Project description:PRKAR1A inactivating mutations are responsible for primary pigmented nodular adrenocortical disease (PPNAD) whereas somatic GNAS activating mutations cause macronodular disease in the context of McCune-Albright syndrome (MAS), ACTH-independent hyperplasia (AIMAH) and, rarely, cortisol-producing adenomas (CPA). The whole-genome expression profile (WGEP) of normal (pooled) adrenals, PRKAR1A- (3) and GNAS-mutant (3) was studied.
Project description:PRKAR1A inactivating mutations are responsible for primary pigmented nodular adrenocortical disease (PPNAD) whereas somatic GNAS activating mutations cause macronodular disease in the context of McCune-Albright syndrome (MAS), ACTH-independent hyperplasia (AIMAH) and, rarely, cortisol-producing adenomas (CPA). The whole-genome expression profile (WGEP) of normal (pooled) adrenals, PRKAR1A- (3) and GNAS-mutant (3) was studied. Total RNA obtained from adrenal tumors were compared to those samples obtained from normal adrenal pools
Project description:A ""Cartes d'Identite des Tumeurs"" (CIT) project from the french Ligue Nationale Contre le Cancer (http://cit.ligue-cancer.net). 92 samples on Affymetrix HG-U133 Plus 2.0 GeneChips arrays for 92 patients with Adrenocortical Tumors (ACT). 4 normal adrenal samples from the same batch are also included. 10 ACTH-independant Macronodular Adrenal Hyperplasia (AIMAH) from the same batch are also included.
Project description:ACTH-independent macronodular adrenal hyperplasia (AIMAH) is a clinically and genetically heterogeneous disorder that can be associated with aberrant hormone receptors. Whole-genome expression profiling was analyzed in samples of different nodules from a patient with AIMAH.
Project description:ACTH-independent macronodular adrenal hyperplasia (AIMAH) is a clinically and genetically heterogeneous disorder that can be associated with aberrant hormone receptors. Whole-genome expression profiling was analyzed in samples of different nodules from a patient with AIMAH. Total RNA obtained from adrenal nodules were compared to those samples obtained normal adrenal pools
Project description:The mechanisms responsible for the ectopic adrenal expression of glucose-dependent insulinotropic peptide (GIP) receptor (GIPR) in GIP-dependent Cushing's syndrome (CS) are unknown. Chronic adrenal stimulation by ACTH in Cushing's disease or GIP in GIP-dependent ACTH-independent macronodular adrenal hyperplasia both lead to the induction of genes implicated in adrenal proliferation and steroidogenesis. OBJECTIVE: The objective of the study was to identify genes differentially expressed specifically in GIP-dependent CS that could be implicated in the ectopic expression of GIPR. METHODS: We used the Affymetrix U133 plus 2.0 microarray oligochips to compare the whole genome expression profile of adrenal tissues from five cases of GIP-dependent bilateral ACTH-independent macronodular adrenal hyperplasia with CS, one case of GIP-dependent unilateral adenoma with CS, five cases of ACTH-dependent hyperplasias, and a pool of adrenals from 62 normal individuals. RESULTS: After data normalization and statistical filtering, 723 genes with differential expression were identified, including 461 genes or sequences with a known functional implication, classified in eight dominant functional classes. Specific findings include repression of perilipin, the overexpression of 13 G protein-coupled receptors, and the potential involvement of Rho-GTPases. We also isolated 94 probe sets potentially linked to the formation of GIP-dependent nodules adjacent to the diffuse hyperplasia. These included probe sets related to the linker histone H1 and repression of RXRa and CCND2. The expression profiles for eight genes were confirmed by real-time RT-PCR. CONCLUSION: This study identified an extensive series of potentially novel target candidate genes that could be implicated in the molecular mechanisms of ectopic expression of the GIPR as well as in the multistep progression of GIP-dependent CS.
Project description:Analysis of ACTH-regulation on adrenocortical cells at gene expression level. The hypothesis tested in the present study was that ACTH increases chronic cell growth and steroidogenesis in adrenal glands by changing the gene expression profile. Results provide important information on the changes of gene expression of adrenocortical cells after chronic ACTH treatment.
Project description:Analysis of ACTH-regulation on adrenocortical cells at gene expression level. The hypothesis tested in the present study was that ACTH increases chronic cell growth and steroidogenesis in adrenal glands by changing the gene expression profile. Results provide important information of the response of adrenocortical cells gene expression to chronic ACTH treatment.
Project description:Analysis of ACTH-regulation on adrenocortical cells at gene expression level. The hypothesis tested in the present study was that ACTH increases chronic cell growth and steroidogenesis in adrenal glands by changing the gene expression profile. Results provide important information of the response of adrenocortical cells gene expression to chronic ACTH treatment. Total RNA obtained from primary cultured adult adrenal cells subjected to 48 hours in vitro treatment of ACTH compared to untreated control cell.
