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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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  • [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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  • [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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  • [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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4. Tomkova K, Tomka M, Zajac V: Contribution of p53, p63, and p73 to the developmental diseases and cancer. Neoplasma; 2008;55(3):177-81
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  • [Title] Contribution of p53, p63, and p73 to the developmental diseases and cancer.
  • Tumor suppressor TP53 gene is one of the most mutated genes in human genome.
  • This syndrome is characterized by the early onset of different types of cancers including soft-tissue sarcomas, breast and brain cancers, leukemias, lung, laryngeal cancers, and adrenocortical carcinomas.
  • The key role of p53 in tumor suppression has been confirmed in animal models as well.
  • The p53 -knock-out and knock-in animals were born alive but were tumor prone.
  • On one hand, there are evidences that both, p63 and p73-deficient animals are not tumor prone; on the other hand, there is evidence that such animals develop tumors later during their life.
  • [MeSH-major] DNA-Binding Proteins / genetics. Genes, p53. Membrane Proteins / genetics. Neoplasms / genetics. Nuclear Proteins / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Animals. Embryonic Development. Genes, Tumor Suppressor. Germ-Line Mutation. Humans. Mutation

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  • (PMID = 18348649.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / CKAP4 protein, human; 0 / DNA-Binding Proteins; 0 / Membrane Proteins; 0 / Nuclear Proteins; 0 / Tumor Suppressor Proteins
  • [Number-of-references] 63
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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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  • [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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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  • [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
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] England
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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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  • (PMID = 18670617.001).
  • [ISSN] 1687-4757
  • [Journal-full-title] PPAR research
  • [ISO-abbreviation] PPAR Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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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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  • (PMID = 16320017.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Hormonal; 0O54ZQ14I9 / Aminoglutethimide; 9002-60-2 / Adrenocorticotropic Hormone
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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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