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At least 217 records · Page 12Linked to original sources
PubMed2002

Expression of prolactin-releasing peptide and its receptor in the human adrenal glands and tumor tissues of adrenocortical tumors, pheochromocytomas and neuroblastomas.

Adrenal tumors, such as pheochromocytomas, are known to express various peptides and their receptors. Prolactin-releasing peptide (PrRP) is a novel neuropeptide isolated from bovine hypothalamic tissues. In the present study, expression of PrRP receptor was studied in the human brain, pituitaries, adrenal glands and tumor tissues of adrenocortical tumors, pheochromocytomas, a ganglioneuroblastoma and neuroblastomas by reverse transcriptase polymerase chain reaction (RT-PCR) and Northern blot analysis. The presence of immunoreactive-PrRP in the adrenal glands and in these tumor tissues was studied by radioimmunoassay. Human brain tissues and pituitaries were obtained at autopsy. Normal portions of adrenal glands and tumor tissues were obtained at surgery. RT-PCR analysis showed expression of PrRP receptor in the human brain, pituitaries, normal portions of adrenal glands and various tumor tissues. Northern blot analysis showed high expression of PrRP receptor only in tumor tissues of pheochromocytomas, indicating that PrRP receptor expression is high in pheochromocytomas. Immunoreactive-PrRP was detected in normal portions of adrenal glands (0.162+/-0.024 pmol/g wet weight, n=4, mean+/-S.E.M.), four out of six cases of pheochromocytomas (0.050-7.9 pmol/g wet weight), one neuroblastoma and some adrenocortical tumors. The present study has shown that PrRP receptor mRNA was widely expressed in the brain tissues, pituitaries, adrenal glands and various tumors. The high expression of PrRP receptor in pheochromocytomas suggests potential pathophysiological roles of PrRP in these tumors.

Adrenal Cortex Neoplasms↗
PubMed1979

Myelolipoma in adenoma of accessory adrenal gland.

A tumor was incidentally found at autopsy in the vicinity of the right adrenal gland of a 69-year-old man who had died of liver cirrhosis with hepatoma. Microscopic examination disclosed a myelolipoma associated with a cortical adenoma occurring in an accessory adrenal gland. No evidence of hormonal abnormalities was found in the clinical record of the patient. The association of myelolipoma with cortical adenoma occurring in an accessory adrenal gland seems very unusual, and the present case is believed to be the first reported of this type of association.

Adenoma↗
PubMed1989

Immunohistochemical demonstration of cholesterol side-chain cleavage cytochrome P-450 in bovine and human adrenals.

Cytochrome P-450 specific for cholesterol side-chain cleavage (P-450SCC) was purified from the bovine adrenal and a specific antibody was raised in rabbits. The antiserum was applied for immunohistochemical visualization of the P-450SCC in the bovine and human adrenal cortex. The immunoreactivity was intense in the zona fasciculata (ZF) and reticularis (ZR) while weak in the zona glomerulosa (ZG) in the normal adrenals. In adrenocortical hyperplasia, a marked immunoreactivity was observed in the ZG in idiopathic hyperaldosteronism and the inner ZF and reticularis particularly in cells of micronodules in Cushing's disease, corresponding to cells with active steroidogenesis. In aldosteronoma and adenoma with Cushing's syndrome, P-450SCC was generally present in compact cells of adenomas.

Adenoma↗
PubMed1996

Corticomedullary tumors of the adrenal glands. Report of two cases. Association of corticomedullary tumor with spindle cell sarcoma.

We describe two cases of corticomedullary tumors of the adrenal gland. The patients suffered from Cushings syndrome and paroxysmal hypertension. The corticomedullary tumors consisted of benign looking cortical adenoma cells growing on the background of the pheochromocytoma cells. We further present the ultrastructural and immunohistochemical features of these tumors. Focally a spindle cell sarcoma arising from the corticomedullary tumor was found in one case. The spindle cell sarcoma was immunohistochemically negative with antibodies to chromogranin, synaptophysin, cytokeratin and S-100 protein. Ultrastructurally the sarcoma was composed of undifferentiated primitive cells poorly endowed with cytoplasmic organelles. Focal transitions of the pheochromocytoma into the spindle cell sarcoma were seen. It is hypothesized that the spindle cell sarcoma was arising from the pheochromocytoma component of the corticomedullary tumor.

Adrenal Cortex Neoplasms↗
PubMed2000

Radiology of the adrenal.

Adrenal incidentalomas are commonly noted on abdominal cross-sectional imaging studies. Most of these lesions are benign, non-functional adrenal adenomas. Certain adrenal lesions have such characteristic radiologic findings that their diagnosis can be made with virtual certainty. This article reviews the radiologic evaluation of adrenal tumors, with particular emphasis on incidentalomas.

Adenoma↗
PubMed1998

Unique association of pheochromocytoma with contralateral nonfunctioning adrenal cortical adenoma.

A 57-year-old woman complaining of hypertensive attacks associated with headache and palpitation was admitted to our hospital for examination of bilateral adrenal tumors in 1985. After right pheochromocytoma was diagnosed, right adrenalectomy was performed. The left adrenal tumor was small; thus, the left adrenal tumor was preserved to avoid adrenal insufficiency, although left adrenal pheochromocytoma could not be denied. In 1995, she was referred to our clinic again because of recurrent headache and palpitation, and enlargement of the left adrenal tumor. Although pheochromocytoma was suspected again, the enlarged left adrenal turned out to be a nonfunctioning cortical adenoma. This case was interesting, not only because of difficulty in identifying the left adrenal tumor, but also because of the rare coexistence of a pheochromocytoma and a nonfunctioning adrenal cortical tumor.

Adrenal Cortex Neoplasms↗
PubMed2002

Normal adrenal gland: in vivo observations, and high-resolution in vitro chemical shift MR imaging-histologic correlation.

RATIONALE AND OBJECTIVES: The purpose of this study was to determine whether adrenal cortical lipid affects signal intensity on magnetic resonance (MR) images and to evaluate contrast between cortex and medulla. MATERIALS AND METHODS: From their clinical database, the authors selected 37 MR imaging studies of patients with adrenal adenomas. Two independent readers compared in-phase and fat-suppressed T1-weighted images, looking for visible lipid-induced signal intensity loss in the adrenal gland. Six adrenal gland specimens obtained after radical nephrectomy were also studied with high-resolution MR imaging, including in-phase, opposed-phase, and fat-suppressed T1-weighted images, and T2-weighted images. Adjacent histologic sections were stained with oil red O for neutral fats and with hematoxylin-eosin, and they were also viewed with polarization light microscopy. The relative amount of lipid was graded as mild, moderate, or intense, and the appearance of the cortex and medulla was compared with that on the MR images. RESULTS: On the 37 clinical MR studies, there was no visible signal intensity loss within the limbs of the ipsilateral adrenal glands. T2-weighted images of the adrenal specimens showed a thin high-intensity band, corresponding to the appearance of medulla on histologic slices. This could not be seen on any of the T1-weighted images. Region-of-interest measurements were nearly identical for in-phase and opposed-phase images. Histologic analysis showed abundant cortical lipid. CONCLUSION: Adrenal corticomedullary contrast can be depicted on high-resolution T2-weighted images but not on any T1-weighted images. There is abundant cortical lipid in adrenal specimens, but comparison of in-phase with opposed-phase MR images does not depict it.

Adrenal Cortex Neoplasms↗
PubMed2004

Serum interleukin-6 in patients with adrenal tumors.

The mean blood content of interleukin-6 in patients with adrenal tumors was much higher than in healthy donors. No correlations were revealed between interleukin-6 level, patients sex and age, stage and duration of the disease. Interleukin-6 concentration was maximum in patients with adrenocortical cancer. A negative correlation was found between interleukin-6 level and blood cortisol concentration in patients with cortisol-producing adenoma. In patients with aldosterone-producing adenoma, interleukin-6 level tended to correlate negatively with plasma renin activity.

Adenoma↗
PubMed2003

Concomitant surgery with laparoscopic live donor nephrectomy.

Routine live donor evaluations reveal unexpected silent pathologies. Herein, we describe our experience treating such pathologies at the time of laparoscopic donor nephrectomy. We have not encountered any previous reports of such an approach. We prospectively collected data on 321 donors. Concomitant surgeries at the time of procurement included two laparoscopic adrenalectomies, one colposuspension, one laparoscopic cholecystectomy, and one liver biopsy. Mean operative time was 321 min (range 230-380), with a mean blood loss of 280 mL (range 150-500). No blood transfusions were required. The left kidney was procured in four cases. The right kidney was obtained on one occasion. Mean hospital stay was 3 days (median 3, range 2-4). No short- or long-term complications have been identified. Mean follow-up time was 2.63 years (median 2.76, range 2.23-2.99). Four of the five kidney recipients were first-time transplants who had not yet started dialysis. Simultaneous surgical interventions at the time of laparoscopic live kidney donation are safe and can be undertaken in selected cases. This practice is beneficial to both the donor and the recipient, and is likely to become more commonplace with changing practice patterns involving donor evaluation and management.

Adenoma↗
PubMed2006

Mechanisms of disease: the adrenocorticotropin receptor and disease.

The action of the peptide hormone adrenocorticotropin (ACTH) to stimulate glucocorticoid production by the adrenal gland is an essential physiologic process, yet is dependent on a single unique genetic component--the ACTH receptor or melanocortin 2 receptor. Genetic defects that cause abnormalities in this receptor or in a protein required for its expression at the cell surface result in a potentially fatal disease (familial glucocorticoid deficiency). Overexpression of this receptor or inability to desensitize it is found in adrenal adenomas or hyperplasia associated with glucocorticoid overproduction (Cushing syndrome). These disorders are uncommon, but there are considerable data to show that the hypothalamo-pituitary-adrenal axis is overactive, or in some circumstances underactive, in more common situations including depressive illness and septic shock. The origin of these latter disturbances is undoubtedly complex and multifactorial, but there is good evidence that a component of this phenomenon is an altered responsiveness of the ACTH receptor to ACTH. Understanding the basis of ACTH responsiveness might, therefore, contribute to the understanding of disorders such as these and perhaps enable the hypothalamo-pituitary-adrenal axis to be manipulated beneficially in these circumstances.

Adrenal Cortex Neoplasms↗
PubMed2003

High levels of luteinizing hormone analog stimulate gonadal and adrenal tumorigenesis in mice transgenic for the mouse inhibin-alpha-subunit promoter/Simian virus 40 T-antigen fusion gene.

Transgenic (TG) mice expressing the Simian virus 40 T-antigen under the control of the murine inhibin-alpha promoter (Inhalpha/Tag) develop granulosa and Leydig cell tumors at the age of 5-6 months, with 100% penetrance. When these mice are gonadectomized, they develop adrenocortical tumors. Suppression of gonadotropin secretion inhibits the tumorigenesis in the gonads of intact animals and in the adrenals after gonadectomy. To study further the role of luteinizing hormone (LH) in gonadal and adrenal tumorigenesis, a double TG mouse model was generated by crossing the Inhalpha/Tag mice with mice producing constitutively elevated levels of LH (bLHbeta-CTP mice). Our results show that in double TG mice (bLHbeta-CTP/Inhalpha/Tag), gonadal tumorigenesis starts earlier and progresses faster than in Inhalpha/Tag mice. Both ovarian and testicular tumors were histologically comparable with the tumors found in Inhalpha/Tag mice. In addition, adrenal tumorigenesis was found in intact double TG females, but not in Inhalpha/Tag females. Inhibin-alpha and LH receptor (LHR) were highly expressed in tumorigenic gonadal tissues, and the elevated LH levels were shown to be associated with ectopic LHR and high inhibin-alpha expression in the female adrenals. We conclude that in the Inhalpha/Tag tumor mouse model, elevated LH levels act as a tumor promoter, advancing gonadal and adrenal tumorigenesis.

Adrenal Cortex Neoplasms↗
PubMed2004

Gene array analysis of macronodular adrenal hyperplasia confirms clinical heterogeneity and identifies several candidate genes as molecular mediators.

Corticotropin (ACTH)-independent macronodular adrenal hyperplasia (AIMAH) is a heterogeneous condition in which cortisol secretion may be mediated by gastrointestinal peptide (GIP), vasopressin, catecholamines and other hormones. We studied the expression profile of AIMAH by genomic cDNA microarray analysis. Total RNA was extracted from eight tissues (three GIP-dependent) and compared to total RNA obtained from adrenal glands from 62 normal subjects. Genes had to be altered in 75% of the patients, and be up- or downregulated at a cutoff ratio of at least 2.0; 82 and 31 genes were found to be consistently up- and downregulated, respectively. Among the former were regulators of transcription, chromatin remodeling, and cell cycle and adhesion. Downregulated sequences included genes involved in immune responses and insulin signaling. Hierarchical clustering correlated with the two main AIMAH diagnostic groups: GIP-dependent and non-GIP-dependent. The genes encoding the 7B2 protein (SGNE1) and WNT1-inducible signaling pathway protein 2 (WISP2) were specifically overexpressed in the GIP-dependent AIMAH. For these, and six more genes, the data were validated by semiquantitative amplification in samples from a total of 32 patients (the original eight, six more cases of AIMAH, and 18 other adrenocortical hyperplasias and tumors) and the H295R adrenocortical cancer cell line. In conclusion, our data confirmed AIMAH's clinical heterogeneity by identifying molecularly distinct diagnostic subgroups. Several candidate genes that may be responsible for AIMAH formation and/or progression were also identified, suggesting pathways that affect the cell cycle, adhesion and transcription as possible mediators of adrenocortical hyperplasia.

Adrenal Cortex Neoplasms↗