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1. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Peroxisome proliferator-activated receptor-gamma agonists suppress adrenocortical tumor cell proliferation and induce differentiation.
  • Adrenocortical carcinoma (ACC) is a rare tumor entity with poor prognosis due to its highly malignant phenotype and lack of effective treatment options.
  • OBJECTIVE: The purpose of this study was to investigate effects of TZDs on adrenocortical cancer cells.
  • RESULTS: PPARgamma mRNA expression was detectable in all adrenocortical tumors including ACCs at similar levels.
  • Furthermore, incubation of the adrenocortical tumor cell line NCI h295 with the PPARgamma agonist rosiglitazone led to a decrease in cell viability, a decrease of cellular proliferation, and an increase in apoptosis as well as steroidogenesis.
  • On the molecular level, NCI h295 cells expressed higher levels of ACTH receptor (melanocortin receptor-2) mRNA upon treatment, whereas cyclin E mRNA was reduced, thus reflecting a shift toward an expression pattern found in less aggressive adrenocortical tumors in vivo.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. PPAR gamma / agonists. Thiazolidinediones / pharmacology
  • [MeSH-minor] Adult. Aged. Anilides / pharmacology. Apoptosis / drug effects. Cell Differentiation. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin E / genetics. Dose-Response Relationship, Drug. Female. Humans. Insulin-Like Growth Factor II / genetics. Male. Middle Aged. Promoter Regions, Genetic. RNA, Messenger / analysis. Receptor, Melanocortin, Type 2 / genetics

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  • (PMID = 15886257.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-chloro-5-nitrobenzanilide; 0 / Anilides; 0 / Cyclin E; 0 / PPAR gamma; 0 / RNA, Messenger; 0 / Receptor, Melanocortin, Type 2; 0 / Thiazolidinediones; 05V02F2KDG / rosiglitazone; 67763-97-7 / Insulin-Like Growth Factor II
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2. Ziegler CG, Brown JW, Schally AV, Erler A, Gebauer L, Treszl A, Young L, Fishman LM, Engel JB, Willenberg HS, Petersenn S, Eisenhofer G, Ehrhart-Bornstein M, Bornstein SR: Expression of neuropeptide hormone receptors in human adrenal tumors and cell lines: antiproliferative effects of peptide analogues. Proc Natl Acad Sci U S A; 2009 Sep 15;106(37):15879-84
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  • [Title] Expression of neuropeptide hormone receptors in human adrenal tumors and cell lines: antiproliferative effects of peptide analogues.
  • Peptide analogues targeting various neuropeptide receptors have been used effectively in cancer therapy.
  • A hallmark of adrenocortical tumor formation is the aberrant expression of peptide receptors relating to uncontrolled cell proliferation and hormone overproduction.
  • Our microarray results have also demonstrated a differential expression of neuropeptide hormone receptors in tumor subtypes of human pheochromocytoma.
  • In light of these findings, we performed a comprehensive analysis of relevant receptors in both human adrenomedullary and adrenocortical tumors and tested the antiproliferative effects of peptide analogues targeting these receptors.
  • Specifically, we examined the receptor expression of somatostatin-type-2 receptor, growth hormone-releasing hormone (GHRH) receptor or GHRH receptor splice variant-1 (SV-1) and luteinizing hormone-releasing hormone (LHRH) receptor at the mRNA and protein levels in normal human adrenal tissues, adrenocortical and adrenomedullary tumors, and cell lines.
  • Cytotoxic derivatives of somatostatin AN-238 and, to a lesser extent, AN-162, reduced cell numbers of uninduced and NGF-induced adrenomedullary pheochromocytoma cells and adrenocortical cancer cells.
  • Both the splice variant of GHRH receptor SV-1 and the LHRH receptor were also expressed in adrenocortical cancer cell lines but not in the pheochromocytoma cell line.
  • The GHRH receptor antagonist MZ-4-71 and LHRH antagonist Cetrorelix both significantly reduced cell growth in the adrenocortical cancer cell line.
  • In conclusion, the expression of receptors for somatostatin, GHRH, and LHRH in the normal human adrenal and in adrenal tumors, combined with the growth-inhibitory effects of the antitumor peptide analogues, may make possible improved treatment approaches to adrenal tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / drug therapy. Adrenal Gland Neoplasms / metabolism. Neuropeptides / pharmacology. Receptors, Neuropeptide / metabolism
  • [MeSH-minor] 2-Hydroxyphenethylamine / analogs & derivatives. 2-Hydroxyphenethylamine / pharmacology. Adrenal Glands / metabolism. Aniline Compounds / pharmacology. Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Cytostatic Agents / pharmacology. Doxorubicin / analogs & derivatives. Doxorubicin / pharmacology. Gene Expression. Humans. Oligonucleotide Array Sequence Analysis. PC12 Cells. Pyrroles / pharmacology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Receptors, LHRH / genetics. Receptors, LHRH / metabolism. Receptors, Somatostatin / genetics. Receptors, Somatostatin / metabolism. Somatostatin / analogs & derivatives. Somatostatin / pharmacology

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  • (PMID = 19717419.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AN 238; 0 / Aniline Compounds; 0 / Cytostatic Agents; 0 / Neuropeptides; 0 / Pyrroles; 0 / RNA, Messenger; 0 / Receptors, LHRH; 0 / Receptors, Neuropeptide; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 2PK59M9GFF / vapreotide; 33189-65-0 / N-(2-diethylaminoethyl)-N-(2-hydroxy-2-phenylethyl)-2,5-dichloroaniline; 51110-01-1 / Somatostatin; 7568-93-6 / 2-Hydroxyphenethylamine; 80168379AG / Doxorubicin
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3. 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.
  • Complete resection by an expert surgeon is the only potentially curative treatment for ACC, and tumor spillage should be avoided.
  • Histopathology is important for diagnosis, but immunohistochemistry markers and gene profiling of the resected tumor may become superior to current staging systems to stratify prognosis.
  • Careful replacement of glucocorticoid and mineralocorticoid deficiency after surgery or mitotane therapy is important; steroid excess from remaining tumor burden should also be controlled to avoid its morbidities.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenocortical Carcinoma / surgery

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

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  • (PMID = 19849700.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / Z01 HD000642; United States / Intramural NIH HHS / / Z01 HD000642-11; United States / NICHD NIH HHS / HD / Z01-HD-000642-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Validation Studies
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MicroRNAs
  • [Other-IDs] NLM/ NIHMS154316; NLM/ PMC3003432
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5. Kouidou S, Malousi A, Kyventidis A, Fragou A, Maglaveras N: G:C > A:T mutations and potential epigenetic regulation of p53 in breast cancer. Breast Cancer Res Treat; 2007 Dec;106(3):351-60
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  • [Title] G:C > A:T mutations and potential epigenetic regulation of p53 in breast cancer.
  • Analysis of germline p53 mutations in breast cancer reveals that the Li-Fraumeni and Li-Fraumeni-like syndromes are mostly related to the loss of initiation codon 133 of regulatory TP53 isoforms (Delta133p53).
  • In eight codons of exons 5-8 (including 133), mutations are frequent in Li-Fraumeni-related, but scarce in sporadic breast cancer, while in six more codons they are frequent both in familial and sporadic breast cancers.
  • At the proximity of these codons, we observed in somatic mutation databases, 16 codons (minihotspots mostly in exons 7, 8) which undergo frequent G:C > A:T transitions (non-CpG) in all sporadic cancers.
  • In addition, in sporadic breast cancer we observed 35 adjacent codons in which the following types of mutation are observed: frequent G:C > A:T transitions at CCs/GGs, frequent silent mutations in exons 5,6 and suppressed nonsense mutations (5 codons, few records).
  • Non-CpG G:C > A:T transitions in the 35 codons are rare in familial cancers (p53, BRCA1, or BRCA2-related), but frequent in sporadic cancers in organs where Li-Fraumeni-related carcinogenesis is common e.g. adrenal cortex, soft tissues.
  • These data are in support of the following tissue-specific processes: in sporadic breast cancer (sarcomas etc.
  • Frequent C > T activation at non-CpG is also observed in prostate sporadic cancer, which similarly to breast, undergoes age-related crisis.


6. Mitra S, Roy SG, Sur PK: Adrenocortical carcinoma with skeletal metastases in a postmenopausal woman. Indian J Med Paediatr Oncol; 2009 Jan;30(1):24-7
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  • [Title] Adrenocortical carcinoma with skeletal metastases in a postmenopausal woman.
  • Adrenocortical cancer is a very rare tumor with a poor prognosis.
  • CT-guided fine-needle aspiration cytology of an abdominal mass revealed the presence of a carcinoma of the left adrenal cortex.

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  • (PMID = 20668603.001).
  • [ISSN] 0975-2129
  • [Journal-full-title] Indian journal of medical and paediatric oncology : official journal of Indian Society of Medical & Paediatric Oncology
  • [ISO-abbreviation] Indian J Med Paediatr Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC2902211
  • [Keywords] NOTNLM ; Adrenocortical carcinoma / androgen secreting tumors / mitotane
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7. Daffara F, De Francia S, Reimondo G, Zaggia B, Aroasio E, Porpiglia F, Volante M, Termine A, Di Carlo F, Dogliotti L, Angeli A, Berruti A, Terzolo M: Prospective evaluation of mitotane toxicity in adrenocortical cancer patients treated adjuvantly. Endocr Relat Cancer; 2008 Dec;15(4):1043-53
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  • [Title] Prospective evaluation of mitotane toxicity in adrenocortical cancer patients treated adjuvantly.
  • Seventeen consecutive patients who were treated with mitotane after radical resection of adrenocortical cancer (ACC) from 1999 to 2005 underwent physical examination, routine laboratory evaluation, monitoring of mitotane concentrations, and a hormonal work-up at baseline and every 3 months till ACC relapse or study end (December 2007).
  • Mitotane affected adrenal steroidogenesis with a more remarkable inhibition of cortisol and DHEAS than aldosterone.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Mitotane / therapeutic use
  • [MeSH-minor] Adult. Chemotherapy, Adjuvant. Chromatography, High Pressure Liquid. Female. Humans. Hydrocortisone / metabolism. Hypothyroidism / etiology. Male. Middle Aged. Neoplasm Staging. Prospective Studies. Survival Rate. Testosterone / metabolism. Young Adult

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  • (PMID = 18824557.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 3XMK78S47O / Testosterone; 78E4J5IB5J / Mitotane; WI4X0X7BPJ / Hydrocortisone
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8. Carmona-Bayonas A, Soler IO, Gómez FI, Billalabeitia EG, Saura HP, Tafalla MS, Díaz MP: Tailored hormonal therapy in secretory adrenocortical cancer. Ann Oncol; 2007 Jul;18(7):1281
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tailored hormonal therapy in secretory adrenocortical cancer.

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  • (PMID = 17675396.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiotensin-Converting Enzyme Inhibitors; 0 / Anti-Inflammatory Agents; 0 / Antifungal Agents; 0 / Antineoplastic Agents, Hormonal; 0 / Mineralocorticoid Receptor Antagonists; 27O7W4T232 / Spironolactone; 4964P6T9RB / Aldosterone; 6PLQ3CP4P3 / Etoposide; 78E4J5IB5J / Mitotane; 80168379AG / Doxorubicin; 9G64RSX1XD / Captopril; Q20Q21Q62J / Cisplatin; R9400W927I / Ketoconazole; RWP5GA015D / Potassium; WI4X0X7BPJ / Hydrocortisone
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9. 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.
  • 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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10. de Reyniès A, Assié G, Rickman DS, Tissier F, Groussin L, René-Corail F, Dousset B, Bertagna X, Clauser E, Bertherat J: Gene expression profiling reveals a new classification of adrenocortical tumors and identifies molecular predictors of malignancy and survival. J Clin Oncol; 2009 Mar 1;27(7):1108-15
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  • [Title] Gene expression profiling reveals a new classification of adrenocortical tumors and identifies molecular predictors of malignancy and survival.
  • PURPOSE: Adrenocortical tumors, especially cancers, remain challenging both for their diagnosis and prognosis assessment.
  • PATIENTS AND METHODS: One hundred fifty-three unilateral adrenocortical tumors were studied by microarray (n = 92) or reverse transcription quantitative polymerase chain reaction (n = 148).
  • Similarly, for malignant tumors, a two-gene predictor of survival was built using the overall survival as the end point in a training cohort (n = 23), then tested in an independent validation cohort (n = 35).
  • RESULTS: Unsupervised clustering analysis discriminated robustly the malignant and benign tumors, and identified two groups of malignant tumors with very different outcome.
  • Among the malignant tumors, the combined expression of BUB1B and PINK1 was the best predictor of overall survival (P < 2 x 10(-6)), and remained significant after adjusting for MacFarlane staging (P < .005).
  • CONCLUSION: Gene expression analysis unravels two distinct groups of adrenocortical carcinomas.
  • The molecular predictors of malignancy and of survival are reliable and provide valuable independent information in addition to pathology and tumor staging.
  • These original tools should provide important improvements for adrenal tumors management.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Biomarkers, Tumor / genetics. Neoplasm Proteins / genetics. Protein Kinases / genetics. Protein-Serine-Threonine Kinases / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cluster Analysis. Diagnosis, Differential. Disease-Free Survival. Female. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Proportional Hazards Models. Prospective Studies. Reproducibility of Results. Survival Analysis

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  • (PMID = 19139432.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DLGAP5 protein, human; 0 / Neoplasm Proteins; EC 2.7.- / Protein Kinases; EC 2.7.11.1 / Bub1 spindle checkpoint protein; EC 2.7.11.1 / PTEN-induced putative kinase; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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11. Libé R, Bertherat J: Molecular genetics of adrenocortical tumours, from familial to sporadic diseases. Eur J Endocrinol; 2005 Oct;153(4):477-87
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  • [Title] Molecular genetics of adrenocortical tumours, from familial to sporadic diseases.
  • Adrenal masses can be detected in up to 4% of the population, and are mostly of adrenocortical origin.
  • Adrenocortical tumours (ACTs) may be responsible for excess steroid production and, in the case of adrenocortical cancers, for morbidity or mortality due to tumour growth.
  • The familial diseases concerned are Li-Fraumeni syndrome, which may be due to germline mutation of the tumour-suppressor gene TP53 and Beckwith-Wiedemann syndrome, which is caused by dys-regulation of the imprinted IGF-II locus at 11p15.
  • ACTs also occur in type 1 multiple endocrine neoplasia (MEN 1), which is characterized by a germline mutation of the menin gene.
  • Cushing's syndrome due to primary pigmented nodular adrenocortical disease (PPNAD) has been observed in Carney complex patients presenting inactivating germline PRKAR1A mutations.
  • Interestingly, allelic losses at 17p13 and 11p15 have been demonstrated in sporadic adrenocortical cancer and somatic PRKAR1A mutations have been found in secreting adrenocortical adenomas.
  • The genetics of another group of adrenal diseases that can lead to adrenal nodular hyperplasia -- congenital adrenal hyperplasia (CAH) and glucocorticoid-remediable aldosteronism (GRA) -- have also been studied extensively.
  • This review summarizes recent advances in the genetics of ACTs, highlighting both improvements in our understanding of the pathophysiology and the diagnosis of these tumours.

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  • (PMID = 16189167.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 97
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12. Poon D, Cheung YB, Tay MH, Lim WT, Lim ST, Wong NS, Koo WH: Adrenal insufficiency in intestinal obstruction from carcinomatosis peritonei--a factor of potential importance in symptom palliation. J Pain Symptom Manage; 2005 Apr;29(4):411-8
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  • [Title] Adrenal insufficiency in intestinal obstruction from carcinomatosis peritonei--a factor of potential importance in symptom palliation.
  • There is considerable overlap in the symptoms experienced in IO and functional adrenal insufficiency (AI).
  • The aim of this preliminary study was to evaluate the incidence of functional adrenal insufficiency in patients with IO and its relation to clinical outcome and symptom control.
  • Twenty-nine consecutive patients with IO and carcinomatosis peritonei from gastrointestinal cancers admitted to our inpatient service between January and October 2002 were analyzed.
  • Differences in characteristics of patients with normal adrenal function (Group 1) and adrenal insufficiency (Group 2) were not statistically significant.
  • Functional AI may be caused by cytokines produced in advanced cancer mediating direct adrenal suppression.
  • [MeSH-major] Adrenal Insufficiency / mortality. Carcinoma / mortality. Intestinal Obstruction / mortality. Palliative Care / methods. Peritoneal Neoplasms / mortality. Risk Assessment / methods
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Adult. Aged. Aged, 80 and over. Comorbidity. Diagnosis, Differential. Female. Humans. Incidence. Male. Middle Aged. Prognosis. Risk Factors. Singapore / epidemiology. Survival Analysis

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  • (PMID = 15857745.001).
  • [ISSN] 0885-3924
  • [Journal-full-title] Journal of pain and symptom management
  • [ISO-abbreviation] J Pain Symptom Manage
  • [Language] eng
  • [Publication-type] Clinical Trial; Controlled Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
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13. Cerquetti L, Sampaoli C, Amendola D, Bucci B, Misiti S, Raza G, De Paula U, Marchese R, Brunetti E, Toscano V, Stigliano A: Mitotane sensitizes adrenocortical cancer cells to ionizing radiations by involvement of the cyclin B1/CDK complex in G2 arrest and mismatch repair enzymes modulation. Int J Oncol; 2010 Aug;37(2):493-501
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  • [Title] Mitotane sensitizes adrenocortical cancer cells to ionizing radiations by involvement of the cyclin B1/CDK complex in G2 arrest and mismatch repair enzymes modulation.
  • It also has a cytotoxic effect on the adrenocortical cells and represents a primary drug used in the adrenocortical carcinoma (ACC).
  • H295R and SW13 cell lines were treated with mitotane 10(-5) M and ionizing radiations (IR) in combination therapy, inducing an irreversible inhibition of cell growth in both adrenocortical cancer cells.
  • [MeSH-major] Adrenal Cortex Neoplasms / radiotherapy. Adrenocortical Carcinoma / radiotherapy. Cyclin B / metabolism. Cyclin-Dependent Kinases / metabolism. DNA Repair Enzymes / metabolism. Mitotane / pharmacology
  • [MeSH-minor] Cell Proliferation / drug effects. Cell Proliferation / radiation effects. DNA Mismatch Repair / drug effects. DNA Mismatch Repair / physiology. Drug Evaluation, Preclinical. G2 Phase / drug effects. G2 Phase / physiology. Humans. Multiprotein Complexes / metabolism. Protein Kinase Inhibitors / pharmacology. Purines / pharmacology. Radiation, Ionizing. Radiation-Sensitizing Agents / pharmacology. Tumor Cells, Cultured

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  • (PMID = 20596677.001).
  • [ISSN] 1791-2423
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / 6-((3-chloro)anilino)-2-(isopropyl-2-hydroxyethylamino)-9-isopropylpurine; 0 / Cyclin B; 0 / Multiprotein Complexes; 0 / Protein Kinase Inhibitors; 0 / Purines; 0 / Radiation-Sensitizing Agents; 78E4J5IB5J / Mitotane; EC 2.7.11.22 / Cyclin-Dependent Kinases; EC 6.5.1.- / DNA Repair Enzymes
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14. Mathurin P: [Alcohol and the liver]. Gastroenterol Clin Biol; 2009 Aug-Sep;33(8-9):840-9
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  • The role of alcohol in mouth, oropharynx and oesophageal cancers is clearly established.
  • The evidence for the role of alcohol in breast cancer has become clear.
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Alcoholism / complications. Humans. Severity of Illness Index

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  • (PMID = 19729258.001).
  • [ISSN] 0399-8320
  • [Journal-full-title] Gastroentérologie clinique et biologique
  • [ISO-abbreviation] Gastroenterol. Clin. Biol.
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
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15. Dempsey OJ: Clinical review: idiopathic pulmonary fibrosis--past, present and future. Respir Med; 2006 Nov;100(11):1871-85
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  • It has a median mortality of only 3 years, worse than many cancers, and its incidence continues to rise.
  • [MeSH-minor] Administration, Oral. Adrenal Cortex Hormones / administration & dosage. Anti-Inflammatory Agents / administration & dosage. Combined Modality Therapy. Cortisone / administration & dosage. Humans. Prognosis


16. Montanaro D, Maggiolini M, Recchia AG, Sirianni R, Aquila S, Barzon L, Fallo F, Andò S, Pezzi V: Antiestrogens upregulate estrogen receptor beta expression and inhibit adrenocortical H295R cell proliferation. J Mol Endocrinol; 2005 Oct;35(2):245-56
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  • [Title] Antiestrogens upregulate estrogen receptor beta expression and inhibit adrenocortical H295R cell proliferation.
  • The molecular mechanisms involved in adrenocortical tumorigenesis are still not completely understood.
  • In this study, using the H295R cell line as a model system, we investigated the role of estrogens and estrogen receptor (ER) alpha and ER beta in the growth regulation of adrenocortical tumors.
  • Moreover, this study points towards a role for ER beta as an important mediator of the repressive effects exerted by antiestrogens on H295R cells; however, further studies are needed to clarify its role in the control of adrenocortical cell proliferation and on the potential benefits of antiestrogens for treatment of adrenocortical cancer.
  • [MeSH-major] Adrenal Cortex / cytology. Cell Proliferation. Estrogen Receptor Modulators / metabolism. Estrogen Receptor beta / metabolism
  • [MeSH-minor] Adrenal Cortex Neoplasms / metabolism. Adrenal Cortex Neoplasms / pathology. Androgens / metabolism. Antigens, CD95 / metabolism. Apoptosis. Aromatase / metabolism. Aromatase Inhibitors / metabolism. Autocrine Communication. Caspases / metabolism. Cell Line, Tumor. Colforsin / metabolism. Estradiol / metabolism. Estrogen Receptor alpha / genetics. Estrogen Receptor alpha / metabolism. Fas Ligand Protein. Humans. Membrane Glycoproteins / genetics. Membrane Glycoproteins / metabolism. Nitriles / metabolism. Promoter Regions, Genetic. RNA, Messenger / metabolism. Triazoles / metabolism. Tumor Necrosis Factors / genetics. Tumor Necrosis Factors / metabolism

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  • (PMID = 16216906.001).
  • [ISSN] 0952-5041
  • [Journal-full-title] Journal of molecular endocrinology
  • [ISO-abbreviation] J. Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / Antigens, CD95; 0 / Aromatase Inhibitors; 0 / Estrogen Receptor Modulators; 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Membrane Glycoproteins; 0 / Nitriles; 0 / RNA, Messenger; 0 / Triazoles; 0 / Tumor Necrosis Factors; 1F7A44V6OU / Colforsin; 4TI98Z838E / Estradiol; 7LKK855W8I / letrozole; EC 1.14.14.1 / Aromatase; EC 3.4.22.- / Caspases
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17. Sticchi D, Fassina A, Ganzaroli C, Pasqualetto C, Pessina AC, Nussdorfer GG, Rossi GP: Expression of telomerase (hTERT) in aldosterone-producing adrenocortical tumors. Int J Mol Med; 2006 Mar;17(3):469-74
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  • [Title] Expression of telomerase (hTERT) in aldosterone-producing adrenocortical tumors.
  • Telomerase was found in cancers and immortalized cell lines, but only occasionally in normal tissues, thus suggesting that measurement of its hTERT subunit might help distinguishing benign from malignant tumors.
  • Data on hTERT expression in adrenocortical tumors are scant and mostly confined to non-functioning tumors.
  • Therefore, we investigated whether hTERT expression may predict malignancy in aldosterone producing adrenocortical tumors.
  • We also studied two rare aldosterone-producing carcinomas (APCs), eight adrenocortical carcinomas (ACs), twelve normal adrenal cortexes, and two malignant cell lines (NCI-295H and SW-13).
  • Of interest, we detected hTERT mRNA in 58% of APAs at levels similar to those of malignant tumors, which all consistently showed hTERT expression.
  • No hTERT expression was found in the normal adrenocortical tissue.
  • In conclusion, RT-PCR measurement of hTERT mRNA is a hallmark of malignant adrenocortical tumors, but identifies also a subset of hTERT-expressing APAs that might show metastatic spread at long-term follow-up.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / secretion. Aldosterone / secretion. Telomerase / genetics

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  • (PMID = 16465394.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / RNA, Messenger; 4964P6T9RB / Aldosterone; EC 2.7.7.49 / Telomerase
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18. Hong DS, Sebti SM, Newman RA, Blaskovich MA, Ye L, Gagel RF, Moulder S, Wheler JJ, Naing A, Tannir NM, Ng CS, Sherman SI, El Naggar AK, Khan R, Trent J, Wright JJ, Kurzrock R: Phase I trial of a combination of the multikinase inhibitor sorafenib and the farnesyltransferase inhibitor tipifarnib in advanced malignancies. Clin Cancer Res; 2009 Nov 15;15(22):7061-8
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  • Interestingly, six of eight patients with medullary thyroid cancer had durable stable disease (n = 3) or partial remissions (n = 3), lasting 12 to 26+ months.
  • Prolonged (> or =6 months) stable disease was also seen in nine patients as follows: papillary thyroid cancer (n = 4; 18+ to 27+ months), adrenocortical cancer (n = 2; 7 and 11 months), and one each of melanoma (platelet-derived growth factor receptor mutation positive; 14 months), renal (6 months), and pancreatic cancer (6 months).
  • Activity was seen, especially in patients with medullary thyroid cancer, a tumor characterized by RET mutations.

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  • (PMID = 19903778.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA062461-10; United States / NCI NIH HHS / CA / U01 CA062461; United States / NCI NIH HHS / CA / 5 U01 CA062461; United States / NCI NIH HHS / CA / U01 CA062461-10
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzenesulfonates; 0 / Phenylurea Compounds; 0 / Pyridines; 0 / Quinolones; 192185-72-1 / tipifarnib; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 2.5.1.29 / Farnesyltranstransferase; EC 2.7.10.1 / Proto-Oncogene Proteins c-ret; EC 2.7.10.1 / RET protein, human
  • [Other-IDs] NLM/ NIHMS140339; NLM/ PMC2784003
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19. Ismail A, Bateman A: Expression of TBX2 promotes anchorage-independent growth and survival in the p53-negative SW13 adrenocortical carcinoma. Cancer Lett; 2009 Jun 18;278(2):230-40
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  • [Title] Expression of TBX2 promotes anchorage-independent growth and survival in the p53-negative SW13 adrenocortical carcinoma.
  • The transcriptional regulator TBX2 is genetically amplified in several cancers and has, in addition, important roles in development.
  • Here we used SW13 carcinoma cells which express inactive p53 and have no detectable p16 or p21 CDK-inhibitors as a model to study these functions.
  • This is a cell type-dependent effect as TBX2 overexpression in PANC1 pancreatic cancer cells which are p53-negative has no effect on colony formation or survival after irradiation.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. T-Box Domain Proteins / physiology. Tumor Suppressor Protein p53 / physiology
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation. Cell Survival / drug effects. Cell Survival / radiation effects. Doxorubicin / pharmacology. Endoplasmic Reticulum / metabolism. Humans. Phosphatidylinositol 3-Kinases / physiology

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  • (PMID = 19216023.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / T-Box Domain Protein 2; 0 / T-Box Domain Proteins; 0 / Tumor Suppressor Protein p53; 80168379AG / Doxorubicin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
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20. Paramonova I, Haase M, Mülders-Opgenoorth B, Ansurudeen-Rafi I, Bornstein SR, Papewalis C, Schinner S, Schott M, Scherbaum WA, Willenberg HS: The effects of the endothelium on adrenal steroidogenesis and growth are mainly mediated by proteins other than endothelin-1. Horm Metab Res; 2010 Nov;42(12):840-5
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  • [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.
  • [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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21. Lodish MB, Stratakis CA: Rare and unusual endocrine cancer syndromes with mutated genes. Semin Oncol; 2010 Dec;37(6):680-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rare and unusual endocrine cancer syndromes with mutated genes.
  • The study of a number of rare familial syndromes associated with endocrine tumor development has led to the identification of genes involved in the development of these tumors.
  • Major advances have expanded our understanding of the pathophysiology of these rare endocrine tumors, resulting in the elucidation of causative genes in rare familial diseases and a better understanding of the signaling pathways implicated in endocrine cancers.
  • Recognition of the familial syndrome associated with a particular patient's endocrine tumor has important implications in terms of prognosis, screening of family members, and screening for associated conditions.
  • [MeSH-major] Endocrine Gland Neoplasms / diagnosis. Endocrine Gland Neoplasms / genetics. Neoplastic Syndromes, Hereditary / diagnosis. Neoplastic Syndromes, Hereditary / genetics
  • [MeSH-minor] Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / genetics. Carney Complex / diagnosis. Carney Complex / genetics. Hamartoma / diagnosis. Hamartoma / genetics. Humans. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / genetics. Rare Diseases

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  • [Copyright] Published by Elsevier Inc.
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  • (PMID = 21167385.001).
  • [ISSN] 1532-8708
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 HD999999
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS246989; NLM/ PMC3053053
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22. Coulter CL: Fetal adrenal development: insight gained from adrenal tumors. Trends Endocrinol Metab; 2005 Jul;16(5):235-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fetal adrenal development: insight gained from adrenal tumors.
  • Conversely, tumor progression and the development of cancer probably occur through a process of dysregulation and dedifferentiation.
  • Similarities exist between normal human fetal adrenal cortex and adrenal cancers, such as high expression of growth factors, including insulin-like growth factor II.
  • Therefore, we might gain insight into factors involved in adrenocortical development through better understanding the development and progression of adrenocortical tumors.
  • This review is prompted by recent gene profiling studies that have identified genes differentially expressed between normal and abnormal adrenal glands.
  • Several of these genes are specific growth factors or key cell cycle regulators, in addition to genes not previously associated with adrenal growth or function.
  • [MeSH-major] Adrenal Gland Neoplasms / pathology. Adrenal Glands / embryology

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  • (PMID = 15949953.001).
  • [ISSN] 1043-2760
  • [Journal-full-title] Trends in endocrinology and metabolism: TEM
  • [ISO-abbreviation] Trends Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Somatomedins
  • [Number-of-references] 62
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23. Iyoda A, Moriya Y, Hiroshima K, Shibuya K, Yoshino I: Successful management of postoperative acute respiratory distress syndrome in a patient with lung cancer. Gen Thorac Cardiovasc Surg; 2008 Jul;56(7):354-6
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  • [Title] Successful management of postoperative acute respiratory distress syndrome in a patient with lung cancer.
  • Acute respiratory distress syndrome after pulmonary resection for lung cancer frequently has a lethal outcome.
  • A 74-year-old man was diagnosed with lung cancer and referred to the outpatient department of Chiba University Hospital with double primary lung cancers located in the right upper lobe that were staged at T2N0M0 (stage IB).
  • [MeSH-major] Adrenal Cortex Hormones / therapeutic use. Glycine / analogs & derivatives. Lung Neoplasms / surgery. Pneumonectomy / adverse effects. Proteinase Inhibitory Proteins, Secretory / therapeutic use. Respiratory Distress Syndrome, Adult / drug therapy. Sulfonamides / therapeutic use

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24. Szabó PM, Wiener Z, Tömböl Z, Kovács A, Pócza P, Horányi J, Kulka J, Riesz P, Tóth M, Patócs A, Gaillard RC, Falus A, Rácz K, Igaz P: Differences in the expression of histamine-related genes and proteins in normal human adrenal cortex and adrenocortical tumors. Virchows Arch; 2009 Aug;455(2):133-42
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  • [Title] Differences in the expression of histamine-related genes and proteins in normal human adrenal cortex and adrenocortical tumors.
  • Histamine is involved in the pathogenesis of several tumors; however, there are no data on its possible involvement in human adrenocortical tumorigenesis.
  • The expression of genes and proteins involved in the biosynthesis (histidine decarboxylase, HDC), action (histamine receptors: HRH1-HRH4), and metabolism of histamine is largely unknown both in the normal human adrenal cortex and in adrenocortical tumors.
  • In this study, we examined the expression of histamine-related genes and proteins and histamine content in normal adrenal cortex, benign adrenocortical adenomas, and malignant adrenocortical cancer (ACC).
  • We found that all proteins involved in histamine biosynthesis and action are present both in the normal adrenal cortex and in the tumors studied.
  • Adrenocortical tumorigenesis might, thus, be characterized by reduced histamine biosynthesis; furthermore, different adrenocortical tumor subtypes may show unique histamine receptor expression profiles.
  • [MeSH-major] Adrenal Cortex / metabolism. Adrenal Cortex Neoplasms / metabolism. Adrenocortical Adenoma / metabolism. Histamine / metabolism. Histidine Decarboxylase / metabolism. Receptors, Histamine / metabolism

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

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

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  • (PMID = 16378774.001).
  • [ISSN] 1555-7162
  • [Journal-full-title] The American journal of medicine
  • [ISO-abbreviation] Am. J. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 9002-60-2 / Adrenocorticotropic Hormone; R9400W927I / Ketoconazole
  • [Number-of-references] 100
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27. Kanczkowski W, Morawietz H, Ziegler CG, Funk RH, Schmitz G, Zacharowski K, Mohn CE, Ehrhart-Bornstein M, Bornstein SR: Pam3CSK4 and LTA-TLRs ligands associated with microdomains induce IL8 production in human adrenocortical cancer cells. Horm Metab Res; 2007 Jun;39(6):457-60
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  • [Title] Pam3CSK4 and LTA-TLRs ligands associated with microdomains induce IL8 production in human adrenocortical cancer cells.
  • Bacterially derived ligands, Pam3CSK4 and LPS, can directly impact adrenal glands steroidogenesis through microdomain-related TLR1/2 and 4, respectively, and indirectly via immune cell-derived cytokines.
  • CXC chemokine-dependent immune cell infiltration into adrenocortical carcinomas (ACC), which correlates with poor prognosis, is a common phenomenon.
  • Recently, IL8 was identified in ACC and NCI-H295R cells, and was found to contribute to ACC tumour growth.
  • This is the first study to demonstrate the expression of several TLRs including TLR1, 3, 6, 7 and 9 in human adrenocortical cells by using the RT-PCR approach.
  • Our data suggest that gram-positive bacteria-related TLR1/2/6 ligands might contribute to adrenal gland tumorigenesis via IL8 production.
  • [MeSH-major] Adrenal Cortex Neoplasms / immunology. Interleukin-8 / biosynthesis. Lipopolysaccharides / pharmacology. Peptides / pharmacology. Teichoic Acids / pharmacology. Toll-Like Receptors / physiology

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  • (PMID = 17578764.001).
  • [ISSN] 0018-5043
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Interleukin-8; 0 / Ligands; 0 / Lipopeptides; 0 / Lipopolysaccharides; 0 / Pam(3)CSK(4) peptide; 0 / Peptides; 0 / Teichoic Acids; 0 / Toll-Like Receptors; 56411-57-5 / lipoteichoic acid
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28. Balasubramaniam S, Fojo T: Practical considerations in the evaluation and management of adrenocortical cancer. Semin Oncol; 2010 Dec;37(6):619-26
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  • [Title] Practical considerations in the evaluation and management of adrenocortical cancer.
  • Adrenocortical cancer (ACC) is a rare, challenging disease with a broad range of clinical presentations.
  • Often presenting in an advanced stage with a large, locally invasive primary tumor or with Cushing's syndrome, it requires a multidisciplinary approach to treatment.
  • Biopsies should be performed only when metastatic disease is present and a primary tumor has not been clearly established.
  • [MeSH-major] Adrenocortical Carcinoma / pathology. Adrenocortical Carcinoma / therapy

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  • [Copyright] Published by Elsevier Inc.
  • (PMID = 21167380.001).
  • [ISSN] 1532-8708
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 5W494URQ81 / Streptozocin; 78E4J5IB5J / Mitotane
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29. Nychytaĭlo ME, Diachenko VV, Litvinenko AN, Gul'ko ON, Bulik II, Lukecha II: [Experience of performance of laparoscopic adrenalectomy using lateral transabdominal approach]. Klin Khir; 2008 Sep;(9):41-4
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  • In 2002-2008 yrs. in the Department of Laparoscopic Surgery and Cholelithiasis in 52 patients laparoscopic adrenalectomy (LA) was accomplished, performed for different diseases of suprarenal glands.
  • Incidentaloma was diagnosed in 8, fibroma--in 4, pheokhromocytoma--in 10, aldosteroma--in 11, adrenocortical cancer--in 3, corticosteroma--in 13, suprarenal gland cyst--in 3 patients.
  • The operation time in right-sided and left-sided LA had constituted accordingly 85 and 118 minutes.
  • In 1 (2.4%) observation hemoperitoneum had occurred as a result of traumatic damage of spleen during performance of left-sided LA.

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  • (PMID = 19278040.001).
  • [ISSN] 0023-2130
  • [Journal-full-title] Klinichna khirurhiia
  • [ISO-abbreviation] Klin Khir
  • [Language] RUS
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Ukraine
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30. Toumi S, Ghnaya H, Braham A, Harrabi I, Laouani-Kechrid C, Groupe tunisien d'étude des myosites inflammatoires: [Polymyositis and dermatomyositis in adults. Tunisian multicentre study]. Rev Med Interne; 2009 Sep;30(9):747-53
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  • [Transliterated title] Les polymyosites et dermatomyosites de l'adulte. Etude multicentrique tunisienne.
  • The mean age at diagnosis was 40.7 years.
  • Malignant disease was found in 12.8% of the patients (mainly gynecological and nasopharyngeal cancers).
  • CONCLUSION: The particularities of PM and DM in Tunisia are the preponderance of DM, early onset of the disease and high frequency of the nasopharyngeal cancer.

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  • (PMID = 19683369.001).
  • [ISSN] 0248-8663
  • [Journal-full-title] La Revue de medecine interne
  • [ISO-abbreviation] Rev Med Interne
  • [Language] FRE
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Multicenter Study
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Anti-Inflammatory Agents; 0 / Glucocorticoids; 0 / Immunosuppressive Agents; X4W7ZR7023 / Methylprednisolone
  • [Investigator] Ajili F; Azzabi S; Bahri F; Béji M; Ben Abdelhafidh N; Ben Dridi M; Ben Hassine L; Bouajina I; Bougacha N; Darghouthi S; Ghannouchi N; Hamdoun S; Hammami S; Hmidi A; Houman MH; Khalfallah N; Khanfir M; Ksontini I; Mahfoudhi M; Mahjoub S; Mahmoud I; Mkhinini M; Nouira R; Othmani S; Rokbani L; Romdhane H; Saidane O; Soltani I
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31. Bauditz J, Quinkler M, Beyersdorff D, Wermke W: Improved detection of hepatic metastases of adrenocortical cancer by contrast-enhanced ultrasound. Oncol Rep; 2008 May;19(5):1135-9
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  • [Title] Improved detection of hepatic metastases of adrenocortical cancer by contrast-enhanced ultrasound.
  • Adrenocortical carcinoma (ACC) is a rare and heterogeneous malignancy whose pathogenesis and poor prognosis is poorly understood.
  • Computerized tomography (CT) and magnetic resonance imaging (MRI) are routinely performed for the imaging of the adrenal mass and for standard staging of the chest and abdomen as the lung and liver are the primary organs for metastasis in ACC.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Contrast Media / pharmacology. Liver Neoplasms / secondary. Liver Neoplasms / ultrasonography. Ultrasonography / methods
  • [MeSH-minor] Adult. Aged. Female. Humans. Magnetic Resonance Imaging / methods. Male. Middle Aged. Neoplasm Metastasis. Retrospective Studies. Sensitivity and Specificity. Tomography, X-Ray Computed / methods

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  • (PMID = 18425368.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Contrast Media
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32. Portnov BA, Barchana M, Dubnov J: Exploratory analysis of potential risk factors of a rare disease: spatial distribution of adrenocortical carcinoma in Israel as a case study. Sci Total Environ; 2009 Feb 15;407(5):1738-43
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  • [Title] Exploratory analysis of potential risk factors of a rare disease: spatial distribution of adrenocortical carcinoma in Israel as a case study.
  • In the present study, the performance of proposed approach is investigated by cross-examination of the spatial patterns of three widespread cancers--lung, larynx and colorectal (CRC)--with that of a rare malignant disease--Adrenocortical Carcinoma (ACC).
  • [MeSH-major] Adrenal Cortex Neoplasms / epidemiology. Adrenocortical Carcinoma / epidemiology. Colorectal Neoplasms / epidemiology. Laryngeal Neoplasms / epidemiology. Lung Neoplasms / epidemiology


33. Sidhu S, Martin E, Gicquel C, Melki J, Clark SJ, Campbell P, Magarey CJ, Schulte KM, Röher HD, Delbridge L, Robinson BG: Mutation and methylation analysis of TP53 in adrenal carcinogenesis. Eur J Surg Oncol; 2005 Jun;31(5):549-54
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  • [Title] Mutation and methylation analysis of TP53 in adrenal carcinogenesis.
  • AIM: To investigate the role of coding region mutation and promoter hypermethylation of TP53 in adrenocortical cancer formation.
  • METHODS: Twenty sporadic adrenocortical cancers (ACCs) and five normal adrenal tissue samples were available for analysis.
  • In 10 ACCs and five normal adrenal tissue specimens, methylation of the 16 CpG sites within the TP53 promoter was examined using bisulphite methylation sequencing.
  • Four of 5 patients with a TP53 mutation had metastases at diagnosis or detected soon thereafter and 3 of 4 died of disease within 12 months of surgical resection.
  • No methylation was seen in the TP53 promoter in 10 ACC and the five normal adrenal tissues examined.
  • Promoter methylation of TP53 is not present in ACC as a mechanism for tumour suppressor gene (TSG) inactivation and, therefore, other genes in the 17p13 region are implicated in adrenal carcinogenesis.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Adrenal Gland Neoplasms / metabolism. DNA Methylation. Genes, p53. Mutation. Promoter Regions, Genetic

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  • (PMID = 15922892.001).
  • [ISSN] 0748-7983
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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34. Elad S, Levitt M, M Y S: [Chronic graft-versus-host-disease involving the oral mucosa: clinical presentation and treatment]. Refuat Hapeh Vehashinayim (1993); 2008 Nov;25(4):19-27, 72
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  • The chronic syndrome of GVHD (cGVHD) occurs in approximately 50% of patients post hematopoietic stem cell transplantation (HSCT) and remains the leading cause of non-malignant mortality.
  • In addition to impaired oral functions, cGVHD may lead to secondary malignancies in the form of solid cancers, particularly squamous cell carcinomas of the oral cavity.
  • The NIH consensus paper referred to standard criteria for diagnosis, classification, and response to treatment.
  • [MeSH-major] Graft vs Host Disease / diagnosis. Mouth Diseases / diagnosis
  • [MeSH-minor] Administration, Buccal. Adrenal Cortex Hormones / therapeutic use. Carcinoma, Squamous Cell / diagnosis. Chronic Disease. Glucocorticoids / therapeutic use. Hematopoietic Stem Cell Transplantation / adverse effects. Humans. Immunosuppressive Agents / therapeutic use. Lichenoid Eruptions / diagnosis. Mouth Mucosa / pathology. Mouth Neoplasms / diagnosis. Neoplasms, Second Primary / diagnosis. Oral Ulcer / diagnosis. Phototherapy

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  • (PMID = 19263864.001).
  • [ISSN] 0792-9935
  • [Journal-full-title] Refuʼat ha-peh ṿeha-shinayim (1993)
  • [ISO-abbreviation] Refuat Hapeh Vehashinayim (1993)
  • [Language] heb
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Israel
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Glucocorticoids; 0 / Immunosuppressive Agents
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36. Mannelli M, Cantini G, Poli G, Mangoni M, Nesi G, Canu L, Rapizzi E, Borgogni E, Ercolino T, Piccini V, Luconi M: Role of the PPAR-γ system in normal and tumoral pituitary corticotropic cells and adrenal cells. Neuroendocrinology; 2010;92 Suppl 1:23-7
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  • [Title] Role of the PPAR-γ system in normal and tumoral pituitary corticotropic cells and adrenal cells.
  • In this minireview, we summarize the current knowledge on PPAR-γ in normal and tumoral corticotropic pituitary and adrenal cells.
  • The receptor expression has been shown in ACTH-secreting cells in both normal and adenomal pituitary as well as in normal and tumor adrenal cortex.
  • Preclinical studies conducted both in vitro on tumor cells and in vivo on xenograft tumor models obtained by subcutaneous injection of cancer cells have evidenced the anticancer properties of TZD, in particular rosiglitazone (RGZ) and pioglitazone (PIO).
  • In both pituitary and adrenocortical cancer, RGZ treatment results in inhibition of cell proliferation, through G0/G1 cell-cycle arrest and induction of cell apoptosis, leading to significant inhibition of tumor growth in the xenograft tumor models.
  • [MeSH-major] Adrenal Cortex / metabolism. Corticotrophs / metabolism. PPAR gamma / metabolism. Pituitary ACTH Hypersecretion / metabolism. Pituitary Gland / metabolism
  • [MeSH-minor] Adrenal Cortex Neoplasms / drug therapy. Adrenal Cortex Neoplasms / metabolism. Humans. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / metabolism. Thiazolidinediones / therapeutic use

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  • [Copyright] Copyright © 2010 S. Karger AG, Basel.
  • (PMID = 20829614.001).
  • [ISSN] 1423-0194
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / PPAR gamma; 0 / Thiazolidinediones; X4OV71U42S / pioglitazone
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37. 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.
  • In sporadic ACC, some molecular modifications are commonly observed (i.e., overexpression of insulin-like growth factor II or vascular endothelial growth factor and somatic mutations of tumor protein 53).
  • When surgical resection of the tumor is impossible or ineffective, chemotherapy with etoposide, doxorubicin and cisplatin plus mitotane or with streptozotocin plus mitotane is frequently used; however, the overall survival rates are disappointing.
  • New treatments, such as insulin-like growth factor I receptor antibodies, tyrosine kinase inhibitors and other antiangiogenic compounds, are now being intensively investigated to identify better therapies for this extremely severe malignant neoplasia.
  • [MeSH-major] Adrenal Cortex Neoplasms / therapy. Adrenocortical Carcinoma / therapy

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

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  • (PMID = 16551738.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 156
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39. Yang JY, Yang MQ, Luo Z, Ma Y, Li J, Deng Y, Huang X: A hybrid machine learning-based method for classifying the Cushing's Syndrome with comorbid adrenocortical lesions. BMC Genomics; 2008;9 Suppl 1:S23
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  • [Title] A hybrid machine learning-based method for classifying the Cushing's Syndrome with comorbid adrenocortical lesions.
  • BACKGROUND: The prognosis for many cancers could be improved dramatically if they could be detected while still at the microscopic disease stage.
  • It follows from a comprehensive statistical analysis that a number of antigens such as hTERT, PCNA and Ki-67 can be considered as cancer markers, while another set of antigens such as P27KIP1 and FHIT are possible markers for normal tissue.
  • Because more than one marker must be considered to obtain a classification of cancer or no cancer, and if cancer, to classify it as malignant, borderline, or benign, we must develop an intelligent decision system that can fullfill such an unmet medical need.
  • We have also used immunohistochemistry techniques to measure the gene expression profiles from a number of antigens such as cyclin E, P27KIP1, FHIT, Ki-67, PCNA, Bax, Bcl-2, P53, Fas, FasL and hTERT in several particular types of neuroendocrine tumors such as pheochromocytomas, paragangliomas, and the adrenocortical carcinomas (ACC), adenomas (ACA), and hyperplasia (ACH) involved with Cushing's syndrome.
  • We provided statistical evidence that higher expression levels of hTERT, PCNA and Ki-67 etc. are associated with a higher risk that the tumors are malignant or borderline as opposed to benign.
  • While no significant difference was found between cell-arrest antigens such as P27KIP1 for malignant, borderline, and benign tumors, there was a significant difference between expression levels of such antigens in normal adrenal medulla samples and in adrenomedullary tumors.
  • This research has many potential applications; it might provide an alternative diagnostic tool and a better understanding of the mechanisms involved in malignant transformation as well as information that is useful for treatment planning and cancer prevention.
  • [MeSH-major] Adrenal Cortex Neoplasms / classification. Algorithms. Artificial Intelligence. Biomarkers, Tumor / metabolism. Cushing Syndrome / classification


40. Brown KL, Bacal D: Large adrenocortical carcinoma. J Natl Med Assoc; 2009 Dec;101(12):1287-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Large adrenocortical carcinoma.
  • Adrenal cortical carcinomas (ACCs) are rare, highly malignant tumors that carry a poor prognosis.
  • The goal of this report is to enrich the growing body of knowledge concerning the presentation, evaluation, and surgical intervention of these rare cancers.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / surgery. Adrenocortical Carcinoma / diagnosis. Adrenocortical Carcinoma / surgery
  • [MeSH-minor] Diagnosis, Differential. Diagnostic Imaging. Humans. Male. Middle Aged

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  • (PMID = 20070018.001).
  • [ISSN] 1943-4693
  • [Journal-full-title] Journal of the National Medical Association
  • [ISO-abbreviation] J Natl Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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46. 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.
  • Somatic mutations of the tumour suppressor gene TP53 are observed in a third of ACCs.
  • This recent progress in the molecular genetics of ACC has led to the development of new molecular markers for the diagnosis of malignancy; these might also help to identify prognostic markers of ACC and may ultimately lead to novel therapeutic approaches.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology

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  • (PMID = 19500768.001).
  • [ISSN] 1878-1594
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 67
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47. Turner DJ, Miskulin J: Management of adrenal lesions. Curr Opin Oncol; 2009 Jan;21(1):34-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Management of 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
  • [MeSH-minor] Biomarkers, Tumor / analysis. Humans

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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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48. Roman S: Adrenocortical carcinoma. Curr Opin Oncol; 2006 Jan;18(1):36-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenocortical carcinoma.
  • PURPOSE OF REVIEW: Adrenocortical carcinoma is a rare malignancy, accounting for 0.02% of all annual cancers reported.
  • Given the generally advanced stage at diagnosis, the overall 5-year survival remains poor, varying between 20 and 45%.
  • RECENT FINDINGS: Recent studies focusing on the tumorigenesis of adrenocortical carcinoma have focused on onco-developmental genes present in the fetal adrenal cortex, as well as local adrenal paracrine and autocrine effects of cellular peptides.
  • SUMMARY: Pre-operative diagnostic advances in positron emission scanning are emerging as promising modalities for confirmation of malignancy of indeterminate adrenal masses.
  • No significant advances in the treatment of adrenocortical carcinoma have been developed.
  • [MeSH-major] Adrenal Cortex Neoplasms. Adrenocortical Carcinoma

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  • (PMID = 16357562.001).
  • [ISSN] 1040-8746
  • [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 / Antineoplastic Agents, Hormonal; 0 / Vascular Endothelial Growth Factor A; 104625-48-1 / Activins; 57285-09-3 / Inhibins; 78E4J5IB5J / Mitotane
  • [Number-of-references] 38
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49. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • Mean tumor size was 132 mm.
  • 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).
  • Neither tumor size, stage, functional status, completeness of surgery, nor plasma level of op'DDD was associated with the occurrence of PC.
  • 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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50. Kumar S, Mandal AK, Acharya N, Thingnam SK, Bhalla V, Singh SK: Superior mesenteric artery injury during en bloc excision of a massive left adrenal tumor. Urol Int; 2007;78(2):182-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Superior mesenteric artery injury during en bloc excision of a massive left adrenal tumor.
  • We report the first case of inadvertent injury of the superior mesenteric artery during surgery of a large malignant adrenocortical tumor with inferior vena cava thrombus.
  • The cause of inadvertent injury was anatomical distortion of the great vessels due to the massive nature of the tumor.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenalectomy. Adrenocortical Carcinoma / surgery. Intraoperative Complications / etiology. Mesenteric Artery, Superior / injuries

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  • [Copyright] 2007 S. Karger AG, Basel
  • (PMID = 17293663.001).
  • [ISSN] 0042-1138
  • [Journal-full-title] Urologia internationalis
  • [ISO-abbreviation] Urol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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51. Luconi M, Mangoni M, Gelmini S, Poli G, Nesi G, Francalanci M, Pratesi N, Cantini G, Lombardi A, Pepi M, Ercolino T, Serio M, Orlando C, Mannelli M: Rosiglitazone impairs proliferation of human adrenocortical cancer: preclinical study in a xenograft mouse model. Endocr Relat Cancer; 2010 Mar;17(1):169-77
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rosiglitazone impairs proliferation of human adrenocortical cancer: preclinical study in a xenograft mouse model.
  • Adrenocortical carcinoma (ACC) is a rare aggressive tumor with a poor prognosis.
  • The lack of a specific and effective medical treatment is due to the poor knowledge of the mechanisms underlying tumor growth.
  • Research on potential drugs able to specifically interfere with tumor proliferation is essential to develop more efficacious therapies.
  • We evaluated for the first time the in vivo effect of rosiglitazone (RGZ), an anti-diabetic drug with in vitro anti-tumor properties, on ACC proliferation in a xenograft model obtained by s.c. injection of human ACC H295R cells in athymic mice.
  • When the tumor size reached 5 mm, animals were allocated to 5 mg/kg RGZ- or water-treated groups.
  • Tumor volume was measured twice a week.
  • A significant reduction of tumor growth in RGZ versus control (control) group was observed and was already maximal following 17 day treatment (1-T/C=75.4% (43.7-93.8%)).
  • After 31 days of treatment, mice were killed and tumor analyzed.
  • Tumor histological evaluation revealed characteristics of invasiveness, richness in small vessels and mitotic figures in control group, while RGZ group tumors presented non infiltrating borders, few vessels, and many apoptotic bodies.
  • Tumor immunohistochemistry showed that Ki-67 was reduced in RGZ versus control group.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Carcinoma / pathology. Cell Proliferation / drug effects. Thiazolidinediones / pharmacology
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Cell Line, Tumor. Female. Gene Expression Regulation, Neoplastic / drug effects. Humans. Hypoglycemic Agents / pharmacology. Hypoglycemic Agents / therapeutic use. Mice. Mice, Nude. Tumor Burden / drug effects. Xenograft Model Antitumor Assays

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  • (PMID = 19955217.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hypoglycemic Agents; 0 / Thiazolidinediones; 05V02F2KDG / rosiglitazone
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52. 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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53. 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.
  • The association between this common polymorphism and risk of different cancers has been extensive studied, however various reports are controversial.
  • We have analyzed the 72Pro polymorphic variant in patients with adrenocortical tumors to evaluate whether 72G--> C substitution at codon 72 of TP53 gene may be associated with increased risk for malignancy in adrenal cortex in comparison to the control group.
  • DNA extracted from peripheral leucocytes of 46 Polish patients with adrenocortical tumors (17 malignant and 29 benign) and 50 controls was examined by PCR-HD method followed by direct sequencing.
  • The genotype Arg/Arg, Arg/Pro and Pro/Pro distribution was respectively 53%/35%/12% for cancers, 72%/28%/0% for benign tumors and 76%/24%/0% for controls.
  • High frequency of 72Pro allele in patients with carcinoma (29%) in comparison to the benign tumors (14%) and controls (12%) was statistically analyzed.
  • Our results suggest that the TP53 codon 72 polymorphism could be associated with susceptibility for adrenocortical cancer in the examined Polish patients.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Genetic Predisposition to Disease. Polymorphism, Genetic. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 16786124.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Codon; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53
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54. Tomkova K, Tomka M, Zajac V: Contribution of p53, p63, and p73 to the developmental diseases and cancer. Neoplasma; 2008;55(3):177-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Contribution of p53, p63, and p73 to the developmental diseases and cancer.
  • Tumor suppressor TP53 gene is one of the most mutated genes in human genome.
  • This syndrome is characterized by the early onset of different types of cancers including soft-tissue sarcomas, breast and brain cancers, leukemias, lung, laryngeal cancers, and adrenocortical carcinomas.
  • The key role of p53 in tumor suppression has been confirmed in animal models as well.
  • The p53 -knock-out and knock-in animals were born alive but were tumor prone.
  • On one hand, there are evidences that both, p63 and p73-deficient animals are not tumor prone; on the other hand, there is evidence that such animals develop tumors later during their life.
  • [MeSH-major] DNA-Binding Proteins / genetics. Genes, p53. Membrane Proteins / genetics. Neoplasms / genetics. Nuclear Proteins / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Animals. Embryonic Development. Genes, Tumor Suppressor. Germ-Line Mutation. Humans. Mutation

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

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

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  • (PMID = 19500766.001).
  • [ISSN] 1878-1594
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 46
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57. Mazzaglia PJ, Vezeridis MP: Laparoscopic adrenalectomy: balancing the operative indications with the technical advances. J Surg Oncol; 2010 Jun 15;101(8):739-44
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  • The adoption of this technique had substantial impact on the management of adrenal incidentalomas.
  • Although laparoscopic adrenalectomy should be in general avoided for known primary adrenal cancers, it is appropriate for metastasectomy of isolated adrenal metastatic disease.
  • [MeSH-major] Adrenal Gland Neoplasms / surgery. Adrenalectomy / methods. Laparoscopy / methods
  • [MeSH-minor] Adrenal Cortex Neoplasms / surgery. Humans. Magnetic Resonance Imaging. Pheochromocytoma / surgery

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  • [Copyright] (c) 2010 Wiley-Liss, Inc.
  • (PMID = 20512951.001).
  • [ISSN] 1096-9098
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 46
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58. Loncarevic IF, Hering A, Posorski N, Linden T, Hoyer H, Bucsky P: Number of genomic imbalances correlates with the overall survival for adrenocortical cancer in childhood. Pediatr Blood Cancer; 2008 Sep;51(3):356-62
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  • [Title] Number of genomic imbalances correlates with the overall survival for adrenocortical cancer in childhood.
  • BACKGROUND: Adrenocortical tumours (ACT) in children are rare and, if malignant, often associated with poor prognosis.
  • PROCEDURES: We analysed 14 adrenocortical cancers (ACC) of children by comparative genomic hybridisation (CGH).
  • RESULTS: The total number of genomic imbalances ranged from 1 to 17 in individual tumour samples.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / mortality. Chromosome Aberrations

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18478573.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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59. Nishikawa T, Saito J, Omura M: [Medical treatment for Cushing's syndrome]. Nihon Rinsho; 2008 Jan;66(1):186-91
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  • Thus, we should treat Cushing's syndrome as soon as possible, since many complications, including cardiovascular diseases and infections, will soon occur when the definite diagnosis is delayed.
  • Adrenalectomy is essential for treatment for Cushing's syndrome even in the patients with pituitary or ectopic ACTH-producing tumor.
  • Medical adrenalectomy is achieved by using with mitotane which is usually used for adrenocortical cancer.
  • We commonly treat the patients with Cushing's syndrome due to adrenal tumor and pituitary or ectopic ACTH producing tumor by using metyrapone which mainly inhibits 11-hydroxylase.
  • Replacement therapy with hydrocortisone should be considered if adrenal failure will occur during treatment with those drugs.

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  • (PMID = 18186263.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Aromatase Inhibitors; 0O54ZQ14I9 / Aminoglutethimide; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase; R9400W927I / Ketoconazole; ZS9KD92H6V / Metyrapone
  • [Number-of-references] 6
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60. Puthenparambil J, Lechner K, Kornek G: Autoimmune hemolytic anemia as a paraneoplastic phenomenon in solid tumors: A critical analysis of 52 cases reported in the literature. Wien Klin Wochenschr; 2010 Apr;122(7-8):229-36
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  • We found that AIHA may occur prior to, concurrent with cancer or well after end of treatment, either as a sign of recurrence or in complete remission of the cancer.
  • AIHA occurred in almost all types of cancers, but it was relatively more common in renal cell cancer and Kaposi sarcoma compared to other cancers.
  • In early stage cancers, in particular in renal cell cancers, curative resection of the cancers led to complete, often sustained remission of AIHA within a short time in a number of patients.
  • Resection of the tumor had also beneficial effects in some metastatic cancers.
  • Patients who had a response to resection of the tumor were often refractory to steroid treatment before surgery, while some responses to steroids were observed in patients with metastatic cancer.
  • The study of cancer patients with autoimmune diseases may provide important insights into the biology of tumors.
  • [MeSH-major] Anemia, Hemolytic, Autoimmune / diagnosis. Neoplasms / diagnosis. Paraneoplastic Syndromes / diagnosis
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Adult. Aged. Autoantibodies / blood. Carcinoma, Renal Cell / diagnosis. Carcinoma, Renal Cell / immunology. Carcinoma, Renal Cell / surgery. Drug Resistance. Erythrocytes / immunology. Female. Humans. Kidney Neoplasms / diagnosis. Kidney Neoplasms / immunology. Kidney Neoplasms / surgery. Male. Middle Aged. Neoplasm Recurrence, Local / diagnosis. Neoplasm Recurrence, Local / immunology. Neoplasm Recurrence, Local / surgery. Prognosis. Sarcoma, Kaposi / diagnosis. Sarcoma, Kaposi / immunology. Sarcoma, Kaposi / surgery

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  • (PMID = 20503022.001).
  • [ISSN] 1613-7671
  • [Journal-full-title] Wiener klinische Wochenschrift
  • [ISO-abbreviation] Wien. Klin. Wochenschr.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Autoantibodies
  • [Number-of-references] 68
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61. Advani A, Johnson SJ, Nicol MR, Papacleovoulou G, Evans DB, Vaikkakara S, Mason JI, Quinton R: Adult-onset hypogonadotropic hypogonadism caused by aberrant expression of aromatase in an adrenocortical adenocarcinoma. Endocr J; 2010;57(7):651-6
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  • [Title] Adult-onset hypogonadotropic hypogonadism caused by aberrant expression of aromatase in an adrenocortical adenocarcinoma.
  • Estrogen-secreting adrenal cancers are extremely rare, with feminizing symptoms attributed to aromatase expression in the adrenal tumor.
  • We describe a case of hypogonadotropic hypogonadism as a consequence of aberrant aromatase expression in a patient with adrenocortical adenocarcinoma.
  • A right adrenal mass was identified on CT scanning and the patient underwent an open adrenalectomy.
  • Immunohistochemistry of the adrenal cancer confirmed aberrant expression of aromatase in most, although not all, carcinoma cells.
  • Transcripts associated with utilization of promoters II, I.1 and I.3 were prominently represented in the tumor aromatase mRNA.
  • This case highlights that clinical features of feminizing adrenocortical carcinomas can be secondary to estrogen production by aberrantly transcribed and translated aromatase within the tumor.
  • The diagnosis of adrenocortical adenocarcinoma should be considered in men presenting with low testosterone and gonadotropins, particularly in the presence of feminizing features.
  • [MeSH-major] Adenocarcinoma / genetics. Adrenal Cortex Neoplasms / genetics. Aromatase / genetics. Hypogonadism / genetics

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  • (PMID = 20467160.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] EC 1.14.14.1 / Aromatase
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62. Alberú J, Urrea EM: [Immunosuppression for kidney transplant recipients: current strategies]. Rev Invest Clin; 2005 Mar-Apr;57(2):213-24
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  • [Transliterated title] Inmunosupresión para receptores de trasplante renal: estrategias actuales.
  • However, long-term use of immunosuppressive drugs convey inherent risks which translate in an increase of cancers and infections, among others.
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Antibodies, Monoclonal / therapeutic use. Azathioprine / pharmacology. Azathioprine / therapeutic use. Calcineurin Inhibitors. Cyclosporine / pharmacology. Cyclosporine / therapeutic use. Graft Rejection / prevention & control. Growth Inhibitors / pharmacology. Growth Inhibitors / therapeutic use. Humans. Immunosuppressive Agents / therapeutic use. Mycophenolic Acid / analogs & derivatives. Mycophenolic Acid / pharmacology. Mycophenolic Acid / therapeutic use. Protein Kinases / drug effects. Receptors, Interleukin-2 / antagonists & inhibitors. Sirolimus / pharmacology. Sirolimus / therapeutic use. TOR Serine-Threonine Kinases. Tacrolimus / pharmacology. Tacrolimus / therapeutic use

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  • (PMID = 16524061.001).
  • [ISSN] 0034-8376
  • [Journal-full-title] Revista de investigación clínica; organo del Hospital de Enfermedades de la Nutrición
  • [ISO-abbreviation] Rev. Invest. Clin.
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Mexico
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Antibodies, Monoclonal; 0 / Calcineurin Inhibitors; 0 / Growth Inhibitors; 0 / Immunosuppressive Agents; 0 / Receptors, Interleukin-2; 83HN0GTJ6D / Cyclosporine; 9242ECW6R0 / mycophenolate mofetil; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; HU9DX48N0T / Mycophenolic Acid; MRK240IY2L / Azathioprine; W36ZG6FT64 / Sirolimus; WM0HAQ4WNM / Tacrolimus
  • [Number-of-references] 81
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63. Ide H, Terado Y, Tokiwa S, Nishio K, Saito K, Isotani S, Kamiyama Y, Muto S, Imamura T, Horie S: Novel germ line mutation p53-P177R in adult adrenocortical carcinoma producing neuron-specific enolase as a possible marker. Jpn J Clin Oncol; 2010 Aug;40(8):815-8
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  • [Title] Novel germ line mutation p53-P177R in adult adrenocortical carcinoma producing neuron-specific enolase as a possible marker.
  • Adrenocortical cancer (ACC) is a rare and aggressive endocrine tumor.
  • The patient presented with a large retroperitoneum tumor and lung metastases.
  • Removal of the adrenocortical tumor with part of the transverse colon and tail of the pancreas, spleen and kidney was successfully performed following chemotherapy.
  • Levels of serum neuron-specific enolase (NSE) were found to be markedly high before surgery and may be clinically useful markers for monitoring tumor status during management.
  • Immunohistochemical studies showed that the cancer cells were positive for NSE and overexpression of p53.
  • The genetic and biochemical data presented in this case confirm the importance of screening for p53 status in ACC with inherited cancer syndrome.
  • [MeSH-major] Adrenal Gland Neoplasms / enzymology. Adrenal Gland Neoplasms / genetics. Adrenocortical Carcinoma / enzymology. Adrenocortical Carcinoma / genetics. Biomarkers, Tumor / blood. Genes, p53 / genetics. Germ-Line Mutation. Phosphopyruvate Hydratase / blood

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  • (PMID = 20421238.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 4.2.1.11 / Phosphopyruvate Hydratase
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64. Gau JT, Acharya U, Khan S, Heh V, Mody L, Kao TC: Pharmacotherapy and the risk for community-acquired pneumonia. BMC Geriatr; 2010;10:45
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  • The controls were patients without the discharge diagnosis of pneumonia or acute exacerbation of chronic obstructive pulmonary disease (COPD) (N = 952).
  • Patients with gastric tube feeding, ventilator support, requiring hemodialysis, metastatic diseases or active lung cancers were excluded.
  • [MeSH-major] Adrenal Cortex Hormones / adverse effects. Antipsychotic Agents / adverse effects. Community-Acquired Infections / chemically induced. Community-Acquired Infections / epidemiology. Pneumonia / chemically induced. Pneumonia / epidemiology

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  • (PMID = 20604960.001).
  • [ISSN] 1471-2318
  • [Journal-full-title] BMC geriatrics
  • [ISO-abbreviation] BMC Geriatr
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / R01 AG032298
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Antipsychotic Agents; 0 / Proton Pump Inhibitors
  • [Other-IDs] NLM/ PMC2909244
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65. Sanderson T, Renaud M, Scholten D, Nijmeijer S, van den Berg M, Cowell S, Guns E, Nelson C, Mutarapat T, Ruchirawat S: Effects of lactone derivatives on aromatase (CYP19) activity in H295R human adrenocortical and (anti)androgenicity in transfected LNCaP human prostate cancer cells. Eur J Pharmacol; 2008 Sep 28;593(1-3):92-8
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  • [Title] Effects of lactone derivatives on aromatase (CYP19) activity in H295R human adrenocortical and (anti)androgenicity in transfected LNCaP human prostate cancer cells.
  • Certain lactone-containing secondary plant metabolites display potent biological effects, including anti-tumor activities.
  • This is of particular interest as these compounds appear effective against hormone-dependent cancers, such as those of breast and prostate, of which the incidence is on the rise.
  • The mechanisms of anti-tumor action of these compounds are largely unknown.
  • Thirteen synthetic lactone derivatives were evaluated for effects on aromatase activity and mRNA expression in H295R human adrenocortical carcinoma cells.
  • The androgen receptor is implicated in mediating hormone-dependent prostate tumor growth, and androgen antagonists are effective in the treatment of these cancers.
  • Thus the (anti)androgenic effects of the lactones were also assessed in LNCaP human prostate cancer cells transfected with human androgen receptor and an androgen receptor-responsive luciferase reporter gene.
  • Lactone moiety-containing molecules may form the structural basis for the development of potent drugs effective against hormone-dependent cancers.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Androgens / biosynthesis. Aromatase Inhibitors. Lactones / pharmacology. Prostatic Neoplasms / metabolism
  • [MeSH-minor] Androgen Receptor Antagonists. Cell Line, Tumor. Cyclic AMP / metabolism. Data Interpretation, Statistical. Genes, Reporter. Humans. Luciferases / genetics. Male. RNA, Neoplasm / biosynthesis. RNA, Neoplasm / genetics. Tetrazolium Salts. Thiazoles. Transfection

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  • (PMID = 18639541.001).
  • [ISSN] 0014-2999
  • [Journal-full-title] European journal of pharmacology
  • [ISO-abbreviation] Eur. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Androgen Receptor Antagonists; 0 / Androgens; 0 / Aromatase Inhibitors; 0 / Lactones; 0 / RNA, Neoplasm; 0 / Tetrazolium Salts; 0 / Thiazoles; 298-93-1 / thiazolyl blue; E0399OZS9N / Cyclic AMP; EC 1.13.12.- / Luciferases
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66. Bakthavathsalam G, Shanmugasundaram VP, Prabakaran J, Venkatesh SP, Sowndaravalli DV, Jain CB: Nonfunctioning adrenocorticalcarcinoma. Int Surg; 2008 Mar-Apr;93(2):81-7
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  • Clinically inapparent adrenal masses detected through imaging for nonadrenal disease, often referred to as adrenal incidentalomas, were first described approximately 20 years ago.
  • Despite the rarity of primary endocrine cancers of the adrenal, adrenal masses are one of the most prevalent of all human tumors.
  • The prevalence of adrenal incidentaloma approaches 3% in middle age and increases to as much as 10% in the elderly.
  • This report describes the case of a 30-year-old man who presented primarily with complaints of deep vein thrombosis of the left leg secondary to a nonfunctioning adrenocortical carcinoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis
  • [MeSH-minor] Adult. Humans. Incidental Findings. Male. Venous Thrombosis / diagnosis

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  • (PMID = 18998286.001).
  • [ISSN] 0020-8868
  • [Journal-full-title] International surgery
  • [ISO-abbreviation] Int Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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67. Wang Y, Nicholls PK, Stanton PG, Harrison CA, Sarraj M, Gilchrist RB, Findlay JK, Farnworth PG: Extra-ovarian expression and activity of growth differentiation factor 9. J Endocrinol; 2009 Sep;202(3):419-30
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  • The present studies confirm GDF9 expression in the mouse testis, pituitary gland and adrenocortical cancer (AC) cells, and establish its expression in L beta T2 gonadotrophs, and in mouse adrenal glands, particularly foetal and neonatal cortical cells.
  • Our findings show that GDF9 regulates the expression of R-SMAD2/3-responsive reporter genes through ALK4, 5 or 7 in extra-ovarian (adrenocortical and Sertoli) cells with similar potency and signalling pathway to its actions on granulosa cells, but suggest that expression of BMPRII, ALK5 (TGFBR1) and R-SMADs 2 and 3 may not be sufficient for a cell to respond to GDF9.
  • [MeSH-major] Adrenal Glands / physiology. Growth Differentiation Factor 9 / genetics. Leydig Cells / physiology. Pituitary Gland / physiology. Sertoli Cells / physiology

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  • (PMID = 19505950.001).
  • [ISSN] 1479-6805
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide; 0 / Benzamides; 0 / Dioxoles; 0 / GDF9 protein, human; 0 / Gdf9 protein, mouse; 0 / Gdf9 protein, rat; 0 / Growth Differentiation Factor 9; 9002-68-0 / Follicle Stimulating Hormone; EC 1.13.12.- / Luciferases
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68. Grogan RH, Mitmaker E, Vriens MR, Harari A, Gosnell JE, Shen WT, Clark OH, Duh QY: Adrenal incidentaloma: does an adequate workup rule out surprises? Surgery; 2010 Aug;148(2):392-7
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  • [Title] Adrenal incidentaloma: does an adequate workup rule out surprises?
  • BACKGROUND: Adrenal incidentaloma remains a diagnostic challenge.
  • METHODS: We catalogued adrenal incidentalomas from a retrospective review of 500 consecutive adrenalectomies at a single institution.
  • The outcome measures studied were patient demographics, preoperative biochemical analysis, imaging characteristics, tumor size, type of operation performed, and postoperative histologic diagnosis.
  • Size was the only significant characteristic that distinguished cortical cancers from benign adenomas.
  • CONCLUSION: Current guidelines accurately predict the functional status of adrenal incidentalomas.
  • However, even with the most up-to-date diagnostic tools available, most adrenal incidentalomas resected are benign tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis. Adrenal Gland Neoplasms / surgery. Adrenalectomy. Incidental Findings
  • [MeSH-minor] Adenoma / diagnosis. Adenoma / pathology. Adenoma / physiopathology. Adenoma / surgery. Adrenal Cortex Hormones / secretion. Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / pathology. Adrenal Cortex Neoplasms / physiopathology. Adrenal Cortex Neoplasms / surgery. Adult. Aged. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Practice Guidelines as Topic. Retrospective Studies

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  • [Copyright] Copyright 2010 Mosby, Inc. All rights reserved.
  • (PMID = 20576282.001).
  • [ISSN] 1532-7361
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
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69. Fujiwara M, Kamma H, Wu W, Yano Y, Homma S, Satoh H: Alternative lengthening of telomeres in the human adrenocortical carcinoma cell line H295R. Int J Oncol; 2006 Aug;29(2):445-51
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  • [Title] Alternative lengthening of telomeres in the human adrenocortical carcinoma cell line H295R.
  • The biological significance and molecular mechanism of ALT have not been well studied in human cancers.
  • It has been reported that clinical samples of adrenocortical carcinoma show a low incidence of telomerase positivity.
  • We characterized an adrenocortical carcinoma cell line, H295R, focusing on the telomere maintenance mechanism, and compared it with telomerase-positive 293 cells and HeLa cells.
  • In conclusion, the H295R adrenocortical carcinoma cell line is negative for telomerase and maintains its telomeres by the ALT mechanism.
  • We anticipate that H295R cells will be a good model for understanding the significance and mechanism of ALT in human cancers.
  • [MeSH-major] Adrenal Cortex Neoplasms / ultrastructure. Carcinoma / ultrastructure. Telomere / ultrastructure
  • [MeSH-minor] Cell Line, Tumor. Cell Nucleus / metabolism. HeLa Cells. Humans. In Situ Hybridization, Fluorescence. Neoplasms / metabolism. Oligonucleotides / chemistry. Phenotype. Reverse Transcriptase Polymerase Chain Reaction. Telomerase / metabolism

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  • (PMID = 16820888.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Oligonucleotides; EC 2.7.7.49 / Telomerase
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70. van Duursen MB, Nijmeijer SM, Ruchirawat S, van den Berg M: Chemopreventive actions by enterolactone and 13 VIOXX-related lactone derivatives in H295R human adrenocortical carcinoma cells. Toxicol Lett; 2010 Feb 15;192(3):271-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemopreventive actions by enterolactone and 13 VIOXX-related lactone derivatives in H295R human adrenocortical carcinoma cells.
  • Cytochrome P450c17 (CYP17) has been linked to various hormone-related diseases, including breast cancer, thus being a potential target for cancer chemoprevention.
  • We conclude that the proposed cancer chemopreventive actions of ENL are not mediated through interaction with CYP17 or cell cycle status.
  • Of the VIOXX-related lactone derivatives, CRI-7 could prove useful in the prevention of hormone-dependent cancers, such as breast cancer, since in vitro it shows low cytotoxicity, it is a potent inhibitor of CYP17 activity and strong inducer of cell cycle arrest.
  • [MeSH-major] 4-Butyrolactone / analogs & derivatives. Adrenal Cortex Neoplasms / enzymology. Adrenocortical Carcinoma / enzymology. Lactones / pharmacology. Lignans / pharmacology. Phytoestrogens / pharmacology. Steroid 17-alpha-Hydroxylase / drug effects. Sulfones / pharmacology
  • [MeSH-minor] Cell Cycle / drug effects. Cell Line, Tumor. Enzyme Induction / drug effects. Flavonoids / pharmacology. Gene Expression / drug effects. Humans. Mitogen-Activated Protein Kinase Kinases / antagonists & inhibitors. Neoplasms, Hormone-Dependent / prevention & control. Protein Processing, Post-Translational / drug effects. Structure-Activity Relationship

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  • [Copyright] Copyright 2009 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 19913079.001).
  • [ISSN] 1879-3169
  • [Journal-full-title] Toxicology letters
  • [ISO-abbreviation] Toxicol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Flavonoids; 0 / Lactones; 0 / Lignans; 0 / Phytoestrogens; 0 / Sulfones; 0QTW8Z7MCR / rofecoxib; EC 1.14.99.9 / Steroid 17-alpha-Hydroxylase; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; OL659KIY4X / 4-Butyrolactone; X01E7E1D6H / 2,3-bis(3'-hydroxybenzyl)butyrolactone
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71. Iorgulescu R, Ilie R, Iorgulescu A, Borca V, Dragomirescu C: [Intraabdominal malignant pathology missed at laparoscopic cholecystectomy]. Chirurgia (Bucur); 2005 Mar-Apr;100(2):121-5
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  • [Title] [Intraabdominal malignant pathology missed at laparoscopic cholecystectomy].
  • [Transliterated title] Patologie malignă abdominală omisă la colecistectomia laparoscopică.
  • Studying the archives of our clinic from January 1995 up to December 2003, we found 15 cases of intraabdominal neoplasia diagnosed in the year that followed laparoscopic cholecystectomy: 7 colorectal cancers, 4 pancreatic cancers, 2 gastric carcinomas, one uterine and one adrenocortical malignancies.
  • [MeSH-major] Abdominal Neoplasms / diagnosis. Cholecystectomy, Laparoscopic. Diagnostic Errors
  • [MeSH-minor] Adrenal Cortex Neoplasms / diagnosis. Adult. Aged. Colorectal Neoplasms / diagnosis. Female. Humans. Male. Medical Records. Middle Aged. Pancreatic Neoplasms / diagnosis. Retrospective Studies. Stomach Neoplasms / diagnosis. Uterine Neoplasms / diagnosis

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  • (PMID = 15957452.001).
  • [ISSN] 1221-9118
  • [Journal-full-title] Chirurgia (Bucharest, Romania : 1990)
  • [ISO-abbreviation] Chirurgia (Bucur)
  • [Language] rum
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Romania
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72. Sanderson JT: The steroid hormone biosynthesis pathway as a target for endocrine-disrupting chemicals. Toxicol Sci; 2006 Nov;94(1):3-21
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  • Interferences with steroid biosynthesis may result in impaired reproduction, alterations in (sexual) differentiation, growth, and development and the development of certain cancers.
  • Particularly aromatase (CYP19), the enzyme that converts androgens to estrogens, has been the subject of studies into the mechanisms by which chemicals interfere with sex steroid hormone homeostasis and function, often related to (de)feminization and (de)masculinazation processes.
  • Studies in vivo and in vitro have focussed on ovarian and testicular function, with less attention given to other steroidogenic organs, such as the adrenal cortex.

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  • (PMID = 16807284.001).
  • [ISSN] 1096-6080
  • [Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology
  • [ISO-abbreviation] Toxicol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytochrome P-450 Enzyme Inhibitors; 0 / Endocrine Disruptors; 0 / Gonadal Steroid Hormones; 9035-51-2 / Cytochrome P-450 Enzyme System
  • [Number-of-references] 173
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73. Wandoloski M, Bussey KJ, Demeure MJ: Adrenocortical cancer. Surg Clin North Am; 2009 Oct;89(5):1255-67
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  • [Title] Adrenocortical cancer.
  • Adrenocortical carcinoma (ACC) is a rare endocrine malignancy causing up to 0.2% of all cancer deaths This article reviews the incidence, presentation, and pathology of ACC.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Combined Modality Therapy. Diagnosis, Differential. Diagnostic Imaging. Genetic Predisposition to Disease. Humans. Mitotane / therapeutic use

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  • (PMID = 19836496.001).
  • [ISSN] 1558-3171
  • [Journal-full-title] The Surgical clinics of North America
  • [ISO-abbreviation] Surg. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 78E4J5IB5J / Mitotane
  • [Number-of-references] 51
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74. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Somatic TP53 mutations are relatively rare among adrenocortical cancers with the frequent 17p13 loss of heterozygosity.
  • PURPOSE: Allelic losses [loss of heterozygosity (LOH)] at the 17p13 locus are frequent (85%) in adrenocortical cancers.
  • The tumor suppressor gene TP53 is located at 17p13.
  • The aim of the study was to determine the frequency of TP53 somatic inactivating mutations in adrenocortical tumors with 17p13 LOH and their clinico-biological correlations.
  • EXPERIMENTAL DESIGN: TP53 somatic mutations, intragenic LOH (VNTR1 marker), and p53 overexpression were studied in 36 adrenocortical tumors with 17p13 LOH determined by Southern blot.
  • TP53-mutant tumors were significantly larger than wild-type TP53 tumors (median tumor weight: 640 versus 185 g; P=0.02), were associated with a more advanced stage of tumor progression (MacFarlane stage IV; P=0.01), and had a shorter disease-free survival (P=0.03).
  • CONCLUSIONS: The finding that only a minority of adrenocortical tumors with 17p13 LOH had either a VNTR1 LOH or a TP53 mutation indicates that TP53 might not be the only or major tumor suppressor gene at 17p13 involved in adrenocortical cancer progression.
  • We suggest that a genetic instability of the 17p13 region, occurring early in adrenocortical cancer development, involves various genes located in this region.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Chromosomes, Human, Pair 17. Genes, p53. Loss of Heterozygosity. Minisatellite Repeats / genetics. Mutation
  • [MeSH-minor] Adult. Alleles. Disease Progression. Female. Humans. Immunohistochemistry. Male. Middle Aged. RNA, Neoplasm / chemistry

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  • (PMID = 17289876.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Neoplasm
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75. Gaujoux S, Tissier F, Groussin L, Libé R, Ragazzon B, Launay P, Audebourg A, Dousset B, Bertagna X, Bertherat J: Wnt/beta-catenin and 3',5'-cyclic adenosine 5'-monophosphate/protein kinase A signaling pathways alterations and somatic beta-catenin gene mutations in the progression of adrenocortical tumors. J Clin Endocrinol Metab; 2008 Oct;93(10):4135-40
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  • [Title] Wnt/beta-catenin and 3',5'-cyclic adenosine 5'-monophosphate/protein kinase A signaling pathways alterations and somatic beta-catenin gene mutations in the progression of adrenocortical tumors.
  • BACKGROUND: The Wnt/beta-catenin and cAMP signaling pathways play an important role in adrenal cortex tumorigenesis.
  • Somatic activating mutations of the beta-catenin gene (CTNNB1) are the most frequent genetic defects identified both in adrenocortical adenomas (ACAs) and adrenocortical cancers (ACCs).
  • PRKAR1A mutations leading to cAMP pathway dysregulation are observed in primary pigmented nodular adrenocortical diseases (PPNADs) and some sporadic ACAs.
  • OBJECTIVE: The objective of the investigation was to study Wnt/beta-catenin dysregulation in adrenocortical tumors (ACTs) with cAMP pathway genetic alteration and search for secondary CTNNB1 somatic mutations in heterogeneous tumors.
  • PATIENTS AND METHODS: Nine PPNADs, including five with macronodules, three ACAs with PRKAR1A somatic mutations, and one heterogeneous tumor with ACC developed within an ACA, were studied by immunohistochemistry and DNA sequencing.
  • RESULTS: beta-Catenin accumulation was observed in all PPNADs, ACAs with PRKAR1A mutations, and the ACC component of the heterogeneous tumor.
  • CTNNB1 somatic activating mutations were found in the macronodule of two of the five macronodular PPNADs, in one ACA with a PRKAR1A somatic mutation, and in the malignant part of the heterogeneous ACT.
  • This underlines the importance of the Wnt/beta-catenin pathway in adrenal cortex tumorigenesis and the importance of genetic accumulation in the progression of ACTs.
  • [MeSH-major] Adenoma / genetics. Adrenal Cortex Neoplasms / genetics. Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / genetics. Mutation. Signal Transduction / genetics. Wnt Proteins / genetics. beta Catenin / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Cyclic AMP / metabolism. DNA Mutational Analysis. Disease Progression. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Neoplasm Invasiveness. Tumor Burden / genetics

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  • (PMID = 18647815.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human; 0 / Wnt Proteins; 0 / beta Catenin; E0399OZS9N / Cyclic AMP
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76. Lawnicka H, Kowalewicz-Kulbat M, Sicinska P, Kazimierczuk Z, Grieb P, Stepien H: Anti-neoplastic effect of protein kinase CK2 inhibitor, 2-dimethylamino-4,5,6,7-tetrabromobenzimidazole (DMAT), on growth and hormonal activity of human adrenocortical carcinoma cell line (H295R) in vitro. Cell Tissue Res; 2010 May;340(2):371-9
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  • [Title] Anti-neoplastic effect of protein kinase CK2 inhibitor, 2-dimethylamino-4,5,6,7-tetrabromobenzimidazole (DMAT), on growth and hormonal activity of human adrenocortical carcinoma cell line (H295R) in vitro.
  • CK2 kinase (casein kinase-2) has been suggested to be a constituent of a neoplastic milleu, and its inhibition might represent a new approach to cancer therapy.
  • Adrenocortical carcinomas (ACCs) are highly malignant neoplasms with poor overall prognosis.
  • We have examined the effects of 2-dimethylamino-4,5,6,7-tetrabromobenzimidazole (DMAT), a potent CK2 inhibitor, on the H295R human adrenocortical cancer cell line.
  • [MeSH-major] Adrenal Cortex Hormones / secretion. Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Benzimidazoles / pharmacology. Casein Kinase II / antagonists & inhibitors. Cell Proliferation / drug effects. Protein Kinase Inhibitors / pharmacology
  • [MeSH-minor] 17-alpha-Hydroxyprogesterone / metabolism. Aldosterone / secretion. Antineoplastic Agents / pharmacology. Cell Cycle / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Dehydroepiandrosterone Sulfate / metabolism. Drug Screening Assays, Antitumor. Humans. Hydrocortisone / secretion

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  • (PMID = 20383646.001).
  • [ISSN] 1432-0878
  • [Journal-full-title] Cell and tissue research
  • [ISO-abbreviation] Cell Tissue Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / 4,5,6,7-tetrabromobenzimidazole; 0 / Adrenal Cortex Hormones; 0 / Antineoplastic Agents; 0 / Benzimidazoles; 0 / Protein Kinase Inhibitors; 4964P6T9RB / Aldosterone; 57B09Q7FJR / Dehydroepiandrosterone Sulfate; 68-96-2 / 17-alpha-Hydroxyprogesterone; EC 2.7.11.1 / Casein Kinase II; WI4X0X7BPJ / Hydrocortisone
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77. Ragazzon B, Libé R, Gaujoux S, Assié G, Fratticci A, Launay P, Clauser E, Bertagna X, Tissier F, de Reyniès A, Bertherat J: Transcriptome analysis reveals that p53 and {beta}-catenin alterations occur in a group of aggressive adrenocortical cancers. Cancer Res; 2010 Nov 1;70(21):8276-81
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  • [Title] Transcriptome analysis reveals that p53 and {beta}-catenin alterations occur in a group of aggressive adrenocortical cancers.
  • Adrenocortical carcinoma (ACC) is a rare disease with an overall poor but heterogeneous prognosis.
  • This heterogeneity could reflect different mechanisms of tumor development.
  • Somatic inactivating mutations of the tumor suppressor gene TP53 and activating mutations of the proto-oncogene β-catenin (CTNNB1) are the most frequent mutations identified in ACC.
  • Analysis of p53 and β-catenin target gene expressions in each cluster confirmed a profound and anticipated effect on tumor biology, with distinct profiles logically associated with the respective pathway alterations.
  • [MeSH-major] Adrenocortical Carcinoma / genetics. Biomarkers, Tumor / genetics. Gene Expression Profiling. Mutation / genetics. Tumor Suppressor Protein p53 / genetics. beta Catenin / genetics


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

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

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

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  • [ISSN] 1687-4757
  • [Journal-full-title] PPAR research
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  • [Language] eng
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81. Boudou-Rouquette P, Alexandre J, Soubrane O, Bertagna X, Goldwasser F: Antitumoral effect of the bisphosphonate zoledronic acid against visceral metastases in an adrenocortical cancer patient. Ann Oncol; 2009 Oct;20(10):1747
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  • [Title] Antitumoral effect of the bisphosphonate zoledronic acid against visceral metastases in an adrenocortical cancer patient.

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  • [CommentIn] Ann Oncol. 2009 Dec;20(12):2019; author reply 2019 [19752002.001]
  • (PMID = 19633056.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid
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82. 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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  • [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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83. Gaujoux S, Pinson S, Gimenez-Roqueplo AP, Amar L, Ragazzon B, Launay P, Meatchi T, Libé R, Bertagna X, Audebourg A, Zucman-Rossi J, Tissier F, Bertherat J: Inactivation of the APC gene is constant in adrenocortical tumors from patients with familial adenomatous polyposis but not frequent in sporadic adrenocortical cancers. Clin Cancer Res; 2010 Nov 1;16(21):5133-41
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  • [Title] Inactivation of the APC gene is constant in adrenocortical tumors from patients with familial adenomatous polyposis but not frequent in sporadic adrenocortical cancers.
  • PURPOSE: In adrenocortical tumors (ACT), Wnt/β-catenin pathway activation can be explained by β-catenin somatic mutations only in a subset of tumors.
  • EXPERIMENTAL DESIGN: ACTs from patients with FAP and sporadic adrenocortical carcinomas (ACC) with abnormal β-catenin localization on immunohistochemistry but no somatic β-catenin mutations were studied.
  • RESULTS: Four ACTs were observed in three patients with FAP and were ACC, adrenocortical adenoma, and bilateral macronodular adrenocortical hyperplasia, all with abnormal β-catenin localization.
  • CONCLUSIONS: ACT should be considered a FAP tumor.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Gene Silencing. Genes, APC
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Adenomatous Polyposis Coli Protein / genetics. Adenomatous Polyposis Coli Protein / metabolism. Adult. Aged. DNA Mutational Analysis. Family. Female. Gene Frequency. Humans. Male. Middle Aged. Tumor Suppressor Proteins / genetics. Tumor Suppressor Proteins / metabolism. beta Catenin / genetics. beta Catenin / metabolism

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  • [Copyright] ©2010 AACR.
  • (PMID = 20978149.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AMER1 protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / Adenomatous Polyposis Coli Protein; 0 / Tumor Suppressor Proteins; 0 / beta Catenin
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84. Skrepnek GH, Seal B, Tangirala M, Jeffcoat MK, Watts NB, Hay JW: Adverse events and intravenous versus oral bisphosphonate use in patients with osteoporosis and cancer in the U.S. Gen Dent; 2010 Nov-Dec;58(6):484-92; quiz 493-4
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  • [Title] Adverse events and intravenous versus oral bisphosphonate use in patients with osteoporosis and cancer in the U.S.
  • Patients diagnosed with osteoporosis or various cancers were categorized according to bisphosphonate use (via IV, oral, or none).
  • Continuous enrollment for at least six months pre- and post-index diagnosis was required.
  • After controlling for numerous demographic, clinical, and instrumental variables, this study found significant relationships between IV bisphosphonate use and both inflammatory conditions of the jaw and major jaw surgery for necrotic or inflammatory conditions in patients with osteoporosis or various cancers.
  • [MeSH-minor] Administration, Oral. Adrenal Cortex Hormones / therapeutic use. Aged. Alendronate / administration & dosage. Alendronate / adverse effects. Breast Neoplasms / drug therapy. Databases as Topic. Etidronic Acid / administration & dosage. Etidronic Acid / adverse effects. Female. Humans. Imidazoles / administration & dosage. Imidazoles / adverse effects. Injections, Intravenous / statistics & numerical data. Jaw Diseases / chemically induced. Jaw Diseases / epidemiology. Lung Neoplasms / drug therapy. Male. Middle Aged. Multiple Myeloma / drug therapy. Oral Surgical Procedures / statistics & numerical data. Osteitis / chemically induced. Osteitis / epidemiology. Osteomyelitis / chemically induced. Osteomyelitis / epidemiology. Prevalence. Prostatic Neoplasms / drug therapy. Risk Factors. United States / epidemiology

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  • (PMID = 21062718.001).
  • [ISSN] 0363-6771
  • [Journal-full-title] General dentistry
  • [ISO-abbreviation] Gen Dent
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Bone Density Conservation Agents; 0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid; M2F465ROXU / Etidronic Acid; OYY3447OMC / pamidronate; X1J18R4W8P / Alendronate
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85. Porpiglia F, Fiori C, Daffara F, Zaggia B, Bollito E, Volante M, Berruti A, Terzolo M: Retrospective evaluation of the outcome of open versus laparoscopic adrenalectomy for stage I and II adrenocortical cancer. Eur Urol; 2010 May;57(5):873-8
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  • [Title] Retrospective evaluation of the outcome of open versus laparoscopic adrenalectomy for stage I and II adrenocortical cancer.
  • BACKGROUND: Although there is consensus that laparoscopy is the standard of care for the resection of benign adrenal tumours, there is controversy regarding the role of laparoscopy for the resection of adrenocortical cancer (ACC).
  • OBJECTIVE: The aim of the present study was to review the ACC database of the San Luigi Hospital to compare the oncologic effectiveness of open adrenalectomy (OA) versus laparoscopic adrenalectomy (LA) in the treatment of patients with stage I and II ACC.
  • The "open group" consisted of patients treated with OA; the "lap group" consisted of patients treated with LA.
  • MEASUREMENTS: Oncologic effectiveness of the procedures was tested comparing the recurrence-free survival of patients treated with OA versus LA.
  • CONCLUSIONS: The present findings provide interesting evidence that OA and LA may be comparable in terms of recurrence-free survival for patients with stage I and II ACC when the principles of surgical oncology are respected.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenal Cortex Neoplasms / surgery. Adrenalectomy / methods. Laparoscopy
  • [MeSH-minor] Adult. Aged. Female. Humans. Male. Middle Aged. Neoplasm Staging. Retrospective Studies. Treatment Outcome. Young Adult

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  • [Copyright] Copyright © 2010 European Association of Urology. Published by Elsevier B.V. All rights reserved.
  • (PMID = 20137850.001).
  • [ISSN] 1873-7560
  • [Journal-full-title] European urology
  • [ISO-abbreviation] Eur. Urol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
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86. Doghman M, Madoux F, Hodder P, Lalli E: Identification and characterization of steroidogenic factor-1 inverse agonists. Methods Enzymol; 2010;485:3-23
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  • Furthermore, SF-1 is amplified and overexpressed in most cases of adrenocortical tumor occurring in children; studies performed in transgenic mice have shown that an increased SF-1 dosage triggers tumor formation in the adrenal cortex.
  • For these reasons, drugs interfering with SF-1 action would represent a promising tool to be added to the current pharmacological protocols in the therapy of adrenocortical cancer.
  • These compounds have the attributes to inhibit the increase in proliferation triggered by an augmented SF-1 dosage in adrenocortical tumor cells and to reduce their steroid production.
  • This latter property may also reveal beneficial for drugs used in the therapy of adrenocortical tumors to alleviate symptoms of virilization and Cushing often associated with tumor burden.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 21050908.001).
  • [ISSN] 1557-7988
  • [Journal-full-title] Methods in enzymology
  • [ISO-abbreviation] Meth. Enzymol.
  • [Language] ENG
  • [Grant] United States / NIMH NIH HHS / MH / U54 MH084512; United States / NIMH NIH HHS / MH / MH077624; United States / NIMH NIH HHS / MH / MH084512
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Isoquinolines; 0 / Steroidogenic Factor 1; 0 / Steroids
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87. Lai M, Lü B, Xing X, Xu E, Ren G, Huang Q: Secretagogin, a novel neuroendocrine marker, has a distinct expression pattern from chromogranin A. Virchows Arch; 2006 Oct;449(4):402-9
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  • Preliminary data suggest that secretagogin (SCGN), a calcium-binding protein identified from our previous proteomics study of colorectal cancers, is a potentially useful neuroendocrine marker.
  • In this study, we further analyzed SCGN expression in normal and tumor tissues from various organ sites compared with three other conventional neuroendocrine markers [chromogranin A (CgA), neuron specific enolase, and synaptophysin].
  • We found strong SCGN staining in most normal neuroendocrine tissues except in the adrenal cortex.
  • In a subset of neuroendocrine tumors, such as gastric neuroendocrine cancers and typical carcinoid tumors of rectum and ovary, SCGN showed strong staining while CgA expression was often negative.
  • It is intriguing to note that SCGN staining was positive in 26 out of 31 small cell lung cancers, more frequently than the other three markers.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Calcium-Binding Proteins / metabolism. Chromogranin A / metabolism. Neuroendocrine Tumors / metabolism. Neurosecretory Systems / metabolism. Pathology, Surgical / methods

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  • (PMID = 16955307.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Calcium-Binding Proteins; 0 / Chromogranin A; 0 / SCGN protein, human; 0 / Secretagogins; 0 / Synaptophysin; EC 4.2.1.11 / Phosphopyruvate Hydratase
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88. Clavère P, Bonnafoux-Clavère A, Bonnetblanc JM: [Radiation induced skin reactions]. Ann Dermatol Venereol; 2008 Jan;Spec No 1:1-4
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  • [Transliterated title] Réactions cutanées induites par la radiothérapie.
  • Radiotherapy is one of the most important treatment modality of cancers.
  • [MeSH-minor] Adjuvants, Immunologic / therapeutic use. Adrenal Cortex Hormones / therapeutic use. Age Factors. Anti-Ulcer Agents / therapeutic use. Humans. Hyaluronic Acid / therapeutic use. Pentoxifylline / therapeutic use. Radiation-Protective Agents / therapeutic use. Risk Factors. Sucralfate / therapeutic use. Time Factors. Vitamin E / therapeutic use

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  • (PMID = 18342110.001).
  • [ISSN] 0151-9638
  • [Journal-full-title] Annales de dermatologie et de vénéréologie
  • [ISO-abbreviation] Ann Dermatol Venereol
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Adrenal Cortex Hormones; 0 / Anti-Ulcer Agents; 0 / Radiation-Protective Agents; 1406-18-4 / Vitamin E; 54182-58-0 / Sucralfate; 9004-61-9 / Hyaluronic Acid; SD6QCT3TSU / Pentoxifylline
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89. Soon PS, McDonald KL, Robinson BG, Sidhu SB: Molecular markers and the pathogenesis of adrenocortical cancer. Oncologist; 2008 May;13(5):548-61
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  • [Title] Molecular markers and the pathogenesis of adrenocortical cancer.
  • Adrenal tumors are common, with an estimated incidence of 7.3% in autopsy cases, while adrenocortical carcinomas (ACCs) are rare, with an estimated prevalence of 4-12 per million population.
  • Because the prognoses for adrenocortical adenomas (ACAs) and ACCs are vastly different, it is important to be able to accurately differentiate the two tumor types.
  • Advancement in the understanding of the pathophysiology of ACCs is essential for the development of more sensitive means of diagnosis and treatment, resulting in better clinical outcome.
  • Adrenocortical tumors (ACTs) occur as a component of several hereditary tumor syndromes, which include the Li-Fraumeni syndrome, Beckwith-Wiedemann syndrome, multiple endocrine neoplasia 1, Carney complex, and congenital adrenal hyperplasia.
  • The adrenocorticotropic hormone-cAMP-protein kinase A and Wnt pathways are also implicated in adrenocortical tumorigenesis.
  • The aim of this review is to summarize the current knowledge on the molecular mechanisms involved in adrenocortical tumorigenesis, including results of comparative genomic hybridization, loss of heterozygosity, and microarray gene-expression profiling studies.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics. Adrenocortical Carcinoma / genetics. Neoplastic Syndromes, Hereditary / genetics
  • [MeSH-minor] Adrenocorticotropic Hormone / genetics. Adrenocorticotropic Hormone / metabolism. Animals. Gene Expression Profiling. Genes, Tumor Suppressor. Humans. Loss of Heterozygosity. Molecular Biology

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

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

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

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  • (PMID = 16912591.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 6PLQ3CP4P3 / Etoposide; 78E4J5IB5J / Mitotane; 80168379AG / Doxorubicin; Q20Q21Q62J / Cisplatin
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93. Delaney HM, Prauner RD, Person DA: Germline p53 mutation in a Micronesian child with adrenocortical carcinoma and subsequent osteosarcoma. J Pediatr Hematol Oncol; 2008 Nov;30(11):803-6
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  • [Title] Germline p53 mutation in a Micronesian child with adrenocortical carcinoma and subsequent osteosarcoma.
  • In 1990, an 18-month-old Micronesian girl was initially diagnosed with a right adrenocortical carcinoma.
  • Given this child's remarkable history of malignancy, she underwent testing for a genetic mutation that is associated with increased cancer formation.
  • One such cancer syndrome is called Li-Fraumeni syndrome where approximately 70% of patients carry a genetic mutation in the p53 tumor suppressor gene.
  • Patients with LFS are at risk for developing cancers of the breast, soft tissues, brain, bone, adrenal gland, and blood cells.
  • Mutational analysis of our patient did reveal the presence of a germline mutation of the p53 tumor suppressor gene.
  • She was found to have a base pair change (A-->C) at nucleotide 394 resulting in a lysine to glutamine amino acid change at codon 132 (K132Q), which remarkably has never been described in association with either adrenocortical carcinoma or osteosarcoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Bone Neoplasms / genetics. Germ-Line Mutation / genetics. Neoplasms, Second Primary / genetics. Osteosarcoma / genetics. Tumor Suppressor Protein p53 / genetics


94. Britvin TA, Kazantseva IA, Kalinin AP, Kushlinskii NE: Vascular endothelium growth factor in the sera of patients with adrenal tumors. Bull Exp Biol Med; 2005 Aug;140(2):228-30
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  • [Title] Vascular endothelium growth factor in the sera of patients with adrenal tumors.
  • Serum levels of vascular endothelium growth factor were measured in 43 patients with adrenal tumors and 25 healthy subjects.
  • The mean blood levels of the factor in patients with adrenal tumors significantly surpassed the control.
  • The levels of this factor were maximum in patients with adrenocortical cancer, but its mean level differed negligibly from that in other morphological variants of tumors.
  • The level of vascular endothelium growth factor tended to increase with increasing the stage of adrenocortical cancer.
  • A direct correlation was revealed between the level of vascular endothelium growth factor and tumor size in adrenocortical cancer and aldosterone-producing adenoma.
  • Presumably, vascular endothelium growth factor is involved into mechanisms of growth, invasion, and metastatic growth of adrenocortical cancer.
  • [MeSH-major] Adrenal Gland Neoplasms / blood. Gene Expression Regulation, Neoplastic. Vascular Endothelial Growth Factor A / blood
  • [MeSH-minor] Adult. Aged. Case-Control Studies. Female. Humans. Male. Middle Aged. Neoplasm Metastasis

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  • (PMID = 16283008.001).
  • [ISSN] 0007-4888
  • [Journal-full-title] Bulletin of experimental biology and medicine
  • [ISO-abbreviation] Bull. Exp. Biol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A
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95. Schroeder SA, Swift M, Sandoval C, Langston C: Interstitial lung disease in patients with ataxia-telangiectasia. Pediatr Pulmonol; 2005 Jun;39(6):537-43
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  • Ataxia-telangiectasia (A-T) is an autosomal-recessive multiorgan disease characterized by progressive neurologic deterioration in which the most common causes of death are diseases of the respiratory system and cancers.
  • [MeSH-minor] Adolescent. Adrenal Cortex Hormones / therapeutic use. Adult. Bronchoalveolar Lavage / statistics & numerical data. Child. Comorbidity. Female. Humans. Immunoglobulins / blood. Lung / pathology. Male. Outcome and Process Assessment (Health Care). Radiography, Thoracic / statistics & numerical data. Retrospective Studies. Survival Analysis. Treatment Outcome. United States / epidemiology


96. Lee HG, Lee B, Kim SM, Suh BJ, Yu HJ: A case of gastric adenocarcinoma presenting as meningeal carcinomatosis. Korean J Intern Med; 2007 Dec;22(4):304-7
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  • Leptomeningeal carcinomatosis occurs in approximately 5% of patients with cancer.
  • The most common cancers involving the leptomeninges are breast, lung cancer and melanoma.
  • We report a case of leptomeningeal metastasis that presented as a gastric cancer.
  • The endoscopy showed a thickening of the folds of the stomach compatible with the diagnosis of a Borrman type IV gastric cancer.
  • The biopsy revealed a signet ring cell carcinoma.
  • The cytology examination of the cerebrospinal fluid supported the diagnosis of metastatic signet ring cell carcinoma.
  • [MeSH-major] Carcinoma, Signet Ring Cell / diagnosis. Meningeal Neoplasms / diagnosis. Stomach Neoplasms / diagnosis
  • [MeSH-minor] Adrenal Cortex Hormones. Female. Humans. Mannitol. Middle Aged

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  • (PMID = 18309694.001).
  • [ISSN] 1226-3303
  • [Journal-full-title] The Korean journal of internal medicine
  • [ISO-abbreviation] Korean J. Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 3OWL53L36A / Mannitol
  • [Other-IDs] NLM/ PMC2687665
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97. 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
  • [MeSH-minor] Chemotherapy, Adjuvant. Humans. Multivariate Analysis. Neoplasm Recurrence, Local / epidemiology. Neoplasm Recurrence, Local / prevention & control. Retrospective Studies. Survival Analysis


98. Frederiks WM, Kümmerlin IP, Bosch KS, Vreeling-Sindelárová H, Jonker A, Van Noorden CJ: NADPH production by the pentose phosphate pathway in the zona fasciculata of rat adrenal gland. J Histochem Cytochem; 2007 Sep;55(9):975-80
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  • [Title] NADPH production by the pentose phosphate pathway in the zona fasciculata of rat adrenal gland.
  • Biosynthesis of steroid hormones in the cortex of the adrenal gland takes place in smooth endoplasmic reticulum and mitochondria and requires NADPH.
  • However, the contribution of each enzyme to NADPH production in the cortex of adrenal gland has not been established.
  • Therefore, activity of G6PD, PGD, MDH, and ICDH was localized and quantified in rat adrenocortical tissue using metabolic mapping, image analysis, and electron microscopy.
  • The four enzymes have similar localization patterns in adrenal gland with highest activities in the zona fasciculata of the cortex.
  • It is concluded that G6PD and PGD provide the major part of NADPH in adrenocortical cells.

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  • (PMID = 17533217.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0U46U6E8UK / NAD; C24W7J5D5R / Androsterone; EC 1.1.1.37 / Malate Dehydrogenase; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.43 / Phosphogluconate Dehydrogenase; EC 1.1.1.49 / Glucosephosphate Dehydrogenase
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99. 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.
  • [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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100. Zhang C, Mattern J, Haferkamp A, Pfitzenmaier J, Hohenfellner M, Rittgen W, Edler L, Debatin KM, Groene E, Herr I: Corticosteroid-induced chemotherapy resistance in urological cancers. Cancer Biol Ther; 2006 Jan;5(1):59-64
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  • [Title] Corticosteroid-induced chemotherapy resistance in urological cancers.
  • PURPOSE: Glucocorticoids such as dexamethasone are widely used for medication of urological diseases, e.g., as cotreatment of advanced prostate cancer, to improve appetite, weight loss, fatigue, relieve bone pain, diminish ureteric obstruction, to reduce the production of adrenal androgens, as an antiemetic in patients undergoing chemo- and/or radiotherapy together with serving as "standard" therapy arm in randomized studies.
  • While the potent pro-apoptotic properties and the supportive effects of glucocorticoids to tumor therapy in lymphoid cells are well studied, the impact to growth of prostate and other urological carcinomas is unknown.
  • No difference in dexamethasone-mediated protection was found in normal, benign and malignant prostate tumors.
  • CONCLUSIONS: These data show for the first time that dexamethasone induced therapy resistance in urological carcinomas is not the exception but a more common phenomenon and implicate that glucocorticoids may have two faces in cancer therapy, a beneficial and a dangerous one.
  • [MeSH-major] Adrenal Cortex Hormones / adverse effects. Dexamethasone / adverse effects. Drug Resistance, Neoplasm / drug effects. Urologic Neoplasms / therapy

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  • (PMID = 16294015.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 7S5I7G3JQL / Dexamethasone
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