Ontology highlight
ABSTRACT:
PROVIDER: PRJNA761730 | ENA |
REPOSITORIES: ENA
Dataset's files
| 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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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).
2023-04-03 | GSE201125 | GEO
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: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.
2013-11-28 | GSE42171 | GEO
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. Copy number and LOH analysis of Affymetrix SNP6 arrays was performed for AIMAH nodules from 26 patients, including 18 with paired leucocyte and nodules (1 to 4 nodules per patient), and 8 with a single nodule (no paired leucocyte available)
2013-11-28 | E-GEOD-42171 | biostudies-arrayexpress
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.
2007-10-02 | E-GEOD-4060 | biostudies-arrayexpress
Project description:Our study showed that the steroidogenic capacity firstly decreased without tissue change (the first hit) and secondarily declined with tissue change (the second hit) in the adrenal cortex of lipoid congenital adrenal hyperplasia. The key feature of the secondary decline of steroidogenic capacity might be the decreased gene expression related to steroid biosynthesis following the lipid accumulation exacerbated by ACTH hypersecretion.
2018-12-04 | GSE123300 | GEO
Project description:Purpose: Ectopic Rspo1 expression in the mouse adrenal gland (driven by Sf1-Cre) leads to a sexually dimorphic phenotype of adrenocortical hyperplasia and tissue degeneration. In order to gain a mechanistic understanding of the sexual dimorphism, we compared the gene expression profiles of Rspo1-overexpressing animals (Rspo1 GOF) with control littermates. Methods: Total RNA was extracted from whole adrenals of male and female, control and Rspo1GOF mice during puberty (4 weeks). mRNA sequencing and differential gene expression analysis was conducted by Novogene Co. Hierarchical clustering and principal component analysis were conducted using Phantasus. Gene set enrichment analysis was performed using Broad's institute GSEA and the Molecular Signatures database. Conclusions: After Rspo1 transgene expression, sex is the second most important component that explains variability among the experimental groups. Genes specifically upregulated in female Rspo1GOF adrenals vs all the other groups are enriched in DNA proliferation and cell cycle genes, targets of E2F transcription factros and the DREAM complex. Genes specifically upregulated in male Rspo1GOF adrenals are related to immune system regulation. Verification of the RNA Seq results by experimental methods has showed that ectopic proliferation in the mutant adrenals is female-specific and that androgen receptor signalling plays a role in proliferation arrest in male animals. Moreover, accumulation of abnormal foamy-like macrophages in the male adrenals leads to tissue degeneration.
2021-06-27 | GSE178958 | GEO