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ABSTRACT: Morphologic and molecular characterization of adrenals and adrenal rest affected by congenital adrenal hyperplasia

PROVIDER: PRJNA761730 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15819973_1.fastq.gz	Fastqsanger.gz
	SRR15819973_2.fastq.gz	Fastqsanger.gz
	SRR15819974_1.fastq.gz	Fastqsanger.gz
	SRR15819974_2.fastq.gz	Fastqsanger.gz
	SRR15819975_1.fastq.gz	Fastqsanger.gz

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Senescence-Induced Immune Remodeling Facilitates Metastatic Adrenal Cancer in a Sex-Dimorphic Manner [bulk RNA-seq]

Project description:Using the adrenal gland as a model, we investigated the interplay between genetic Znrf3 inactivation and the aging microenvironment. We hypothesized that SF1-Cre-driven Znrf3 cKO mice would progress from adrenal hyperplasia to carcinoma with age. Unexpectedly, after an initial phase of hyperplasia, we found that Znrf3 cKO adrenals steadily regress over time. We demonstrate this phenotypic switch from hyperplasia to regression is driven by activation of cellular senescence and a subsequent senescence-associated secretory phenotype (SASP).

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Project description:Variants causing lipoid congenital adrenal hyperplasia

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Activation of cyclic AMP signaling leads to different pathway alterations in lesions of the adrenal cortex caused by germline PRKAR1A defects versus those due to somatic GNAS mutations

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

2011-11-15 | E-GEOD-33694 | biostudies-arrayexpress

Project description:long-read sequencing of congenital adrenal hyperplasia

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Affymetrix SNP6 array data for ACTH-Independent Macronodular Adrenal Hyperplasia (AIMAH) samples

Project description:AIMAH is an ACTH-independent bilateral enlargement of the adrenal cortex occuring during adulthood. The enlargment is related to the growth of multiple benign nodules. This condition is associated with various degrees of cortisol hypersecretion. The occurence of several nodules in both adrenals, and the existence of familial forms, suggest the existence of a germline genetic predisposition. To find the gene(s), the aim of the project was to look for recurrent chromosomal alterations in the AIMAH nodules. Extensive mapping of somatic gains, losses and copy-neutral loss of heterozygosity (LOH) was performed with Affymetrix SNP6 arrays. A copy neutral LOH of 16p, occuring in 7 of 26 patients, was one of the only recurrent alterations, pointing towards a candidate gene in this region. Of note this condition differs from the congenital adrenal hyperplasias, related to genetic alterations of steroidogenesis (the latter is an ACTH dependent adrenal hyperplasia). Affymetrix SNP6 arrays were performed according to the manufacturer's directions on DNA extracted from cryopreserved tumor samples or peripheral blood samples.

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Affymetrix SNP6 array data for ACTH-Independent Macronodular Adrenal Hyperplasia (AIMAH) samples

2013-11-28 | E-GEOD-42171 | biostudies-arrayexpress

Transcription profiling of human glucose-dependent insulinotropic peptide (GIP)- and adrenocorticotropin-dependent adrenal hyperplasias reveals novel targets for the study of GIP-dependent Cushings syndrome.

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.

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