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

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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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2. 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

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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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3. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • 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).
  • In patients with metastatic or progressive disease, medical treatment is started with mitotane that requires a close monitoring of its blood level.
  • Local treatment (radiofrequency, chemoembolization, and radiation therapy) can have some indications for metastatic disease.
  • In patients with disease progression cytotoxic chemotherapy can be used.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / therapy

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  • (PMID = 17395972.001).
  • [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; Review
  • [Publication-country] England
  • [Number-of-references] 127
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4. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

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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
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Cytotoxins; 78E4J5IB5J / Mitotane
  • [Other-IDs] NLM/ PMC2966201
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5. 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).
  • We demonstrate a high expression of IGF-IR in the two cell lines and in ACC.
  • Cell proliferation is stimulated by IGF-I in a dose- and time-dependent manner and is inhibited by RGZ.
  • In conclusion, our results suggest that RGZ exerts an inhibitory effect on human ACC cell proliferation by interfering with the PI3K/Akt and ERK1/2 signaling pathways downstream of the activated IGF-IR.

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  • (PMID = 18670617.001).
  • [ISSN] 1687-4757
  • [Journal-full-title] PPAR research
  • [ISO-abbreviation] PPAR Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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6. 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.
  • [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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7. Waalkes MP, Liu J, Ward JM, Diwan BA: Enhanced urinary bladder and liver carcinogenesis in male CD1 mice exposed to transplacental inorganic arsenic and postnatal diethylstilbestrol or tamoxifen. Toxicol Appl Pharmacol; 2006 Sep 15;215(3):295-305
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  • Arsenic alone increased hepatocellular carcinoma (14%), adenoma (23%) and total tumors (31%) compared to control (0, 2 and 2%, respectively).
  • Arsenic alone also increased lung adenocarcinoma, adrenal cortical adenoma and renal cystic tubular hyperplasia compared to control.
  • The treatments alone did not impact urinary bladder carcinogenesis, but arsenic plus TAM significantly increased formation of urinary bladder transitional cell tumors (papilloma and carcinoma; 13%) compared to control (0%).
  • Urinary bladder lesions and hepatocellular carcinoma induced by arsenic plus TAM and/or DES overexpressed estrogen receptor-alpha, indicating that aberrant estrogen signaling may have been a factor in the enhanced carcinogenic response.
  • Thus, in male CD1 mice, gestational arsenic exposure alone induced liver adenoma and carcinoma, lung adenocarcinoma, adrenal adenoma and renal cystic hyperplasia.

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  • (PMID = 16712894.001).
  • [ISSN] 0041-008X
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CO / N01-CO-12400; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Estrogens, Non-Steroidal; 0 / Selective Estrogen Receptor Modulators; 094ZI81Y45 / Tamoxifen; 731DCA35BT / Diethylstilbestrol; N712M78A8G / Arsenic
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8. Szabó D, Zsippai A, Bendes M, Tömböl Z, Szabó PM, Rácz K, Igaz P: [Pathogenesis of adrenocortical cancer]. Orv Hetil; 2010 Jul 18;151(29):1163-70
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  • [Title] [Pathogenesis of adrenocortical cancer].
  • [Transliterated title] A mellékvesekéreg-carcinoma molekuláris patogenezise.
  • Adrenocortical cancer is a rare tumor with poor prognosis.
  • The hereditary syndromes associated with adrenocortical cancer are: Li-Fraumeni's syndrome, Beckwith-Wiedemann's syndrome and familial adenomatous polyposis, whereas multiple endocrine neoplasia type 1, Carney's complex and McCune-Albright's syndrome mostly predispose to benign adrenocortical tumors.
  • Options for medical treatment of adrenocortical cancer are rather limited.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / metabolism
  • [MeSH-minor] Adenomatous Polyposis Coli / genetics. Beckwith-Wiedemann Syndrome / genetics. Carney Complex / genetics. Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / metabolism. Fibrous Dysplasia, Polyostotic / genetics. Gene Expression Regulation, Neoplastic. Genes, p53. Genetic Predisposition to Disease. Humans. Insulin-Like Growth Factor II / metabolism. Li-Fraumeni Syndrome / genetics. Multiple Endocrine Neoplasia Type 1 / genetics. Mutation. Proto-Oncogene Proteins / genetics. Signal Transduction. Up-Regulation. Wnt Proteins / metabolism. beta Catenin / metabolism

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  • (PMID = 20591784.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Wnt Proteins; 0 / beta Catenin; 67763-97-7 / Insulin-Like Growth Factor II
  • [Number-of-references] 37
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9. 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.
  • Particular attention is paid to the molecular oncogenesis of this disease, and the surgical and therapeutic options available for its cure.
  • [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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10. 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.
  • As shown in a previous report, mitotane/IR combination treatment induced a cell accumulation in the G2 phase.
  • Here, we report the radiosensitizing properties of mitotane in two different ACC cell lines.
  • Indeed, treatment with purvalanol, a cdc2-inhibitor prevents cell cycle arrest, triggering the G2/M transition.
  • The observation that mitotane and IR in combination treatment amplifies the activation level of cyclin B/cdc2 complexes contributing to cell cycle arrest, suggests that the MPF could function as a master signal for controlling the temporal order of different mitotic events.
  • [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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11. 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.
  • Biopsies should be performed only when metastatic disease is present and a primary tumor has not been clearly established.
  • The use of mitotane in patients without evidence of disease remains controversial.
  • Systemic chemotherapy is effective in patients with widely metastatic disease or as an adjunct to a surgical intervention and should focus on regimens that have been shown to effect responses; "novel targeted therapies" should not be employed as first-line treatment.
  • Finally, physicians caring for these patients need to recognize that Cushing's disease is a debilitating problem that should be managed aggressively; expecting chemotherapy to solve this complication is not appropriate.
  • [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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12. Patalano A, Brancato V, Mantero F: Adrenocortical cancer treatment. Horm Res; 2009 Jan;71 Suppl 1:99-104
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • Although most cases of ACC are of sporadic origin, they may also occur as part of a congenital or familial disease in which the genetic abnormalities are well established.
  • 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
  • [MeSH-minor] Algorithms. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Diagnostic Imaging / methods. Genetic Predisposition to Disease. Humans. Mitotane / administration & dosage. Prognosis. Streptozocin / administration & dosage. Syndrome

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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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13. Coli A, Di Giorgio A, Castri F, Destito C, Marin AW, Bigotti G: Sarcomatoid carcinoma of the adrenal gland: A case report and review of literature. Pathol Res Pract; 2010 Jan 15;206(1):59-65
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sarcomatoid carcinoma of the adrenal gland: A case report and review of literature.
  • Reports about adrenocortical carcinomas (AC) mixed with sarcomatous areas are very rare.
  • Herein, we report a case of sarcomatoid carcinoma of the adrenal gland in a 75-year-old woman who presented with left abdominal pain of one month's standing.
  • The results of abdominal ultrasonography and computed tomography (CT) showed the presence of a large heterogeneous adrenal mass.
  • Histologically, the neoplasm showed areas of adrenocortical carcinoma and areas of sarcomatoid spindle cell proliferation.
  • Twelve months after removal of the primary tumor, the patient died of her disease.
  • To the best of our knowledge, only seven cases of adrenal sarcomatoid carcinoma have been reported in the medical literature.
  • We review the reported cases according to the 2004 classification of the World Health Organization (WHO) of lung tumors, and highlight the histogenesis, diagnosis, and clinical course of this very aggressive tumor.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Carcinosarcoma / secondary. Liver Neoplasms / secondary

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  • [Copyright] Copyright 2009 Elsevier GmbH. All rights reserved.
  • (PMID = 19369012.001).
  • [ISSN] 1618-0631
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Neoplasm Proteins
  • [Number-of-references] 16
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14. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The TP53 codon 72 polymorphism and predisposition to adrenocortical cancer in Polish patients.
  • 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.
  • 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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15. Kvacheniuk AN: [Surgical treatment of adrenocortical cancer: significance of systematic lymphodissection]. Klin Khir; 2008 Mar;(3):34-7

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

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

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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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17. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • O, P'-DDD, MeSO2-DDE, or oil (control) was administered i. p., either simultaneously with cell injection at day 0 (mimicking adjuvant treatment), or at day 48 (established tumors).
  • 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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18. Matsuoka T, Morikage N, Kuga T, Nakayama T, Fujii Y: [Metastatic carcinoma of the adrenal gland from large cell neuroendocrine carcinoma; report of a case]. Kyobu Geka; 2005 Jun;58(6):499-503
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Metastatic carcinoma of the adrenal gland from large cell neuroendocrine carcinoma; report of a case].
  • A 69-year-old man had undertaken left upper lobectomy (ND 2 a) with partial resection of the left lower lobe under the diagnosis of a primary lung cancer, T2N0M0, stage IB in June, 2002.
  • The histopathological diagnosis was large cell neuroendocrine carcinoma (LCNEC), T3N0M0, stage IIB.
  • Abdominal computed tomography (CT) revealed an enhanced tumor in the left adrenal lesion, 3 cm in diameter, in October, 2003.
  • Although a prognosis of LCNEC is poor in general, we should consider the resection of metastatic carcinoma of the adrenal gland from LCNEC for long-term survival expectantly.
  • [MeSH-major] Adrenal Gland Neoplasms / secondary. Carcinoma, Large Cell / pathology. Carcinoma, Large Cell / secondary. Carcinoma, Neuroendocrine / pathology. Lung Neoplasms / pathology

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  • (PMID = 15957427.001).
  • [ISSN] 0021-5252
  • [Journal-full-title] Kyobu geka. The Japanese journal of thoracic surgery
  • [ISO-abbreviation] Kyobu Geka
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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19. Przybylik-Mazurek E, Darczuk A, Huszno B, Budzyński A, Rembiasz K, Gałazka K, Wierzchowski W, Giza A, Jurczak W, Skotnicki AB, Sztuk S, Urbanik A: [Primary adrenal lymphoma in incidentally discovered adrenal tumour]. Przegl Lek; 2006;63(8):701-5
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  • [Title] [Primary adrenal lymphoma in incidentally discovered adrenal tumour].
  • [Transliterated title] Pierwotny chłoniak w przypadkowo wykrytym guzie nadnercza.
  • The new imaging techniques used during the last several years: ultrasound, computed tomography and magnetic resonance imaging have improved detection of non-functional adrenal tumours s.c. "incidentaloma".
  • Incidence of adrenal incidentaloma is not very low.
  • In most of cases incidentaloma are benign and gave no clinical signs; however primary adrenal cortex cancer and metastases of different cancers are not uncommon.
  • The primary adrenal lymphoma is an extremely rare disease.
  • Most frequently both adrenal glands are affected and signs of adrenal insufficiency (despite weakness, fever and loss of weight) are present.
  • The diagnosis was made by histological examination and adjuvant chemotherapy was administrated.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis. Adrenal Gland Neoplasms / surgery. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Non-Hodgkin / diagnosis. Lymphoma, Non-Hodgkin / surgery

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  • (PMID = 17441388.001).
  • [ISSN] 0033-2240
  • [Journal-full-title] Przegla̧d lekarski
  • [ISO-abbreviation] Prz. Lek.
  • [Language] pol
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide
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20. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

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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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21. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • 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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22. Ferruzzi P, Ceni E, Tarocchi M, Grappone C, Milani S, Galli A, Fiorelli G, Serio M, Mannelli M: Thiazolidinediones inhibit growth and invasiveness of the human adrenocortical cancer cell line H295R. J Clin Endocrinol Metab; 2005 Mar;90(3):1332-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Thiazolidinediones inhibit growth and invasiveness of the human adrenocortical cancer cell line H295R.
  • In the present study, we evaluated PPARgamma mRNA and protein expression in tissue samples of human adrenocortical carcinomas (ACCs), normal adrenal glands, and the human ACC cell line H295R.
  • PPARgamma mRNA was expressed in six of eight ACC, two of three normal adrenal glands and the H295R cells.
  • Western blot analysis showed that TZDs increased the expression of the cell cycle inhibitors p21 and p27 and reduced the expression of cyclin D1.
  • These data suggest that TZDs reduce the malignant potential of the H295R ACC cell line and, therefore, might potentially constitute a novel tool in the medical treatment of human ACCs.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Hypoglycemic Agents / pharmacology. Thiazolidinediones / pharmacology
  • [MeSH-minor] Adrenal Glands / cytology. Adrenal Glands / pathology. Adult. Aged. Cell Division / drug effects. Cell Line, Tumor. Female. Humans. Matrix Metalloproteinase 2 / metabolism. Middle Aged. Neoplasm Invasiveness. PPAR gamma / genetics. PPAR gamma / metabolism. RNA, Messenger / analysis. Tumor Cells, Cultured

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  • (PMID = 15585569.001).
  • [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 / Hypoglycemic Agents; 0 / PPAR gamma; 0 / RNA, Messenger; 0 / Thiazolidinediones; 05V02F2KDG / rosiglitazone; EC 3.4.24.24 / Matrix Metalloproteinase 2; X4OV71U42S / pioglitazone
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23. Bertherat J, Bertagna X: Pathogenesis of adrenocortical cancer. Best Pract Res Clin Endocrinol Metab; 2009 Apr;23(2):261-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pathogenesis of adrenocortical cancer.
  • The study of the clonality of adrenocortical tumours (ACTs) has shown that adrenocortical cancers (ACCs) are of monoclonal origin.
  • Numerous chromosomal alterations have been observed in ACCs, and they are much more frequent than in adrenocortical adenomas.
  • This recent progress in the molecular genetics of ACC has led to the development of new molecular markers for the diagnosis of malignancy; these might also help to identify prognostic markers of ACC and may ultimately lead to novel therapeutic approaches.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology

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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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24. Abiven G, Coste J, Groussin L, Anract P, Tissier F, Legmann P, Dousset B, Bertagna X, Bertherat J: Clinical and biological features in the prognosis of adrenocortical cancer: poor outcome of cortisol-secreting tumors in a series of 202 consecutive patients. J Clin Endocrinol Metab; 2006 Jul;91(7):2650-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical and biological features in the prognosis of adrenocortical cancer: poor outcome of cortisol-secreting tumors in a series of 202 consecutive patients.
  • CONTEXT: Adrenocortical carcinomas (ACC) are rare tumors with a poor prognosis.
  • DESIGN AND SETTING: This study is a descriptive and multivariate analysis of a cohort from a single endocrinology center.
  • Mean age at diagnosis was 44 +/- 16 yr (range, 11-88 yr).
  • We found that 154 patients (76%) had hypersecreting tumors [mostly cortisol and androgens (47%), cortisol alone (27%), or androgens alone (6%)] and 43 patients (21%) had metastases at diagnosis.
  • Multivariate analysis identified the following independent prognostic factors associated with shorter survival: older age at diagnosis [hazard ratio (HR), 1.03; P < 0.0001], initial MacFarlane extension stages 3 (HR, 4.42; P = 0.005) and 4 (HR, 7.93; P < 0.0001), and cortisol hypersecretion (HR, 3.90; P < 0.0001).
  • [MeSH-major] Adrenal Cortex Neoplasms / secretion. Hydrocortisone / secretion

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  • (PMID = 16670169.001).
  • [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 / Androgens; 0 / Antineoplastic Agents, Hormonal; 78E4J5IB5J / Mitotane; WI4X0X7BPJ / Hydrocortisone
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25. Sudhakar MK, Kallarakkal JT, Damodharan J, Sahib K, Mahajan A, Kannan R: Sweet's syndrome preceding carcinoma of the adrenal cortex. J Indian Med Assoc; 2005 Aug;103(8):433-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sweet's syndrome preceding carcinoma of the adrenal cortex.
  • A case of Sweet's syndrome preceding carcinoma of the adrenal cortex is reported.
  • Sweet's syndrome can be a rare premalignant manifestation of carcinoma of adrenal cortex.
  • [MeSH-major] Adrenal Cortex Neoplasms / epidemiology. Sweet Syndrome / epidemiology

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  • (PMID = 16363199.001).
  • [ISSN] 0019-5847
  • [Journal-full-title] Journal of the Indian Medical Association
  • [ISO-abbreviation] J Indian Med Assoc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
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26. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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).
  • The median number was 4 in the eight patients, who remain in remission more than 51 months and 15.5 in the six patients, who have died from the disease within 44 months.
  • Moreover, all seven patients with less than 10 individual imbalances were in remission (median follow-up 72 months), while all but one patient with 10 and more individual imbalances (n = 7) have died from the disease (median survival time 30 months).
  • [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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27. Fulmer BR: Diagnosis and management of adrenal cortical carcinoma. Curr Urol Rep; 2007 Jan;8(1):77-82

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnosis and management of adrenal cortical carcinoma.
  • Adrenal cortical carcinoma is a relatively uncommon malignancy that represents a significant clinical challenge for the development of optimal treatment strategies.
  • Although the framework of a successful treatment paradigm still relies on these steps, advances in diagnostic imaging have led to increased accuracy in diagnosis, and advances in laparoscopic surgical technique have served to reduce morbidity for patients facing treatment.
  • This review focuses on a discussion of advances in modalities for the diagnosis and treatment of adrenal cortical carcinoma amenable to curative therapy.
  • Patients that present with metastatic or locally advanced disease generally are treated with mitotane-based chemotherapy with or without the addition of cytotoxic drugs.
  • Contemporary results of this treatment approach are presented in this review as well as a discussion of further directions for the treatment of patients with advanced disease.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / therapy. Adrenocortical Carcinoma / diagnosis. Adrenocortical Carcinoma / therapy

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  • (PMID = 17239320.001).
  • [ISSN] 1534-6285
  • [Journal-full-title] Current urology reports
  • [ISO-abbreviation] Curr Urol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 50
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28. Xiao ZJ, Li CL: [Combined therapy of advanced adrenal cortical adenocarcinoma]. Zhonghua Yi Xue Za Zhi; 2010 Aug 10;90(30):2123-5

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  • [Title] [Combined therapy of advanced adrenal cortical adenocarcinoma].
  • OBJECTIVE: To analyze the clinical efficacy of combined therapy in the treatment of advanced adrenal cortical adenocarcinoma.
  • METHODS: The clinical data of 12 cases with advanced adrenal cortical adenocarcinoma at our hospital from 1986 - 2006 were analyzed.
  • Pathological diagnosis was all of adrenal cortical adenocarcinoma.
  • According to evaluation criterion of chemotherapeutic effect by WHO in 1987, the results were: CR (complete remission) (n = 0), PR (partial remission) (n = 7), SD (stable disease) (n = 3) and PD (progressive disease) (n = 2).
  • CONCLUSION: Combined therapy of adrenal cortical adenocarcinoma is effective to prolong the patient lifespan.
  • Making an early diagnosis and offering a novel therapy yield a better outcome.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenal Cortex Neoplasms / therapy. Adrenocortical Carcinoma / pathology. Adrenocortical Carcinoma / therapy

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  • (PMID = 21029628.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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29. 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.
  • 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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30. Gonzalez RJ, Shapiro S, Sarlis N, Vassilopoulou-Sellin R, Perrier ND, Evans DB, Lee JE: Laparoscopic resection of adrenal cortical carcinoma: a cautionary note. Surgery; 2005 Dec;138(6):1078-85; discussion 1085-6
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  • [Title] Laparoscopic resection of adrenal cortical carcinoma: a cautionary note.
  • BACKGROUND: While laparoscopic removal of small, benign, functioning adrenal tumors is accepted, laparoscopic resection of adrenal tumors that may be adrenal cortical carcinoma (ACC) remains controversial.
  • Open adrenalectomy remains the standard of care for patients presenting with an adrenal cortical tumor for which ACC is in the differential diagnosis.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenalectomy. Carcinoma / surgery. Laparoscopy. Neoplasm Recurrence, Local / epidemiology

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  • (PMID = 16360394.001).
  • [ISSN] 0039-6060
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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31. Li SH, Huang CH, Ko SF, Chou FF, Huang SC: Extended survival in a patient with recurrent and metastatic adrenal cortical carcinoma by aggressive transarterial embolization--a case report. J Surg Oncol; 2005 May 1;90(2):101-5
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  • [Title] Extended survival in a patient with recurrent and metastatic adrenal cortical carcinoma by aggressive transarterial embolization--a case report.
  • The prognosis of inoperable recurrent or metastatic adrenal cortical carcinoma is poor due to lack of effective treatment modalities.
  • We report a case of recurrent and metastatic adrenal cortical carcinoma in which prolonged survival of 58 months was achieved with aggressive three sequential transarterial embolization.
  • A 60-year-old man received operation for left adrenal cortical carcinoma.
  • Aggressive transarterial embolization seems to be a safe and effective procedure for symptoms relief, and may prolong survival in the management of inoperable adrenal cortical carcinoma.
  • It can be considered in any patient with inoperable adrenal cortical carcinoma if not contraindicated.
  • [MeSH-major] Adrenal Cortex Neoplasms / therapy. Adrenocortical Carcinoma / therapy. Embolization, Therapeutic. Liver Neoplasms / secondary. Neoplasm Recurrence, Local / therapy. Splenic Neoplasms / secondary

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  • (PMID = 15844181.001).
  • [ISSN] 0022-4790
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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32. 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.
  • 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

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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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33. 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].
  • [Transliterated title] Rozsiany rak kory nadnercza.
  • 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.
  • Most of the carcinomas (60%) are functional and usually the first manifestation is Cushing's syndrome with virilization.
  • 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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34. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • Integrity of BMP-dependent pathways in these cell lines could be shown by activation of the Smad1/5/8 pathway with subsequent increase of ID protein expression upon incubation with BMP2 or BMP5.
  • On a functional level, BMP treatment resulted in inhibition of cell proliferation and viability in a dose- and time-dependent manner.
  • 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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35. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

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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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36. Capone G, Della Pepa GM, Sabatino G, Bartoccioni E, Albanese A, Mannino S, Maira G: A rare bone-leptomeningeal metastasis from an adrenal cortical carcinoma. J Clin Neurosci; 2009 Jul;16(7):977-80
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  • [Title] A rare bone-leptomeningeal metastasis from an adrenal cortical carcinoma.
  • We report a rare bone-leptomeningeal metastasis from an adrenal cortical carcinoma (ACC).
  • Thus, the patient underwent excision of the mass; histopathological diagnosis confirmed that it was an ACC metastasis.
  • At post-operative follow-up, the patient was in a good neurological condition with no radiological evidence of a cranial recurrence; however, there was a voluminous abdominal regrowth of the primary tumor.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Bone Neoplasms / secondary. Meningeal Carcinomatosis / secondary

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  • (PMID = 19375918.001).
  • [ISSN] 0967-5868
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Scotland
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37. 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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  • [Cites] N Engl J Med. 2007 Jun 7;356(23):2372-80 [17554118.001]
  • [Cites] Endocr Relat Cancer. 2007 Mar;14(1):13-28 [17395972.001]
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  • [Cites] Surgery. 2003 Dec;134(6):874-80; discussion 880 [14668717.001]
  • (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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38. Feng YC, Yang ZG, Chen TW, Su XY, Deng W, Wang QL: Adrenal sarcomatoid carcinoma: a rare case depicted on multi-detector row computed tomography. Indian J Med Sci; 2010 Jan;64(1):37-40
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  • [Title] Adrenal sarcomatoid carcinoma: a rare case depicted on multi-detector row computed tomography.
  • Primary adrenal sarcomatoid carcinoma is rare malignant tumor with the characteristics of carcinoma and sarcoma.
  • To date, only one case of primary sarcomatoid carcinoma in the adrenal gland was reported.
  • We present here computed tomography appearance and pathological features of the case with primary adrenal sarcomatoid carcinoma confirmed by pathology.
  • [MeSH-major] Adrenal Gland Neoplasms / radiography. Carcinosarcoma / radiography. Multidetector Computed Tomography / methods. Radiographic Image Enhancement

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  • (PMID = 22301808.001).
  • [ISSN] 1998-3654
  • [Journal-full-title] Indian journal of medical sciences
  • [ISO-abbreviation] Indian J Med Sci
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Contrast Media
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39. 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.
  • Removal of the adrenocortical tumor with part of the transverse colon and tail of the pancreas, spleen and kidney was successfully performed following chemotherapy.
  • 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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40. Sturgeon C, Shen WT, Clark OH, Duh QY, Kebebew E: Risk assessment in 457 adrenal cortical carcinomas: how much does tumor size predict the likelihood of malignancy? J Am Coll Surg; 2006 Mar;202(3):423-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Risk assessment in 457 adrenal cortical carcinomas: how much does tumor size predict the likelihood of malignancy?
  • STUDY DESIGN: Adrenocortical carcinomas (ACC) recorded in the Surveillance, Epidemiology, and End Results (SEER) database (1988 to 2000) were compared with benign functional or nonfunctional adrenal cortical adenomas (excluding aldosteronomas) operated on at our institution between January 1, 1993, and July 1, 2003.
  • RESULTS: We identified 457 patients with ACC and 47 patients with adrenal cortical adenomas; 376 and 44 neoplasms, respectively, had tumor size data available.
  • For ACC presenting with local disease, the sensitivity, specificity, and likelihood ratios of tumor size to predict malignancy were 96%, 52%, and 2.0, respectively, for tumors > or = 4 cm; 90%, 80%, and 4.4 for tumors > or = 6 cm; 77%, 95%, and 16.9 for tumors > or = 8 cm; and 55%, 98%, and 24.4 for tumors > or = 10 cm.
  • Assuming a pretest probability of malignancy of 5%, the likelihood ratios derived from this study yield a posttest probability of 10%, 19%, and 47% for cancer in adrenal cortical tumors > or = 4 cm, > or = 6 cm, and > or = 8 cm, respectively.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Diagnosis, Differential. Female. Humans. Infant. Infant, Newborn. Male. Middle Aged. Neoplasm Staging. Prevalence. Probability. Prognosis. Retrospective Studies. Risk Assessment. SEER Program / statistics & numerical data. Severity of Illness Index

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  • (PMID = 16500246.001).
  • [ISSN] 1072-7515
  • [Journal-full-title] Journal of the American College of Surgeons
  • [ISO-abbreviation] J. Am. Coll. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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41. Soga H, Takenaka A, Ooba T, Nakano Y, Miyake H, Takeda M, Tanaka K, Hara I, Fujisawa M: A twelve-year experience with adrenal cortical carcinoma in a single institution: long-term survival after surgical treatment and transcatheter arterial embolization. Urol Int; 2009;82(2):222-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A twelve-year experience with adrenal cortical carcinoma in a single institution: long-term survival after surgical treatment and transcatheter arterial embolization.
  • INTRODUCTION: We retrospectively analyzed 6 cases of adrenal cortical carcinoma (ACC) treated during a 12-year period at a single institution.
  • The mean age at diagnosis was 53.3 years (range 36-72).
  • [MeSH-major] Adrenal Cortex Neoplasms / therapy. Adrenalectomy. Adrenocortical Carcinoma / therapy. Chemoembolization, Therapeutic

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19322014.001).
  • [ISSN] 1423-0399
  • [Journal-full-title] Urologia internationalis
  • [ISO-abbreviation] Urol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
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42. 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.
  • Cell growth as measured by the MTT and 5-bromo-2'-deoxyuridine incorporation assays is inhibited, and cell cycle analysis has revealed a slight induction of apoptosis.
  • [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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43. Ishida M, Yoshida K, Miyamoto K, Iwai M, Miyahira Y, Kushima R, Okabe H: Cytological features of myxoid adrenocortical adenoma with a pseudoglandular component: a case report with differential diagnostic considerations. Diagn Cytopathol; 2008 Aug;36(8):576-80

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytological features of myxoid adrenocortical adenoma with a pseudoglandular component: a case report with differential diagnostic considerations.
  • Myxoid adrenocortical tumors are extremely rare neoplasms with only nine adenomas and eleven carcinomas reported in the literature.
  • They occasionally have a pseudoglandular component resembling metastatic mucinous adenocarcinoma in the adrenal gland.
  • We report here the first cytopathological study of a myxoid adrenocortical adenoma with a pseudoglandular component, contributing especially to the differential diagnosis from metastatic mucinous adenocarcinoma.
  • Two major cytopathological features distinguishing myxoid adrenocortical adenoma from metastatic mucinous adenocarcinoma in the adrenal gland are:.
  • Careful observation of these cytological features and positive immunoreactivity to Melan A, alpha-inhibin and synaptophysin can lead to the correct diagnosis.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / diagnosis. Adrenocortical Adenoma / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Diagnosis, Differential. Female. Humans. Male. Middle Aged

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  • (PMID = 18618725.001).
  • [ISSN] 1097-0339
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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44. Lacroix A: Approach to the patient with adrenocortical carcinoma. J Clin Endocrinol Metab; 2010 Nov;95(11):4812-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • 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.
  • Some retrospective studies indicate that adjuvant mitotane therapy prolongs disease-free survival, leading several centers to recommend its administration; prospective studies are under way to provide future evidence-based recommendations.
  • For metastatic disease, combination chemotherapy should be administered, if possible, in the context of multicenter collaborative research protocols.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenocortical Carcinoma / surgery
  • [MeSH-minor] Disease Progression. Female. Humans. Prognosis. Treatment Outcome. Young Adult

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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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45. Abbasova SG, Vysotskii MM, Ovchinnikova LK, Obusheva MN, Digaeva MA, Britvin TA, Bahoeva KA, Karabekova ZK, Kazantzeva IA, Mamedov UR, Manuchin IB, Davidov MI: Cancer and soluble FAS. Bull Exp Biol Med; 2009 Oct;148(4):638-42
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  • [Title] Cancer and soluble FAS.
  • A test system developed by the authors was used to measure serum concentrations of soluble Fas in patients with malignant and benign tumors of different location and morphology.
  • Relationships between soluble Fas levels and the main clinical and morphological characteristics of cancer were evaluated.
  • No appreciable differences in the concentrations of soluble Fas were detected in malignant and benign tumors of the mammary gland, bones, ovaries, and adrenals.
  • In thyroid cancer, soluble Fas levels were higher than in benign and hyperplastic processes in this organ.
  • High level of soluble Fas is associated with late stages of the disease (ovarian cancer, cancer of the corpus uteri, adrenocortical and colorectal cancer) and with poor differentiation of the tumor (ovarian cancer and cancer of the corpus uteri), with local metastases (colorectal and adrenocortical cancer), and with tumor invasion into the myometrial tissue, intestinal wall, and adjacent tissues (cancer of the corpus uteri and colorectal cancer).
  • A significantly high level of soluble Fas was detected in colorectal and adrenocortical cancer in the presence of at least 2 local metastases.
  • Soluble Fas levels depended on tumor histogenesis in malignant and benign ovarian tumors.
  • High concentration of soluble Fas was detected in large tumors in patients with ovarian cancer, cancer of the corpus uteri, colorectal cancer, thyroid cancer and adenoma, and in adrenocortical cancer.
  • The overall 5-year survival of patients with low levels of soluble Fas is better in osteosarcoma, cancer of the corpus uteri, ovarian and adrenocortical cancer.

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  • (PMID = 20396760.001).
  • [ISSN] 1573-8221
  • [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 / Antigens, CD95
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46. Tadjine M, Lampron A, Ouadi L, Bourdeau I: Frequent mutations of beta-catenin gene in sporadic secreting adrenocortical adenomas. Clin Endocrinol (Oxf); 2008 Feb;68(2):264-70

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

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  • (PMID = 17854394.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / beta Catenin
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47. 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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48. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of the zinc-finger transcription factor Snail in adrenocortical carcinoma is associated with decreased survival.
  • In this study, we evaluate whether Snail is expressed in adrenocortical cancer (ACC) and if its expression is related to patient outcome.
  • Snail expression was neither detected in normal adrenocortical tissue, nor in benign adrenocortical adenomas.
  • Survival rates were significantly decreased in Snail-positive tumours compared to Snail-negative tumours: 10 out of 16 vs one out of eight patients succumbed to disease after a median follow up of 14.5 and 28.5 months, respectively (P=0.03).
  • Patients with Snail-expressing ACCs presented in advanced disease (11 out of 12 vs 6 out of 14, P=0.01) and tend to develop distant metastases more frequently than patients with negative staining (7 out of 11 vs two out of eight, P=0.19).
  • Furthermore, Snail expression is associated with decreased survival, advanced disease and higher risk of developing distant metastases.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenocortical Carcinoma / metabolism. Biomarkers, Tumor / analysis. Transcription Factors / biosynthesis

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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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49. Miller BS, Ammori JB, Gauger PG, Broome JT, Hammer GD, Doherty GM: Laparoscopic resection is inappropriate in patients with known or suspected adrenocortical carcinoma. World J Surg; 2010 Jun;34(6):1380-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Laparoscopic resection is inappropriate in patients with known or suspected adrenocortical carcinoma.
  • BACKGROUND: Complete surgical resection is the mainstay of treatment for patients with adrenocortical cancer (ACC).
  • Seventeen patients underwent laparoscopic adrenalectomy (LA).
  • Median tumor size of those who underwent LA was 7.0 (range, 4-14) cm versus 12.3 (range, 5-27) cm for OR.
  • Recurrent disease in the laparoscopic group occurred in 63% versus 65% in the open group.
  • Mean time to first recurrence for those who underwent LA was 9.6 months (+/-14) versus 19.2 months (+/-37.5) in the open group (p < 0.005).
  • Fifty percent of patients who underwent LA had positive margins or notation of intraoperative tumor spill versus 18% of those who underwent OR (p = 0.01).
  • CONCLUSIONS: ACC continues to be a deadly disease, and little to no progress has been made from a treatment standpoint in the past 20 years.
  • Although feasible in many cases and tempting, laparoscopic resection should not be attempted in patients with tumors suspicious for or known to be adrenocortical carcinoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenocortical Carcinoma / surgery. Laparoscopy / contraindications

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  • (PMID = 20372905.001).
  • [ISSN] 1432-2323
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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50. Bertagna X, Groussin L, Libe R, Bertherat J: [Adrenal cortical carcinoma: advances in the pathophysiology and management of this malignancy]. Bull Acad Natl Med; 2008 Jan;192(1):87-102; discussion 102-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Adrenal cortical carcinoma: advances in the pathophysiology and management of this malignancy].
  • [Transliterated title] Le corticosurrénalome: progrès dans la physiopathologie et la prise en charge d'un cancer rare.
  • Adrenal cortical carcinoma is a rare malignancy, with only one or two new cases being diagnosed per million subjects per year.
  • Most often, however, the diagnosis is made when the tumor is already invasive and non secretory Clinical, hormonal and imaging features, including 18-fluorodeoxyglucose PET scan, can provide strong evidence of malignancy and indicate open surgical excision in expert hands.
  • Recent advances in the genetics of adrenal cortical carcinomas have identified molecular factors that can be used as diagnostic and prognostic markers.
  • [MeSH-major] Adrenal Cortex Neoplasms / therapy. Carcinoma / therapy

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  • (PMID = 18663984.001).
  • [ISSN] 0001-4079
  • [Journal-full-title] Bulletin de l'Académie nationale de médecine
  • [ISO-abbreviation] Bull. Acad. Natl. Med.
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 30
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51. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of telomere length maintenance mechanisms in adrenocortical carcinoma.
  • CONTEXT: Adrenocortical cancer (ACC) is a rare disease with an often fatal outcome.
  • The clinical and pathological diagnosis of a malignant vs. benign adrenocortical tumor is sometimes challenging.
  • Telomere maintenance mechanisms (TMMs) are critical for the persistence of the malignant phenotype, but little is known about these mechanisms or their diagnostic value in adrenocortical lesions.
  • OBJECTIVE: Tissue samples of diagnostically known adrenocortical neoplasms were evaluated for parameters of known TMMs, telomerase activity (TA), and alternative telomere lengthening (ALT).
  • DESIGN: The study analyzed retrospectively collected frozen adrenocortical tissue samples from the University of Michigan Health System.
  • PATIENT SAMPLES: Samples included 24 ACCs, 11 adrenocortical adenomas (ACAs), and three normal adrenal tissues.
  • 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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52. Zardi EM, Santini D, Vincenzi B, Galati G, Tonini G, Zobel BB, Afeltra A: Surgical complications after resection of adrenal carcinoma. J Exp Clin Cancer Res; 2006 Sep;25(3):449-51
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  • [Title] Surgical complications after resection of adrenal carcinoma.
  • Sonographic and tomographic examinations showed the presence of a large adrenal gland tumor and the promptly performed adrenalectomy and splenectomy proved that the lesion was an adrenal gland carcinoma infiltrating the spleen.
  • One month after surgical treatment, the patient's general condition dramatically worsened due to development of perirenal abscess and renal infarction; finally, the patient died.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenocortical Carcinoma / surgery. Postoperative Complications / surgery

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  • (PMID = 17167987.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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53. Leboulleux S, Deandreis D, Al Ghuzlan A, Aupérin A, Goéré D, Dromain C, Elias D, Caillou B, Travagli JP, De Baere T, Lumbroso J, Young J, Schlumberger M, Baudin E: Adrenocortical carcinoma: is the surgical approach a risk factor of peritoneal carcinomatosis? Eur J Endocrinol; 2010 Jun;162(6):1147-53
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  • [Title] Adrenocortical carcinoma: is the surgical approach a risk factor of peritoneal carcinomatosis?
  • CONTEXT: Peritoneal carcinomatosis (PC) is a rare site of distant metastases in patients with adrenocortical cancer (ACC).
  • One preliminary study suggests an increased risk of PC after laparoscopic adrenalectomy (LA) for ACC.
  • Patients had stage I disease in 2 cases, stage II disease in 32 cases, stage III disease in 7 cases, stage IV disease in 21 cases, and unknown stage disease in 2 cases.
  • It was present at initial diagnosis in three cases and occurred during follow-up in 15 cases.
  • The only risk factor of PC occurring during follow-up was the surgical approach with a 4-year rate of PC of 67% (95% confidence interval (CI), 30-90%) for LA and 27% (95% CI, 15-44%) for open adrenalectomy (P=0.016).
  • CONCLUSION: We found an increased risk of PC after LA for ACC.

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  • (PMID = 20348273.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
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54. 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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  • [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


55. 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.
  • A recently used technique for the isolation of this cell population is through exclusion of the vital dye Hoechst 33342, which defines the so-called side population (SP).
  • 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.
  • Furthermore, re-sorting and tracing experiments revealed the capacity for both cell types to give rise to the original SP- and non-SP-containing cell population.
  • 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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56. 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).
  • Of the 3 patients who are alive at the time of report, 1 patient has been without disease for 16 months, and 2 patients have progressive disease.
  • All patients had recurrent metastatic disease (2 to 9 times).
  • [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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57. 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.
  • 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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58. 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.
  • Moreover, recent evidence has suggested that TZDs might have favorable effects in the treatment of a variety of tumors as differentiation-inducing agents.
  • 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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59. Turner DJ, Miskulin J: Management of adrenal lesions. Curr Opin Oncol; 2009 Jan;21(1):34-40
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  • [Title] Management of adrenal lesions.
  • PURPOSE OF REVIEW: Adrenal lesions are commonly seen on modern imaging modalities, and although the majority are benign, potentially lethal entities necessitate exclusion.
  • The purpose of this review is to summarize recent advances in diagnosis and therapies for adrenal lesions.
  • RECENT FINDINGS: New tumor markers and genetic risk factors continue to be discovered, and improved diagnostic techniques have made adrenal incidentalomas more common than ever before.
  • Laparoscopic approaches for adrenal lesions continue to evolve for functional lesions, and also for lesions 12 cm and larger.
  • Open adrenalectomy continues to be the most appropriate for adrenocortical cancer.
  • SUMMARY: All adrenal lesions should prompt a functional hormonal assessment and additional imaging to determine malignancy employed.
  • [MeSH-major] Adrenal Gland Diseases / diagnosis. Adrenal Gland Diseases / surgery. Adrenal Gland Neoplasms / diagnosis. Adrenal Gland Neoplasms / surgery

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  • (PMID = 19125016.001).
  • [ISSN] 1531-703X
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 41
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60. 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.
  • Histopathology is crucial for the diagnosis of malignancy and may also provide important prognostic information.
  • Surgery also plays a role in local tumor recurrence and metastatic disease.
  • In advanced disease, the most promising therapeutic options (etoposide, doxorubicin, cisplatin plus mitotane, and streptozotocin plus mitotane) are currently being compared in an international phase III trial (www.firm-act.org).
  • 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

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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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61. Bovio S, Porpiglia F, Bollito E, Allasino B, Reimondo G, Rovero E, Perazzolo L, Angeli A, Papotti M, Terzolo M: Adrenal pseudocyst mimicking cancer: a case report. J Endocrinol Invest; 2007 Mar;30(3):256-8
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  • [Title] Adrenal pseudocyst mimicking cancer: a case report.
  • Adrenal cysts are infrequently observed, since less than 500 cases have been reported in Western literature.
  • Adrenal cysts are conventionally divided into four categories: epithelial, parasitic, endothelial, and hemorrhagic.
  • We report herein the case of an adrenal hemorrhagic pseudocyst that simulated adrenocortical cancer and argue on the clinical clues for a differential diagnosis with other adrenal tumors.
  • [MeSH-major] Adrenal Gland Diseases / diagnosis. Adrenal Gland Neoplasms / diagnosis. Cysts / diagnosis
  • [MeSH-minor] Adrenal Glands / pathology. Adrenal Glands / surgery. Aged. Diagnosis, Differential. Female. Humans

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  • (PMID = 17505162.001).
  • [ISSN] 1720-8386
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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62. Paton BL, Novitsky YW, Zerey M, Harrell AG, Norton HJ, Asbun H, Kercher KW, Heniford BT: Outcomes of adrenal cortical carcinoma in the United States. Surgery; 2006 Dec;140(6):914-20; discussion 919-20
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  • [Title] Outcomes of adrenal cortical carcinoma in the United States.
  • BACKGROUND: Improvements in the sensitivity of radiographic imaging have lead to an increase in the number of adrenal masses diagnosed.
  • The purpose of this study is to determine if technologic advancements have resulted in the diagnosis of earlier-staged adrenal cortical cancer (ACC) and to determine if the survival of patients with ACC has improved over the past 15 years.
  • Two hundred thirty-eight (39.5%) patients presented with localized disease (stages I and II), and 311 (52%) patients presented with advanced disease (stages III and IV).
  • Patients with masses less than 5 cm were statistically more likely to have localized disease (P <. 001).
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / pathology. Neoplasm Staging. SEER Program / statistics & numerical data
  • [MeSH-minor] Adrenal Glands / pathology. Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Prognosis. Survival Rate. United States / epidemiology

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  • (PMID = 17188138.001).
  • [ISSN] 0039-6060
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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63. Meyer A, Behrend M: State of the art management of adrenal masses--"how to do it?". Eur J Med Res; 2006 Sep 29;11(9):397-404
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  • [Title] State of the art management of adrenal masses--"how to do it?".
  • By the frequent use of computed tomography or ultrasound the detection of incidentally found adrenal tumours has become a common problem.
  • Most incidentally-found adrenal tumours are benign non-functioning cortical adenomas.
  • But benign functioning tumours producing aldosterone, cortisol or catecholamines, adrenocortical carcinoma or adrenal gland metastasis can also be found.
  • Surgical therapy is always indicated in case of hormonal overproduction or in case of suspected adrenocortical carcinoma; in all other cases the correct and adequate therapeutic approach is still under debate and a controversial topic of discussion.
  • This review deals with the different forms of adrenal tumours regarding the optimal diagnostic and therapeutic approach to give physicians an easy-to-follow guideline.
  • [MeSH-major] Adrenal Gland Neoplasms / therapy

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  • (PMID = 17101464.001).
  • [ISSN] 0949-2321
  • [Journal-full-title] European journal of medical research
  • [ISO-abbreviation] Eur. J. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 50
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64. 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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65. D'Antonio A, Caleo A, Caleo O, De Dominicis G, Boscaino A: Monotypic epithelioid angiomyolipoma of the adrenal gland: an unusual site for a rare extrarenal tumor. Ann Diagn Pathol; 2009 Oct;13(5):347-50
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  • [Title] Monotypic epithelioid angiomyolipoma of the adrenal gland: an unusual site for a rare extrarenal tumor.
  • Epithelioid angiomyolipoma (AML) is an uncommon renal mesenchymal tumor with malignant potential and is frequently associated with tuberous sclerosis.
  • Extrarenal AMLs are rare, and to the best of our knowledge, this is the first reported case of a primary monotypic epithelioid AML of adrenal gland in a patient without evidence of tuberous sclerosis.
  • The patient is a 42-year old man who presented with retroperitoneal hemorrhage resulting from spontaneous rupture of adrenal mass.
  • Differential diagnosis from renal cell carcinoma, adrenal gland carcinoma, and metastatic carcinoma is often challenging because of its epithelioid morphology.
  • Because primary and secondary malignant tumors are much more common and aggressive neoplasms, establishing the correct diagnosis has important therapeutic and prognostic implications.
  • [MeSH-major] Adrenal Gland Neoplasms / pathology. Angiomyolipoma / pathology
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adrenalectomy. Adult. Biomarkers, Tumor / analysis. Carcinoma, Renal Cell / diagnosis. Diagnosis, Differential. Disease-Free Survival. Epithelioid Cells / chemistry. Epithelioid Cells / pathology. Hemorrhage / etiology. Hemorrhage / pathology. Humans. Male. Neoplasm Metastasis. Nephrectomy. Retroperitoneal Space / pathology. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 19751913.001).
  • [ISSN] 1532-8198
  • [Journal-full-title] Annals of diagnostic pathology
  • [ISO-abbreviation] Ann Diagn Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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66. Lee JA, Duh QY: Reoperation for adrenocortical neoplasms. Curr Treat Options Oncol; 2006 Jul;7(4):320-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reoperation for adrenocortical neoplasms.
  • Adrenocortical cancer is a highly lethal malignancy.
  • Surgical resection remains the only potential modality for cure or appreciable disease-free intervals.
  • Even with radical resection, most patients will recur or have metastatic disease.
  • For these patients, surgical re-resection of local recurrence and metastases is the best chance of controlling disease and prolonging survival.
  • 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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67. 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 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.
  • RESULTS: TP53 mutations were detected in 33% of the tumors, and VNTR1 LOH was present in 44% of the cases and did not always correlate with the presence of a TP53 mutation.
  • 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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68. 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.
  • Also the management of this condition is largely empirical, and data are insufficient to indicate the superiority of a surgical or non-surgical approach to managing patients with subclinical Cushing's syndrome.
  • [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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69. Bertherat J, Gimenez-Roqueplo AP: New insights in the genetics of adrenocortical tumors, pheochromocytomas and paragangliomas. Horm Metab Res; 2005 Jun;37(6):384-90
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  • [Title] New insights in the genetics of adrenocortical tumors, pheochromocytomas and paragangliomas.
  • Recent advances in the molecular genetic of adrenal tumors give new insights in the pathophysiology of these neoplasms in both hereditary and sporadic cases.
  • The practice of genetic counselling in patients with adrenal tumors have been recently changed by the identification and the understanding of new specific hereditary cancer susceptibility syndromes.
  • In the case of sporadic adrenocortical tumors these progress also offer new prognosis predictors.
  • The genetic predisposition to adrenocortical cancer in children has been well established in the Li-Fraumeni and Beckewith-Wiedeman syndromes due to germline p53 mutation located at 17p13 and dysregulation of the imprinted IGF-2 locus at 11p15, respectively.
  • Adrenocortical tumors are also observed in Multiple Endocrine Neoplasia type I syndrome.
  • Cushing's syndrome due to primary pigmented nodular adrenocortical disease have been observed in patients with germline PRKAR1A inactivating mutations.
  • Interestingly allelic loss at 17p13 and 11p15 have been observed in sporadic adrenocortical cancer and somatic PRKAR1A mutations in secreting adrenocortical adenomas.
  • The potential interest of these finding for the diagnosis of these tumors will be discussed.
  • Up to date, four diagnosis of familal disease (multiple endocrine neoplasia type II, von Hippel Lindau disease, neurofibromatosis type 1 and hereditary paraganglioma) should be discussed and causative mutations in six different phaechomocytoma susceptibility genes (RET, VHL, NF1, SDHB, SDHD, SDHC) could be identified.
  • We will suggest guidelines for the practice of the phaeochomocytoma genetic testing in the patients and their families, and for an early detection of tumors in the patients or in individuals determined to be at-risk of disease by the presymptomatic genetic testing.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Gene Expression Regulation, Neoplastic / genetics. Paraganglioma / genetics. Pheochromocytoma / genetics

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  • (PMID = 16001332.001).
  • [ISSN] 0018-5043
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Number-of-references] 53
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70. Ren R, Guo M, Sneige N, Moran CA, Gong Y: Fine-needle aspiration of adrenal cortical carcinoma: cytologic spectrum and diagnostic challenges. Am J Clin Pathol; 2006 Sep;126(3):389-98

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fine-needle aspiration of adrenal cortical carcinoma: cytologic spectrum and diagnostic challenges.
  • We reviewed the cytologic features of 20 adrenal cortical carcinomas (ACCs; 9 primary and 11 metastatic) from 19 patients and highlighted diagnostic pitfalls.
  • Primary and metastatic ACCs were cytologically similar and showed a wide range of features varying from well-differentiated tumor resembling a benign cortical lesion or low-grade neuroendocrine tumor to poorly differentiated pleomorphic tumor mimicking poorly differentiated carcinoma, melanoma, or high-grade sarcoma.
  • Cytologic, immunophenotypic, and ultrastructural findings should be correlated with clinical and radiologic information for achieving a proper cytologic diagnosis.
  • [MeSH-major] Adrenal Cortex / pathology. Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology

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  • (PMID = 16880150.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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71. 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.
  • In addition, since RGZ can reduce ACTH and corticosterone secretion in mouse corticotropic pituitary tumors, both RGZ and PIO have been used in the treatment of Cushing's disease with variable but generally unsatisfactory results.
  • [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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72. Nishikawa T, Saito J, Omura M: [Medical treatment for Cushing's syndrome]. Nihon Rinsho; 2008 Jan;66(1):186-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • It is well known that the development of the microvascular disease of various organs such as the heart and kidney, in patients with diabetes mellitus, hyperlipidemia and hypertension of which disorders are frequently associated with Cushing's syndrome.
  • 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.
  • 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.
  • Metyrapone is also recommended to treat the patients who are not well differentiated Cushing's disease from ectopic ACTH syndrome.
  • 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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73. Lin J, Wasco MJ, Korobkin M, Doherty G, Giordano TJ: Leiomyoma of the adrenal gland presenting as a non-functioning adrenal incidentaloma: case report and review of the literature. Endocr Pathol; 2007;18(4):239-43
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  • [Title] Leiomyoma of the adrenal gland presenting as a non-functioning adrenal incidentaloma: case report and review of the literature.
  • A 31-year-old woman was incidentally found to have a large right adrenal mass by computed tomography imaging and underwent a workup that included endocrinological evaluation and positron emission tomography imaging.
  • Because of concern for adrenal cortical carcinoma, the patient underwent a successful right adrenalectomy.
  • The diagnosis of leiomyoma was supported by a panel of immunohistochemical stains.
  • Adrenal leiomyomas have been reported in the literature, although most are small and not preoperatively suspicious for malignancy.
  • This case illustrates that benign tumors such as leiomyomas, when large and heterogeneous on imaging, can clinically mimic adrenal cortical carcinomas and should be included in the differential diagnosis of adrenal incidentalomas.
  • [MeSH-major] Adrenal Gland Neoplasms / pathology. Incidental Findings. Leiomyoma / pathology
  • [MeSH-minor] Adrenocortical Carcinoma / pathology. Adult. Diagnosis, Differential. Female. Humans. Positron-Emission Tomography. Tomography, X-Ray Computed

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  • (PMID = 18197480.001).
  • [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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74. Cerquetti L, Bucci B, Marchese R, Misiti S, De Paula U, Miceli R, Muleti A, Amendola D, Piergrossi P, Brunetti E, Toscano V, Stigliano A: Mitotane increases the radiotherapy inhibitory effect and induces G2-arrest in combined treatment on both H295R and SW13 adrenocortical cell lines. Endocr Relat Cancer; 2008 Jun;15(2):623-34
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  • [Title] Mitotane increases the radiotherapy inhibitory effect and induces G2-arrest in combined treatment on both H295R and SW13 adrenocortical cell lines.
  • This drug and radiotherapy are used also in adrenal cancer treatment even if their biological action in this neoplasia remains unknown.
  • We investigated the effects of o,p'-DDD and ionizing radiations (IR) on cell growth inhibition and cell cycle perturbation in H295R and SW13 adrenocortical cancer cells.
  • Both cell lines were irradiated at a 6 Gy dose and were treated with o,p'-DDD 10(-5) M separately and with IR/o,p'-DDD in combination.
  • This combination treatment induced an irreversible inhibition of cell growth in both adrenocortical cancer cells.
  • Cell cycle analysis showed that IR alone and IR/o,p'-DDD in combination induced the cell accumulation in the G2 phase.
  • In order to study the molecular mechanism involved in the G2 irreversible arrest, we have considered the H295R cell line showing the highest inhibition of cell proliferation associated with a noteworthy G2 arrest.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Antineoplastic Agents, Hormonal / pharmacology. Mitotane / pharmacology. Radiotherapy
  • [MeSH-minor] CDC2 Protein Kinase / metabolism. Cell Division / drug effects. Cell Division / radiation effects. Cell Line, Tumor. Cyclin B / metabolism. Cyclin B1. G2 Phase / drug effects. G2 Phase / radiation effects. Humans. RNA, Messenger / metabolism. Steroids / pharmacology. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 18509009.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / CCNB1 protein, human; 0 / Cyclin B; 0 / Cyclin B1; 0 / RNA, Messenger; 0 / Steroids; 0 / Tumor Suppressor Protein p53; 78E4J5IB5J / Mitotane; EC 2.7.11.22 / CDC2 Protein Kinase
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75. 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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  • [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

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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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76. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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77. Doghman M, El Wakil A, Cardinaud B, Thomas E, Wang J, Zhao W, Peralta-Del Valle MH, Figueiredo BC, Zambetti GP, Lalli E: Regulation of insulin-like growth factor-mammalian target of rapamycin signaling by microRNA in childhood adrenocortical tumors. Cancer Res; 2010 Jun 1;70(11):4666-75
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  • [Title] Regulation of insulin-like growth factor-mammalian target of rapamycin signaling by microRNA in childhood adrenocortical tumors.
  • Here, we report the identification of a set of miRNAs that are differentially regulated in childhood adrenocortical tumors (ACT), including miR-99a and miR-100.
  • Functional analysis of these miRNAs in ACT cell lines showed that they coordinately regulate expression of the insulin-like growth factor-mammalian target of rapamycin (mTOR)-raptor signaling pathway through binding sites in their 3'-untranslated regions.
  • In these cells, the active Ser(2448)-phosphorylated form of mTOR is present only in mitotic cells in association with the mitotic spindle and midbody in the G(2)-M phases of the cell cycle.
  • Pharmacologic inhibition of mTOR signaling by everolimus greatly reduces tumor cell growth in vitro and in vivo.
  • Our results reveal a novel mechanism of regulation of mTOR signaling by miRNAs, and they lay the groundwork for clinical evaluation of drugs inhibiting the mTOR pathway for treatment of adrenocortical cancer.

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  • (PMID = 20484036.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM083159; United States / NCI NIH HHS / CA / P01 CA071907; United States / NIGMS NIH HHS / GM / GM083159; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / CA071907-060006; United States / NCI NIH HHS / CA / P01 CA071907-060006
  • [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 / Intracellular Signaling Peptides and Proteins; 0 / MicroRNAs; 0 / Somatomedins; 9HW64Q8G6G / Everolimus; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ NIHMS192514; NLM/ PMC2880211
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78. Yang WH, Heaton JH, Brevig H, Mukherjee S, Iñiguez-Lluhí JA, Hammer GD: SUMOylation inhibits SF-1 activity by reducing CDK7-mediated serine 203 phosphorylation. Mol Cell Biol; 2009 Feb;29(3):613-25
Hazardous Substances Data Bank. Corticotropin .

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  • Steroidogenic factor 1 (SF-1) is an orphan nuclear receptor selectively expressed in the adrenal cortex and gonads, where it mediates the hormonal stimulation of multiple genes involved in steroid hormone biosynthesis.
  • Based on these observations, we propose a coordinated modification model in which inhibition of SF-1-mediated transcription by SUMOylation in adrenocortical cancer cells is mediated through reduced CDK7-induced phosphorylation of SF-1.

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  • (PMID = 19015234.001).
  • [ISSN] 1098-5549
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK61656; United States / NIDDK NIH HHS / DK / R01 DK061656; United States / NIDDK NIH HHS / DK / P60 DK20572; United States / NIDDK NIH HHS / DK / DK62027; United States / NIDDK NIH HHS / DK / R56 DK061656; United States / NIDDK NIH HHS / DK / R01 DK062027; United States / NIDDK NIH HHS / DK / P60 DK020572; United States / NCI NIH HHS / CA / T32 CA009676
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Small Ubiquitin-Related Modifier Proteins; 0 / Steroidogenic Factor 1; 17885-08-4 / Phosphoserine; 9002-60-2 / Adrenocorticotropic Hormone; EC 2.7.11.22 / Cyclin-Dependent Kinases; EC 2.7.11.22 / cyclin-dependent kinase 7, mouse; K3Z4F929H6 / Lysine
  • [Other-IDs] NLM/ PMC2630698
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79. 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
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • RESULTS: IGFBP-2 mRNA level distinguished between the two genetic subtypes of this disease; increased IGFBP-2 expression in PRKAR1A mutation-positive PPNAD tissues was also confirmed by immunohistochemistry.
  • 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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80. Nieman LK, Ilias I: Evaluation and treatment of Cushing's syndrome. Am J Med; 2005 Dec;118(12):1340-6
Hazardous Substances Data Bank. Corticotropin .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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.
  • 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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81. El Kochairi I, Letovanec I, Uffer S, Munier FL, Chaubert P, Schorderet DF: Systemic investigation of keratoepithelin deposits in TGFBI/BIGH3-related corneal dystrophy. Mol Vis; 2006;12:461-6
Hazardous Substances Data Bank. (L)-ARGININE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Eighteen different tissues or organs, including brain, heart, lung, kidney, liver, lymph nodes, spleen, aorta, esophagus, bone marrow, urinary bladder (including a papillary urothelial carcinoma), samples of a metastatic squamous cell carcinoma, adrenal gland, parathyroid gland, muscle, prostate, and cornea were investigated, and sections from the tissues were labeled with KE2 rabbit TGFBI/BIGH3 antiserum.
  • RESULTS: The patient, diagnosed with LCDI and Alzheimer's disease, died at 79 years of age from a complicated chronic obstructive lung disease.
  • [MeSH-minor] Aged. Arginine. Cornea / metabolism. Cornea / pathology. Cysteine. DNA Mutational Analysis. Exons. Humans. Immunohistochemistry. Male. Pulmonary Disease, Chronic Obstructive / complications. Tissue Distribution

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  • (PMID = 16710170.001).
  • [ISSN] 1090-0535
  • [Journal-full-title] Molecular vision
  • [ISO-abbreviation] Mol. Vis.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Extracellular Matrix Proteins; 0 / Transforming Growth Factor beta; 148710-76-3 / betaIG-H3 protein; 94ZLA3W45F / Arginine; K848JZ4886 / Cysteine
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82. Libé R, Fratticci A, Coste J, Tissier F, Horvath A, Ragazzon B, Rene-Corail F, Groussin L, Bertagna X, Raffin-Sanson ML, Stratakis CA, Bertherat J: Phosphodiesterase 11A (PDE11A) and genetic predisposition to adrenocortical tumors. Clin Cancer Res; 2008 Jun 15;14(12):4016-24

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phosphodiesterase 11A (PDE11A) and genetic predisposition to adrenocortical tumors.
  • PURPOSE: We have reported previously nonsense inactivating mutations of the phosphodiesterase 11A (PDE11A) gene in patients with micronodular adrenocortical hyperplasia and Cushing syndrome.
  • The aim of this study is to investigate the presence of somatic or germ-line PDE11A mutations in various types of adrenocortical tumors: ACTH-independent macronodular adrenocortical hyperplasia (AIMAH), adrenocortical adenoma (ACA), and adrenocortical cancer (ACC).
  • EXPERIMENTAL DESIGN: PDE11A was sequenced in 117 adrenocortical tumors and 192 controls subjects; immunohistochemistry for PDE11A and tumor cyclic AMP levels were studied in a subgroup of adrenocortical tumors.
  • RESULTS: One PDE11A inactivating mutation (R307X) was found in one ACA, 22 germ-line missense variants (18.8%) were found in adrenocortical tumors, and only 11 missense variants (5.7%) were found in controls.
  • By comparing the common mutations, a higher frequency of mutations in adrenocortical tumors than in age/sex-matched controls were observed [16% versus 10% in ACC, 19% versus 10% in ACA, and 24% versus 9% in AIMAH; odds ratio (OR), 3.53; P = 0.05].
  • Somatic DNA from adrenocortical tumors with missense variants showed a wild-type allelic loss.
  • In AIMAH/ACA, cyclic AMP levels were higher than in normal adrenals and decreased PDE11A immunostaining was present in adrenocortical tumors with PDE11A variants.
  • CONCLUSIONS: The present investigation of a large cohort of adrenocortical tumors suggests that PDE11A sequence defects predispose to a variety of lesions (beyond micronodular adrenocortical hyperplasia) and may contribute to the development of these tumors in the general population.

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  • (PMID = 18559625.001).
  • [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 / NICHD NIH HHS / HD / Z01 HD000642; United States / Intramural NIH HHS / / ZIA HD000642-13
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.1.4.- / Phosphoric Diester Hydrolases; EC 3.1.4.35 / PDE11A protein, human
  • [Other-IDs] NLM/ NIHMS306040; NLM/ PMC3134879
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83. Doghman M, Madoux F, Hodder P, Lalli E: Identification and characterization of steroidogenic factor-1 inverse agonists. Methods Enzymol; 2010;485:3-23

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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84. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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
  • [MeSH-minor] Cell Line. Cholesterol Side-Chain Cleavage Enzyme / genetics. Cholesterol Side-Chain Cleavage Enzyme / metabolism. Cytochrome P-450 CYP11B2 / genetics. Cytochrome P-450 CYP11B2 / metabolism. Gene Expression Regulation / drug effects. Humans. Steroid 11-beta-Hydroxylase / genetics. Steroid 11-beta-Hydroxylase / metabolism

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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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85. Stratakis CA: Cushing syndrome caused by adrenocortical tumors and hyperplasias (corticotropin- independent Cushing syndrome). Endocr Dev; 2008;13:117-32
SciCrunch. KEGG: Data: Disease Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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86. Szabó PM, Wiener Z, Tömböl Z, Kovács A, Pócza P, Horányi J, Kulka J, Riesz P, Tóth M, Patócs A, Gaillard RC, Falus A, Rácz K, Igaz P: Differences in the expression of histamine-related genes and proteins in normal human adrenal cortex and adrenocortical tumors. Virchows Arch; 2009 Aug;455(2):133-42
Hazardous Substances Data Bank. HISTAMINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differences in the expression of histamine-related genes and proteins in normal human adrenal cortex and adrenocortical tumors.
  • Histamine is involved in the pathogenesis of several tumors; however, there are no data on its possible involvement in human adrenocortical tumorigenesis.
  • The expression of genes and proteins involved in the biosynthesis (histidine decarboxylase, HDC), action (histamine receptors: HRH1-HRH4), and metabolism of histamine is largely unknown both in the normal human adrenal cortex and in adrenocortical tumors.
  • In this study, we examined the expression of histamine-related genes and proteins and histamine content in normal adrenal cortex, benign adrenocortical adenomas, and malignant adrenocortical cancer (ACC).
  • We found that all proteins involved in histamine biosynthesis and action are present both in the normal adrenal cortex and in the tumors studied.
  • 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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87. Menéndez Calderón MJ, Casal F, Prieto J, Cacho L, Tusón C: [Adrenocortical carcinoma. A retrospective analysis of five cases]. An Med Interna; 2006 Nov;23(11):533-6
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  • [Title] [Adrenocortical carcinoma. A retrospective analysis of five cases].
  • [Transliterated title] Carcinoma suprarrenal. Análisis retrospectivo de cinco casos.
  • We present five cases of adrenal cortical carcinoma, diagnosed in our hospital and we describe the clinical presentation, diagnostic methods and treatment.
  • The diagnosis is based on the biochemical characterization of the hormonal profile and on imaging techniques, especially computed tomography and magnetic resonance.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology

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  • (PMID = 17222069.001).
  • [ISSN] 0212-7199
  • [Journal-full-title] Anales de medicina interna (Madrid, Spain : 1984)
  • [ISO-abbreviation] An Med Interna
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
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88. Gasilionis V, Ersahin C, Gabram S, Bova D, Branch J, Rajan P: Adrenal cortical carcinoma metastatic to the breast. J Clin Pathol; 2006 May;59(5):546-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenal cortical carcinoma metastatic to the breast.
  • A 56 year old woman was diagnosed with adrenal cortical carcinoma in May 2003, for which she underwent left radical adrenalectomy.
  • A diagnosis of metastatic adrenal cortical carcinoma was made on core biopsy.
  • Subsequently, the patient underwent a lumpectomy of the mass, which confirmed the diagnosis.
  • To our knowledge, this is the first case report of adrenal cortical carcinoma metastatic to the breast.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Breast Neoplasms / secondary. Carcinoma / secondary

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  • (PMID = 16644887.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1860300
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89. Gatta G, Ciccolallo L, Kunkler I, Capocaccia R, Berrino F, Coleman MP, De Angelis R, Faivre J, Lutz JM, Martinez C, Möller T, Sankila R, EUROCARE Working Group: Survival from rare cancer in adults: a population-based study. Lancet Oncol; 2006 Feb;7(2):132-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Survival from rare cancer in adults: a population-based study.
  • BACKGROUND: Rare cancers are a challenge to clinical practice, and treatment experience, even in major cancer centres to which rare cancers are usually referred, is often limited.
  • We also estimated the adjusted relative excess risk of death for every rare cancer.
  • FINDINGS: Overall 5-year relative survival was good (ie, >65%) for placental choriocarcinoma (85.4% [95% CI 81.4-89.5]), thyroid medullary carcinoma (72.4% [69.2-75.5]), ovarian germ-cell cancer (73.0% [70.0-76.0]), lung carcinoid (70.1% [67.3-72.9]), and cervical adenocarcinoma (65.5% [64.3-66.6]); intermediate (ie, 35-65%) for testicular cancer at age 65 years or older (64.0% [59.3-68.7]), sarcoma of extremities (60.0% [58.9-61.2]), digestive-system endocrine cancers (55.6% [54.9-56.3]), anal squamous-cell carcinoma (53.1% [51.5-54.8]), and uterine sarcoma (43.5% [42.0-44.9]); low for carcinoma of adrenal-gland cortex (32.7% [28.3-37.2]) and bladder squamous-cell carcinoma (20.4% [18.8-22.0]); and poor for angiosarcoma of liver (6.4% [1.8-11.0]) and mesothelioma (4.7% [4.3-5.2]).
  • Survival significantly improved over time for ovarian germ-cell cancer, sarcomas of extremities, digestive-system endocrine tumours, anal squamous-cell carcinoma, and angiosarcoma of liver.

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  • (PMID = 16455477.001).
  • [ISSN] 1470-2045
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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90. 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
Hazardous Substances Data Bank. HYDROCORTISONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • It was also shown that the ET-1 does not mediate the effect of ECCM on the NCI-H295R cell line.
  • [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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91. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mechanisms of disease: adrenocortical tumors--molecular advances and clinical perspectives.
  • Most adrenocortical tumors are benign, unilateral, adrenocortical adenomas that are often discovered incidentally.
  • Adrenocortical cancer is rare.
  • Exceptionally, adrenocortical tumors can be bilateral.
  • Although most adrenocortical tumors occur sporadically, they may also feature in congenital and/or familial disease.
  • The identification of germline genetic defects in familial diseases associated with adrenocortical tumors helped to define the somatic alterations in sporadic disease: for example, overexpression of insulin-like growth factor 2 and alterations at the 11p15 locus (observed in Beckwith-Wiedemann syndrome) are also found in most adrenocortical cancers.
  • Similarly, inactivating mutations of the TP53 gene, located at 17p13 (observed in Li-Fraumeni syndrome), can also be found at the somatic level in sporadic adrenocortical cancers, as can 17p13 allelic losses.
  • Components of the cyclic AMP signaling pathway--for example, adrenocorticotropic hormone receptors and other membrane receptors, Gs proteins and protein kinase A--can be altered to various degrees in adrenocortical tumors.
  • More recently, gene profiling and genetic studies have shown that the Wnt-beta-catenin signaling pathway is frequently activated in adrenocortical tumors.
  • These research findings already have profound implications for clinical management of patients with adrenocortical tumors, for example in unraveling the genetic origin of the disease in some patients, and in the development of molecular markers for diagnosis and prognosis.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics

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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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92. Grubbs EG, Callender GG, Xing Y, Perrier ND, Evans DB, Phan AT, Lee JE: Recurrence of adrenal cortical carcinoma following resection: surgery alone can achieve results equal to surgery plus mitotane. Ann Surg Oncol; 2010 Jan;17(1):263-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurrence of adrenal cortical carcinoma following resection: surgery alone can achieve results equal to surgery plus mitotane.
  • BACKGROUND: A recent nonrandomized interinstitutional study reported that adjuvant mitotane following surgery for adrenocortical carcinoma (ACC) was associated with decreased recurrence.
  • SI patients had a superior disease-free survival compared with SO patients (median 25 versus 12 months, P = 0.003), and SI patients also had a superior overall survival compared with SO patients (median not reached versus 44 months, P = 0.02).
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenocortical Carcinoma / surgery. Antineoplastic Agents, Hormonal / therapeutic use. Mitotane / therapeutic use. Neoplasm Recurrence, Local / diagnosis

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  • (PMID = 19851811.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 78E4J5IB5J / Mitotane
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93. Hennings J, Lindhe O, Bergström M, Långström B, Sundin A, Hellman P: [11C]metomidate positron emission tomography of adrenocortical tumors in correlation with histopathological findings. J Clin Endocrinol Metab; 2006 Apr;91(4):1410-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [11C]metomidate positron emission tomography of adrenocortical tumors in correlation with histopathological findings.
  • CONTEXT: Adrenal incidentalomas are common findings necessitating extensive laboratory work-up and repetitive radiological examinations.
  • Positron emission tomography (PET) using (11)C-labeled metomidate (MTO) has previously been described as a tool for specific adrenocortical imaging.
  • OBJECTIVE: We evaluated 212 MTO-PET examinations in 173 patients to identify its role in the management of adrenal tumors.
  • PATIENTS: Patients who were operated or biopsied due to adrenal tumors had histopathological diagnoses of adrenocortical adenoma (n = 26), adrenocortical cancer (ACC; n = 13), adrenocortical hyperplasia (n = 8), pheochromocytoma (n = 6), metastasis (n = 3), and tumors of nonadrenal origin (n = 19).
  • The hypothesis that MTO-PET is of value in the management of adrenal tumors, especially incidentaloma, was stated before data collection.
  • RESULTS: Sensitivity was 0.89 and specificity was 0.96 for MTO-PET in proving adrenocortical origin of the lesions.
  • Pheochromocytomas, metastases to the adrenal gland, and nonadrenal masses were all MTO negative.
  • PET measurements using standardized uptake values (SUV) in pathological adrenocortical tissue could differentiate lesions larger than 1-1.5 cm from normal adrenocortical tissue.
  • SUV was higher in aldosterone-hypersecreting adenomas, and the SUV ratio between the tumor and the contralateral gland was significantly higher in all hormonally hypersecreting adenomas as well as in ACC.
  • CONCLUSION: MTO-PET is a specific and sensitive method for diagnosing adrenocortical tumors.
  • MTO-PET is useful in the imaging work-up of adrenal incidentalomas and may be beneficial for the examination of patients with primary aldosteronism or ACC.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenal Cortex Neoplasms / radionuclide imaging. Antineoplastic Agents. Etomidate / analogs & derivatives

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  • (PMID = 16403816.001).
  • [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 / Antineoplastic Agents; 0 / Radiopharmaceuticals; 5377-20-8 / metomidate; Z22628B598 / Etomidate
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94. Aumo L, Rusten M, Mellgren G, Bakke M, Lewis AE: Functional roles of protein kinase A (PKA) and exchange protein directly activated by 3',5'-cyclic adenosine 5'-monophosphate (cAMP) 2 (EPAC2) in cAMP-mediated actions in adrenocortical cells. Endocrinology; 2010 May;151(5):2151-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Functional roles of protein kinase A (PKA) and exchange protein directly activated by 3',5'-cyclic adenosine 5'-monophosphate (cAMP) 2 (EPAC2) in cAMP-mediated actions in adrenocortical cells.
  • In the adrenal cortex, the biosynthesis of steroid hormones is controlled by the pituitary-derived hormone ACTH.
  • In the present study, we demonstrate the occurrence of the EPAC2 splicing variant EPAC2B in adrenocortical cancer cells.
  • Using the cAMP analogs 8-p-chlorophenylthio-2'-O-methyl-cAMP and N6-benzoyl-cAMP, which specifically activate EPAC1/2 and PKA, respectively, we evaluated the contribution of these factors in steroid hormone production, cell morphology, actin reorganization, and migration.
  • In contrast, both PKA- and EPAC-specific cAMP analogs induced cell rounding, loss of stress fibers, and blocked migration.
  • Taken together, the presented data confirm PKA as the central cAMP mediator in steroid hormone production and reveal the involvement of EPAC2B in cAMP-induced effects on cytoskeleton integrity and cell migration.
  • [MeSH-major] Cell Nucleus / metabolism. Cyclic AMP / metabolism. Cyclic AMP-Dependent Protein Kinases / metabolism. Guanine Nucleotide Exchange Factors / physiology
  • [MeSH-minor] Adrenal Cortex / metabolism. Adrenal Cortex / pathology. Aldosterone / biosynthesis. Alternative Splicing. Animals. Blotting, Western. COS Cells. Cell Line. Cell Line, Tumor. Cell Movement / drug effects. Cell Shape / drug effects. Cercopithecus aethiops. Cytoskeleton / drug effects. Cytoskeleton / metabolism. Humans. Hydrocortisone / biosynthesis. Immunohistochemistry. Microscopy, Confocal. Protein Isoforms / genetics. Protein Isoforms / metabolism. Protein Isoforms / physiology. Reverse Transcriptase Polymerase Chain Reaction. rap1 GTP-Binding Proteins / metabolism

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  • (PMID = 20233795.001).
  • [ISSN] 1945-7170
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Guanine Nucleotide Exchange Factors; 0 / Protein Isoforms; 0 / RAPGEF4 protein, human; 4964P6T9RB / Aldosterone; E0399OZS9N / Cyclic AMP; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 3.6.5.2 / rap1 GTP-Binding Proteins; WI4X0X7BPJ / Hydrocortisone
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95. 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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  • Cushing's syndrome is a rare disease with significant morbidity and mortality.
  • It is not uncommon, however, that surgery fails to cure or control the disease.
  • 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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96. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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97. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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).
  • CONCLUSIONS: MicroRNAs appear to have distinct regulatory effects in MMAD, including an association with clinical presentation and severity of the disease, expressed by the degree of hypercortisolism.
  • This is the first investigation of microRNAs in MMAD, a disease with complex pathogenesis; the data indicate that specific microRNAs such as miR-200b may play a significant role in MMAD formation and/or progression.

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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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98. 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.
  • 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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99. Menon V, Krishnamurthy SV: Adrenocortical carcinomas: a 12-year clinicopathologic study of 15 cases. Indian J Pathol Microbiol; 2006 Jan;49(1):7-11

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenocortical carcinomas: a 12-year clinicopathologic study of 15 cases.
  • Adrenal cortical carcinomas are rare neoplasms and the definitive diagnostic criteria are distant metastasis and / or local invasion.
  • Due to advances in imaging techniques, adrenal cortical neoplasms are discovered earlier and are smaller, increasing the need for more accurate diagnosis and pathologic indicators of prognosis.
  • A twelve year retrospective clinicopathologic analysis of 15 histopathologically proven cases of adrenocortical carcinomas was done.
  • Clinical details including radiologic findings, endocrine manifestations and gross finding were analysed.
  • Functional tumors showed a greater representation of mixed cell type.
  • It was concluded that Weiss criteria is easy to apply and that a combined evaluation of clinical features, size, weight and microscopic appearance seems necessary for the diagnosis of adrenocortical carcinomas.
  • [MeSH-major] Adrenal Cortex / pathology. Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology

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  • (PMID = 16625963.001).
  • [ISSN] 0377-4929
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
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100. Stránský P, Hora M, Eret V, Klecka J, Urge T, Grégrová H, Dvoráková E, Hes O, Chudácek Z, Kreuzberg B: [Laparoscopic adrenalectomy]. Rozhl Chir; 2009 Sep;88(9):514-20

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: Laparoscopy has become the gold standard for the treatment of adrenal tumours in urology.
  • We evaluate our experience with laparoscopic adrenalectomy (LA) in this work.
  • MATERIAL, METHODS: We performed 38 LA between 2003-2008.
  • Nine LA were made in men (24%), in women 29 (76%).
  • There were histologically 15 cortical adenomas, 5 nodular cortical hyperplasia, 1 calcificated hematoma, 3 cysts, 2 potentional malignant tumours on interface between adenoma and carcinoma, 1 cortical carcinoma and 7 pheochromocytoma.
  • We found 3 metastases of renal carcinoma in adrenal gland and one metastasis mesenchymal chondrosarcoma too.
  • CONCLUSION: LA is a quick and safe procedure with minimal morbidity and mortality.
  • Especially benign tumours of smaller size (by 8 cm) are indicated, extensive and especially malignant tumours remain a domain of open approach.
  • Previous operations in abdominal cavity do not have to be a contraindication for LA and operation is possible in patients with monster obesity.
  • [MeSH-minor] Adrenal Gland Neoplasms / surgery. Adult. Aged. Female. Humans. Male. Middle Aged

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  • (PMID = 20052929.001).
  • [ISSN] 0035-9351
  • [Journal-full-title] Rozhledy v chirurgii : měsíčník Československé chirurgické společnosti
  • [ISO-abbreviation] Rozhl Chir
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Czech Republic
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