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1. 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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2. 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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3. 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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4. 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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5. Jurczyńska J, Stepień T, Lawnicka H, Stepień H, Krupiński R, Kołomecki K, Kuzdak K, Komorowski J: Peripheral blood concentrations of vascular endothelial growth factor and its soluble receptors (R1 and R2) in patients with adrenal cortex tumours treated by surgery. Endokrynol Pol; 2009 Jan-Feb;60(1):9-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Peripheral blood concentrations of vascular endothelial growth factor and its soluble receptors (R1 and R2) in patients with adrenal cortex tumours treated by surgery.
  • INTRODUCTION: Neoangiogenesis appears to be an important event in tumour invasion and in the formation of metastases in many endocrine-related human cancers.
  • The aim of the study was to evaluate the plasma blood concentrations of VEGF, sVEGFR1, and sVEGFR2 in patients with benign and malignant adrenal tumours treated by surgery.
  • MATERIAL AND METHODS: We studied the blood before surgery of 41 patients with adrenal cortex tumours and 10 normal subjects without hormonal or CT/USG pathology of the adrenal glands (controls).
  • We studied the blood after adrenalectomy of 16 patients with tumours of the adrenal cortex.
  • VEGF blood concentrations before surgery did not differ in the patients with the cortical tumours as compared to the controls.
  • After surgery VEGF concentrations decreased among the patients, taken in total, with adrenal cortex tumours and cortical adenomas.
  • After surgery, sVEGFR1 concentrations decreased significantly in the group with cortical adenomas only.
  • CONCLUSIONS: Peripheral blood concentrations of VEGF and its receptors cannot be clinically valuable markers that discriminate between benign and malignant adrenocortical tumours before and after adrenalectomy.
  • [MeSH-major] Adrenal Gland Neoplasms / blood. Adrenal Gland Neoplasms / diagnosis. Biomarkers, Tumor / blood. Vascular Endothelial Growth Factor A / blood. Vascular Endothelial Growth Factor Receptor-1 / blood. Vascular Endothelial Growth Factor Receptor-2 / blood
  • [MeSH-minor] Adrenal Gland Diseases / blood. Adrenal Gland Diseases / diagnosis. Adrenalectomy. Adult. Aged. Diagnosis, Differential. Female. Humans. Male. Middle Aged

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  • (PMID = 19224499.001).
  • [ISSN] 0423-104X
  • [Journal-full-title] Endokrynologia Polska
  • [ISO-abbreviation] Endokrynol Pol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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6. Sticchi D, Fassina A, Ganzaroli C, Pasqualetto C, Pessina AC, Nussdorfer GG, Rossi GP: Expression of telomerase (hTERT) in aldosterone-producing adrenocortical tumors. Int J Mol Med; 2006 Mar;17(3):469-74
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  • [Title] Expression of telomerase (hTERT) in aldosterone-producing adrenocortical tumors.
  • Telomerase was found in cancers and immortalized cell lines, but only occasionally in normal tissues, thus suggesting that measurement of its hTERT subunit might help distinguishing benign from malignant tumors.
  • Data on hTERT expression in adrenocortical tumors are scant and mostly confined to non-functioning tumors.
  • Therefore, we investigated whether hTERT expression may predict malignancy in aldosterone producing adrenocortical tumors.
  • We also studied two rare aldosterone-producing carcinomas (APCs), eight adrenocortical carcinomas (ACs), twelve normal adrenal cortexes, and two malignant cell lines (NCI-295H and SW-13).
  • Of interest, we detected hTERT mRNA in 58% of APAs at levels similar to those of malignant tumors, which all consistently showed hTERT expression.
  • No hTERT expression was found in the normal adrenocortical tissue.
  • In conclusion, RT-PCR measurement of hTERT mRNA is a hallmark of malignant adrenocortical tumors, but identifies also a subset of hTERT-expressing APAs that might show metastatic spread at long-term follow-up.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / secretion. Aldosterone / secretion. Telomerase / genetics

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  • (PMID = 16465394.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / RNA, Messenger; 4964P6T9RB / Aldosterone; EC 2.7.7.49 / Telomerase
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7. 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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8. 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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9. 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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10. 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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11. Yang JY, Yang MQ, Luo Z, Ma Y, Li J, Deng Y, Huang X: A hybrid machine learning-based method for classifying the Cushing's Syndrome with comorbid adrenocortical lesions. BMC Genomics; 2008;9 Suppl 1:S23
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  • [Title] A hybrid machine learning-based method for classifying the Cushing's Syndrome with comorbid adrenocortical lesions.
  • BACKGROUND: The prognosis for many cancers could be improved dramatically if they could be detected while still at the microscopic disease stage.
  • It follows from a comprehensive statistical analysis that a number of antigens such as hTERT, PCNA and Ki-67 can be considered as cancer markers, while another set of antigens such as P27KIP1 and FHIT are possible markers for normal tissue.
  • Because more than one marker must be considered to obtain a classification of cancer or no cancer, and if cancer, to classify it as malignant, borderline, or benign, we must develop an intelligent decision system that can fullfill such an unmet medical need.
  • We have also used immunohistochemistry techniques to measure the gene expression profiles from a number of antigens such as cyclin E, P27KIP1, FHIT, Ki-67, PCNA, Bax, Bcl-2, P53, Fas, FasL and hTERT in several particular types of neuroendocrine tumors such as pheochromocytomas, paragangliomas, and the adrenocortical carcinomas (ACC), adenomas (ACA), and hyperplasia (ACH) involved with Cushing's syndrome.
  • We provided statistical evidence that higher expression levels of hTERT, PCNA and Ki-67 etc. are associated with a higher risk that the tumors are malignant or borderline as opposed to benign.
  • While no significant difference was found between cell-arrest antigens such as P27KIP1 for malignant, borderline, and benign tumors, there was a significant difference between expression levels of such antigens in normal adrenal medulla samples and in adrenomedullary tumors.
  • This research has many potential applications; it might provide an alternative diagnostic tool and a better understanding of the mechanisms involved in malignant transformation as well as information that is useful for treatment planning and cancer prevention.
  • [MeSH-major] Adrenal Cortex Neoplasms / classification. Algorithms. Artificial Intelligence. Biomarkers, Tumor / metabolism. Cushing Syndrome / classification


12. 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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13. 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


14. 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


15. 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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16. 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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17. Hamrahian AH, Ioachimescu AG, Remer EM, Motta-Ramirez G, Bogabathina H, Levin HS, Reddy S, Gill IS, Siperstein A, Bravo EL: Clinical utility of noncontrast computed tomography attenuation value (hounsfield units) to differentiate adrenal adenomas/hyperplasias from nonadenomas: Cleveland Clinic experience. J Clin Endocrinol Metab; 2005 Feb;90(2):871-7
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  • [Title] Clinical utility of noncontrast computed tomography attenuation value (hounsfield units) to differentiate adrenal adenomas/hyperplasias from nonadenomas: Cleveland Clinic experience.
  • Radiological characterization of an adrenal tumor as adenoma may decrease the need for follow-up imaging studies, biopsies, and unnecessary adrenalectomies.
  • We retrospectively reviewed 299 adrenalectomies in 290 patients at Cleveland Clinic Foundation over a recent 5-yr period to assess the value of noncontrast Hounsfield units (HU) in characterizing whether an adrenal mass is adenoma or nonadenoma.
  • The mean (+/- SD) HU value for the adrenocortical adenoma/hyperplasia group was 16.2 +/- 13.6 and significantly lower (P < 0.0001) than primary adrenocortical cancers (36.9 +/- 4.1), metastases (39.2 +/- 15.2), and pheochromocytomas (38.6 +/- 8.2).
  • The size of the adrenal tumor had less value with only 40.7 and 81.3% sensitivity and 94.7 and 61.4% specificity for 2- and 4-cm cutoff values.
  • A combination of less than or equal to 4-cm adrenal mass size and noncontrast computed tomography HU less than or equal to 20 had 42.1% sensitivity and 100% specificity.
  • Our study, the largest with surgical histopathology as the gold standard for diagnosis, supports a noncontrast computed tomography attenuation value of 10 HU as a safe cutoff value to differentiate adrenal adenomas/hyperplasias from nonadenomas.
  • [MeSH-major] Adenoma / radiography. Adrenal Gland Neoplasms / radiography. Adrenocortical Hyperfunction / radiography
  • [MeSH-minor] Adolescent. Adult. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Retrospective Studies. Tomography, X-Ray Computed

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  • (PMID = 15572420.001).
  • [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
  • [Publication-country] United States
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18. 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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19. 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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20. Portnov BA, Barchana M, Dubnov J: Exploratory analysis of potential risk factors of a rare disease: spatial distribution of adrenocortical carcinoma in Israel as a case study. Sci Total Environ; 2009 Feb 15;407(5):1738-43
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  • [Title] Exploratory analysis of potential risk factors of a rare disease: spatial distribution of adrenocortical carcinoma in Israel as a case study.
  • In the present study, the performance of proposed approach is investigated by cross-examination of the spatial patterns of three widespread cancers--lung, larynx and colorectal (CRC)--with that of a rare malignant disease--Adrenocortical Carcinoma (ACC).
  • [MeSH-major] Adrenal Cortex Neoplasms / epidemiology. Adrenocortical Carcinoma / epidemiology. Colorectal Neoplasms / epidemiology. Laryngeal Neoplasms / epidemiology. Lung Neoplasms / epidemiology


21. Tadjine M, Lampron A, Ouadi L, Bourdeau I: Frequent mutations of beta-catenin gene in sporadic secreting adrenocortical adenomas. Clin Endocrinol (Oxf); 2008 Feb;68(2):264-70
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  • [Title] Frequent mutations of beta-catenin gene in sporadic secreting adrenocortical adenomas.
  • OBJECTIVE: Molecular alterations remain largely unknown in most sporadic adrenocortical tumours and hyperplasias.
  • In our previous work, we demonstrated the differential expression of several Wnt/beta-catenin signalling-related genes implicated in ACTH-independent macronodular adrenal hyperplasias (AIMAH).
  • To better understand the role of Wnt/beta-catenin signalling in adrenocortical tumours, we performed mutational analysis of the beta-catenin gene.
  • METHODS: We studied 53 human adrenocortical samples (33 adenomas, 4 carcinomas, 13 AIMAH, 3 ACTH-dependent adrenal hyperplasias) and the human adrenocortical cancer cell line NCI-H295R.
  • RESULTS: No mutations were detected in adrenocortical carcinomas, AIMAH and ACTH-dependent hyperplasias.
  • CONCLUSIONS: Activating mutations of exon 3 of the beta-catenin gene are frequent in adrenocortical adenomas, and further characterization of the Wnt/beta-catenin signalling pathway should lead to a better understanding of adrenal tumourigenesis.
  • [MeSH-major] Adrenocortical Adenoma / genetics. Adrenocortical Adenoma / metabolism. beta Catenin / genetics. beta Catenin / metabolism

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  • (PMID = 17854394.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / beta Catenin
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22. Abbasova SG, Vysotskii MM, Ovchinnikova LK, Obusheva MN, Digaeva MA, Britvin TA, Bahoeva KA, Karabekova ZK, Kazantzeva IA, Mamedov UR, Manuchin IB, Davidov MI: Cancer and soluble FAS. Bull Exp Biol Med; 2009 Oct;148(4):638-42
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  • [Title] Cancer and soluble FAS.
  • A test system developed by the authors was used to measure serum concentrations of soluble Fas in patients with malignant and benign tumors of different location and morphology.
  • Relationships between soluble Fas levels and the main clinical and morphological characteristics of cancer were evaluated.
  • No appreciable differences in the concentrations of soluble Fas were detected in malignant and benign tumors of the mammary gland, bones, ovaries, and adrenals.
  • In thyroid cancer, soluble Fas levels were higher than in benign and hyperplastic processes in this organ.
  • High level of soluble Fas is associated with late stages of the disease (ovarian cancer, cancer of the corpus uteri, adrenocortical and colorectal cancer) and with poor differentiation of the tumor (ovarian cancer and cancer of the corpus uteri), with local metastases (colorectal and adrenocortical cancer), and with tumor invasion into the myometrial tissue, intestinal wall, and adjacent tissues (cancer of the corpus uteri and colorectal cancer).
  • A significantly high level of soluble Fas was detected in colorectal and adrenocortical cancer in the presence of at least 2 local metastases.
  • Soluble Fas levels depended on tumor histogenesis in malignant and benign ovarian tumors.
  • High concentration of soluble Fas was detected in large tumors in patients with ovarian cancer, cancer of the corpus uteri, colorectal cancer, thyroid cancer and adenoma, and in adrenocortical cancer.
  • The overall 5-year survival of patients with low levels of soluble Fas is better in osteosarcoma, cancer of the corpus uteri, ovarian and adrenocortical cancer.

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  • (PMID = 20396760.001).
  • [ISSN] 1573-8221
  • [Journal-full-title] Bulletin of experimental biology and medicine
  • [ISO-abbreviation] Bull. Exp. Biol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95
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23. Chou SH, Tseleni-Balafouta S, Moon HS, Chamberland JP, Liu X, Kavantzas N, Mantzoros CS: Adiponectin receptor expression in human malignant tissues. Horm Cancer; 2010 Jun;1(3):136-45
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  • [Title] Adiponectin receptor expression in human malignant tissues.
  • We describe herein the expression of AdipoR1 and AdipoR2 in several cancers not previously studied.
  • We used immunohistochemistry to assess expression of adiponectin receptors in archival specimens of renal cell carcinoma (n = 64), hepatocellular carcinoma (n = 123), melanoma (n = 20), cholangiocarcinoma (n = 20), transitional cell carcinoma of the bladder (n = 24), ovarian epithelial carcinoma (n = 63), cervical squamous cell carcinoma (n = 49), and adrenocortical carcinoma (n = 48).
  • To compare expression in malignant versus nonmalignant tissues, we also studied AdipoR1 and AdipoR2 expression in pairs of renal cell carcinoma and adjacent healthy kidney tissue specimens by immunohistochemistry.
  • We also studied mRNA expression in 45 specimens of renal cell carcinoma by real-time polymerase chain reaction.
  • Finally, we utilized Western blotting to confirm the presence of adiponectin receptors and subsequently studied cell signaling pathways of adiponectin in the renal cancer cell line 786-O.
  • Cancers associated with obesity were significantly more likely to express AdipoR1 than cancers not associated with obesity.
  • Of the specimens of renal cell carcinoma, which is strongly associated with obesity, 93.8% expressed AdipoR1 compared to 44.9% of the specimens of cervical cell carcinoma, which is not associated with obesity (p < 0.001).
  • There was no difference in the expression of adiponectin receptors or their mRNA between malignant and benign kidney tissue specimens.
  • Overall, there were no correlations between expression of adiponectin receptors or their mRNA and tumor prognostic factors.
  • Finally, Western blotting confirmed the presence of AdipoR1 in the renal cancer cell line 786-O, and adiponectin activates in vitro several signaling pathways in this cell line.
  • In summary, we report for the first time expression of AdipoR1 and AdipoR2 in the above cancers and that AdipoR1 is more ubiquitously expressed in obesity-associated cancers.
  • [MeSH-minor] Adult. Aged. Blotting, Western. Carcinoma, Renal Cell / metabolism. Female. Humans. Immunohistochemistry. Kidney Neoplasms / metabolism. Male. Middle Aged. Obesity / complications. Obesity / metabolism. RNA, Messenger / analysis. Real-Time Polymerase Chain Reaction

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  • (PMID = 21761356.001).
  • [ISSN] 1868-8500
  • [Journal-full-title] Hormones & cancer
  • [ISO-abbreviation] Horm Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptors, Adiponectin
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24. Stelow EB, Debol SM, Stanley MW, Mallery S, Lai R, Bardales RH: Sampling of the adrenal glands by endoscopic ultrasound-guided fine-needle aspiration. Diagn Cytopathol; 2005 Jul;33(1):26-30
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  • [Title] Sampling of the adrenal glands by endoscopic ultrasound-guided fine-needle aspiration.
  • Endoscopic ultrasound (EUS)-guided fine-needle aspiration (FNA) has proven to be a valuable modality for the primary diagnosis and staging of gastrointestinal, and perigastrointestinal malignancy.
  • Aside from assessing thoracic and abdominal lymph nodes and the liver for metastases, EUS can assess and sample the adrenal glands, which are frequently involved by metastatic disease, but can also harbor benign primary neoplasms.
  • The cytology files at our institution were reviewed for all cases of EUS-guided FNA of the adrenal glands.
  • Results were compared with overall EUS-guided FNA performance and the performance of non-EUS-guided FNA of the adrenal.
  • Between 1/1/00 and 5/15/04 there were 24 cases of EUS-guided FNA of the adrenal gland from 22 different patients (13 men; 9 women) at our institution.
  • This represented 1.4% of overall EUS-guided FNA and 77% of adrenal gland FNA.
  • Most patients had other cancers or mass lesions and were being staged at the time of the procedure (19 of 22).
  • Almost all FNAs were of the left adrenal gland (23 of 24).
  • Final diagnoses were as follows: cortical tissue consistent with cortical adenoma (19), metastatic adenocarcinoma (3), pheochromocytoma (1), and adrenal cortical carcinoma (1).
  • EUS-guided FNA of the adrenal gland is primarily used in the staging of other malignancies when lesions of the left adrenal are recognized sonographically.
  • Diagnostic tissue is easily obtained, including material for cell block IHC, which allows definitive diagnosis in cases that present difficult differential diagnoses.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis. Adrenal Glands / pathology. Biopsy, Fine-Needle / methods. Endosonography / methods
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenoma / diagnosis. Adrenocortical Carcinoma / diagnosis. Adult. Aged. Aged, 80 and over. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Pheochromocytoma / diagnosis. Sensitivity and Specificity

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  • [Copyright] 2005 Wiley-Liss, Inc
  • (PMID = 15945088.001).
  • [ISSN] 8755-1039
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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25. Miller BS, Ammori JB, Gauger PG, Broome JT, Hammer GD, Doherty GM: Laparoscopic resection is inappropriate in patients with known or suspected adrenocortical carcinoma. World J Surg; 2010 Jun;34(6):1380-5
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  • [Title] Laparoscopic resection is inappropriate in patients with known or suspected adrenocortical carcinoma.
  • BACKGROUND: Complete surgical resection is the mainstay of treatment for patients with adrenocortical cancer (ACC).
  • Seventeen patients underwent laparoscopic adrenalectomy (LA).
  • Median tumor size of those who underwent LA was 7.0 (range, 4-14) cm versus 12.3 (range, 5-27) cm for OR.
  • Mean time to first recurrence for those who underwent LA was 9.6 months (+/-14) versus 19.2 months (+/-37.5) in the open group (p < 0.005).
  • Fifty percent of patients who underwent LA had positive margins or notation of intraoperative tumor spill versus 18% of those who underwent OR (p = 0.01).
  • Although feasible in many cases and tempting, laparoscopic resection should not be attempted in patients with tumors suspicious for or known to be adrenocortical carcinoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenocortical Carcinoma / surgery. Laparoscopy / contraindications
  • [MeSH-minor] Adolescent. Adrenalectomy / methods. Adult. Aged. Aged, 80 and over. Chi-Square Distribution. Female. Humans. Male. Middle Aged. Neoplasm Recurrence, Local. Neoplasm Staging. Retrospective Studies. Treatment Outcome

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  • (PMID = 20372905.001).
  • [ISSN] 1432-2323
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
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26. Aumo L, Rusten M, Mellgren G, Bakke M, Lewis AE: Functional roles of protein kinase A (PKA) and exchange protein directly activated by 3',5'-cyclic adenosine 5'-monophosphate (cAMP) 2 (EPAC2) in cAMP-mediated actions in adrenocortical cells. Endocrinology; 2010 May;151(5):2151-61
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  • [Title] Functional roles of protein kinase A (PKA) and exchange protein directly activated by 3',5'-cyclic adenosine 5'-monophosphate (cAMP) 2 (EPAC2) in cAMP-mediated actions in adrenocortical cells.
  • In the adrenal cortex, the biosynthesis of steroid hormones is controlled by the pituitary-derived hormone ACTH.
  • In the present study, we demonstrate the occurrence of the EPAC2 splicing variant EPAC2B in adrenocortical cancer cells.
  • [MeSH-minor] Adrenal Cortex / metabolism. Adrenal Cortex / pathology. Aldosterone / biosynthesis. Alternative Splicing. Animals. Blotting, Western. COS Cells. Cell Line. Cell Line, Tumor. Cell Movement / drug effects. Cell Shape / drug effects. Cercopithecus aethiops. Cytoskeleton / drug effects. Cytoskeleton / metabolism. Humans. Hydrocortisone / biosynthesis. Immunohistochemistry. Microscopy, Confocal. Protein Isoforms / genetics. Protein Isoforms / metabolism. Protein Isoforms / physiology. Reverse Transcriptase Polymerase Chain Reaction. rap1 GTP-Binding Proteins / metabolism

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  • (PMID = 20233795.001).
  • [ISSN] 1945-7170
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Guanine Nucleotide Exchange Factors; 0 / Protein Isoforms; 0 / RAPGEF4 protein, human; 4964P6T9RB / Aldosterone; E0399OZS9N / Cyclic AMP; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 3.6.5.2 / rap1 GTP-Binding Proteins; WI4X0X7BPJ / Hydrocortisone
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27. 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
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Cytotoxins; 78E4J5IB5J / Mitotane
  • [Other-IDs] NLM/ PMC2966201
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28. 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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29. Freddi S, Arnaldi G, Fazioli F, Scarpelli M, Appolloni G, Mancini T, Kola B, Bertagna X, Mantero F, Collu R, Boscaro M: Expression of growth hormone-releasing hormone receptor splicing variants in human primary adrenocortical tumours. Clin Endocrinol (Oxf); 2005 May;62(5):533-8
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  • [Title] Expression of growth hormone-releasing hormone receptor splicing variants in human primary adrenocortical tumours.
  • OBJECTIVE: Several splice variants (SVs) of GHRH receptor (GHRH-R) have been identified in various human cancers through which GHRH antagonists may exert their IGF-II-mediated antiproliferative action.
  • Because the overexpression of the IGF-II gene is a frequent feature of adrenal carcinoma, we searched for the presence of GHRH-R SVs in these tumours.
  • METHODS AND RESULTS: The expression of GHRH-R SVs was assessed by nested PCR in 45 human adrenocortical tumours.
  • SV2 was detected in five of 24 cancers examined, whereas the incidence of SV1 and SV4 was lower.
  • Their simultaneous expression was observed in one carcinoma.
  • No PCR products for SV3 or wild-type GHRH-R were found in carcinomas; mRNA for wild-type GHRH-R or SVs of GHRH-R were not observed either in adenomas or in normal adrenal or in NCI-H295R cells.
  • CONCLUSION: This is the first time that the expression of splice variants of GHRH-R has been demonstrated in human adrenal carcinoma.
  • This study raises the possibility that splice variants might play a role in adrenal carcinogenesis and might offer the possibility for new therapeutic strategies at least in a subgroup of adrenal carcinomas.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Alternative Splicing. Carcinoma / genetics. Polymorphism, Genetic. RNA, Messenger / analysis. Receptors, Neuropeptide / genetics. Receptors, Pituitary Hormone-Regulating Hormone / genetics
  • [MeSH-minor] Adenoma / genetics. Adenoma / metabolism. Adolescent. Adult. Aged. Base Sequence. Cell Line, Tumor. Female. Humans. Male. Middle Aged. Molecular Sequence Data. Reverse Transcriptase Polymerase Chain Reaction. Sequence Analysis, DNA. Tumor Cells, Cultured

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  • (PMID = 15853821.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptors, Neuropeptide; 0 / Receptors, Pituitary Hormone-Regulating Hormone; 0 / somatotropin releasing hormone receptor
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30. Roman S: Adrenocortical carcinoma. Curr Opin Oncol; 2006 Jan;18(1):36-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenocortical carcinoma.
  • PURPOSE OF REVIEW: Adrenocortical carcinoma is a rare malignancy, accounting for 0.02% of all annual cancers reported.
  • Given the generally advanced stage at diagnosis, the overall 5-year survival remains poor, varying between 20 and 45%.
  • RECENT FINDINGS: Recent studies focusing on the tumorigenesis of adrenocortical carcinoma have focused on onco-developmental genes present in the fetal adrenal cortex, as well as local adrenal paracrine and autocrine effects of cellular peptides.
  • SUMMARY: Pre-operative diagnostic advances in positron emission scanning are emerging as promising modalities for confirmation of malignancy of indeterminate adrenal masses.
  • No significant advances in the treatment of adrenocortical carcinoma have been developed.
  • [MeSH-major] Adrenal Cortex Neoplasms. Adrenocortical Carcinoma

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  • (PMID = 16357562.001).
  • [ISSN] 1040-8746
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Vascular Endothelial Growth Factor A; 104625-48-1 / Activins; 57285-09-3 / Inhibins; 78E4J5IB5J / Mitotane
  • [Number-of-references] 38
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31. Porpiglia F, Fiori C, Daffara F, Zaggia B, Bollito E, Volante M, Berruti A, Terzolo M: Retrospective evaluation of the outcome of open versus laparoscopic adrenalectomy for stage I and II adrenocortical cancer. Eur Urol; 2010 May;57(5):873-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Retrospective evaluation of the outcome of open versus laparoscopic adrenalectomy for stage I and II adrenocortical cancer.
  • BACKGROUND: Although there is consensus that laparoscopy is the standard of care for the resection of benign adrenal tumours, there is controversy regarding the role of laparoscopy for the resection of adrenocortical cancer (ACC).
  • OBJECTIVE: The aim of the present study was to review the ACC database of the San Luigi Hospital to compare the oncologic effectiveness of open adrenalectomy (OA) versus laparoscopic adrenalectomy (LA) in the treatment of patients with stage I and II ACC.
  • The "open group" consisted of patients treated with OA; the "lap group" consisted of patients treated with LA.
  • MEASUREMENTS: Oncologic effectiveness of the procedures was tested comparing the recurrence-free survival of patients treated with OA versus LA.
  • CONCLUSIONS: The present findings provide interesting evidence that OA and LA may be comparable in terms of recurrence-free survival for patients with stage I and II ACC when the principles of surgical oncology are respected.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenal Cortex Neoplasms / surgery. Adrenalectomy / methods. Laparoscopy
  • [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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32. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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33. Przybylik-Mazurek E, Darczuk A, Huszno B, Budzyński A, Rembiasz K, Gałazka K, Wierzchowski W, Giza A, Jurczak W, Skotnicki AB, Sztuk S, Urbanik A: [Primary adrenal lymphoma in incidentally discovered adrenal tumour]. Przegl Lek; 2006;63(8):701-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Primary adrenal lymphoma in incidentally discovered adrenal tumour].
  • The new imaging techniques used during the last several years: ultrasound, computed tomography and magnetic resonance imaging have improved detection of non-functional adrenal tumours s.c. "incidentaloma".
  • Incidence of adrenal incidentaloma is not very low.
  • In most of cases incidentaloma are benign and gave no clinical signs; however primary adrenal cortex cancer and metastases of different cancers are not uncommon.
  • The primary adrenal lymphoma is an extremely rare disease.
  • Most frequently both adrenal glands are affected and signs of adrenal insufficiency (despite weakness, fever and loss of weight) are present.
  • Hormonal examinations were normal, but the tumour size was indication for surgery treatment.
  • The diagnosis was made by histological examination and adjuvant chemotherapy was administrated.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis. Adrenal Gland Neoplasms / surgery. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Non-Hodgkin / diagnosis. Lymphoma, Non-Hodgkin / surgery

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  • (PMID = 17441388.001).
  • [ISSN] 0033-2240
  • [Journal-full-title] Przegla̧d lekarski
  • [ISO-abbreviation] Prz. Lek.
  • [Language] pol
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide
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34. Achatz MI, Olivier M, Le Calvez F, Martel-Planche G, Lopes A, Rossi BM, Ashton-Prolla P, Giugliani R, Palmero EI, Vargas FR, Da Rocha JC, Vettore AL, Hainaut P: The TP53 mutation, R337H, is associated with Li-Fraumeni and Li-Fraumeni-like syndromes in Brazilian families. Cancer Lett; 2007 Jan 8;245(1-2):96-102
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A TP53 germline mutation, R337H, has been previously described in children from southern Brazil with adrenocortical tumours but no documented familial history of other cancers.
  • Families with the R337H mutation presented a wide spectrum of tumours, including breast cancers (30.4%), brain cancers (10.7%), soft tissue sarcomas (10.7%) and adrenocortical carcinomas (8.9%).
  • Testing of 53 Brazilian subjects with no cancer history showed that R337H was not a common polymorphism in that population.
  • [MeSH-major] Germ-Line Mutation. Li-Fraumeni Syndrome / genetics. Tumor Suppressor Protein p53 / genetics

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  • [CommentIn] Cancer Lett. 2007 Mar 18;247(2):353-5; author reply 356-8 [16750598.001]
  • (PMID = 16494995.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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35. Farnworth PG, Wang Y, Escalona R, Leembruggen P, Ooi GT, Findlay JK: Transforming growth factor-beta blocks inhibin binding to different target cell types in a context-dependent manner through dual mechanisms involving betaglycan. Endocrinology; 2007 Nov;148(11):5355-68
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  • To clarify the nature and extent of interactions between inhibin and TGF-beta, we therefore examined 1) the mutual competition between these ligands for binding, 2) the regulation of endogenous betaglycan expression by inhibin and TGF-beta isoforms, and 3) the consequences of such betaglycan regulation for subsequent inhibin binding in mouse Leydig (TM3), Sertoli (TM4), adrenocortical cancer (AC), and gonadotroph (LbetaT2) cell lines, chosen to model cellular targets for local and endocrine actions of inhibin.

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  • (PMID = 17656464.001).
  • [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 / Proteoglycans; 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta; 145170-29-2 / betaglycan; 57285-09-3 / Inhibins
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36. Carmona-Bayonas A, Soler IO, Gómez FI, Billalabeitia EG, Saura HP, Tafalla MS, Díaz MP: Tailored hormonal therapy in secretory adrenocortical cancer. Ann Oncol; 2007 Jul;18(7):1281
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tailored hormonal therapy in secretory adrenocortical cancer.

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  • (PMID = 17675396.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiotensin-Converting Enzyme Inhibitors; 0 / Anti-Inflammatory Agents; 0 / Antifungal Agents; 0 / Antineoplastic Agents, Hormonal; 0 / Mineralocorticoid Receptor Antagonists; 27O7W4T232 / Spironolactone; 4964P6T9RB / Aldosterone; 6PLQ3CP4P3 / Etoposide; 78E4J5IB5J / Mitotane; 80168379AG / Doxorubicin; 9G64RSX1XD / Captopril; Q20Q21Q62J / Cisplatin; R9400W927I / Ketoconazole; RWP5GA015D / Potassium; WI4X0X7BPJ / Hydrocortisone
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37. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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38. Soon PS, McDonald KL, Robinson BG, Sidhu SB: Molecular markers and the pathogenesis of adrenocortical cancer. Oncologist; 2008 May;13(5):548-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular markers and the pathogenesis of adrenocortical cancer.
  • Adrenal tumors are common, with an estimated incidence of 7.3% in autopsy cases, while adrenocortical carcinomas (ACCs) are rare, with an estimated prevalence of 4-12 per million population.
  • Because the prognoses for adrenocortical adenomas (ACAs) and ACCs are vastly different, it is important to be able to accurately differentiate the two tumor types.
  • Advancement in the understanding of the pathophysiology of ACCs is essential for the development of more sensitive means of diagnosis and treatment, resulting in better clinical outcome.
  • Adrenocortical tumors (ACTs) occur as a component of several hereditary tumor syndromes, which include the Li-Fraumeni syndrome, Beckwith-Wiedemann syndrome, multiple endocrine neoplasia 1, Carney complex, and congenital adrenal hyperplasia.
  • The adrenocorticotropic hormone-cAMP-protein kinase A and Wnt pathways are also implicated in adrenocortical tumorigenesis.
  • The aim of this review is to summarize the current knowledge on the molecular mechanisms involved in adrenocortical tumorigenesis, including results of comparative genomic hybridization, loss of heterozygosity, and microarray gene-expression profiling studies.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics. Adrenocortical Carcinoma / genetics. Neoplastic Syndromes, Hereditary / genetics
  • [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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39. Doghman M, El Wakil A, Cardinaud B, Thomas E, Wang J, Zhao W, Peralta-Del Valle MH, Figueiredo BC, Zambetti GP, Lalli E: Regulation of insulin-like growth factor-mammalian target of rapamycin signaling by microRNA in childhood adrenocortical tumors. Cancer Res; 2010 Jun 1;70(11):4666-75
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  • [Title] Regulation of insulin-like growth factor-mammalian target of rapamycin signaling by microRNA in childhood adrenocortical tumors.
  • Here, we report the identification of a set of miRNAs that are differentially regulated in childhood adrenocortical tumors (ACT), including miR-99a and miR-100.
  • Pharmacologic inhibition of mTOR signaling by everolimus greatly reduces tumor cell growth in vitro and in vivo.
  • Our results reveal a novel mechanism of regulation of mTOR signaling by miRNAs, and they lay the groundwork for clinical evaluation of drugs inhibiting the mTOR pathway for treatment of adrenocortical cancer.

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  • [Copyright] Copyright 2010 AACR.
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  • (PMID = 20484036.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM083159; United States / NCI NIH HHS / CA / P01 CA071907; United States / NIGMS NIH HHS / GM / GM083159; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / CA071907-060006; United States / NCI NIH HHS / CA / P01 CA071907-060006
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / MicroRNAs; 0 / Somatomedins; 9HW64Q8G6G / Everolimus; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ NIHMS192514; NLM/ PMC2880211
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40. Cerquetti L, Bucci B, Marchese R, Misiti S, De Paula U, Miceli R, Muleti A, Amendola D, Piergrossi P, Brunetti E, Toscano V, Stigliano A: Mitotane increases the radiotherapy inhibitory effect and induces G2-arrest in combined treatment on both H295R and SW13 adrenocortical cell lines. Endocr Relat Cancer; 2008 Jun;15(2):623-34
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  • [Title] Mitotane increases the radiotherapy inhibitory effect and induces G2-arrest in combined treatment on both H295R and SW13 adrenocortical cell lines.
  • This drug and radiotherapy are used also in adrenal cancer treatment even if their biological action in this neoplasia remains unknown.
  • We investigated the effects of o,p'-DDD and ionizing radiations (IR) on cell growth inhibition and cell cycle perturbation in H295R and SW13 adrenocortical cancer cells.
  • This combination treatment induced an irreversible inhibition of cell growth in both adrenocortical cancer cells.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. Antineoplastic Agents, Hormonal / pharmacology. Mitotane / pharmacology. Radiotherapy
  • [MeSH-minor] CDC2 Protein Kinase / metabolism. Cell Division / drug effects. Cell Division / radiation effects. Cell Line, Tumor. Cyclin B / metabolism. Cyclin B1. G2 Phase / drug effects. G2 Phase / radiation effects. Humans. RNA, Messenger / metabolism. Steroids / pharmacology. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 18509009.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / CCNB1 protein, human; 0 / Cyclin B; 0 / Cyclin B1; 0 / RNA, Messenger; 0 / Steroids; 0 / Tumor Suppressor Protein p53; 78E4J5IB5J / Mitotane; EC 2.7.11.22 / CDC2 Protein Kinase
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41. Hennings J, Lindhe O, Bergström M, Långström B, Sundin A, Hellman P: [11C]metomidate positron emission tomography of adrenocortical tumors in correlation with histopathological findings. J Clin Endocrinol Metab; 2006 Apr;91(4):1410-4
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  • [Title] [11C]metomidate positron emission tomography of adrenocortical tumors in correlation with histopathological findings.
  • CONTEXT: Adrenal incidentalomas are common findings necessitating extensive laboratory work-up and repetitive radiological examinations.
  • Positron emission tomography (PET) using (11)C-labeled metomidate (MTO) has previously been described as a tool for specific adrenocortical imaging.
  • OBJECTIVE: We evaluated 212 MTO-PET examinations in 173 patients to identify its role in the management of adrenal tumors.
  • PATIENTS: Patients who were operated or biopsied due to adrenal tumors had histopathological diagnoses of adrenocortical adenoma (n = 26), adrenocortical cancer (ACC; n = 13), adrenocortical hyperplasia (n = 8), pheochromocytoma (n = 6), metastasis (n = 3), and tumors of nonadrenal origin (n = 19).
  • The hypothesis that MTO-PET is of value in the management of adrenal tumors, especially incidentaloma, was stated before data collection.
  • RESULTS: Sensitivity was 0.89 and specificity was 0.96 for MTO-PET in proving adrenocortical origin of the lesions.
  • Pheochromocytomas, metastases to the adrenal gland, and nonadrenal masses were all MTO negative.
  • PET measurements using standardized uptake values (SUV) in pathological adrenocortical tissue could differentiate lesions larger than 1-1.5 cm from normal adrenocortical tissue.
  • SUV was higher in aldosterone-hypersecreting adenomas, and the SUV ratio between the tumor and the contralateral gland was significantly higher in all hormonally hypersecreting adenomas as well as in ACC.
  • CONCLUSION: MTO-PET is a specific and sensitive method for diagnosing adrenocortical tumors.
  • MTO-PET is useful in the imaging work-up of adrenal incidentalomas and may be beneficial for the examination of patients with primary aldosteronism or ACC.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenal Cortex Neoplasms / radionuclide imaging. Antineoplastic Agents. Etomidate / analogs & derivatives

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  • (PMID = 16403816.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Radiopharmaceuticals; 5377-20-8 / metomidate; Z22628B598 / Etomidate
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42. Shah MA, Kortmansky J, Motwani M, Drobnjak M, Gonen M, Yi S, Weyerbacher A, Cordon-Cardo C, Lefkowitz R, Brenner B, O'Reilly E, Saltz L, Tong W, Kelsen DP, Schwartz GK: A phase I clinical trial of the sequential combination of irinotecan followed by flavopiridol. Clin Cancer Res; 2005 May 15;11(10):3836-45
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  • PURPOSE: Flavopiridol potently enhances the effect of irinotecan with cures in colorectal cancer xenografts, and is associated with modulation of several molecular targets, including p21, Differentiation-related gene 1 (Drg1), and p53.
  • At the maximal tolerated dose, the pharmacokinetic analysis was expanded and pre- and posttreatment tumor biopsies were done.
  • We observed partial responses in three patients and prolonged stable disease (i.e., >6 months) in 36% of patients including adrenocortical cancer and hepatocellular cancer.
  • [MeSH-minor] Adult. Aged. Bilirubin / analysis. Cell Cycle Proteins / biosynthesis. Cyclin-Dependent Kinase Inhibitor p21. Drug Administration Schedule. Drug Interactions. Female. Flavonoids / administration & dosage. Flavonoids / adverse effects. Flavonoids / pharmacokinetics. Humans. Intracellular Signaling Peptides and Proteins. Male. Maximum Tolerated Dose. Middle Aged. Piperidines / administration & dosage. Piperidines / adverse effects. Piperidines / pharmacokinetics. Treatment Outcome. Tumor Suppressor Protein p53 / biosynthesis

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  • (PMID = 15897584.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 067819
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Flavonoids; 0 / Intracellular Signaling Peptides and Proteins; 0 / N-myc downstream-regulated gene 1 protein; 0 / Piperidines; 0 / Tumor Suppressor Protein p53; 45AD6X575G / alvocidib; 7673326042 / irinotecan; RFM9X3LJ49 / Bilirubin; XT3Z54Z28A / Camptothecin
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43. Gonzalez K, Fong C, Buzin C, Sommer SS, Saldivar JS: p53 Testing for Li-Fraumeni and Li-Fraumeni-like syndromes. Curr Protoc Hum Genet; 2008 Apr;Chapter 10:Unit 10.10
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  • Li-Fraumeni Syndrome (LFS; OMIM #151623) is an autosomal dominant cancer predisposition syndrome characterized by early onset tumors including sarcomas, breast cancer, leukemia, brain tumors, and adrenocortical carcinoma.
  • Li-Fraumeni syndrome is primarily attributed to germline mutations in the p53 tumor suppressor gene, which encodes tumor protein 53.
  • In addition to germline p53 mutations, the p53 gene is the most commonly mutated gene in human cancers, with as much as 50% of tumors containing somatic p53 mutations.

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  • [Copyright] Copyright 2008 by John Wiley & Sons, Inc.
  • (PMID = 18428420.001).
  • [ISSN] 1934-8258
  • [Journal-full-title] Current protocols in human genetics
  • [ISO-abbreviation] Curr Protoc Hum Genet
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA, Neoplasm
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44. Libé R, Fratticci A, Coste J, Tissier F, Horvath A, Ragazzon B, Rene-Corail F, Groussin L, Bertagna X, Raffin-Sanson ML, Stratakis CA, Bertherat J: Phosphodiesterase 11A (PDE11A) and genetic predisposition to adrenocortical tumors. Clin Cancer Res; 2008 Jun 15;14(12):4016-24
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  • [Title] Phosphodiesterase 11A (PDE11A) and genetic predisposition to adrenocortical tumors.
  • PURPOSE: We have reported previously nonsense inactivating mutations of the phosphodiesterase 11A (PDE11A) gene in patients with micronodular adrenocortical hyperplasia and Cushing syndrome.
  • The aim of this study is to investigate the presence of somatic or germ-line PDE11A mutations in various types of adrenocortical tumors: ACTH-independent macronodular adrenocortical hyperplasia (AIMAH), adrenocortical adenoma (ACA), and adrenocortical cancer (ACC).
  • EXPERIMENTAL DESIGN: PDE11A was sequenced in 117 adrenocortical tumors and 192 controls subjects; immunohistochemistry for PDE11A and tumor cyclic AMP levels were studied in a subgroup of adrenocortical tumors.
  • RESULTS: One PDE11A inactivating mutation (R307X) was found in one ACA, 22 germ-line missense variants (18.8%) were found in adrenocortical tumors, and only 11 missense variants (5.7%) were found in controls.
  • By comparing the common mutations, a higher frequency of mutations in adrenocortical tumors than in age/sex-matched controls were observed [16% versus 10% in ACC, 19% versus 10% in ACA, and 24% versus 9% in AIMAH; odds ratio (OR), 3.53; P = 0.05].
  • Somatic DNA from adrenocortical tumors with missense variants showed a wild-type allelic loss.
  • In AIMAH/ACA, cyclic AMP levels were higher than in normal adrenals and decreased PDE11A immunostaining was present in adrenocortical tumors with PDE11A variants.
  • CONCLUSIONS: The present investigation of a large cohort of adrenocortical tumors suggests that PDE11A sequence defects predispose to a variety of lesions (beyond micronodular adrenocortical hyperplasia) and may contribute to the development of these tumors in the general population.

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  • (PMID = 18559625.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / Z01 HD000642; United States / Intramural NIH HHS / / ZIA HD000642-13
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.1.4.- / Phosphoric Diester Hydrolases; EC 3.1.4.35 / PDE11A protein, human
  • [Other-IDs] NLM/ NIHMS306040; NLM/ PMC3134879
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45. Bovio S, Porpiglia F, Bollito E, Allasino B, Reimondo G, Rovero E, Perazzolo L, Angeli A, Papotti M, Terzolo M: Adrenal pseudocyst mimicking cancer: a case report. J Endocrinol Invest; 2007 Mar;30(3):256-8
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  • [Title] Adrenal pseudocyst mimicking cancer: a case report.
  • Adrenal cysts are infrequently observed, since less than 500 cases have been reported in Western literature.
  • Adrenal cysts are conventionally divided into four categories: epithelial, parasitic, endothelial, and hemorrhagic.
  • We report herein the case of an adrenal hemorrhagic pseudocyst that simulated adrenocortical cancer and argue on the clinical clues for a differential diagnosis with other adrenal tumors.
  • [MeSH-major] Adrenal Gland Diseases / diagnosis. Adrenal Gland Neoplasms / diagnosis. Cysts / diagnosis
  • [MeSH-minor] Adrenal Glands / pathology. Adrenal Glands / surgery. Aged. Diagnosis, Differential. Female. Humans


46. Lin MT, Shieh JJ, Chang JH, Chang SW, Chen TC, Hsu WH: Early detection of adrenocortical carcinoma in a child with Li-Fraumeni syndrome. Pediatr Blood Cancer; 2009 Apr;52(4):541-4
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  • [Title] Early detection of adrenocortical carcinoma in a child with Li-Fraumeni syndrome.
  • We report an early detection of cancer in a child with Li-Fraumeni syndrome.
  • The proband was a 3-year-old male with a primitive mesenchymal tumor.
  • The younger sister at risk was followed, and an asymptomatic adrenal cortical carcinoma was detected 3 years later.
  • The report highlights the importance of genetic counseling and provides an example of early detection of cancers in childhood LFS carriers.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenocortical Carcinoma / diagnosis. Early Detection of Cancer. Genetic Predisposition to Disease. Li-Fraumeni Syndrome / genetics
  • [MeSH-minor] Child, Preschool. DNA Mutational Analysis. Female. Genetic Counseling. Germ-Line Mutation. Humans. Male. Pedigree. Point Mutation. Tumor Suppressor Protein p53 / genetics

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  • [Copyright] Copyright 2008 Wiley-Liss, Inc.
  • (PMID = 19101993.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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47. 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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48. Szabó D, Zsippai A, Bendes M, Tömböl Z, Szabó PM, Rácz K, Igaz P: [Pathogenesis of adrenocortical cancer]. Orv Hetil; 2010 Jul 18;151(29):1163-70
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  • [Title] [Pathogenesis of adrenocortical cancer].
  • [Transliterated title] A mellékvesekéreg-carcinoma molekuláris patogenezise.
  • Adrenocortical cancer is a rare tumor with poor prognosis.
  • Whereas most cases occur in a sporadic setting, there are very rare hereditary forms that are important for the understanding of tumor pathogenesis.
  • The hereditary syndromes associated with adrenocortical cancer are: Li-Fraumeni's syndrome, Beckwith-Wiedemann's syndrome and familial adenomatous polyposis, whereas multiple endocrine neoplasia type 1, Carney's complex and McCune-Albright's syndrome mostly predispose to benign adrenocortical tumors.
  • Options for medical treatment of adrenocortical cancer are rather limited.
  • In this study, the pathogenesis of hereditary tumor syndromes, the alterations in sporadic tumors and the most recent molecular-bioinformatical observations are discussed.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / metabolism
  • [MeSH-minor] Adenomatous Polyposis Coli / genetics. Beckwith-Wiedemann Syndrome / genetics. Carney Complex / genetics. Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / metabolism. Fibrous Dysplasia, Polyostotic / genetics. Gene Expression Regulation, Neoplastic. Genes, p53. Genetic Predisposition to Disease. Humans. Insulin-Like Growth Factor II / metabolism. Li-Fraumeni Syndrome / genetics. Multiple Endocrine Neoplasia Type 1 / genetics. Mutation. Proto-Oncogene Proteins / genetics. Signal Transduction. Up-Regulation. Wnt Proteins / metabolism. beta Catenin / metabolism

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  • (PMID = 20591784.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Wnt Proteins; 0 / beta Catenin; 67763-97-7 / Insulin-Like Growth Factor II
  • [Number-of-references] 37
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49. Shi Z, Henwood MJ, Bannerman P, Batista D, Horvath A, Guttenberg M, Stratakis CA, Grimberg A: Primary pigmented nodular adrenocortical disease reveals insulin-like growth factor binding protein-2 regulation by protein kinase A. Growth Horm IGF Res; 2007 Apr;17(2):113-21
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  • [Title] Primary pigmented nodular adrenocortical disease reveals insulin-like growth factor binding protein-2 regulation by protein kinase A.
  • OBJECTIVE: Primary pigmented nodular adrenocortical disease (PPNAD) can occur as an isolated trait or part of Carney complex, a familial lentiginosis-multiple endocrine neoplasia syndrome frequently caused by mutations in PRKAR1A, which encodes the 1alpha regulatory subunit of protein kinase A (PKA).
  • Because alterations in the insulin-like growth factor (IGF) axis, particularly IGF-II and IGF binding protein (IGFBP)-2 overexpression, have been implicated in sporadic adrenocortical tumors, we sought to examine the IGF axis in PPNAD.
  • NCI-H295R cells were used to study PKA and IGF axis signaling in adrenocortical cells in vitro.
  • Moreover, PKA inhibitors increased IGFBP-2 expression in NCI-H295R adrenocortical cells, and anti-IGFBP-2 antibody reduced their proliferation.
  • CONCLUSIONS: IGFBP-2 expression is increased in PPNAD caused by PRKAR1A mutations, and in adrenocortical cancer cells.
  • This is the first evidence for PKA-dependent regulation of IGFBP-2 expression in adrenocortical cells.

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  • (PMID = 17280861.001).
  • [ISSN] 1096-6374
  • [Journal-full-title] Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society
  • [ISO-abbreviation] Growth Horm. IGF Res.
  • [Language] ENG
  • [Databank-accession-numbers] OMIM/ 160980
  • [Grant] United States / NIDDK NIH HHS / DK / T32 DK63688; United States / NIDDK NIH HHS / DK / T32 DK063688; United States / NICHD NIH HHS / HD / Z01 HD000642-04; United States / NIDDK NIH HHS / DK / 5 K08 DK64352; United States / NICHD NIH HHS / HD / Z01 HD000642; United States / NIDDK NIH HHS / DK / K08 DK064352
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / Insulin-Like Growth Factor Binding Protein 2; 0 / PRKAR1A protein, human; 0 / Protein Kinase Inhibitors; 0 / RNA, Messenger; 67763-97-7 / Insulin-Like Growth Factor II; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
  • [Other-IDs] NLM/ NIHMS22924; NLM/ PMC2577759
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50. Igaz P, Tömböl Z, Szabó PM, Likó I, Rácz K: Steroid biosynthesis inhibitors in the therapy of hypercortisolism: theory and practice. Curr Med Chem; 2008;15(26):2734-47
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  • A few drugs inhibiting single or multiple steps in adrenal steroid biosynthesis can be used in clinical practice.
  • Besides blocking multiple steps in adrenal steroid biosynthesis, the DDT (insecticide) analogue mitotane also has adrenolytic properties by inducing mitochondrial degeneration that renders it superior to other drugs in the treatment of adrenocortical cancer.

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  • (PMID = 18991633.001).
  • [ISSN] 0929-8673
  • [Journal-full-title] Current medicinal chemistry
  • [ISO-abbreviation] Curr. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Steroids
  • [Number-of-references] 153
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51. Cavlan D, Bharwani N, Grossman A: Androgen- and estrogen-secreting adrenal cancers. Semin Oncol; 2010 Dec;37(6):638-48
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  • [Title] Androgen- and estrogen-secreting adrenal cancers.
  • Androgen-secreting adrenal cancers are extremely rare malignancies, accounting for only a tiny proportion of the total number of women presenting with signs of androgen excess.
  • Estrogen-secreting adrenal cancers are rarer still.
  • Understanding how these tumors work benefits from an appreciation of adrenal steroid biosynthesis, as it is said that secretion in cancers is an anarchic version of normal adrenal function.
  • When an adrenal tumor is found to secrete androgens or estrogens to excess, it can be difficult to confirm that it is a cancer, as there is significant overlap in the secretory patterns and imaging appearances of benign and malignant disease.
  • [MeSH-major] Adrenal Gland Neoplasms / secretion. Androgens / secretion. Estrogens / secretion
  • [MeSH-minor] Adrenalectomy. Adrenocortical Carcinoma / diagnosis. Adrenocortical Carcinoma / secretion. Adrenocortical Carcinoma / therapy. Adult. Algorithms. Antineoplastic Agents, Hormonal / therapeutic use. Child. Diagnostic Imaging / methods. Female. Humans. Mitotane / therapeutic use. Prognosis. Virilism / etiology

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 21167382.001).
  • [ISSN] 1532-8708
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents, Hormonal; 0 / Estrogens; 78E4J5IB5J / Mitotane
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52. Berbel Tornero O, Ortega García JA, Ferrís i Tortajada J, García Castell J, Donat i Colomer J, Soldin OP, Fuster Soler JL: [Neonatal tumours and congenital malformations]. An Pediatr (Barc); 2008 Jun;68(6):589-95
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  • INTRODUCTION: The association between pediatric cancer and congenital abnormalities is well known but, there is no exclusive data on the neonatal period and the underlying etiopathogenic mechanisms are unknown.
  • MATERIALS AND METHOD: Historical series of neonatal tumours from La Fe University Children's Hospital in Valencia (Spain), from January 1990 to December 1999.
  • The search profile used was the combination of "neonatal/congenital-tumors/cancer/neoplasms" and "congenital malformations/birth defects".
  • RESULTS: 72 neonatal tumours were identified (2.8% of all pediatric cancers diagnosed in our hospital) and in 15 cases (20.8%) there was some associated malformation, disease or syndrome.
  • d) one tumour of the central nervous system with Bochdaleck hernia;.
  • g) kidney tumour in one case with triventricular hydrocephaly, and h) adrenocortical tumour: hemihypertrophy.
  • CONCLUSIONS: Neonatal tumours are more often associated to congenital abnormalities than other pediatric cancers.

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  • (PMID = 18559198.001).
  • [ISSN] 1695-4033
  • [Journal-full-title] Anales de pediatría (Barcelona, Spain : 2003)
  • [ISO-abbreviation] An Pediatr (Barc)
  • [Language] spa
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR020359
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
  • [Other-IDs] NLM/ NIHMS459185; NLM/ PMC3635533
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53. 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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54. Willenberg HS, Ansurudeen I, Schebesta K, Haase M, Wess B, Schinner S, Raffel A, Schott M, Scherbaum WA: The endothelium secretes interleukin-6 (IL-6) and induces IL-6 and aldosterone generation by adrenocortical cells. Exp Clin Endocrinol Diabetes; 2008 Sep;116 Suppl 1:S70-4
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  • [Title] The endothelium secretes interleukin-6 (IL-6) and induces IL-6 and aldosterone generation by adrenocortical cells.
  • Endothelial cells have been shown to induce adrenal steroidogenesis and to enhance aldosterone secretion via angiotensin II and endothelin 1-independent mechanisms.
  • It has been demonstrated that endothelial cells and adrenocortical cells are capable of producing interleukin-6 (IL-6) and IL-6 is a factor known to stimulate adrenal cortisol secretion.
  • We therefore asked whether endothelial cells have an effect on adrenal IL-6 generation and whether IL-6 mediates biosynthesis of aldosterone as is observed after exposure of adrenocortical cells to endothelial cell-conditioned medium (ECCM).
  • Cells from the adrenocortical cancer cell line NCI-H295R were incubated with ECCM produced from human umbilical vein endothelial cells at increasing concentrations.
  • As detected by an enzyme-linked immunosorbent assay, pure ECCM significantly increased IL-6 protein secretion by cultured adrenocortical cells in a dose-dependent fashion, to a 18.0+/-2.0 pg/mL (mean+/-SEM).
  • Pure ECCM also induced aldosterone secretion by adrenocortical cells more than three times that of controls with serum-free medium.
  • These data suggest that endothelial cells secrete IL-6 and that endothelial cell-derived factors regulate adrenal IL-6 synthesis which does not alter adrenal aldosterone secretion.
  • Our findings support the hypothesis that the endothelium and the adrenal gland may play a role in the development of some forms of hypertension and - more speculative - inflammation.
  • [MeSH-major] Adrenal Cortex / metabolism. Aldosterone / biosynthesis. Endothelium, Vascular / secretion. Interleukin-6 / biosynthesis. Interleukin-6 / secretion

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  • (PMID = 18777460.001).
  • [ISSN] 0947-7349
  • [Journal-full-title] Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
  • [ISO-abbreviation] Exp. Clin. Endocrinol. Diabetes
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Interleukin-6; 4964P6T9RB / Aldosterone
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55. Hahner S, Stürmer A, Fassnacht M, Hartmann RW, Schewe K, Cochran S, Zink M, Schirbel A, Allolio B: Etomidate unmasks intraadrenal regulation of steroidogenesis and proliferation in adrenal cortical cell lines. Horm Metab Res; 2010 Jun;42(7):528-34
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  • [Title] Etomidate unmasks intraadrenal regulation of steroidogenesis and proliferation in adrenal cortical cell lines.
  • To characterize intraadrenal adaptations for inhibition of cortisol synthesis, we analyzed the effects of etomidate (ETO) on steroid hormone secretion and expression of key regulators of steroidogenesis and proliferation in human NCI-h295 adrenocortical cancer cells.
  • In summary, ETO exhibits pleiotropic effects on adrenal function in vitro.
  • These changes reflect adaptations to maintain steroidogenesis at the cost of adrenal proliferation.
  • [MeSH-major] Adrenal Cortex / cytology. Adrenal Cortex / metabolism. Cell Proliferation / drug effects. Etomidate / pharmacology. Steroids / biosynthesis

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  • [Copyright] Georg Thieme Verlag KG Stuttgart * New York.
  • (PMID = 20352599.001).
  • [ISSN] 1439-4286
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Steroids; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase; EC 1.14.15.6 / Cholesterol Side-Chain Cleavage Enzyme; Z22628B598 / Etomidate
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56. Taja-Chayeb L, Vidal-Millán S, Gutiérrez-Hernández O, Trejo-Becerril C, Pérez-Cárdenas E, Chávez-Blanco A, de la Cruz-Hernández E, Dueñas-González A: Identification of a novel germ-line mutation in the TP53 gene in a Mexican family with Li-Fraumeni syndrome. World J Surg Oncol; 2009;7:97
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  • BACKGROUND: Germ-line mutations of the TP53 gene are known to cause Li-Fraumeni syndrome, an autosomal, dominantly inherited, high-penetrance cancer-predisposition syndrome characterized by the occurrence of a variety of cancers, mainly soft tissue sarcomas, adrenocortical carcinoma, leukemia, breast cancer, and brain tumors.
  • [MeSH-major] Germ-Line Mutation / genetics. Li-Fraumeni Syndrome / genetics. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 20017945.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ PMC2806269
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57. Abiven G, Coste J, Groussin L, Anract P, Tissier F, Legmann P, Dousset B, Bertagna X, Bertherat J: Clinical and biological features in the prognosis of adrenocortical cancer: poor outcome of cortisol-secreting tumors in a series of 202 consecutive patients. J Clin Endocrinol Metab; 2006 Jul;91(7):2650-5
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  • [Title] Clinical and biological features in the prognosis of adrenocortical cancer: poor outcome of cortisol-secreting tumors in a series of 202 consecutive patients.
  • CONTEXT: Adrenocortical carcinomas (ACC) are rare tumors with a poor prognosis.
  • Mean age at diagnosis was 44 +/- 16 yr (range, 11-88 yr).
  • We found that 154 patients (76%) had hypersecreting tumors [mostly cortisol and androgens (47%), cortisol alone (27%), or androgens alone (6%)] and 43 patients (21%) had metastases at diagnosis.
  • Multivariate analysis identified the following independent prognostic factors associated with shorter survival: older age at diagnosis [hazard ratio (HR), 1.03; P < 0.0001], initial MacFarlane extension stages 3 (HR, 4.42; P = 0.005) and 4 (HR, 7.93; P < 0.0001), and cortisol hypersecretion (HR, 3.90; P < 0.0001).
  • [MeSH-major] Adrenal Cortex Neoplasms / secretion. Hydrocortisone / secretion
  • [MeSH-minor] Adult. Analysis of Variance. Androgens / secretion. Antineoplastic Agents, Hormonal / therapeutic use. Bone Neoplasms / secondary. Chemotherapy, Adjuvant. Female. Humans. Liver Neoplasms / secondary. Lung Neoplasms / secondary. Male. Middle Aged. Mitotane / therapeutic use. Neoplasm Staging. Prognosis. Survival Rate

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  • (PMID = 16670169.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents, Hormonal; 78E4J5IB5J / Mitotane; WI4X0X7BPJ / Hydrocortisone
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58. Leboulleux S, Dromain C, Bonniaud G, Aupérin A, Caillou B, Lumbroso J, Sigal R, Baudin E, Schlumberger M: Diagnostic and prognostic value of 18-fluorodeoxyglucose positron emission tomography in adrenocortical carcinoma: a prospective comparison with computed tomography. J Clin Endocrinol Metab; 2006 Mar;91(3):920-5
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  • [Title] Diagnostic and prognostic value of 18-fluorodeoxyglucose positron emission tomography in adrenocortical carcinoma: a prospective comparison with computed tomography.
  • OBJECTIVE: Patients with adrenocortical cancer are submitted to multiple imaging procedures for diagnosis of recurrence and staging.
  • METHODS: Twenty-eight consecutive patients with adrenocortical cancer referred from November 2003 to December 2004 to the Institut Gustave Roussy were included.
  • The sensitivities for the detection of distinct lesions and the diagnosis of metastatic organs were 90 and 93% for PET/CT and 88 and 82% for TAP-CT, respectively.
  • Tumor size and mitotic rate were significantly associated with FDG uptake.
  • CONCLUSIONS: We show that FDG-PET/CT is complementary to TAP-CT and of special interest in the diagnosis of local relapses.
  • [MeSH-major] Adrenal Cortex Neoplasms / radiography. Adrenal Cortex Neoplasms / radionuclide imaging. Fluorodeoxyglucose F18
  • [MeSH-minor] Adult. Aged. Female. Humans. Image Processing, Computer-Assisted. Male. Middle Aged. Neoplasm Metastasis. Positron-Emission Tomography. Prognosis. Radiopharmaceuticals. Survival Analysis. Tomography, X-Ray Computed

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

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  • (PMID = 19022344.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Interleukin-8; 0 / NF-kappa B; 0 / Protein Isoforms; 0 / Toll-Like Receptors; 0 / Tumor Necrosis Factor-alpha
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60. 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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61. Johnsen IK, Kappler R, Auernhammer CJ, Beuschlein F: Bone morphogenetic proteins 2 and 5 are down-regulated in adrenocortical carcinoma and modulate adrenal cell proliferation and steroidogenesis. Cancer Res; 2009 Jul 15;69(14):5784-92
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  • [Title] Bone morphogenetic proteins 2 and 5 are down-regulated in adrenocortical carcinoma and modulate adrenal cell proliferation and steroidogenesis.
  • Quantitative PCR analysis revealed down-regulation of BMP2 and BMP5 in tissue samples from adrenocortical carcinoma and adrenocortical tumor cell lines compared with normal adrenal glands.
  • Taken together, we show that loss of expression of members of the BMP family of ligands is a common finding in adrenocortical tumors and we provide evidence that BMP-dependent pathways are likely to be involved in the modulation of the malignant and functional phenotype of adrenocortical cancer cells.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Bone Morphogenetic Protein 2 / genetics. Bone Morphogenetic Protein 5 / genetics
  • [MeSH-minor] Aldosterone / metabolism. Blotting, Western. Bone Morphogenetic Protein Receptors / genetics. Bone Morphogenetic Protein Receptors / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Colforsin / pharmacology. Dose-Response Relationship, Drug. Down-Regulation / drug effects. GATA6 Transcription Factor / genetics. GATA6 Transcription Factor / metabolism. Humans. Hydrocortisone / metabolism. Insulin-Like Growth Factor I / genetics. Insulin-Like Growth Factor I / pharmacology. Phosphorylation / drug effects. Proto-Oncogene Proteins c-akt / metabolism. Recombinant Proteins / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Steroid 17-alpha-Hydroxylase / genetics. Steroid 17-alpha-Hydroxylase / metabolism. Time Factors. Tretinoin / pharmacology. Tumor Cells, Cultured

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  • (PMID = 19584291.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bone Morphogenetic Protein 2; 0 / Bone Morphogenetic Protein 5; 0 / GATA6 Transcription Factor; 0 / GATA6 protein, human; 0 / Recombinant Proteins; 1F7A44V6OU / Colforsin; 4964P6T9RB / Aldosterone; 5688UTC01R / Tretinoin; 67763-96-6 / Insulin-Like Growth Factor I; EC 1.14.99.9 / Steroid 17-alpha-Hydroxylase; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.30 / Bone Morphogenetic Protein Receptors; WI4X0X7BPJ / Hydrocortisone
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62. Coulter CL: Fetal adrenal development: insight gained from adrenal tumors. Trends Endocrinol Metab; 2005 Jul;16(5):235-42
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  • [Title] Fetal adrenal development: insight gained from adrenal tumors.
  • Conversely, tumor progression and the development of cancer probably occur through a process of dysregulation and dedifferentiation.
  • Similarities exist between normal human fetal adrenal cortex and adrenal cancers, such as high expression of growth factors, including insulin-like growth factor II.
  • Therefore, we might gain insight into factors involved in adrenocortical development through better understanding the development and progression of adrenocortical tumors.
  • This review is prompted by recent gene profiling studies that have identified genes differentially expressed between normal and abnormal adrenal glands.
  • Several of these genes are specific growth factors or key cell cycle regulators, in addition to genes not previously associated with adrenal growth or function.
  • [MeSH-major] Adrenal Gland Neoplasms / pathology. Adrenal Glands / embryology

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  • (PMID = 15949953.001).
  • [ISSN] 1043-2760
  • [Journal-full-title] Trends in endocrinology and metabolism: TEM
  • [ISO-abbreviation] Trends Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Somatomedins
  • [Number-of-references] 62
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63. Palmero EI, Schüler-Faccini L, Caleffi M, Achatz MI, Olivier M, Martel-Planche G, Marcel V, Aguiar E, Giacomazzi J, Ewald IP, Giugliani R, Hainaut P, Ashton-Prolla P: Detection of R337H, a germline TP53 mutation predisposing to multiple cancers, in asymptomatic women participating in a breast cancer screening program in Southern Brazil. Cancer Lett; 2008 Mar 8;261(1):21-5
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  • [Title] Detection of R337H, a germline TP53 mutation predisposing to multiple cancers, in asymptomatic women participating in a breast cancer screening program in Southern Brazil.
  • Germline TP53 mutations predispose to a rare familial cancer syndrome, the Li-Fraumeni Syndrome (LFS), characterized by the early onset of multiple cancers including childhood adrenocortical carcinomas, sarcomas and brain tumors, and breast and colon cancer in young adults.
  • An identical germline mutation at codon 337 in TP53 (R337H) has been shown to be causally related to an increased risk of multiple cancers in unrelated subjects with familial cancer risk in Southern Brazil.
  • Here we have assessed the prevalence of R337H in 750 healthy women participating in a community-based breast cancer screening program in the area of Porto Alegre.
  • The mutant was detected in two participants (0.3%) who were fourth-degree relatives and reported a familial history of cancer at multiple sites that did not match classical criteria for LFS and its variants.
  • Testing in additional family members detected the mutation in three subjects, one of whom developed breast cancer at the age of 36.
  • These findings indicate that R337H may be a low penetrance mutant which predisposes to multiple cancers and occurs in the population of Southern Brazil at a frequency 10-20 times higher than other TP53 mutants commonly associated with LFS.
  • [MeSH-minor] Adult. Aged. Brazil. Breast Neoplasms / diagnosis. Female. Genetic Testing. Humans. Li-Fraumeni Syndrome / genetics. Middle Aged. Pedigree

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  • (PMID = 18248785.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
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64. Betz MJ, Shapiro I, Fassnacht M, Hahner S, Reincke M, Beuschlein F, German and Austrian Adrenal Network: Peroxisome proliferator-activated receptor-gamma agonists suppress adrenocortical tumor cell proliferation and induce differentiation. J Clin Endocrinol Metab; 2005 Jul;90(7):3886-96
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  • [Title] Peroxisome proliferator-activated receptor-gamma agonists suppress adrenocortical tumor cell proliferation and induce differentiation.
  • Adrenocortical carcinoma (ACC) is a rare tumor entity with poor prognosis due to its highly malignant phenotype and lack of effective treatment options.
  • OBJECTIVE: The purpose of this study was to investigate effects of TZDs on adrenocortical cancer cells.
  • RESULTS: PPARgamma mRNA expression was detectable in all adrenocortical tumors including ACCs at similar levels.
  • Furthermore, incubation of the adrenocortical tumor cell line NCI h295 with the PPARgamma agonist rosiglitazone led to a decrease in cell viability, a decrease of cellular proliferation, and an increase in apoptosis as well as steroidogenesis.
  • On the molecular level, NCI h295 cells expressed higher levels of ACTH receptor (melanocortin receptor-2) mRNA upon treatment, whereas cyclin E mRNA was reduced, thus reflecting a shift toward an expression pattern found in less aggressive adrenocortical tumors in vivo.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. PPAR gamma / agonists. Thiazolidinediones / pharmacology
  • [MeSH-minor] Adult. Aged. Anilides / pharmacology. Apoptosis / drug effects. Cell Differentiation. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin E / genetics. Dose-Response Relationship, Drug. Female. Humans. Insulin-Like Growth Factor II / genetics. Male. Middle Aged. Promoter Regions, Genetic. RNA, Messenger / analysis. Receptor, Melanocortin, Type 2 / genetics

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  • (PMID = 15886257.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-chloro-5-nitrobenzanilide; 0 / Anilides; 0 / Cyclin E; 0 / PPAR gamma; 0 / RNA, Messenger; 0 / Receptor, Melanocortin, Type 2; 0 / Thiazolidinediones; 05V02F2KDG / rosiglitazone; 67763-97-7 / Insulin-Like Growth Factor II
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65. Chen YF, Wang JY, Wu CH, Chen FM, Cheng TL, Lin SR: Detection of circulating cancer cells with K-ras oncogene using membrane array. Cancer Lett; 2005 Nov 8;229(1):115-22
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  • [Title] Detection of circulating cancer cells with K-ras oncogene using membrane array.
  • K-ras oncogene is frequently found in human cancers and thus may serve as a potential diagnostic marker for cancer cells in circulation.
  • So far, there is no reliable method for detecting cancer cells with K-ras oncogene in peripheral blood.
  • In our previous study, cDNA microarray analysis showed that there were 94 genes differentially expressed in K-ras mutant stably transfected adrenocortical cells.
  • A number as low as 5 cancer cells bearing K-ras oncogene in 1 ml of blood could be distinctively detected.
  • Then, we collected blood specimens from 76 cancer patients.
  • [MeSH-major] DNA, Neoplasm / analysis. Genes, ras. Neoplastic Cells, Circulating. Oligonucleotide Array Sequence Analysis
  • [MeSH-minor] Computational Biology. DNA Mutational Analysis. Humans. Neoplasms / blood. Neoplasms / diagnosis. Neoplasms / genetics. Reproducibility of Results. Sensitivity and Specificity. Up-Regulation. ras Proteins / biosynthesis. ras Proteins / genetics

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  • (PMID = 16157223.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 3.6.5.2 / ras Proteins
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66. Ziegler CG, Brown JW, Schally AV, Erler A, Gebauer L, Treszl A, Young L, Fishman LM, Engel JB, Willenberg HS, Petersenn S, Eisenhofer G, Ehrhart-Bornstein M, Bornstein SR: Expression of neuropeptide hormone receptors in human adrenal tumors and cell lines: antiproliferative effects of peptide analogues. Proc Natl Acad Sci U S A; 2009 Sep 15;106(37):15879-84
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  • [Title] Expression of neuropeptide hormone receptors in human adrenal tumors and cell lines: antiproliferative effects of peptide analogues.
  • Peptide analogues targeting various neuropeptide receptors have been used effectively in cancer therapy.
  • A hallmark of adrenocortical tumor formation is the aberrant expression of peptide receptors relating to uncontrolled cell proliferation and hormone overproduction.
  • Our microarray results have also demonstrated a differential expression of neuropeptide hormone receptors in tumor subtypes of human pheochromocytoma.
  • In light of these findings, we performed a comprehensive analysis of relevant receptors in both human adrenomedullary and adrenocortical tumors and tested the antiproliferative effects of peptide analogues targeting these receptors.
  • Specifically, we examined the receptor expression of somatostatin-type-2 receptor, growth hormone-releasing hormone (GHRH) receptor or GHRH receptor splice variant-1 (SV-1) and luteinizing hormone-releasing hormone (LHRH) receptor at the mRNA and protein levels in normal human adrenal tissues, adrenocortical and adrenomedullary tumors, and cell lines.
  • Cytotoxic derivatives of somatostatin AN-238 and, to a lesser extent, AN-162, reduced cell numbers of uninduced and NGF-induced adrenomedullary pheochromocytoma cells and adrenocortical cancer cells.
  • Both the splice variant of GHRH receptor SV-1 and the LHRH receptor were also expressed in adrenocortical cancer cell lines but not in the pheochromocytoma cell line.
  • The GHRH receptor antagonist MZ-4-71 and LHRH antagonist Cetrorelix both significantly reduced cell growth in the adrenocortical cancer cell line.
  • In conclusion, the expression of receptors for somatostatin, GHRH, and LHRH in the normal human adrenal and in adrenal tumors, combined with the growth-inhibitory effects of the antitumor peptide analogues, may make possible improved treatment approaches to adrenal tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / drug therapy. Adrenal Gland Neoplasms / metabolism. Neuropeptides / pharmacology. Receptors, Neuropeptide / metabolism
  • [MeSH-minor] 2-Hydroxyphenethylamine / analogs & derivatives. 2-Hydroxyphenethylamine / pharmacology. Adrenal Glands / metabolism. Aniline Compounds / pharmacology. Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Cytostatic Agents / pharmacology. Doxorubicin / analogs & derivatives. Doxorubicin / pharmacology. Gene Expression. Humans. Oligonucleotide Array Sequence Analysis. PC12 Cells. Pyrroles / pharmacology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Receptors, LHRH / genetics. Receptors, LHRH / metabolism. Receptors, Somatostatin / genetics. Receptors, Somatostatin / metabolism. Somatostatin / analogs & derivatives. Somatostatin / pharmacology

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

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

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  • (PMID = 19849700.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / Z01 HD000642; United States / Intramural NIH HHS / / Z01 HD000642-11; United States / NICHD NIH HHS / HD / Z01-HD-000642-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Validation Studies
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MicroRNAs
  • [Other-IDs] NLM/ NIHMS154316; NLM/ PMC3003432
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69. Acar C, Akkas BE, Sen I, Sozen S, Kitapci MT: False positive 18F-FDG PET scan in adrenal oncocytoma. Urol Int; 2008;80(4):444-7
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  • [Title] False positive 18F-FDG PET scan in adrenal oncocytoma.
  • 18F-FDG whole-body positron emulsion tomography (18F-FDG PET) has become an established imaging modality for a variety of cancers.
  • Today, 18F-FDG PET is utilized to differentiate benign from malignant non-functioning adrenal masses.
  • Abdominal CT revealed a left 6.5 x 4.5 cm adrenal mass with regular margins and focal calcification.
  • To make a differential diagnosis, 18F-FDG PET was performed.
  • The final pathologic evaluation revealed adrenal oncocytoma.
  • We present the disassociation between preoperative 18F-FDG PET and pathologic findings of a benign adrenocortical oncocytoma.
  • [MeSH-major] Adenoma, Oxyphilic / pathology. Adenoma, Oxyphilic / radionuclide imaging. Adrenal Gland Neoplasms / pathology. Adrenal Gland Neoplasms / radionuclide imaging. Positron-Emission Tomography / methods
  • [MeSH-minor] Adrenalectomy / methods. Adult. Diagnosis, Differential. False Positive Reactions. Female. Fluorodeoxyglucose F18. Follow-Up Studies. Humans. Immunohistochemistry. Neoplasm Staging. Preoperative Care / methods. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.
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  • [Copyright] 2008 S. Karger AG, Basel.
  • (PMID = 18587259.001).
  • [ISSN] 1423-0399
  • [Journal-full-title] Urologia internationalis
  • [ISO-abbreviation] Urol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0Z5B2CJX4D / Fluorodeoxyglucose F18
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70. Figueiredo BC, Sandrini R, Zambetti GP, Pereira RM, Cheng C, Liu W, Lacerda L, Pianovski MA, Michalkiewicz E, Jenkins J, Rodriguez-Galindo C, Mastellaro MJ, Vianna S, Watanabe F, Sandrini F, Arram SB, Boffetta P, Ribeiro RC: Penetrance of adrenocortical tumours associated with the germline TP53 R337H mutation. J Med Genet; 2006 Jan;43(1):91-6
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  • [Title] Penetrance of adrenocortical tumours associated with the germline TP53 R337H mutation.
  • BACKGROUND: An inherited germline P53 mutation has been identified in cases of childhood adrenocortical carcinoma (ACT), a neoplasm with a high incidence in southern Brazil.
  • CONCLUSIONS: The TP53 R337H mutation dramatically increases predisposition to childhood ACT but not to other cancers, and explains the increased frequency of ACT observed in this geographic region.

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  • (PMID = 16033918.001).
  • [ISSN] 1468-6244
  • [Journal-full-title] Journal of medical genetics
  • [ISO-abbreviation] J. Med. Genet.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / CA-71907
  • [Publication-type] Letter; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ PMC2564508
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71. Lindhe O, Skogseid B: Mitotane effects in a H295R xenograft model of adjuvant treatment of adrenocortical cancer. Horm Metab Res; 2010 Sep;42(10):725-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mitotane effects in a H295R xenograft model of adjuvant treatment of adrenocortical cancer.
  • Adrenocortical cancer is one of the most aggressive endocrine malignancies.
  • Growth through the capsule or accidental release of cancer cells during surgery frequently results in metastatic disease.
  • We investigated the antitumoral effect of 2 adrenocorticolytic compounds, O, P'-DDD and MeSO2-DDE, in the adrenocortical cell line H295R both in vitro and as a xenograft model in vivo.
  • Tumor growth was significantly inhibited when O, P'-DDD was given at the same time as injection of tumor cells.
  • We suggest that FLT may be a potential PET biomarker when assessing adrenocortical cancer treatment with O,P'-DDD.
  • [MeSH-major] Adjuvants, Pharmaceutic / therapeutic use. Adrenal Cortex Neoplasms / drug therapy. Mitotane / therapeutic use. Xenograft Model Antitumor Assays
  • [MeSH-minor] Animals. Cell Aggregation / drug effects. Cell Count. Cell Proliferation / drug effects. Female. Humans. Mice. Positron-Emission Tomography. Radioactive Tracers. Spheroids, Cellular / drug effects. Spheroids, Cellular / pathology. Time Factors. Tumor Burden / drug effects. Tumor Cells, Cultured

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  • (PMID = 20665429.001).
  • [ISSN] 1439-4286
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Adjuvants, Pharmaceutic; 0 / Radioactive Tracers; 78E4J5IB5J / Mitotane
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72. 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


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

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  • (PMID = 20668603.001).
  • [ISSN] 0975-2129
  • [Journal-full-title] Indian journal of medical and paediatric oncology : official journal of Indian Society of Medical & Paediatric Oncology
  • [ISO-abbreviation] Indian J Med Paediatr Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC2902211
  • [Keywords] NOTNLM ; Adrenocortical carcinoma / androgen secreting tumors / mitotane
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74. Lee JA, Duh QY: Reoperation for adrenocortical neoplasms. Curr Treat Options Oncol; 2006 Jul;7(4):320-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reoperation for adrenocortical neoplasms.
  • Adrenocortical cancer is a highly lethal malignancy.
  • Patients with widely metastatic disease or those with tumors not amenable to re-resection may benefit from tumor debulking to help control symptoms associated with oversecretion syndromes.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery

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  • (PMID = 16916492.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 35
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75. Guerrero MA, Kebebew E: Adrenocortical carcinoma and synchronous malignancies. J Cancer; 2010;1:108-11
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  • [Title] Adrenocortical carcinoma and synchronous malignancies.
  • OBJECTIVE: Adrenocortical carcinoma (ACC) is an aggressive tumor that accounts for 0.02% of all reported cancers.
  • Regardless of the setting, ACC rarely arises concurrent with other malignant tumors.
  • We also provide a literature review of the past 20 years to identify other patients with ACC and synchronous malignant tumors, and those with familial syndromes associated with an increased risk of developing ACC.
  • RESULTS AND CONCLUSIONS: To our knowledge this is the first report of a patient with synchronous malignant tumors of the uterus, ovary and adrenal gland.
  • Review of the literature revealed only 5 other cases in which a patient had concurrent ACC and malignant tumors in other organs.

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  • (PMID = 20842232.001).
  • [ISSN] 1837-9664
  • [Journal-full-title] Journal of Cancer
  • [ISO-abbreviation] J Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Other-IDs] NLM/ PMC2938073
  • [Keywords] NOTNLM ; Adrenocortical carcinoma / Ovarian cancer / Synchronous malignancies / Uterine cancer / and Hereditary syndrome
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76. Achatz MI, Hainaut P, Ashton-Prolla P: Highly prevalent TP53 mutation predisposing to many cancers in the Brazilian population: a case for newborn screening? Lancet Oncol; 2009 Sep;10(9):920-5
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  • [Title] Highly prevalent TP53 mutation predisposing to many cancers in the Brazilian population: a case for newborn screening?
  • The unusually high population frequency of a germline TP53 mutation (R337H) predisposing to early cancer has led to mass newborn testing for this mutation in the State of Paraná, southern Brazil.
  • Newborn screening for inherited cancer risk is complex and controversial.
  • R337H has been identified in Brazilian families with Li-Fraumeni or related syndromes predisposing to cancers in childhood (ie, brain, renal, and adrenocortical carcinomas), adolescence (ie, soft tissue and bone sarcomas), and young adulthood (ie, breast cancer).
  • R337H has also been detected in children with adrenocortical carcinoma without a documented family history of cancer.
  • The mutation is estimated to occur in about 0.3% of the population in southern Brazil and is associated with increased cancer risk throughout life.
  • Cancer patterns in families positive for R337H suggest strong genetic modifying effects, making it difficult to predict individual risk.
  • Because protocols for cancer-risk management in Li-Fraumeni or related syndromes are debatable, extreme care should prevail in predictive testing of children for R337H.


77. Martarelli D, Pompei P, Baldi C, Mazzoni G: Mebendazole inhibits growth of human adrenocortical carcinoma cell lines implanted in nude mice. Cancer Chemother Pharmacol; 2008 Apr;61(5):809-17
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  • [Title] Mebendazole inhibits growth of human adrenocortical carcinoma cell lines implanted in nude mice.
  • Adrenocortical carcinoma is a rare tumor of the adrenal gland which requires new therapeutic approaches as its early diagnosis is difficult and prognosis poor despite therapies used.
  • Recently, mebendazole has been proved to be effective against different cancers.
  • The aim of our study was to evaluate whether mebendazole may result therapeutically useful in the treatment of human adrenocortical carcinoma.
  • We analyzed the effect of mebendazole on human adrenocortical carcinoma cells in vitro and after implantation in nude mice.
  • Mebendazole significantly inhibited cancer cells growth, both in vitro and in vivo, the effects being due to the induction of apoptosis.
  • Moreover, mebendazole inhibited invasion and migration of cancer cells in vitro, and metastases formation in vivo.
  • Overall, these data suggest that treatment with mebendazole, also in combination with standard therapies, could provide a new protocol for the inhibition of adrenocortical carcinoma growth.
  • [MeSH-major] Adrenocortical Carcinoma / drug therapy. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Mebendazole / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Movement / drug effects. Cell Proliferation / drug effects. Drug Screening Assays, Antitumor. Humans. In Vitro Techniques. Male. Mice. Mice, Nude. Neoplasm Metastasis / prevention & control. Neoplasm Transplantation. Neovascularization, Pathologic / drug therapy

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  • (PMID = 17581752.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 81G6I5V05I / Mebendazole
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78. Bertherat J, Groussin L, Bertagna X: Mechanisms of disease: adrenocortical tumors--molecular advances and clinical perspectives. Nat Clin Pract Endocrinol Metab; 2006 Nov;2(11):632-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mechanisms of disease: adrenocortical tumors--molecular advances and clinical perspectives.
  • Most adrenocortical tumors are benign, unilateral, adrenocortical adenomas that are often discovered incidentally.
  • Adrenocortical cancer is rare.
  • Exceptionally, adrenocortical tumors can be bilateral.
  • Although most adrenocortical tumors occur sporadically, they may also feature in congenital and/or familial disease.
  • The identification of germline genetic defects in familial diseases associated with adrenocortical tumors helped to define the somatic alterations in sporadic disease: for example, overexpression of insulin-like growth factor 2 and alterations at the 11p15 locus (observed in Beckwith-Wiedemann syndrome) are also found in most adrenocortical cancers.
  • Similarly, inactivating mutations of the TP53 gene, located at 17p13 (observed in Li-Fraumeni syndrome), can also be found at the somatic level in sporadic adrenocortical cancers, as can 17p13 allelic losses.
  • Components of the cyclic AMP signaling pathway--for example, adrenocorticotropic hormone receptors and other membrane receptors, Gs proteins and protein kinase A--can be altered to various degrees in adrenocortical tumors.
  • More recently, gene profiling and genetic studies have shown that the Wnt-beta-catenin signaling pathway is frequently activated in adrenocortical tumors.
  • These research findings already have profound implications for clinical management of patients with adrenocortical tumors, for example in unraveling the genetic origin of the disease in some patients, and in the development of molecular markers for diagnosis and prognosis.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics

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  • (PMID = 17082810.001).
  • [ISSN] 1745-8366
  • [Journal-full-title] Nature clinical practice. Endocrinology & metabolism
  • [ISO-abbreviation] Nat Clin Pract Endocrinol Metab
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 54
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79. Sinha S, Dutta S, Datta K, Ghosh AK, Mukhopadhyay D: Von Hippel-Lindau gene product modulates TIS11B expression in renal cell carcinoma: impact on vascular endothelial growth factor expression in hypoxia. J Biol Chem; 2009 Nov 20;284(47):32610-8
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  • [Title] Von Hippel-Lindau gene product modulates TIS11B expression in renal cell carcinoma: impact on vascular endothelial growth factor expression in hypoxia.
  • TIS11B has been shown to regulate vascular endothelial growth factor (VEGF) mRNA stability in adrenocorticotropic hormone-stimulated primary adrenocortical cells.
  • TIS11B has also been documented as a negative regulator of VEGF during development, but nothing has yet been reported in the context of human cancers.
  • The Von Hippel-Lindau (VHL) tumor suppressor protein regulates VEGF gene expression at both the transcriptional and post-transcriptional levels in normoxia.
  • Here, we report a unique regulatory function of VHL in VEGF expression in hypoxia that is mediated through modulation of TIS11B protein levels in renal cancer cells.
  • In normoxia, we detected increased expression of the microRNA hsa-miR-29b in the VHL-overexpressing renal cancer cell line 786-O.

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  • (PMID = 19801654.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA078383; United States / NCI NIH HHS / CA / R29 CA078383; United States / NCI NIH HHS / CA / CA78383
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Butyrate Response Factor 1; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; 0 / ZFP36L1 protein, human; EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein; S88TT14065 / Oxygen
  • [Other-IDs] NLM/ PMC2781675
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80. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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81. Ismail A, Bateman A: Expression of TBX2 promotes anchorage-independent growth and survival in the p53-negative SW13 adrenocortical carcinoma. Cancer Lett; 2009 Jun 18;278(2):230-40
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  • [Title] Expression of TBX2 promotes anchorage-independent growth and survival in the p53-negative SW13 adrenocortical carcinoma.
  • The transcriptional regulator TBX2 is genetically amplified in several cancers and has, in addition, important roles in development.
  • Here we used SW13 carcinoma cells which express inactive p53 and have no detectable p16 or p21 CDK-inhibitors as a model to study these functions.
  • This is a cell type-dependent effect as TBX2 overexpression in PANC1 pancreatic cancer cells which are p53-negative has no effect on colony formation or survival after irradiation.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology. T-Box Domain Proteins / physiology. Tumor Suppressor Protein p53 / physiology
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation. Cell Survival / drug effects. Cell Survival / radiation effects. Doxorubicin / pharmacology. Endoplasmic Reticulum / metabolism. Humans. Phosphatidylinositol 3-Kinases / physiology

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  • (PMID = 19216023.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / T-Box Domain Protein 2; 0 / T-Box Domain Proteins; 0 / Tumor Suppressor Protein p53; 80168379AG / Doxorubicin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
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82. de Reyniès A, Assié G, Rickman DS, Tissier F, Groussin L, René-Corail F, Dousset B, Bertagna X, Clauser E, Bertherat J: Gene expression profiling reveals a new classification of adrenocortical tumors and identifies molecular predictors of malignancy and survival. J Clin Oncol; 2009 Mar 1;27(7):1108-15
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression profiling reveals a new classification of adrenocortical tumors and identifies molecular predictors of malignancy and survival.
  • PURPOSE: Adrenocortical tumors, especially cancers, remain challenging both for their diagnosis and prognosis assessment.
  • PATIENTS AND METHODS: One hundred fifty-three unilateral adrenocortical tumors were studied by microarray (n = 92) or reverse transcription quantitative polymerase chain reaction (n = 148).
  • Similarly, for malignant tumors, a two-gene predictor of survival was built using the overall survival as the end point in a training cohort (n = 23), then tested in an independent validation cohort (n = 35).
  • RESULTS: Unsupervised clustering analysis discriminated robustly the malignant and benign tumors, and identified two groups of malignant tumors with very different outcome.
  • Among the malignant tumors, the combined expression of BUB1B and PINK1 was the best predictor of overall survival (P < 2 x 10(-6)), and remained significant after adjusting for MacFarlane staging (P < .005).
  • CONCLUSION: Gene expression analysis unravels two distinct groups of adrenocortical carcinomas.
  • The molecular predictors of malignancy and of survival are reliable and provide valuable independent information in addition to pathology and tumor staging.
  • These original tools should provide important improvements for adrenal tumors management.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Biomarkers, Tumor / genetics. Neoplasm Proteins / genetics. Protein Kinases / genetics. Protein-Serine-Threonine Kinases / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cluster Analysis. Diagnosis, Differential. Disease-Free Survival. Female. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Proportional Hazards Models. Prospective Studies. Reproducibility of Results. Survival Analysis

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  • (PMID = 19139432.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DLGAP5 protein, human; 0 / Neoplasm Proteins; EC 2.7.- / Protein Kinases; EC 2.7.11.1 / Bub1 spindle checkpoint protein; EC 2.7.11.1 / PTEN-induced putative kinase; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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83. Rivest P, Devine PJ, Sanderson JT: Evaluation of a bioluminescent mouse model expressing aromatase PII-promoter-controlled luciferase as a tool for the study of endocrine disrupting chemicals. Toxicol Appl Pharmacol; 2010 Nov 15;249(1):33-40
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  • Dysfunction of the enzyme aromatase (CYP19) is associated with endocrine pathologies such as osteoporosis, impaired fertility and development of hormone-dependent cancers.
  • We studied the effects of forskolin, pregnant mare serum gonadotropin and atrazine in this model (atrazine was previously shown to induced pII-promoter-driven aromatase expression in H295R human adrenocortical carcinoma cells).

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20723554.001).
  • [ISSN] 1096-0333
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Endocrine Disruptors; 0 / Luminescent Proteins; EC 1.13.12.- / Luciferases; EC 1.14.14.1 / Aromatase
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84. Montanaro D, Maggiolini M, Recchia AG, Sirianni R, Aquila S, Barzon L, Fallo F, Andò S, Pezzi V: Antiestrogens upregulate estrogen receptor beta expression and inhibit adrenocortical H295R cell proliferation. J Mol Endocrinol; 2005 Oct;35(2):245-56
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  • [Title] Antiestrogens upregulate estrogen receptor beta expression and inhibit adrenocortical H295R cell proliferation.
  • The molecular mechanisms involved in adrenocortical tumorigenesis are still not completely understood.
  • In this study, using the H295R cell line as a model system, we investigated the role of estrogens and estrogen receptor (ER) alpha and ER beta in the growth regulation of adrenocortical tumors.
  • Moreover, this study points towards a role for ER beta as an important mediator of the repressive effects exerted by antiestrogens on H295R cells; however, further studies are needed to clarify its role in the control of adrenocortical cell proliferation and on the potential benefits of antiestrogens for treatment of adrenocortical cancer.
  • [MeSH-major] Adrenal Cortex / cytology. Cell Proliferation. Estrogen Receptor Modulators / metabolism. Estrogen Receptor beta / metabolism
  • [MeSH-minor] Adrenal Cortex Neoplasms / metabolism. Adrenal Cortex Neoplasms / pathology. Androgens / metabolism. Antigens, CD95 / metabolism. Apoptosis. Aromatase / metabolism. Aromatase Inhibitors / metabolism. Autocrine Communication. Caspases / metabolism. Cell Line, Tumor. Colforsin / metabolism. Estradiol / metabolism. Estrogen Receptor alpha / genetics. Estrogen Receptor alpha / metabolism. Fas Ligand Protein. Humans. Membrane Glycoproteins / genetics. Membrane Glycoproteins / metabolism. Nitriles / metabolism. Promoter Regions, Genetic. RNA, Messenger / metabolism. Triazoles / metabolism. Tumor Necrosis Factors / genetics. Tumor Necrosis Factors / metabolism

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  • (PMID = 16216906.001).
  • [ISSN] 0952-5041
  • [Journal-full-title] Journal of molecular endocrinology
  • [ISO-abbreviation] J. Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / Antigens, CD95; 0 / Aromatase Inhibitors; 0 / Estrogen Receptor Modulators; 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Membrane Glycoproteins; 0 / Nitriles; 0 / RNA, Messenger; 0 / Triazoles; 0 / Tumor Necrosis Factors; 1F7A44V6OU / Colforsin; 4TI98Z838E / Estradiol; 7LKK855W8I / letrozole; EC 1.14.14.1 / Aromatase; EC 3.4.22.- / Caspases
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85. Lachenmayer A, Lichtenauer UD, Cox T, Schott M, Malendowicz LK, Goretzki PE, Cupisti K, Scherbaum WA, Bornstein SR, Willenberg HS: Nestin as a marker in the classification of adrenocortical tumors. Horm Metab Res; 2009 May;41(5):397-401
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nestin as a marker in the classification of adrenocortical tumors.
  • Since adrenocortical carcinoma, a tumor entity still very difficult to classify, may gain the ability to aberrantly express neuroectodermal proteins including chromogranin A and synaptophysin, we asked the question whether nestin might also be detected in adrenocortical carcinomas, and if so, whether it might serve as a tool for clinical pathology.
  • Therefore, we studied the expression of nestin in normal adrenal glands, adrenocortical adenomas, and adrenocortical cancers using specific immunohistochemistry and semi-quantitative reverse transcriptase-polymerase chain reaction.
  • Immunostaining was nestin-positive in 1 out of 9 normal adrenal glands (11%), 2 out of 20 adrenocortical adenomas (10%), and 13 out of 16 adrenocortical carcinomas (81%).
  • We conclude that our findings provide further evidence that nestin, as a marker, is not restricted to neuronal stem cells and nestin expression is worth to be studied in adrenocortical tumors.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / classification. Adrenocortical Carcinoma / pathology. Biomarkers, Tumor / metabolism. Intermediate Filament Proteins / metabolism. Nerve Tissue Proteins / metabolism
  • [MeSH-minor] Adrenal Glands / metabolism. Adult. Aged. Aged, 80 and over. Female. Gene Expression. Humans. Male. Middle Aged. Nestin

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  • (PMID = 19294612.001).
  • [ISSN] 1439-4286
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin
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86. Karakas Z, Tugcu D, Unuvar A, Atay D, Akcay A, Gedik H, Kayserili H, Dogan O, Anak S, Devecioglu O: Li-Fraumeni syndrome in a Turkish family. Pediatr Hematol Oncol; 2010 May;27(4):297-305
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Li-Fraumeni syndrome (LFS) is one of the familial cancers characterized by different tumors and hereditary TP53 mutations.
  • The adrenocortical carcinoma (ACC) association with acute leukemia is unusual in childhood, even in LFS.
  • The authors here present a family with pR337P mutation in TP53 gene who had a child with acute lymphoblastic leukemia (ALL) and associated adrenocortical carcinoma as a case 1 and his cousin with brain tumor as a case 2.
  • A hereditary TP53 mutation supported the diagnosis of LFS in this family.
  • [MeSH-major] Adrenocortical Carcinoma / genetics. Brain Neoplasms / genetics. Li-Fraumeni Syndrome / genetics. Mutation, Missense. Neoplasms, Second Primary / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 20426520.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53
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87. Tissier F, Cavard C, Groussin L, Perlemoine K, Fumey G, Hagneré AM, René-Corail F, Jullian E, Gicquel C, Bertagna X, Vacher-Lavenu MC, Perret C, Bertherat J: Mutations of beta-catenin in adrenocortical tumors: activation of the Wnt signaling pathway is a frequent event in both benign and malignant adrenocortical tumors. Cancer Res; 2005 Sep 1;65(17):7622-7
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  • [Title] Mutations of beta-catenin in adrenocortical tumors: activation of the Wnt signaling pathway is a frequent event in both benign and malignant adrenocortical tumors.
  • Adrenocortical cancer is a rare cancer with a very poor prognosis.
  • The genetic alterations identified to date in adrenocortical tumors are limited.
  • Activating mutations of the Wnt signaling pathway have been observed in more frequent cancers, particularly digestive tract tumors.
  • We investigated whether Wnt pathway activation is involved in adrenocortical tumorigenesis.
  • In a series of 39 adrenocortical tumors, immunohistochemistry revealed abnormal cytoplasmic and/or nuclear accumulation of beta-catenin in 10 of 26 adrenocortical adenomas and in 11 of 13 adrenocortical carcinomas.
  • An activating somatic mutation of the beta-catenin gene was shown in 7 of 26 adrenocortical adenomas and in 4 of 13 adrenocortical carcinomas; these mutations were observed only in adrenocortical tumors with abnormal beta-catenin accumulation and most were point mutations altering the Ser45 of exon 3 (in the consensus GSK3-beta/CK1 phosphorylation site).
  • Functional studies showed that the activating Ser45 beta-catenin mutation found in the adrenocortical cancer H295R cell line leads to constitutive activation of T-cell factor-dependent transcription.
  • This is the first molecular defect to be reported with the same prevalence in both benign (27%) and malignant (31%) adrenocortical tumors. beta-Catenin mutations are also the most frequent genetic defect currently known in adrenocortical adenomas.
  • In adrenocortical adenomas, beta-catenin alterations are more frequent in nonfunctioning tumors, suggesting that beta-catenin pathway activation might be mostly involved in the development of nonsecreting adrenocortical adenomas and adrenocortical carcinomas.
  • The very frequent and substantial accumulation of beta-catenin in adrenocortical carcinomas suggests that other alterations might also be involved.
  • This finding may contribute to new therapeutic approaches targeting the Wnt pathway in malignant adrenocortical tumors, for which limited medical therapy is available.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Cytoskeletal Proteins / genetics. Intercellular Signaling Peptides and Proteins / genetics. Trans-Activators / genetics
  • [MeSH-minor] Adult. Aged. Cell Line, Tumor. Female. Humans. Immunohistochemistry. Male. Middle Aged. Mutation. Signal Transduction. Wnt Proteins. beta Catenin

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  • (PMID = 16140927.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / Cytoskeletal Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Trans-Activators; 0 / Wnt Proteins; 0 / beta Catenin
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88. Hong DS, Sebti SM, Newman RA, Blaskovich MA, Ye L, Gagel RF, Moulder S, Wheler JJ, Naing A, Tannir NM, Ng CS, Sherman SI, El Naggar AK, Khan R, Trent J, Wright JJ, Kurzrock R: Phase I trial of a combination of the multikinase inhibitor sorafenib and the farnesyltransferase inhibitor tipifarnib in advanced malignancies. Clin Cancer Res; 2009 Nov 15;15(22):7061-8
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  • Interestingly, six of eight patients with medullary thyroid cancer had durable stable disease (n = 3) or partial remissions (n = 3), lasting 12 to 26+ months.
  • Prolonged (> or =6 months) stable disease was also seen in nine patients as follows: papillary thyroid cancer (n = 4; 18+ to 27+ months), adrenocortical cancer (n = 2; 7 and 11 months), and one each of melanoma (platelet-derived growth factor receptor mutation positive; 14 months), renal (6 months), and pancreatic cancer (6 months).
  • Activity was seen, especially in patients with medullary thyroid cancer, a tumor characterized by RET mutations.

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  • (PMID = 19903778.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA062461-10; United States / NCI NIH HHS / CA / U01 CA062461; United States / NCI NIH HHS / CA / 5 U01 CA062461; United States / NCI NIH HHS / CA / U01 CA062461-10
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzenesulfonates; 0 / Phenylurea Compounds; 0 / Pyridines; 0 / Quinolones; 192185-72-1 / tipifarnib; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 2.5.1.29 / Farnesyltranstransferase; EC 2.7.10.1 / Proto-Oncogene Proteins c-ret; EC 2.7.10.1 / RET protein, human
  • [Other-IDs] NLM/ NIHMS140339; NLM/ PMC2784003
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89. Libè R, Fratticci A, Bertherat J: Adrenocortical cancer: pathophysiology and clinical management. Endocr Relat Cancer; 2007 Mar;14(1):13-28
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  • [Title] Adrenocortical cancer: pathophysiology and clinical management.
  • Adrenocortical cancer (ACC) is a rare tumor with a poor prognosis.
  • By contrast, benign adrenocortical tumors are frequent, underlying the importance of a correct diagnosis of malignancy of such tumors.
  • ACC can be diagnosed by the investigation of endocrine signs of steroid excess, symptoms due to tumor growth or an adrenal incidentaloma.
  • Imaging by CT-scan or MRI shows a large heterogeneous tumor with a low fat content.
  • Careful pathological investigation with the assessment of the Weiss score is important for the diagnosis of malignancy.
  • Tumors localized to the adrenal gland (McFarlane stages 1 and 2) have a better outcome than invasive and metastatic tumors (stages 3 and 4).
  • Tumor removal by a specialized team is crucial for treatment and should always aim at complete removal.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / therapy
  • [MeSH-minor] Genes, Tumor Suppressor. Humans. Oncogenes / genetics


90. Spiegel AM, Libutti SK: Future diagnostic and therapeutic trends in endocrine cancers. Semin Oncol; 2010 Dec;37(6):691-5
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  • [Title] Future diagnostic and therapeutic trends in endocrine cancers.
  • Current treatment of endocrine cancers relies primarily on surgical resection, which is generally effective only for localized disease.
  • Radioactive iodine treatment is an important modality for those thyroid cancers that maintain the ability to take up iodine.
  • For endocrine cancers that are no longer localized, current modes of therapy, including various combinations of chemotherapy and radiation, are inadequate, posing a major challenge to ongoing research to develop more effective methods for diagnosis and treatment.
  • In this article, we offer some predictions of future trends in the diagnosis and treatment of endocrine cancers.
  • Following a general introduction, we focus on thyroid cancer as a paradigm for what we may expect in future developments, and then add selected comments relevant to parathyroid, adrenocortical, and gastrointestinal and pancreatic neuroendocrine tumors.
  • Rapid, inexpensive whole genome sequencing of both germline and tumor DNA, novel molecular and functional imaging, as well as new biomarkers are expected to enable more precise diagnosis, targeted therapy, and possibly prevention.
  • Translating the coming wave of data on the molecular pathogenesis of endocrine cancers into practical diagnostic and treatment modalities will require new forms of collaboration between investigators, clinicians, and industry.
  • [MeSH-major] Endocrine Gland Neoplasms / diagnosis. Endocrine Gland Neoplasms / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Biomarkers, Tumor. Gastrointestinal Neoplasms / diagnosis. Gastrointestinal Neoplasms / genetics. Gastrointestinal Neoplasms / therapy. Humans. Molecular Probe Techniques. Molecular Targeted Therapy. Neoplastic Syndromes, Hereditary / diagnosis. Neoplastic Syndromes, Hereditary / genetics. Neoplastic Syndromes, Hereditary / therapy. Neuroendocrine Tumors / diagnosis. Neuroendocrine Tumors / genetics. Neuroendocrine Tumors / therapy. Thyroid Neoplasms / diagnosis. Thyroid Neoplasms / genetics. Thyroid Neoplasms / therapy

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 21167386.001).
  • [ISSN] 1532-8708
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor
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91. Paramonova I, Haase M, Mülders-Opgenoorth B, Ansurudeen-Rafi I, Bornstein SR, Papewalis C, Schinner S, Schott M, Scherbaum WA, Willenberg HS: The effects of the endothelium on adrenal steroidogenesis and growth are mainly mediated by proteins other than endothelin-1. Horm Metab Res; 2010 Nov;42(12):840-5
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  • [Title] The effects of the endothelium on adrenal steroidogenesis and growth are mainly mediated by proteins other than endothelin-1.
  • The endothelium releases factors stimulating the adrenal cortex.
  • It is also known that endothelin-1 (ET-1) promotes generation of cortisol and aldosterone, and proliferation of adrenocortical cells.
  • The aim of the study was to find out whether the effect of the endothelium on adrenocortical cells is dominated by the action of ET-1.
  • The effects of endothelial cell-conditioned medium (ECCM), obtained during growth of human umbilical cord vein endothelial cells, on aldosterone and cortisol release by cells of the adrenocortical cancer cell-line NCI-H295R and the promoter activity of steroidogenic acute-regulatory protein (StAR) were studied.
  • The effect of ECCM on proliferation of human primary normal adrenocortical and NCI-H295R cells was also investigated.
  • In conclusion, the cultured endothelial cells secrete a protein that stimulates steroidogenesis in adrenal cells and their growth.
  • [MeSH-major] Adrenal Cortex / cytology. Aldosterone / metabolism. Cell Proliferation. Endothelial Cells / metabolism. Endothelin-1 / metabolism. Hydrocortisone / metabolism. Proteins / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cells, Cultured. Culture Media, Conditioned / metabolism. Humans. Phosphoproteins / genetics. Phosphoproteins / metabolism. Promoter Regions, Genetic

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  • [Copyright] © Georg Thieme Verlag KG Stuttgart · New York.
  • (PMID = 20839150.001).
  • [ISSN] 1439-4286
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Endothelin-1; 0 / Phosphoproteins; 0 / Proteins; 0 / steroidogenic acute regulatory protein; 4964P6T9RB / Aldosterone; WI4X0X7BPJ / Hydrocortisone
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92. 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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93. Libé R, Bertherat J: Molecular genetics of adrenocortical tumours, from familial to sporadic diseases. Eur J Endocrinol; 2005 Oct;153(4):477-87
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  • [Title] Molecular genetics of adrenocortical tumours, from familial to sporadic diseases.
  • Adrenal masses can be detected in up to 4% of the population, and are mostly of adrenocortical origin.
  • Adrenocortical tumours (ACTs) may be responsible for excess steroid production and, in the case of adrenocortical cancers, for morbidity or mortality due to tumour growth.
  • The familial diseases concerned are Li-Fraumeni syndrome, which may be due to germline mutation of the tumour-suppressor gene TP53 and Beckwith-Wiedemann syndrome, which is caused by dys-regulation of the imprinted IGF-II locus at 11p15.
  • ACTs also occur in type 1 multiple endocrine neoplasia (MEN 1), which is characterized by a germline mutation of the menin gene.
  • Cushing's syndrome due to primary pigmented nodular adrenocortical disease (PPNAD) has been observed in Carney complex patients presenting inactivating germline PRKAR1A mutations.
  • Interestingly, allelic losses at 17p13 and 11p15 have been demonstrated in sporadic adrenocortical cancer and somatic PRKAR1A mutations have been found in secreting adrenocortical adenomas.
  • The genetics of another group of adrenal diseases that can lead to adrenal nodular hyperplasia -- congenital adrenal hyperplasia (CAH) and glucocorticoid-remediable aldosteronism (GRA) -- have also been studied extensively.
  • This review summarizes recent advances in the genetics of ACTs, highlighting both improvements in our understanding of the pathophysiology and the diagnosis of these tumours.

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  • (PMID = 16189167.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 97
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94. Han SJ, Kim TS, Jeon SW, Jeong SJ, Yun M, Rhee Y, Kang ES, Cha BS, Lee EJ, Lee HC, Lim SK: Analysis of adrenal masses by 18F-FDG positron emission tomography scanning. Int J Clin Pract; 2007 May;61(5):802-9
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  • [Title] Analysis of adrenal masses by 18F-FDG positron emission tomography scanning.
  • This study aimed to analyse the characteristics of adrenal masses visible in the computerised tomography (CT) scans which have been also evaluated by 2-[18F]fluoro-2-deoxy-D-glucose positron emission tomography (18F-FDG PET), and to characterise the features of 18F-FDG PET scans associated with various adrenal endocrine tumours, especially benign functional tumours.
  • 18F-FDG PET scans of 105 patients with adrenal masses on the CT scan were analysed.
  • Positive uptakes in the 18F-FDG PET scans were seen in 60 malignant tumours (54 metastasic lesions, six primary adrenal cancers) and seven benign tumours.
  • The positive predictive value of 18F-FDG PET imaging to characterise an adrenal mass as a malignant tumour was 90%; the corresponding negative predictive value to rule out malignancy was also 90%.
  • Benign adrenal tumours were smaller than that of malignant lesions (p<0.05).
  • The mean standardised uptake value max (SUVmax) of the metastatic lesions [8.4+/-6.5 (microCi/g)/microCi/kg] was significantly higher than that of the benign adrenal tumours [2.4+/-1.2 (microCi/g)/microCi/kg, p<0.001].
  • Examination of only the primary adrenal lesions revealed that all adrenocortical carcinomas, two of three cases of pheochromocytomas, three of five neuroblastomas and two of four cases of primary aldosteronism showed positive 18F-FDG uptake.
  • In conclusion, for patients presenting adrenal masses with a high probability of malignancy, 18F-FDG PET can be used to differentiate malignant from benign adrenal lesions.
  • This study suggests that 18F-FDG PET scanning can offer supporting data to localise and characterise adrenal tumours.
  • [MeSH-major] Adrenal Gland Neoplasms / radionuclide imaging. Fluorodeoxyglucose F18. Positron-Emission Tomography / methods. Radiopharmaceuticals

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  • (PMID = 17343665.001).
  • [ISSN] 1368-5031
  • [Journal-full-title] International journal of clinical practice
  • [ISO-abbreviation] Int. J. Clin. Pract.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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95. 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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96. Szabó PM, Wiener Z, Tömböl Z, Kovács A, Pócza P, Horányi J, Kulka J, Riesz P, Tóth M, Patócs A, Gaillard RC, Falus A, Rácz K, Igaz P: Differences in the expression of histamine-related genes and proteins in normal human adrenal cortex and adrenocortical tumors. Virchows Arch; 2009 Aug;455(2):133-42
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  • [Title] Differences in the expression of histamine-related genes and proteins in normal human adrenal cortex and adrenocortical tumors.
  • Histamine is involved in the pathogenesis of several tumors; however, there are no data on its possible involvement in human adrenocortical tumorigenesis.
  • The expression of genes and proteins involved in the biosynthesis (histidine decarboxylase, HDC), action (histamine receptors: HRH1-HRH4), and metabolism of histamine is largely unknown both in the normal human adrenal cortex and in adrenocortical tumors.
  • In this study, we examined the expression of histamine-related genes and proteins and histamine content in normal adrenal cortex, benign adrenocortical adenomas, and malignant adrenocortical cancer (ACC).
  • We found that all proteins involved in histamine biosynthesis and action are present both in the normal adrenal cortex and in the tumors studied.
  • Adrenocortical tumorigenesis might, thus, be characterized by reduced histamine biosynthesis; furthermore, different adrenocortical tumor subtypes may show unique histamine receptor expression profiles.
  • [MeSH-major] Adrenal Cortex / metabolism. Adrenal Cortex Neoplasms / metabolism. Adrenocortical Adenoma / metabolism. Histamine / metabolism. Histidine Decarboxylase / metabolism. Receptors, Histamine / metabolism

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

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

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  • (PMID = 16378774.001).
  • [ISSN] 1555-7162
  • [Journal-full-title] The American journal of medicine
  • [ISO-abbreviation] Am. J. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 9002-60-2 / Adrenocorticotropic Hormone; R9400W927I / Ketoconazole
  • [Number-of-references] 100
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99. Daffara F, De Francia S, Reimondo G, Zaggia B, Aroasio E, Porpiglia F, Volante M, Termine A, Di Carlo F, Dogliotti L, Angeli A, Berruti A, Terzolo M: Prospective evaluation of mitotane toxicity in adrenocortical cancer patients treated adjuvantly. Endocr Relat Cancer; 2008 Dec;15(4):1043-53
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  • [Title] Prospective evaluation of mitotane toxicity in adrenocortical cancer patients treated adjuvantly.
  • Seventeen consecutive patients who were treated with mitotane after radical resection of adrenocortical cancer (ACC) from 1999 to 2005 underwent physical examination, routine laboratory evaluation, monitoring of mitotane concentrations, and a hormonal work-up at baseline and every 3 months till ACC relapse or study end (December 2007).
  • Mitotane affected adrenal steroidogenesis with a more remarkable inhibition of cortisol and DHEAS than aldosterone.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Mitotane / therapeutic use
  • [MeSH-minor] Adult. Chemotherapy, Adjuvant. Chromatography, High Pressure Liquid. Female. Humans. Hydrocortisone / metabolism. Hypothyroidism / etiology. Male. Middle Aged. Neoplasm Staging. Prospective Studies. Survival Rate. Testosterone / metabolism. Young Adult

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  • (PMID = 18824557.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 3XMK78S47O / Testosterone; 78E4J5IB5J / Mitotane; WI4X0X7BPJ / Hydrocortisone
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100. Nychytaĭlo ME, Diachenko VV, Litvinenko AN, Gul'ko ON, Bulik II, Lukecha II: [Experience of performance of laparoscopic adrenalectomy using lateral transabdominal approach]. Klin Khir; 2008 Sep;(9):41-4
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  • In 2002-2008 yrs. in the Department of Laparoscopic Surgery and Cholelithiasis in 52 patients laparoscopic adrenalectomy (LA) was accomplished, performed for different diseases of suprarenal glands.
  • Incidentaloma was diagnosed in 8, fibroma--in 4, pheokhromocytoma--in 10, aldosteroma--in 11, adrenocortical cancer--in 3, corticosteroma--in 13, suprarenal gland cyst--in 3 patients.
  • The operation time in right-sided and left-sided LA had constituted accordingly 85 and 118 minutes.
  • In 1 (2.4%) observation hemoperitoneum had occurred as a result of traumatic damage of spleen during performance of left-sided LA.

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  • (PMID = 19278040.001).
  • [ISSN] 0023-2130
  • [Journal-full-title] Klinichna khirurhiia
  • [ISO-abbreviation] Klin Khir
  • [Language] RUS
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Ukraine
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