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National Cancer Institute®
Ultima Vez Modificado: 1 de abril del 2002
UI - 11484289
AU - Shon Ch; Mladenovski V; Petkov R; K'tev N; Mikhailov N; Gavrailov M;
TI - Trifonov D [Diagnosis and surgical treatment of adrenocortical carcinoma. A review of the literature and report of two cases]
SO - Khirurgiia (Sofiia) 2000;56(2):45-9
Adrenocortical carcinomas (ACC) are rare and represent only 0.05 to 0.2% of all cancers. They can be hormonally active, appearing clinically by one or more endocrine syndromes, or can be hormonally non-active. Commonly most of the cases with AC are diagnosed when the neoplastic process have spread out of the suprarenal gland (stage III or IV). Computed tomography and magnetic resonance imaging are the most useful diagnostic methods of ACC but the latter is more accurate, especially in estimation of the local invasion of the tumor. Surgery is the main and the most effective method for treatment of both primary and recurrent ACC, and in selective cases--of metastasis. The chemotherapy with mitotane has a limited role and is indicated in cases of inoperable ACC (primary or recurrent) and/or presence of metastasis. Two cases of ACC treated in our department are reported. Case I: a 26-years-old female with ACC in stage II, which was diagnosed incidentally by ultrasound investigation for other consideration. Although the urine levels of free cortisol were elevated, the woman had no endocrine symptoms. Case II: a 50-years-old female with a second recurrence ACC appeared 5 years after a resection of the first recurrence tumor and 6 years after an operation for the primary tumor. Problems in diagnose and surgical treatment of these cases are discussed.
UI - 11889182
AU - Gao ZH; Suppola S; Liu J; Heikkila P; Janne J; Voutilainen R
TI - Association of H19 promoter methylation with the expression of H19 and IGF-II genes in adrenocortical tumors.
SO - J Clin Endocrinol Metab 2002 Mar;87(3):1170-6
AD - Department of Pathology, University of Helsinki, FIN-00014 Helsinki, Finland.
Low H19 and abundant IGF-II expression may have a role in the development of adrenocortical carcinomas. In the mouse, the H19 promoter area has been found to be methylated when transcription of the H19 gene is silent and unmethylated when it is active. We used PCR-based methylation analysis and bisulfite genomic sequencing to study the cytosine methylation status of the H19 promoter region in 16 normal adrenals and 30 pathological adrenocortical samples. PCR-based analysis showed higher methylation status at three HpaII-cutting CpG sites of the H19 promoter in adrenocortical carcinomas and in a virilizing adenoma than in their adjacent normal adrenal tissues. Bisulfite genomic sequencing revealed a significantly higher mean degree of methylation at each of 12 CpG sites of the H19 promoter in adrenocortical carcinomas than in normal adrenals (P < 0.01 for all sites) or adrenocortical adenomas (P < 0.01, except P < 0.05 for site 12 and P > 0.05 for site 11). The mean methylation degree of the 12 CpG sites was significantly higher in the adrenocortical carcinomas (mean +/- SE, 76 +/- 7%) than in normal adrenals (41 +/- 2%) or adrenocortical adenomas (45 +/- 3%; both P < 0.005). RNA analysis indicated that the adrenocortical carcinomas expressed less H19 but more IGF-II RNAs than normal adrenal tissues did. The mean methylation degree of the 12 H19 promoter CpG sites correlated negatively with H19 RNA levels (r = -0.550; P < 0.01), but positively with IGF-II mRNA levels (r = 0.805; P < 0.001). In the adrenocortical carcinoma cell line NCI-H295R, abundant IGF-II, but minimal H19, RNA expression was detected by Northern blotting. Treatment with a cytosine methylation inhibitor, 5-aza-2'-deoxycytidine, increased H19 RNA expression, whereas it decreased IGF-II mRNA accumulation dose- and time-dependently (both P < 0.005) and reduced cell proliferation to 10% in 7 d. Our results suggest that altered DNA methylation of the H19 promoter is involved in the abnormal expression of both H19 and IGF-II genes in human adrenocortical carcinomas.
UI - 11889190
AU - Lefebvre H; Cartier D; Duparc C; Lihrmann I; Contesse V; Delarue C;
TI - Godin M; Fischmeister R; Vaudry H; Kuhn JM Characterization of serotonin(4) receptors in adrenocortical aldosterone-producing adenomas: in vivo and in vitro studies.
SO - J Clin Endocrinol Metab 2002 Mar;87(3):1211-6
AD - European Institute for Peptide Research (IFRMP 23), Department of Endocrinology, INSERM, U-413, Centre Hospitalo-Universitaire de Rouen, 76031 Rouen, France. firstname.lastname@example.org
We have previously shown that serotonin (5-HT) stimulates aldosterone secretion from the human adrenal gland through activation of 5-HT(4) receptors. The aim of the present study was to investigate in vivo and in vitro the presence of 5-HT(4) receptors in aldosterone-producing adenomas (aldosteronomas). Eight patients with aldosteronoma received a single oral dose of placebo or cisapride (10 mg). Cisapride administration significantly increased plasma aldosterone within 120 min without any significant change in renin, cortisol, or potassium levels. In two patients, a marked decrease in the plasma aldosterone response to cisapride was observed after surgical removal of the tumor. The effects of 5-HT and selective 5-HT(4) ligands on aldosterone production from aldosteronoma tissues were studied in vitro using a perifusion system technique. 5-HT and the 5-HT(4) receptor agonist cisapride (10(-7) M, 20 min) both stimulated aldosterone secretion from aldosteronoma slices. The 5-HT- and cisapride-evoked aldosterone responses were inhibited by concomitant administration of the specific 5-HT(4) receptor antagonist GR 113808 (10(-7) M, 150 min). PCR amplification revealed the expression of 5-HT(4) receptor mRNA in 13 of 14 aldosteronomas studied. Taken together, these data show that most aldosteronomas, like normal glomerulosa cells, express a functional 5-HT(4) receptor. Our results also suggest that 5-HT, which can be locally released by intratumoral mast cells, may play a role in the pathophysiology of these tumors.
UI - 11844057
AU - Honda K; Kashima K; Daa T; Gamachi A; Nakayama I; Yokoyama S
TI - Myxoid adrenal cortical adenoma.
SO - Pathol Int 2001 Nov;51(11):887-91
AD - Department of Pathology, Oita Medical University, Oita, Japan. email@example.com
Myxoid adrenal cortical adenoma is a rare tumor and, to our knowledge, only 16 cases have been reported. We present the case of a 56-year-old Japanese man who was admitted to hospital because of a right adrenal mass that was discovered during a routine physical examination. The resected mass was well circumscribed and contained canary yellow multinodular regions that were surrounded by a brown gelatinous region. Histologically, the multinodular regions resembled a conventional adrenal cortical adenoma, being composed of solid aggregates of large clear or eosinophilic cells. In the gelatinous region, anastomosing small eosinophilic or vesicular cells were visible within a myxoid stroma that contained large amounts of acidic mucopolysaccharides. Light-microscopic findings were consistent with a diagnosis of adenoma. Immunohistochemical staining revealed that a small number of tumor cells were positive for vimentin, and the MIB-1 labeling index was less than 1%. Flow cytometry demonstrated that cells were diploid. At the ultrastructural level, many fat droplets were found in the large clear cells in the multinodular regions. Small eosinophilic cells in the myxoid region contained many mitochondria but few fat droplets. There were no findings suggestive of malignancy. Although the adrenal cortex might have the potential to produce connective tissue-type mucin as a consequence of its mesodermal origin, the mechanism of production of acidic mucopolysaccharides in a myxoid adrenal cortical tumor remains to be clarified.
UI - 11921282
AU - Zhao J; Roth J; Bode-Lesniewska B; Pfaltz M; Heitz PU; Komminoth P
TI - Combined comparative genomic hybridization and genomic microarray for detection of gene amplifications in pulmonary artery intimal sarcomas and adrenocortical tumors.
SO - Genes Chromosomes Cancer 2002 May;34(1):48-57
AD - Department of Pathology, University of Zurich, Zurich, Switzerland. firstname.lastname@example.org
Identification of gene amplifications in human tumors is important for the understanding of tumorigenesis and may lead to discovery of diagnostic and prognostic markers. In this study, we used a microarray-based comparative genomic hybridization (CGH) technique, combined with conventional CGH, to identify gene amplifications in 43 tumors including eight pulmonary artery intimal sarcomas and 35 adrenocortical tumors. Conventional CGH revealed gains or amplifications of 12q13-q15 in six sarcomas and in two adrenocortical carcinomas. Using microarrays, we demonstrated that, among genes located on 12q13-q15, SAS/CDK4 were amplified in six sarcomas, and MDM2 and GLI in five and four sarcomas, respectively. The two adrenocortical tumors showed coamplifications of SAS/CDK4 and MDM2. Furthermore, PDGFRA (located on 4q12) amplification was identified in five sarcomas. Our data demonstrate: (1) amplifications of SAS/CDK4, MDM2, GLI, and PDGFRA are strongly associated with the tumorigenesis of pulmonary artery intimal sarcomas, whereas SAS/CDK4 and MDM2 coamplification may contribute to the progression of adrenocortical tumors; (2) microarray-based CGH is a useful tool for simultaneous detection of multiple gene amplifications, with a high sensitivity and resolution compared to that of conventional CGH. Copyright 2002 Wiley-Liss, Inc.
UI - 11881068
AU - Felmeden DC; Gearty JG; Dawkins DM; Beevers G
TI - Hypertension due to a giant aldosterone-secreting adenoma.
SO - J Renin Angiotensin Aldosterone Syst 2001 Mar;2(1):43-4
AD - Department of Medicine, City Hospital, Brimingham, UK. email@example.com
UI - 11968809
AU - Naruoka T; Suzuki H; Ueda M; Kiyota H; Miki K; Ohishi Y
TI - [A case of adrenocortical carcinoma with masculinization, obtaining long prognosis with surgical treatment alone]
SO - Nippon Hinyokika Gakkai Zasshi 2002 Mar;93(3):499-503
AD - Department of Urology, Fuji General City Hospital.
A 28 year-old woman presented right upper abdominal pain. She had been pointed out her masculinization and amenorrhea. CT scan and magnetic resonance imaging showed right adrenal tumor. In the endocrinological study, the serum cortisol and testosterone was elevated. Transabdominal right adrenalectomy and nephrectomy was carried out and histopathological diagnosis was adrenocortical carcinoma. The masculine symptom had disappeared after the operation and she has been without recurrence for five years.
UI - 11956997
AU - Hirano D; Okada Y; Ishida H; Takimoto Y; Okada K; Jike T
TI - Morphometric analysis, at electron microscope level, combined with hormone assay of nonfunctioning adrenocortical adenomas: comparison with aldosterone-producing adenomas.
SO - Med Electron Microsc 2001 Dec;34(4):240-8
AD - Department of Urology, Nihon University School of Medicine, 30-1 Ooyaguchi Kamimachi, Itabashi-ku, Tokyo 173-8610, Japan. firstname.lastname@example.org
We performed electron microscopic studies of eight nonfunctioning adrenocortical adenomas (NFA) and nine aldosterone-producing adenomas (APA) obtained from surgical specimens. A comparison of these two types of adenomas was conducted by morphometric analysis of random electron micrographs. The organelles measured included mitochondria (M), smooth-surfaced endoplasmic reticulum (SER), rough-surfaced endoplasmic reticulum (RER), lipid vacuoles (LV), and lysosomes (Ly). The content of steroid hormones, including 17-alpha hydroxyprogesterone (17-OHP), aldosterone (Ald), and other steroid hormones, was measured in adenoma tissue from six NFA and eight APA. The percentages of the areas of the organelles M, SER, and RER per total cell area in the NFA were significantly lower than those in the APA. The average content of Ald in adenoma tissues in APA was markedly higher than that in the NFA, while the mean content of 17-OHP in the NFA was significantly higher than that in APA. In conclusion, NFA are morphometrically characterized by a reduction in organelles such as M, SER, and RER, compared with findings in APA. From the quantitative analysis of steroid hormones, it was suggested that NFA produce more precursor substances with less hormone activity than APA and that steroidgenesis in NFA is shifted to a glucocorticoid pathway, as indicated by the elevated 17-OHP concentration.
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