: Antitumoral effect of the bisphosphonate zoledronic acid against visceral metastases in an adrenocortical cancer patient. Ann Oncol; 2009 Oct;20(10):1747
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  • [Title] Antitumoral effect of the bisphosphonate zoledronic acid against visceral metastases in an adrenocortical cancer patient.

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  • [CommentIn] Ann Oncol. 2009 Dec;20(12):2019; author reply 2019 [19752002.001]
  • (PMID = 19633056.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid
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63. Tissier F, Cavard C, Groussin L, Perlemoine K, Fumey G, Hagneré AM, René-Corail F, Jullian E, Gicquel C, Bertagna X, Vacher-Lavenu MC, Perret C, Bertherat J: Mutations of beta-catenin in adrenocortical tumors: activation of the Wnt signaling pathway is a frequent event in both benign and malignant adrenocortical tumors. Cancer Res; 2005 Sep 1;65(17):7622-7
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  • [Title] Mutations of beta-catenin in adrenocortical tumors: activation of the Wnt signaling pathway is a frequent event in both benign and malignant adrenocortical tumors.
  • Adrenocortical cancer is a rare cancer with a very poor prognosis.
  • The genetic alterations identified to date in adrenocortical tumors are limited.
  • Activating mutations of the Wnt signaling pathway have been observed in more frequent cancers, particularly digestive tract tumors.
  • We investigated whether Wnt pathway activation is involved in adrenocortical tumorigenesis.
  • In a series of 39 adrenocortical tumors, immunohistochemistry revealed abnormal cytoplasmic and/or nuclear accumulation of beta-catenin in 10 of 26 adrenocortical adenomas and in 11 of 13 adrenocortical carcinomas.
  • An activating somatic mutation of the beta-catenin gene was shown in 7 of 26 adrenocortical adenomas and in 4 of 13 adrenocortical carcinomas; these mutations were observed only in adrenocortical tumors with abnormal beta-catenin accumulation and most were point mutations altering the Ser45 of exon 3 (in the consensus GSK3-beta/CK1 phosphorylation site).
  • Functional studies showed that the activating Ser45 beta-catenin mutation found in the adrenocortical cancer H295R cell line leads to constitutive activation of T-cell factor-dependent transcription.
  • This is the first molecular defect to be reported with the same prevalence in both benign (27%) and malignant (31%) adrenocortical tumors. beta-Catenin mutations are also the most frequent genetic defect currently known in adrenocortical adenomas.
  • In adrenocortical adenomas, beta-catenin alterations are more frequent in nonfunctioning tumors, suggesting that beta-catenin pathway activation might be mostly involved in the development of nonsecreting adrenocortical adenomas and adrenocortical carcinomas.
  • The very frequent and substantial accumulation of beta-catenin in adrenocortical carcinomas suggests that other alterations might also be involved.
  • This finding may contribute to new therapeutic approaches targeting the Wnt pathway in malignant adrenocortical tumors, for which limited medical therapy is available.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Cytoskeletal Proteins / genetics. Intercellular Signaling Peptides and Proteins / genetics. Trans-Activators / genetics
  • [MeSH-minor] Adult. Aged. Cell Line, Tumor. Female. Humans. Immunohistochemistry. Male. Middle Aged. Mutation. Signal Transduction. Wnt Proteins. beta Catenin

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  • (PMID = 16140927.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / Cytoskeletal Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Trans-Activators; 0 / Wnt Proteins; 0 / beta Catenin
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64. Oller AR, Kirkpatrick DT, Radovsky A, Bates HK: Inhalation carcinogenicity study with nickel metal powder in Wistar rats. Toxicol Appl Pharmacol; 2008 Dec 1;233(2):262-75
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  • Epidemiological studies of nickel refinery workers have demonstrated an association between increased respiratory cancer risk and exposure to certain nickel compounds (later confirmed in animal studies).
  • No increased incidence of neoplasm of the respiratory tract was observed.
  • Adrenal gland pheochromocytomas (benign and malignant) in males and combined cortical adenomas/carcinomas in females were induced in a dose-dependent manner by the nickel metal exposure.
  • Pheochromocytomas appear to be secondary to the lung toxicity associated with the exposure rather than being related to a direct nickel effect on the adrenal glands.
  • The incidence of cortical tumors among 0.4 mg Ni/m(3) females, although statistically higher compared to the concurrent controls, falls within the historical control range; therefore, in the present study, this tumor is of uncertain relationship to nickel metal exposure.
  • [MeSH-minor] Adrenal Cortex Neoplasms / chemically induced. Adrenal Gland Neoplasms / chemically induced. Adrenocortical Adenoma / chemically induced. Adrenocortical Carcinoma / chemically induced. Animals. Dose-Response Relationship, Drug. Female. Male. Models, Animal. Occupational Exposure / adverse effects. Pheochromocytoma / chemically induced. Powders. Rats. Rats, Wistar. Respiratory Tract Neoplasms / epidemiology. Respiratory Tract Neoplasms / etiology. Sex Factors

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  • (PMID = 18822311.001).
  • [ISSN] 1096-0333
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Powders; 7OV03QG267 / Nickel
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65. Else T, Giordano TJ, Hammer GD: Evaluation of telomere length maintenance mechanisms in adrenocortical carcinoma. J Clin Endocrinol Metab; 2008 Apr;93(4):1442-9
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  • [Title] Evaluation of telomere length maintenance mechanisms in adrenocortical carcinoma.
  • CONTEXT: Adrenocortical cancer (ACC) is a rare disease with an often fatal outcome.
  • The clinical and pathological diagnosis of a malignant vs. benign adrenocortical tumor is sometimes challenging.
  • Telomere maintenance mechanisms (TMMs) are critical for the persistence of the malignant phenotype, but little is known about these mechanisms or their diagnostic value in adrenocortical lesions.
  • OBJECTIVE: Tissue samples of diagnostically known adrenocortical neoplasms were evaluated for parameters of known TMMs, telomerase activity (TA), and alternative telomere lengthening (ALT).
  • DESIGN: The study analyzed retrospectively collected frozen adrenocortical tissue samples from the University of Michigan Health System.
  • PATIENT SAMPLES: Samples included 24 ACCs, 11 adrenocortical adenomas (ACAs), and three normal adrenal tissues.
  • None of the normal adrenal tissues (none of three) or ACA (none of 11) samples had signs of an active TMM.
  • Determination of telomere maintenance mechanisms in diagnostically challenging adrenocortical tumors might be of additional diagnostic value in the pathological diagnosis of malignant vs. benign lesions.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Telomere

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  • (PMID = 18198226.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.7.49 / Telomerase
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66. Gaujoux S, Tissier F, Groussin L, Libé R, Ragazzon B, Launay P, Audebourg A, Dousset B, Bertagna X, Bertherat J: Wnt/beta-catenin and 3',5'-cyclic adenosine 5'-monophosphate/protein kinase A signaling pathways alterations and somatic beta-catenin gene mutations in the progression of adrenocortical tumors. J Clin Endocrinol Metab; 2008 Oct;93(10):4135-40
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  • [Title] Wnt/beta-catenin and 3',5'-cyclic adenosine 5'-monophosphate/protein kinase A signaling pathways alterations and somatic beta-catenin gene mutations in the progression of adrenocortical tumors.
  • BACKGROUND: The Wnt/beta-catenin and cAMP signaling pathways play an important role in adrenal cortex tumorigenesis.
  • Somatic activating mutations of the beta-catenin gene (CTNNB1) are the most frequent genetic defects identified both in adrenocortical adenomas (ACAs) and adrenocortical cancers (ACCs).
  • PRKAR1A mutations leading to cAMP pathway dysregulation are observed in primary pigmented nodular adrenocortical diseases (PPNADs) and some sporadic ACAs.
  • OBJECTIVE: The objective of the investigation was to study Wnt/beta-catenin dysregulation in adrenocortical tumors (ACTs) with cAMP pathway genetic alteration and search for secondary CTNNB1 somatic mutations in heterogeneous tumors.
  • PATIENTS AND METHODS: Nine PPNADs, including five with macronodules, three ACAs with PRKAR1A somatic mutations, and one heterogeneous tumor with ACC developed within an ACA, were studied by immunohistochemistry and DNA sequencing.
  • RESULTS: beta-Catenin accumulation was observed in all PPNADs, ACAs with PRKAR1A mutations, and the ACC component of the heterogeneous tumor.
  • CTNNB1 somatic activating mutations were found in the macronodule of two of the five macronodular PPNADs, in one ACA with a PRKAR1A somatic mutation, and in the malignant part of the heterogeneous ACT.
  • This underlines the importance of the Wnt/beta-catenin pathway in adrenal cortex tumorigenesis and the importance of genetic accumulation in the progression of ACTs.
  • [MeSH-major] Adenoma / genetics. Adrenal Cortex Neoplasms / genetics. Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / genetics. Mutation. Signal Transduction / genetics. Wnt Proteins / genetics. beta Catenin / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Cyclic AMP / metabolism. DNA Mutational Analysis. Disease Progression. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Neoplasm Invasiveness. Tumor Burden / genetics

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  • (PMID = 18647815.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human; 0 / Wnt Proteins; 0 / beta Catenin; E0399OZS9N / Cyclic AMP
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67. McNicol AM: Lesions of the adrenal cortex. Arch Pathol Lab Med; 2008 Aug;132(8):1263-71
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  • [Title] Lesions of the adrenal cortex.
  • CONTEXT: In surgical pathology practice adrenal cortical tumors are rare.
  • However, in autopsy series adrenal cortical nodules are found frequently.
  • It is important to differentiate between benign and malignant lesions as adrenal cortical carcinoma is an aggressive tumor.
  • Molecular genetic investigations are providing new information on both pathogenesis of adrenal tumors and basic adrenal development and physiology.
  • OBJECTIVE: To provide an overview of current knowledge on adrenal cortical development and structure that informs our understanding of genetic diseases of the adrenal cortex and adrenal cortical tumors.
  • CONCLUSIONS: The understanding of basic developmental and physiologic processes permits a better understanding of diseases of the adrenal cortex.
  • The information coming from investigation of the molecular pathology of adrenal cortical tumors is beginning to provide additional tests for the assessment of malignant potential in diagnosis but the mainstay remains traditional histologic analysis.
  • [MeSH-major] Adrenal Cortex. Adrenal Gland Diseases
  • [MeSH-minor] Adrenal Cortex Neoplasms / metabolism. Adrenal Cortex Neoplasms / pathology. Growth. Humans. Immunohistochemistry. Prognosis

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  • (PMID = 18684025.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 126
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68. Tomkova K, Tomka M, Zajac V: Contribution of p53, p63, and p73 to the developmental diseases and cancer. Neoplasma; 2008;55(3):177-81
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  • [Title] Contribution of p53, p63, and p73 to the developmental diseases and cancer.
  • Tumor suppressor TP53 gene is one of the most mutated genes in human genome.
  • This syndrome is characterized by the early onset of different types of cancers including soft-tissue sarcomas, breast and brain cancers, leukemias, lung, laryngeal cancers, and adrenocortical carcinomas.
  • The key role of p53 in tumor suppression has been confirmed in animal models as well.
  • The p53 -knock-out and knock-in animals were born alive but were tumor prone.
  • On one hand, there are evidences that both, p63 and p73-deficient animals are not tumor prone; on the other hand, there is evidence that such animals develop tumors later during their life.
  • [MeSH-major] DNA-Binding Proteins / genetics. Genes, p53. Membrane Proteins / genetics. Neoplasms / genetics. Nuclear Proteins / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Animals. Embryonic Development. Genes, Tumor Suppressor. Germ-Line Mutation. Humans. Mutation

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  • (PMID = 18348649.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / CKAP4 protein, human; 0 / DNA-Binding Proteins; 0 / Membrane Proteins; 0 / Nuclear Proteins; 0 / Tumor Suppressor Proteins
  • [Number-of-references] 63
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69. Hemal AK, Singh A, Gupta NP: Whether adrenal mass more than 5 cm can pose problem in laparoscopic adrenalectomy? An evaluation of 22 patients. World J Urol; 2008 Oct;26(5):505-8
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  • [Title] Whether adrenal mass more than 5 cm can pose problem in laparoscopic adrenalectomy? An evaluation of 22 patients.
  • OBJECTIVES: To evaluate technical feasibility and analyze outcome of laparoscopic adrenalectomy (LA) for large adrenal masses more than 5 cm.
  • METHODS: The data of 22 patients (8 men, 14 women), who underwent LA for adrenal masses >5 cm between January 1995 and July 2007 were analyzed for this study.
  • RESULTS: Twenty-two patients with a mean age of 42.5 years underwent LA for large adrenal masses (>5 cm) between January 1995 and July 2007.
  • The mean-operative time, blood loss, tumor size and hospital stay were 149.33 and 132.1 min, 132.33 and 94.28 ml, 7.85 and 5.85 cm and 3.5 and 3.28 days, respectively.
  • Histopathological examination of the specimen confirmed adrenal carcinoma in 5, pheochromocytoma in 14, myelolipoma in 2 and adenoma in 1 patient.
  • CONCLUSIONS: The size of an adrenal mass on preoperative imaging studies alone should not be the primary factor in determining whether LA should be performed.
  • LA for adrenocortical cancers could be performed safely and effectively in the selected group.
  • Transperitoneal approach is most suitable and recommended for large adrenal tumor and adrenal carcinoma to employ laparoscopy.
  • [MeSH-major] Adrenal Gland Neoplasms / pathology. Adrenal Gland Neoplasms / surgery. Adrenalectomy / methods. Laparoscopy

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  • (PMID = 18536881.001).
  • [ISSN] 0724-4983
  • [Journal-full-title] World journal of urology
  • [ISO-abbreviation] World J Urol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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70. Terzolo M, Bovio S, Pia A, Reimondo G, Angeli A: Management of adrenal incidentaloma. Best Pract Res Clin Endocrinol Metab; 2009 Apr;23(2):233-43
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  • [Title] Management of adrenal incidentaloma.
  • Clinically inapparent adrenal masses, or adrenal incidentalomas, are discovered inadvertently in the course of work-up or treatment of unrelated disorders.
  • Cortical adenoma is the most frequent tumour detected incidentally, but adrenocortical cancer, phaeochromocytoma and metastasis are not rare.
  • Two critical questions should be answered before trying to outline the management of adrenal incidentaloma:.
  • (1) identify either primary (adrenocortical cancer) or secondary (adrenal metastasis) malignancy;.
  • Radiological evaluation is the key to the differential diagnosis of benign and malignant tumours.
  • Endocrine testing is necessary to exclude phaeochromocytoma in all patients with an adrenal incidentaloma because this tumour may remain undiagnosed after imaging studies.
  • The management of clinically inapparent adrenal adenomas may vary depending whether or not they are functioning.
  • [MeSH-major] Adrenal Gland Neoplasms / therapy
  • [MeSH-minor] Adenoma / diagnosis. Adenoma / drug therapy. Adenoma / therapy. Animals. Humans. Pheochromocytoma / diagnosis. Pheochromocytoma / therapy

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  • (PMID = 19500766.001).
  • [ISSN] 1878-1594
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 46
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71. Nishikawa T, Saito J, Omura M: [Medical treatment for Cushing's syndrome]. Nihon Rinsho; 2008 Jan;66(1):186-91
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  • Thus, we should treat Cushing's syndrome as soon as possible, since many complications, including cardiovascular diseases and infections, will soon occur when the definite diagnosis is delayed.
  • Adrenalectomy is essential for treatment for Cushing's syndrome even in the patients with pituitary or ectopic ACTH-producing tumor.
  • Medical adrenalectomy is achieved by using with mitotane which is usually used for adrenocortical cancer.
  • We commonly treat the patients with Cushing's syndrome due to adrenal tumor and pituitary or ectopic ACTH producing tumor by using metyrapone which mainly inhibits 11-hydroxylase.
  • Replacement therapy with hydrocortisone should be considered if adrenal failure will occur during treatment with those drugs.

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  • (PMID = 18186263.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Aromatase Inhibitors; 0O54ZQ14I9 / Aminoglutethimide; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase; R9400W927I / Ketoconazole; ZS9KD92H6V / Metyrapone
  • [Number-of-references] 6
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72. Ide H, Terado Y, Tokiwa S, Nishio K, Saito K, Isotani S, Kamiyama Y, Muto S, Imamura T, Horie S: Novel germ line mutation p53-P177R in adult adrenocortical carcinoma producing neuron-specific enolase as a possible marker. Jpn J Clin Oncol; 2010 Aug;40(8):815-8
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  • [Title] Novel germ line mutation p53-P177R in adult adrenocortical carcinoma producing neuron-specific enolase as a possible marker.
  • Adrenocortical cancer (ACC) is a rare and aggressive endocrine tumor.
  • The patient presented with a large retroperitoneum tumor and lung metastases.
  • Removal of the adrenocortical tumor with part of the transverse colon and tail of the pancreas, spleen and kidney was successfully performed following chemotherapy.
  • Levels of serum neuron-specific enolase (NSE) were found to be markedly high before surgery and may be clinically useful markers for monitoring tumor status during management.
  • Immunohistochemical studies showed that the cancer cells were positive for NSE and overexpression of p53.
  • The genetic and biochemical data presented in this case confirm the importance of screening for p53 status in ACC with inherited cancer syndrome.
  • [MeSH-major] Adrenal Gland Neoplasms / enzymology. Adrenal Gland Neoplasms / genetics. Adrenocortical Carcinoma / enzymology. Adrenocortical Carcinoma / genetics. Biomarkers, Tumor / blood. Genes, p53 / genetics. Germ-Line Mutation. Phosphopyruvate Hydratase / blood

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  • (PMID = 20421238.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 4.2.1.11 / Phosphopyruvate Hydratase
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73. Wang Y, Nicholls PK, Stanton PG, Harrison CA, Sarraj M, Gilchrist RB, Findlay JK, Farnworth PG: Extra-ovarian expression and activity of growth differentiation factor 9. J Endocrinol; 2009 Sep;202(3):419-30
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  • The present studies confirm GDF9 expression in the mouse testis, pituitary gland and adrenocortical cancer (AC) cells, and establish its expression in L beta T2 gonadotrophs, and in mouse adrenal glands, particularly foetal and neonatal cortical cells.
  • Our findings show that GDF9 regulates the expression of R-SMAD2/3-responsive reporter genes through ALK4, 5 or 7 in extra-ovarian (adrenocortical and Sertoli) cells with similar potency and signalling pathway to its actions on granulosa cells, but suggest that expression of BMPRII, ALK5 (TGFBR1) and R-SMADs 2 and 3 may not be sufficient for a cell to respond to GDF9.
  • [MeSH-major] Adrenal Glands / physiology. Growth Differentiation Factor 9 / genetics. Leydig Cells / physiology. Pituitary Gland / physiology. Sertoli Cells / physiology

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  • (PMID = 19505950.001).
  • [ISSN] 1479-6805
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide; 0 / Benzamides; 0 / Dioxoles; 0 / GDF9 protein, human; 0 / Gdf9 protein, mouse; 0 / Gdf9 protein, rat; 0 / Growth Differentiation Factor 9; 9002-68-0 / Follicle Stimulating Hormone; EC 1.13.12.- / Luciferases
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74. Ahmed AA: Adrenocortical neoplasms in young children: age as a prognostic factor. Ann Clin Lab Sci; 2009;39(3):277-82
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  • [Title] Adrenocortical neoplasms in young children: age as a prognostic factor.
  • Adrenal cortical neoplasms in pediatric patients are rare.
  • We report 5 cases of adrenocortical neoplasms in young children and review their clinical presentations, pathology, and follow-up data.
  • Imaging studies revealed neoplasms in the left adrenal gland in 3 cases and the right adrenal gland in 2 cases.
  • The tumors were grossly confined to the adrenal glands and ranged in diameter from 3 to 6 cm (mean 4.3 cm).
  • Microscopically, the tumors had histological and immunophenotypic features characteristic of adrenocortical tumors.
  • Despite histological and immunophenotypical evidence of malignancy, these localized adrenocortical neoplasms had a benign clinical course with no evidence of metastasis or recurrence.
  • Because of the discrepancy between pathology and clinical outcome, adrenocortical tumors in this age group should be classified as neoplasms of unknown malignant potential.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis
  • [MeSH-minor] Age Factors. Child, Preschool. Dehydroepiandrosterone / blood. Dehydroepiandrosterone / urine. Female. Humans. Infant. Ki-67 Antigen / metabolism. Male. Prognosis. Testosterone / blood. Tumor Suppressor Protein p53 / metabolism. Virilism / diagnosis. Virilism / etiology

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  • (PMID = 19667412.001).
  • [ISSN] 1550-8080
  • [Journal-full-title] Annals of clinical and laboratory science
  • [ISO-abbreviation] Ann. Clin. Lab. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53; 3XMK78S47O / Testosterone; 459AG36T1B / Dehydroepiandrosterone
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75. Wandoloski M, Bussey KJ, Demeure MJ: Adrenocortical cancer. Surg Clin North Am; 2009 Oct;89(5):1255-67
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  • [Title] Adrenocortical cancer.
  • Adrenocortical carcinoma (ACC) is a rare endocrine malignancy causing up to 0.2% of all cancer deaths This article reviews the incidence, presentation, and pathology of ACC.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Combined Modality Therapy. Diagnosis, Differential. Diagnostic Imaging. Genetic Predisposition to Disease. Humans. Mitotane / therapeutic use

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  • (PMID = 19836496.001).
  • [ISSN] 1558-3171
  • [Journal-full-title] The Surgical clinics of North America
  • [ISO-abbreviation] Surg. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 78E4J5IB5J / Mitotane
  • [Number-of-references] 51
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76. Lawnicka H, Kowalewicz-Kulbat M, Sicinska P, Kazimierczuk Z, Grieb P, Stepien H: Anti-neoplastic effect of protein kinase CK2 inhibitor, 2-dimethylamino-4,5,6,7-tetrabromobenzimidazole (DMAT), on growth and hormonal activity of human adrenocortical carcinoma cell line (H295R) in vitro. Cell Tissue Res; 2010 May;340(2):371-9
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  • [Title] Anti-neoplastic effect of protein kinase CK2 inhibitor, 2-dimethylamino-4,5,6,7-tetrabromobenzimidazole (DMAT), on growth and hormonal activity of human adrenocortical carcinoma cell line (H295R) in vitro.
  • CK2 kinase (casein kinase-2) has been suggested to be a constituent of a neoplastic milleu, and its inhibition might represent a new approach to cancer therapy.
  • Adrenocortical carcinomas (ACCs) are highly malignant neoplasms with poor overall prognosis.
  • We have examined the effects of 2-dimethylamino-4,5,6,7-tetrabromobenzimidazole (DMAT), a potent CK2 inhibitor, on the H295R human adrenocortical cancer cell line.
  • [MeSH-major] Adrenal Cortex Hormones / secretion. Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Benzimidazoles / pharmacology. Casein Kinase II / antagonists & inhibitors. Cell Proliferation / drug effects. Protein Kinase Inhibitors / pharmacology
  • [MeSH-minor] 17-alpha-Hydroxyprogesterone / metabolism. Aldosterone / secretion. Antineoplastic Agents / pharmacology. Cell Cycle / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Dehydroepiandrosterone Sulfate / metabolism. Drug Screening Assays, Antitumor. Humans. Hydrocortisone / secretion

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  • (PMID = 20383646.001).
  • [ISSN] 1432-0878
  • [Journal-full-title] Cell and tissue research
  • [ISO-abbreviation] Cell Tissue Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / 4,5,6,7-tetrabromobenzimidazole; 0 / Adrenal Cortex Hormones; 0 / Antineoplastic Agents; 0 / Benzimidazoles; 0 / Protein Kinase Inhibitors; 4964P6T9RB / Aldosterone; 57B09Q7FJR / Dehydroepiandrosterone Sulfate; 68-96-2 / 17-alpha-Hydroxyprogesterone; EC 2.7.11.1 / Casein Kinase II; WI4X0X7BPJ / Hydrocortisone
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77. Cyriac J, Weizman D, Urbach DR: Laparoscopic adrenalectomy for the management of benign and malignant adrenal tumors. Expert Rev Med Devices; 2006 Nov;3(6):777-86
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  • [Title] Laparoscopic adrenalectomy for the management of benign and malignant adrenal tumors.
  • Laparoscopic adrenalectomy has become the preferred approach for removal of the adrenal gland.
  • Adrenalectomy is usually required for the removal of adrenal tumors causing excess hormone production or because a malignant adrenal tumor cannot be excluded.
  • Current controversies include the appropriateness of laparoscopic adrenalectomy for large or malignant tumors, the role of partial adrenalectomy and the management of some conditions with uncertain natural history (such as subclinical hypercortisolism).
  • With the increased use of sensitive cross-sectional imaging, the detection of clinically inapparent adrenal masses is likely to continue to increase.
  • Due to the fact that malignancy cannot be excluded with certainty in some patients with cortical adenomas, it is expected that the rate of laparoscopic adrenalectomy will continue to increase.
  • [MeSH-major] Adrenal Gland Neoplasms / surgery. Adrenalectomy / methods. Laparoscopy / methods

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  • (PMID = 17280543.001).
  • [ISSN] 1743-4440
  • [Journal-full-title] Expert review of medical devices
  • [ISO-abbreviation] Expert Rev Med Devices
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 63
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78. Ragazzon B, Libé R, Gaujoux S, Assié G, Fratticci A, Launay P, Clauser E, Bertagna X, Tissier F, de Reyniès A, Bertherat J: Transcriptome analysis reveals that p53 and {beta}-catenin alterations occur in a group of aggressive adrenocortical cancers. Cancer Res; 2010 Nov 1;70(21):8276-81
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  • [Title] Transcriptome analysis reveals that p53 and {beta}-catenin alterations occur in a group of aggressive adrenocortical cancers.
  • Adrenocortical carcinoma (ACC) is a rare disease with an overall poor but heterogeneous prognosis.
  • This heterogeneity could reflect different mechanisms of tumor development.
  • Somatic inactivating mutations of the tumor suppressor gene TP53 and activating mutations of the proto-oncogene β-catenin (CTNNB1) are the most frequent mutations identified in ACC.
  • Analysis of p53 and β-catenin target gene expressions in each cluster confirmed a profound and anticipated effect on tumor biology, with distinct profiles logically associated with the respective pathway alterations.
  • [MeSH-major] Adrenocortical Carcinoma / genetics. Biomarkers, Tumor / genetics. Gene Expression Profiling. Mutation / genetics. Tumor Suppressor Protein p53 / genetics. beta Catenin / genetics


79. Aspinall SR, Imisairi AH, Bliss RD, Scott-Coombes D, Harrison BJ, Lennard TW: How is adrenocortical cancer being managed in the UK? Ann R Coll Surg Engl; 2009 Sep;91(6):489-93
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  • [Title] How is adrenocortical cancer being managed in the UK?
  • INTRODUCTION: Adrenocortical carcinomas are rare.
  • This case series is reported to give an overview of how adrenocortical carcinoma is currently managed in the UK.
  • PATIENTS AND METHODS: A retrospective review was made of case notes from patients with adrenocortical carcinomas presenting to the authors (TWJL, RDB, BJH, and DS-C) over the past 10 years in Newcastle, Sheffield and Cardiff.
  • CONCLUSIONS: The size of tumour, stage and mode of presentation, age and overall survival of patients in this study are comparable to published series of adrenocortical carcinomas from major endocrine surgical centres world-wide.
  • The exact role of adjuvant therapy in the management of adrenocortical carcinoma is not as well established as for other more common malignancies.
  • Establishing a database for adrenocortical carcinomas in the UK would contribute to our understanding of the management of this disease.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Adrenocortical Carcinoma / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Mitotane / therapeutic use
  • [MeSH-minor] Adrenalectomy / methods. Antineoplastic Combined Chemotherapy Protocols. Chemotherapy, Adjuvant. Cytotoxins / therapeutic use. Great Britain. Humans. Neoplasm Recurrence, Local. Retrospective Studies. Survival Analysis

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  • (PMID = 19558758.001).
  • [ISSN] 1478-7083
  • [Journal-full-title] Annals of the Royal College of Surgeons of England
  • [ISO-abbreviation] Ann R Coll Surg Engl
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] England
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  • [Other-IDs] NLM/ PMC2966201
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80. Waldmann J, Feldmann G, Slater EP, Langer P, Buchholz M, Ramaswamy A, Saeger W, Rothmund M, Fendrich V: Expression of the zinc-finger transcription factor Snail in adrenocortical carcinoma is associated with decreased survival. Br J Cancer; 2008 Dec 2;99(11):1900-7
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  • [Title] Expression of the zinc-finger transcription factor Snail in adrenocortical carcinoma is associated with decreased survival.
  • In this study, we evaluate whether Snail is expressed in adrenocortical cancer (ACC) and if its expression is related to patient outcome.
  • Increasing evidence suggests that EMT plays a pivotal role in tumour progression and metastatic spread.
  • Seventeen of 26 (65%) ACC tumour samples expressed Snail when assessed by immunohistochemistry.
  • Snail expression was neither detected in normal adrenocortical tissue, nor in benign adrenocortical adenomas.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenocortical Carcinoma / metabolism. Biomarkers, Tumor / analysis. Transcription Factors / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Cadherins / biosynthesis. Female. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Ki-67 Antigen / biosynthesis. Male. Middle Aged. Neoplasm Staging. Prognosis. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19018264.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cadherins; 0 / Ki-67 Antigen; 0 / RNA, Messenger; 0 / Transcription Factors; 0 / snail family transcription factors
  • [Other-IDs] NLM/ PMC2600683
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81. Cantini G, Lombardi A, Piscitelli E, Poli G, Ceni E, Marchiani S, Ercolino T, Galli A, Serio M, Mannelli M, Luconi M: Rosiglitazone inhibits adrenocortical cancer cell proliferation by interfering with the IGF-IR intracellular signaling. PPAR Res; 2008;2008:904041
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  • [Title] Rosiglitazone inhibits adrenocortical cancer cell proliferation by interfering with the IGF-IR intracellular signaling.
  • We investigated RGZ effect on cell proliferation in two cell line models (SW13 and H295R) of human adrenocortical carcinoma (ACC) and its interaction with the signaling pathways of the activated IGF-I receptor (IGF-IR).

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  • (PMID = 18670617.001).
  • [ISSN] 1687-4757
  • [Journal-full-title] PPAR research
  • [ISO-abbreviation] PPAR Res
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  • [Publication-type] Journal Article
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82. Bertherat J, Bertagna X: Pathogenesis of adrenocortical cancer. Best Pract Res Clin Endocrinol Metab; 2009 Apr;23(2):261-71
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  • [Title] Pathogenesis of adrenocortical cancer.
  • The study of the clonality of adrenocortical tumours (ACTs) has shown that adrenocortical cancers (ACCs) are of monoclonal origin.
  • Numerous chromosomal alterations have been observed in ACCs, and they are much more frequent than in adrenocortical adenomas.
  • Somatic mutations of the tumour suppressor gene TP53 are observed in a third of ACCs.
  • This recent progress in the molecular genetics of ACC has led to the development of new molecular markers for the diagnosis of malignancy; these might also help to identify prognostic markers of ACC and may ultimately lead to novel therapeutic approaches.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology

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  • (PMID = 19500768.001).
  • [ISSN] 1878-1594
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 67
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83. Gruschwitz T, Breza J, Wunderlich H, Junker K: Improvement of histopathological classification of adrenal gland tumors by genetic differentiation. World J Urol; 2010 Jun;28(3):329-34
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  • [Title] Improvement of histopathological classification of adrenal gland tumors by genetic differentiation.
  • PURPOSE: There are often problems in differentiating between benign and malignant adrenal gland tumors by imaging and histopathology.
  • On account of considerable differences in the therapy and aftercare of benign and malignant adrenal tumors, correct classification of tumor type is of greatest importance.
  • METHODS: DNA was isolated from tumor areas in paraffin sections and amplified by a modified protocol for DOP-PCR.
  • After labeling of tumor-DNA and normal DNA with biotin-dUTP and digoxigenin-dUTP, respectively, comparative genomic hybridization (CGH) was carried out according to standard protocols.
  • Retrospectively, 26 (16 adenomas and 10 carcinomas) tumors of the adrenal cortex were analyzed.
  • RESULTS: Genetic alterations were found in 5/16 adenomas (31.25%) and in all adrenocortical carcinomas.
  • The mean number of genetic changes per tumor was 8.7 (range 6-12) in carcinomas.
  • The benign cortical tumors present 1.6 changes (range 0-3) per tumor.
  • Only a moderate correlation between number of alterations and size of tumor was seen.
  • CONCLUSIONS: Genetic evaluation facilitates differentiation between adrenal gland tumors.
  • Genetic tests should be used in routine diagnostics of adrenal specimens.
  • Potentially, fine-needle biopsy can be established as standard diagnostics of adrenal tumors with unknown genesis.
  • [MeSH-major] Adenoma / classification. Adenoma / genetics. Adrenal Cortex Neoplasms / classification. Adrenal Cortex Neoplasms / genetics. Carcinoma / genetics
  • [MeSH-minor] Adrenalectomy / methods. Adult. Aged. Biomarkers, Tumor / analysis. Biopsy, Fine-Needle. Chromosome Aberrations. Chromosome Mapping. Cohort Studies. DNA, Neoplasm / analysis. Female. Humans. Immunohistochemistry. Male. Middle Aged. Polymerase Chain Reaction. Retrospective Studies. Sensitivity and Specificity. Statistics, Nonparametric. Young Adult

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  • (PMID = 20364258.001).
  • [ISSN] 1433-8726
  • [Journal-full-title] World journal of urology
  • [ISO-abbreviation] World J Urol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm
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84. Saeger W, Fassnacht M: [Effects of drugs on the adrenal cortex and its tumors]. Pathologe; 2006 Feb;27(1):61-4
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  • [Title] [Effects of drugs on the adrenal cortex and its tumors].
  • [Transliterated title] Wirkungen von Medikamenten auf die Nebennierenrinde und ihre Tumoren.
  • The structure of the normal adrenal cortex is changed by stimulating hormones (ACTH) and inhibiting hormonal drugs (especially glucocorticoids).
  • In the therapy of patients with adrenocortical cancer, mitotane can cause an increase in of necrosis and fibrosis, but also in intracellular lipid.
  • [MeSH-major] Adrenal Cortex / pathology. Adrenal Cortex Neoplasms / drug therapy. Antineoplastic Agents / therapeutic use

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  • (PMID = 16320017.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Hormonal; 0O54ZQ14I9 / Aminoglutethimide; 9002-60-2 / Adrenocorticotropic Hormone
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85. Porpiglia F, Fiori C, Daffara F, Zaggia B, Bollito E, Volante M, Berruti A, Terzolo M: Retrospective evaluation of the outcome of open versus laparoscopic adrenalectomy for stage I and II adrenocortical cancer. Eur Urol; 2010 May;57(5):873-8
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  • [Title] Retrospective evaluation of the outcome of open versus laparoscopic adrenalectomy for stage I and II adrenocortical cancer.
  • BACKGROUND: Although there is consensus that laparoscopy is the standard of care for the resection of benign adrenal tumours, there is controversy regarding the role of laparoscopy for the resection of adrenocortical cancer (ACC).
  • OBJECTIVE: The aim of the present study was to review the ACC database of the San Luigi Hospital to compare the oncologic effectiveness of open adrenalectomy (OA) versus laparoscopic adrenalectomy (LA) in the treatment of patients with stage I and II ACC.
  • The "open group" consisted of patients treated with OA; the "lap group" consisted of patients treated with LA.
  • MEASUREMENTS: Oncologic effectiveness of the procedures was tested comparing the recurrence-free survival of patients treated with OA versus LA.
  • CONCLUSIONS: The present findings provide interesting evidence that OA and LA may be comparable in terms of recurrence-free survival for patients with stage I and II ACC when the principles of surgical oncology are respected.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenal Cortex Neoplasms / surgery. Adrenalectomy / methods. Laparoscopy
  • [MeSH-minor] Adult. Aged. Female. Humans. Male. Middle Aged. Neoplasm Staging. Retrospective Studies. Treatment Outcome. Young Adult

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  • [Copyright] Copyright © 2010 European Association of Urology. Published by Elsevier B.V. All rights reserved.
  • (PMID = 20137850.001).
  • [ISSN] 1873-7560
  • [Journal-full-title] European urology
  • [ISO-abbreviation] Eur. Urol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
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86. Harrison BJ: Surgery of adrenocortical cancer. Ann Endocrinol (Paris); 2009 Jun;70(3):195-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Surgery of adrenocortical cancer.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenalectomy / methods
  • [MeSH-minor] Humans. Laparoscopy / methods. Neoplasm Staging. Risk Factors. Survival Rate. Time Factors

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  • (PMID = 19286159.001).
  • [ISSN] 0003-4266
  • [Journal-full-title] Annales d'endocrinologie
  • [ISO-abbreviation] Ann. Endocrinol. (Paris)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
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87. Doghman M, Madoux F, Hodder P, Lalli E: Identification and characterization of steroidogenic factor-1 inverse agonists. Methods Enzymol; 2010;485:3-23
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  • Furthermore, SF-1 is amplified and overexpressed in most cases of adrenocortical tumor occurring in children; studies performed in transgenic mice have shown that an increased SF-1 dosage triggers tumor formation in the adrenal cortex.
  • For these reasons, drugs interfering with SF-1 action would represent a promising tool to be added to the current pharmacological protocols in the therapy of adrenocortical cancer.
  • These compounds have the attributes to inhibit the increase in proliferation triggered by an augmented SF-1 dosage in adrenocortical tumor cells and to reduce their steroid production.
  • This latter property may also reveal beneficial for drugs used in the therapy of adrenocortical tumors to alleviate symptoms of virilization and Cushing often associated with tumor burden.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 21050908.001).
  • [ISSN] 1557-7988
  • [Journal-full-title] Methods in enzymology
  • [ISO-abbreviation] Meth. Enzymol.
  • [Language] ENG
  • [Grant] United States / NIMH NIH HHS / MH / U54 MH084512; United States / NIMH NIH HHS / MH / MH077624; United States / NIMH NIH HHS / MH / MH084512
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Isoquinolines; 0 / Steroidogenic Factor 1; 0 / Steroids
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88. Slater EP, Diehl SM, Langer P, Samans B, Ramaswamy A, Zielke A, Bartsch DK: Analysis by cDNA microarrays of gene expression patterns of human adrenocortical tumors. Eur J Endocrinol; 2006 Apr;154(4):587-98
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  • [Title] Analysis by cDNA microarrays of gene expression patterns of human adrenocortical tumors.
  • OBJECTIVES: Adrenocortical carcinoma (ACC) is a rare malignant neoplasm with extremely poor prognosis.
  • The molecular mechanisms of adrenocortical tumorigenesis are still not well understood.
  • The comparative analysis by cDNA microarrays of gene-expression patterns of benign and malignant adrenocortical tumors allows us to identify new tumor-suppressor genes and proto-oncogenes underlying adrenocortical tumorigenesis.
  • DESIGN AND METHODS: Total RNA from fresh-frozen tissue of 10 ACC and 10 benign adrenocortical adenomas was isolated after histologic confirmation of neoplastic cellularity of at least 85%.
  • The reference consisted of pooled RNA of 10 normal adrenal cortex samples.
  • Amplified RNA of tumor and reference was used to synthesize Cy3- and Cy5-fluorescently labeled cDNA in a flip-color technique.
  • RESULTS: The comparative analysis of gene expression revealed many genes with more than fourfold expression difference between ACC and normal tissue (42 genes), cortical adenoma and normal tissue (11 genes), and ACC and cortical adenoma (21 genes) respectively.
  • As confirmed by real-time PCR, the IGF2 gene was significantly upregulated in ACCs versus cortical adenomas and normal cortical tissue.
  • Genes that were downregulated in adrenocortical tumors included chromogranin B and early growth response factor 1.
  • CONCLUSIONS: Comprehensive expression profiling of adrenocortical tumors by the cDNA microarray technique is a very powerful tool to elucidate the molecular steps associated with the tumorigenesis of these ill-defined neoplasms.

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  • (PMID = 16556722.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 4964P6T9RB / Aldosterone; WI4X0X7BPJ / Hydrocortisone
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89. Soon PS, McDonald KL, Robinson BG, Sidhu SB: Molecular markers and the pathogenesis of adrenocortical cancer. Oncologist; 2008 May;13(5):548-61
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  • [Title] Molecular markers and the pathogenesis of adrenocortical cancer.
  • Adrenal tumors are common, with an estimated incidence of 7.3% in autopsy cases, while adrenocortical carcinomas (ACCs) are rare, with an estimated prevalence of 4-12 per million population.
  • Because the prognoses for adrenocortical adenomas (ACAs) and ACCs are vastly different, it is important to be able to accurately differentiate the two tumor types.
  • Advancement in the understanding of the pathophysiology of ACCs is essential for the development of more sensitive means of diagnosis and treatment, resulting in better clinical outcome.
  • Adrenocortical tumors (ACTs) occur as a component of several hereditary tumor syndromes, which include the Li-Fraumeni syndrome, Beckwith-Wiedemann syndrome, multiple endocrine neoplasia 1, Carney complex, and congenital adrenal hyperplasia.
  • The adrenocorticotropic hormone-cAMP-protein kinase A and Wnt pathways are also implicated in adrenocortical tumorigenesis.
  • The aim of this review is to summarize the current knowledge on the molecular mechanisms involved in adrenocortical tumorigenesis, including results of comparative genomic hybridization, loss of heterozygosity, and microarray gene-expression profiling studies.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics. Adrenocortical Carcinoma / genetics. Neoplastic Syndromes, Hereditary / genetics
  • [MeSH-minor] Adrenocorticotropic Hormone / genetics. Adrenocorticotropic Hormone / metabolism. Animals. Gene Expression Profiling. Genes, Tumor Suppressor. Humans. Loss of Heterozygosity. Molecular Biology

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  • (PMID = 18515740.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
  • [Number-of-references] 135
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90. Haase M, Schott M, Bornstein SR, Malendowicz LK, Scherbaum WA, Willenberg HS: CITED2 is expressed in human adrenocortical cells and regulated by basic fibroblast growth factor. J Endocrinol; 2007 Feb;192(2):459-65
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  • [Title] CITED2 is expressed in human adrenocortical cells and regulated by basic fibroblast growth factor.
  • CITED2 gene deletion in mice leads to adrenal agenesis.
  • Therefore, we analyzed CITED2, a CBP/p300 interacting transactivator with transforming activity, in the human adrenal gland.
  • In this study, we examined CITED2 expression in human embryonic and adult adrenal glands as well as adrenocortical carcinomas.
  • As ACTH and basic fibroblast growth factor (bFGF) are connected to the physiology and growth of adrenocortical cells we studied the regulation of CITED2 by these factors in the NCI-H295R adrenocortical carcinoma cell line.
  • We found CITED2 expression in the adult adrenal cortex as well in adrenocortical carcinomas.
  • At an early stage of human adrenal organogenesis CITED2 could be located to the definitive zone of the developing adrenal gland using immunohistochemistry.
  • CITED2 is expressed in embryonic and adult human adrenal glands as well as in adrenocortical cancer.
  • This suggests a novel role for CITED2 in human adrenal growth and possibly in adrenal tumorigenesis.
  • [MeSH-major] Adrenal Cortex / metabolism. DNA-Binding Proteins / analysis. Fibroblast Growth Factor 2 / pharmacology. Gene Expression Regulation. Repressor Proteins / analysis. Trans-Activators / analysis
  • [MeSH-minor] Adrenocortical Carcinoma. Adrenocorticotropic Hormone / metabolism. Adrenocorticotropic Hormone / pharmacology. Adult. Cell Line, Tumor. Cells, Cultured. Colforsin / pharmacology. Dose-Response Relationship, Drug. Embryonic Development. Humans. Immunohistochemistry / methods. Microscopy, Fluorescence. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction / methods. Transfection / methods

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  • (PMID = 17283246.001).
  • [ISSN] 0022-0795
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CITED2 protein, human; 0 / DNA-Binding Proteins; 0 / RNA, Messenger; 0 / Repressor Proteins; 0 / Trans-Activators; 103107-01-3 / Fibroblast Growth Factor 2; 1F7A44V6OU / Colforsin; 9002-60-2 / Adrenocorticotropic Hormone
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91. Lichtenauer UD, Shapiro I, Geiger K, Quinkler M, Fassnacht M, Nitschke R, Rückauer KD, Beuschlein F: Side population does not define stem cell-like cancer cells in the adrenocortical carcinoma cell line NCI h295R. Endocrinology; 2008 Mar;149(3):1314-22
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  • [Title] Side population does not define stem cell-like cancer cells in the adrenocortical carcinoma cell line NCI h295R.
  • Recent evidence suggests the existence of a stem cell-like subpopulation of cells in hematological and solid tumor entities, which determine the malignant phenotype of a given tumor through their proliferative potential and chemotherapy resistance.
  • Herein we demonstrate the presence of SP cells in a variety of adrenal specimens, including primary cultures of human adrenocortical tumors and normal adrenal glands as well as established human and murine adrenocortical cancer cell lines by fluorescence-activated cell sorter analysis and confocal microscopy.
  • On a functional level, SP cells from the human adrenocortical tumor cell line NCI h295R revealed an expression pattern consistent with a less differentiated phenotype, including lower expression of steroidogenic enzymes such as steroid acute regulatory protein (StAR) and side-chain cleavage enzyme (P450scc) in comparison with non-SP cells.
  • Similarly to the baseline growth kinetics, no survival benefit was evident in SP cells after treatment with cytotoxic agents commonly used in adrenocortical carcinomas.
  • Taken together, these findings provide evidence that Hoechst dye exclusion, in contrast to what has been reported for other tumor entities, is not a major tumor stem cell defining marker in adrenocortical NCI h295R tumor cells.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Neoplastic Stem Cells / cytology
  • [MeSH-minor] Adrenal Glands / cytology. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Cell Cycle / physiology. Cell Differentiation / physiology. Cell Line, Tumor. Cell Proliferation. Cholesterol Side-Chain Cleavage Enzyme / metabolism. Coloring Agents. Drug Resistance, Neoplasm / physiology. Humans. Phenotype. Phosphoproteins / metabolism. Tumor Cells, Cultured

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  • (PMID = 18063677.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Coloring Agents; 0 / Phosphoproteins; 0 / steroidogenic acute regulatory protein; EC 1.14.15.6 / Cholesterol Side-Chain Cleavage Enzyme
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92. Zancanella P, Pianovski MA, Oliveira BH, Ferman S, Piovezan GC, Lichtvan LL, Voss SZ, Stinghen ST, Callefe LG, Parise GA, Santana MH, Figueiredo BC: Mitotane associated with cisplatin, etoposide, and doxorubicin in advanced childhood adrenocortical carcinoma: mitotane monitoring and tumor regression. J Pediatr Hematol Oncol; 2006 Aug;28(8):513-24
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  • [Title] Mitotane associated with cisplatin, etoposide, and doxorubicin in advanced childhood adrenocortical carcinoma: mitotane monitoring and tumor regression.
  • PURPOSE: To define a mitotane dose for pediatric patients with adrenocortical cancer (ACC) that maintains therapeutic plasma levels (TL) between 14 and 20 microg/mL and to verify its antitumor efficacy in association with 8 cycles of cisplatin, etoposide, and doxorubicin (CED).
  • Minor to partial tumor remission was found in 5 patients (<1 y) and complete remission was found in 2 patients.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Adrenocortical Carcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cisplatin / administration & dosage. Doxorubicin / administration & dosage. Etoposide / administration & dosage. Mitotane / administration & dosage
  • [MeSH-minor] Administration, Oral. Child. Child, Preschool. Disease Progression. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug Monitoring / methods. Drug Therapy, Combination. Female. Follow-Up Studies. Humans. Male. Neoplasm Staging. Prospective Studies. Remission Induction. Survival Rate. Time Factors. Treatment Outcome

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  • (PMID = 16912591.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 6PLQ3CP4P3 / Etoposide; 78E4J5IB5J / Mitotane; 80168379AG / Doxorubicin; Q20Q21Q62J / Cisplatin
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93. Raparia K, Ayala AG, Sienko A, Zhai QJ, Ro JY: Myxoid adrenal cortical neoplasms. Ann Diagn Pathol; 2008 Oct;12(5):344-8
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  • [Title] Myxoid adrenal cortical neoplasms.
  • Myxoid adrenal cortical neoplasms are rare, and to our knowledge, only about 23 cases have been reported in the literature, including 13 carcinomas and 10 adenomas.
  • We recently experienced 4 cases of myxoid adrenal cortical neoplasms (3 benign and 1 borderline malignancy) and studied the clinical, histopathological, and immunohistochemical features of these neoplasms.
  • Histologically, the tumor cells were arranged in delicate arborizing cords or trabecula with myxoid areas varying from 30% to 70%.
  • The tumor cells were positive for vimentin, synaptophysin, and inhibin but negative for cytokeratin.
  • Myxoid changes in adrenal cortical neoplasms are rare but can be seen in both an adenoma and a tumor of uncertain malignant potential.
  • The usual clinical and histological features can be applied to classify the lesions as benign, borderline tumor, or malignant.
  • In our series, there was no case with frank malignant tumor.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / pathology. Adrenocortical Carcinoma / pathology. Mucins / metabolism
  • [MeSH-minor] Adult. Biomarkers, Tumor / metabolism. Female. Humans. Immunoenzyme Techniques. Inhibins / metabolism. Male. Middle Aged. Synaptophysin / metabolism. Vimentin / metabolism

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  • (PMID = 18774497.001).
  • [ISSN] 1532-8198
  • [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 / Mucins; 0 / Synaptophysin; 0 / Vimentin; 57285-09-3 / Inhibins
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94. Takehara K, Sakai H, Shono T, Irie J, Kanetake H: Proliferative activity and genetic changes in adrenal cortical tumors examined by flow cytometry, fluorescence in situ hybridization and immunohistochemistry. Int J Urol; 2005 Feb;12(2):121-7
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  • [Title] Proliferative activity and genetic changes in adrenal cortical tumors examined by flow cytometry, fluorescence in situ hybridization and immunohistochemistry.
  • BACKGROUND: To determine differences in biological features among different adrenal tumors, we investigated the DNA ploidy, numerical chromosomal aberration and proliferative activity in human adrenal cortical neoplasms.
  • METHODS: Our study included six adrenal cortical adenomas with Cushing syndrome, 12 adenomas with hyperaldosteronism, three non-functioning adenomas and three adrenal cortical carcinomas.
  • RESULTS: The mean Ki-67 labeling index (LI) of adrenal cortical carcinomas was markedly higher than that of adrenal cortical adenomas (209.4 vs 8.7).
  • In functional adrenal cortical adenomas, the LI was significantly lower in adenomas with hyperaldosteronism than in those with Cushing syndrome (P = 0.004), although FCM results indicated that tetraploid patterns were more frequently observed in the former type.
  • Tumor size was significantly smaller in adenomas with hyperaldosteronism than in those with Cushing syndrome (P = 0.004).
  • Chromosome 17 showed disomy in all adrenal cortical adenomas, whereas chromosome 17 abnormalities were found in two of three adrenal cortical carcinomas.
  • CONCLUSIONS: Our study characterized various biological features of benign and malignant adrenal cortical tumors.
  • The use of a combination of markers might provide additional information to assist our understanding of the clinical behavior of an individual adrenal cortical tumor.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / metabolism. Flow Cytometry. Immunohistochemistry. In Situ Hybridization, Fluorescence
  • [MeSH-minor] Adenoma / genetics. Adenoma / metabolism. Adenoma / pathology. Adult. Aged. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Carcinoma / genetics. Carcinoma / metabolism. Carcinoma / pathology. Cell Proliferation. Chromosomes, Human, Pair 17. Cushing Syndrome / genetics. Cushing Syndrome / metabolism. Cushing Syndrome / pathology. DNA, Neoplasm / genetics. Female. Humans. Hyperaldosteronism / genetics. Hyperaldosteronism / metabolism. Hyperaldosteronism / pathology. Ki-67 Antigen / metabolism. Male. Middle Aged. Ploidies. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 15733104.001).
  • [ISSN] 0919-8172
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
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95. Stehr C, Velasco S, Velasco A, López M JM: [Is adrenal tumor size related to evolution time or does it represent a biological difference?]. Rev Med Chil; 2007 Dec;135(12):1526-9
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  • [Title] [Is adrenal tumor size related to evolution time or does it represent a biological difference?].
  • [Transliterated title] El tamaño de los tumores suprarrenales ¿está en relación al tiempo de evolución o expresa una diferencia biológica?
  • BACKGROUND: Adrenal tumor (AT) malignancy has been related to tumor size.
  • Since laparoscopic surgery is being used, smaller adrenal tumors are being excised.
  • AIM: To evaluate eventual clinical and histological differences between adrenal tumors smaller than 4 cm. and those larger than 6 cm.
  • PATIENTS AND METHODS: Retrospective review of pathological reports and clinical records of patients operated for adrenal tumors, dividing them in two groups.
  • Nineteen tumors of group 2 were malignant, compared with one of group 1 (p <0.001).
  • CONCLUSIONS: The tumor size of adrenal cortical tumors may represent biological differences, suggesting two different tumor populations.
  • At time of diagnosis adrenal carcinomas are almost always larger than 6 cm.
  • [MeSH-major] Adrenal Gland Neoplasms / pathology. Adrenal Glands / pathology. Carcinoma / pathology
  • [MeSH-minor] Biomarkers, Tumor. Female. Humans. Hyperplasia. Incidental Findings. Male. Middle Aged. Neoplasm Invasiveness. Retrospective Studies. Time Factors

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  • (PMID = 18357352.001).
  • [ISSN] 0034-9887
  • [Journal-full-title] Revista médica de Chile
  • [ISO-abbreviation] Rev Med Chil
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Chile
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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96. Britvin TA, Kazantseva IA, Kalinin AP, Kushlinskii NE: Vascular endothelium growth factor in the sera of patients with adrenal tumors. Bull Exp Biol Med; 2005 Aug;140(2):228-30
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  • [Title] Vascular endothelium growth factor in the sera of patients with adrenal tumors.
  • Serum levels of vascular endothelium growth factor were measured in 43 patients with adrenal tumors and 25 healthy subjects.
  • The mean blood levels of the factor in patients with adrenal tumors significantly surpassed the control.
  • The levels of this factor were maximum in patients with adrenocortical cancer, but its mean level differed negligibly from that in other morphological variants of tumors.
  • The level of vascular endothelium growth factor tended to increase with increasing the stage of adrenocortical cancer.
  • A direct correlation was revealed between the level of vascular endothelium growth factor and tumor size in adrenocortical cancer and aldosterone-producing adenoma.
  • Presumably, vascular endothelium growth factor is involved into mechanisms of growth, invasion, and metastatic growth of adrenocortical cancer.
  • [MeSH-major] Adrenal Gland Neoplasms / blood. Gene Expression Regulation, Neoplastic. Vascular Endothelial Growth Factor A / blood
  • [MeSH-minor] Adult. Aged. Case-Control Studies. Female. Humans. Male. Middle Aged. Neoplasm Metastasis

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  • (PMID = 16283008.001).
  • [ISSN] 0007-4888
  • [Journal-full-title] Bulletin of experimental biology and medicine
  • [ISO-abbreviation] Bull. Exp. Biol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A
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97. Schalin-Jäntti C: [Adrenal incidentaloma--a common dilemma]. Duodecim; 2010;126(9):1037-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Adrenal incidentaloma--a common dilemma].
  • An adrenal incidentaloma is an adrenal tumor larger than 1 cm, incidentally detected in imaging studies carried out for other reasons than adrenal disease.
  • The most frequent explanation is a benign, non-functional adenoma, other frequent diagnoses include cortisol- or aldosterone-secreting adenomas, pheochromocytoma, cortical carcinoma and metastatic lesions.
  • Hormonally active and potentially malignant incidentalomas should be surgically removed.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis
  • [MeSH-minor] Adenoma / diagnosis. Adenoma / surgery. Aldosterone / secretion. Humans. Hydrocortisone / secretion. Incidental Findings. Phenotype. Pheochromocytoma / diagnosis. Pheochromocytoma / surgery. Tomography, X-Ray Computed

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  • (PMID = 20593627.001).
  • [ISSN] 0012-7183
  • [Journal-full-title] Duodecim; lääketieteellinen aikakauskirja
  • [ISO-abbreviation] Duodecim
  • [Language] fin
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Finland
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone; WI4X0X7BPJ / Hydrocortisone
  • [Number-of-references] 21
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98. Jurczyńska J, Stepień T, Lawnicka H, Stepień H, Krupiński R, Kołomecki K, Kuzdak K, Komorowski J: Peripheral blood concentrations of vascular endothelial growth factor and its soluble receptors (R1 and R2) in patients with adrenal cortex tumours treated by surgery. Endokrynol Pol; 2009 Jan-Feb;60(1):9-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Peripheral blood concentrations of vascular endothelial growth factor and its soluble receptors (R1 and R2) in patients with adrenal cortex tumours treated by surgery.
  • INTRODUCTION: Neoangiogenesis appears to be an important event in tumour invasion and in the formation of metastases in many endocrine-related human cancers.
  • The aim of the study was to evaluate the plasma blood concentrations of VEGF, sVEGFR1, and sVEGFR2 in patients with benign and malignant adrenal tumours treated by surgery.
  • MATERIAL AND METHODS: We studied the blood before surgery of 41 patients with adrenal cortex tumours and 10 normal subjects without hormonal or CT/USG pathology of the adrenal glands (controls).
  • We studied the blood after adrenalectomy of 16 patients with tumours of the adrenal cortex.
  • VEGF blood concentrations before surgery did not differ in the patients with the cortical tumours as compared to the controls.
  • After surgery VEGF concentrations decreased among the patients, taken in total, with adrenal cortex tumours and cortical adenomas.
  • After surgery, sVEGFR1 concentrations decreased significantly in the group with cortical adenomas only.
  • CONCLUSIONS: Peripheral blood concentrations of VEGF and its receptors cannot be clinically valuable markers that discriminate between benign and malignant adrenocortical tumours before and after adrenalectomy.
  • [MeSH-major] Adrenal Gland Neoplasms / blood. Adrenal Gland Neoplasms / diagnosis. Biomarkers, Tumor / blood. Vascular Endothelial Growth Factor A / blood. Vascular Endothelial Growth Factor Receptor-1 / blood. Vascular Endothelial Growth Factor Receptor-2 / blood
  • [MeSH-minor] Adrenal Gland Diseases / blood. Adrenal Gland Diseases / diagnosis. Adrenalectomy. Adult. Aged. Diagnosis, Differential. Female. Humans. Male. Middle Aged

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  • (PMID = 19224499.001).
  • [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 / Biomarkers, Tumor; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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99. Caso J, Seigne J, Back M, Spiess PE, Pow-Sang J, Sexton WJ: Circumferential resection of the inferior vena cava for primary and recurrent malignant tumors. J Urol; 2009 Sep;182(3):887-93
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  • [Title] Circumferential resection of the inferior vena cava for primary and recurrent malignant tumors.
  • We explored the oncological effectiveness of inferior vena caval resection, as determined by margin status, cancer recurrence and survival.
  • Primary tumor type was renal cell carcinoma in 7 patients, metastatic testicular cancer in 5, leiomyosarcoma in 3, and adrenal cortical carcinoma, primary retroperitoneal germ cell tumor and upper tract transitional cell carcinoma in 1 each.
  • Data reviewed included preoperative and postoperative sequelae of inferior vena caval obstruction, postoperative complications, pathological results, cancer recurrence, graft requirements and functional outcomes.
  • Cancer recurred locally in 4 of 15 patients who underwent resection.
  • CONCLUSIONS: Local cancer control and potentially increased cancer specific survival can be achieved with successful complete circumferential resection of the inferior vena cava as a component of multimodality care in select patients with locally advanced malignancy.
  • [MeSH-major] Neoplasm Recurrence, Local / surgery. Vascular Neoplasms / surgery. Vena Cava, Inferior / surgery. Venous Insufficiency / surgery

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  • (PMID = 19616230.001).
  • [ISSN] 1527-3792
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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100. Terzolo M, Angeli A, Fassnacht M, Daffara F, Tauchmanova L, Conton PA, Rossetto R, Buci L, Sperone P, Grossrubatscher E, Reimondo G, Bollito E, Papotti M, Saeger W, Hahner S, Koschker AC, Arvat E, Ambrosi B, Loli P, Lombardi G, Mannelli M, Bruzzi P, Mantero F, Allolio B, Dogliotti L, Berruti A: Adjuvant mitotane treatment for adrenocortical carcinoma. N Engl J Med; 2007 Jun 7;356(23):2372-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adjuvant mitotane treatment for adrenocortical carcinoma.
  • BACKGROUND: Adrenocortical carcinoma is a rare neoplasm characterized by a high risk of recurrence after radical resection.
  • METHODS: We performed a retrospective analysis involving 177 patients with adrenocortical cancer who had undergone radical surgery at 8 centers in Italy and 47 centers in Germany between 1985 and 2005.
  • RESULTS: Baseline features in the mitotane group and the control group from Italy were similar; the German patients were significantly older (P=0.03) and had more stage I or II adrenocortical carcinomas (P=0.02) than did patients in the mitotane group.
  • CONCLUSIONS: Adjuvant mitotane may prolong recurrence-free survival in patients with radically resected adrenocortical carcinoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Adrenocortical Carcinoma / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Mitotane / therapeutic use
  • [MeSH-minor] Chemotherapy, Adjuvant. Humans. Multivariate Analysis. Neoplasm Recurrence, Local / epidemiology. Neoplasm Recurrence, Local / prevention & control. Retrospective Studies. Survival Analysis






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