Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA111909 | ENA |
REPOSITORIES: ENA
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Project description:Transcriptional profiling of human adrenocortical tumors. Gene expression profile of normal adrenal cortex, hormonally inactive adenoma, cortisol-secreting Cushing-adenoma and primary adrenocortical cancer tissues were compared. The goal of this study was to identify significant differences in the gene expression of these groups. Further aim was to reveal biologically relevant pathogenetic pathways altered at transcriptional and posttranscriptional level, as well.
2009-07-01 | GSE14922 | GEO
Project description:Adrenocortical tumors are common; their prevalence may reach up to 5-7% in pathological series. Most of them are benign and hormonally inactive, however, rare hormone-secreting (aldosterone and cortisol) and malignant forms are associated with significant morbidity and mortality. The prognosis of adrenocortical cancer (ACC) is poor with an overall five-year survival below 30 %. In this study, CGH analysis was performed on 4 ACC (adrenocortical carcinoma), 4 IA (hormonally inactive adrenocortical adenoma) and 3 CPA (cortisol producing adrenocortical adenoma) samples. Tissue digestion, labeling, hybridization and data analysis of genomic DNA were performed according to the Agilent Technologies (Santa Clara, CA) protocol version 2.0 for 105 K arrays. As expected, many of the observed aberrations were generally consistent with those of other preciously published data and will provide the basis for determination how genomic diversity impacts biological function and human diseases, such as cancer.
2009-08-06 | GSE17396 | GEO
Project description:Adrenocortical tumors are common; their prevalence may reach up to 5-7% in pathological series. Most of them are benign and hormonally inactive, however, rare hormone-secreting (aldosterone and cortisol) and malignant forms are associated with significant morbidity and mortality. The prognosis of adrenocortical cancer (ACC) is poor with an overall five-year survival below 30 %. In this study, CGH analysis was performed on 4 ACC (adrenocortical carcinoma), 4 IA (hormonally inactive adrenocortical adenoma) and 3 CPA (cortisol producing adrenocortical adenoma) samples. Tissue digestion, labeling, hybridization and data analysis of genomic DNA were performed according to the Agilent Technologies (Santa Clara, CA) protocol version 2.0 for 105 K arrays. As expected, many of the observed aberrations were generally consistent with those of other preciously published data and will provide the basis for determination how genomic diversity impacts biological function and human diseases, such as cancer. In this study, biopsies from adrenocortical tumors (4 ACC, 4 IA and 3 CPA samples) were analysed with CGH. Tissue digestion, labeling, hybridization, and data analysis of genomic DNA were performed according to the Agilent Technologies (Santa Clara, CA) protocol version 2.0 for 105 K arrays. Slides were scanned with Agilent Microarray scanner and data were extracted with Feature Extraction software version 9.5.1.1. DNA Analytics software was used (version 4.0.85, Agilent Technologies, Santa Clara, CA) for data analysis. The starting and ending points of the aberrations were confirmed by the ADM-2 algorithm with 6.0 threshold.
2010-05-15 | E-GEOD-17396 | biostudies-arrayexpress
Project description:This data was used in the analysis of the article titled ‘Steroids-producing adrenocortical nodules: a novel two-layered structure as a precursor lesion of cortisol-producing adenoma’.
2023-07-20 | E-MTAB-13109 | biostudies-arrayexpress
Project description:This data was used in the analysis of the article titled: Steroids-producing adrenocortical nodules: a novel two-layered structure as a precursor lesion of cortisol-producing adenoma
2023-06-30 | E-MTAB-13127 | biostudies-arrayexpress
Project description:These data were used in the scRNA-seq analysis of the article titled \\"Steroids-producing adrenocortical nodules: a novel two-layered structure as a precursor lesion of cortisol-producing adenoma\\".
2023-12-28 | E-MTAB-13615 | biostudies-arrayexpress
Project description:Pediatric adrenocortical tumors (ACT) are rare and often fatal malignancies; little is known regarding their etiology and biology. To provide additional insight into the nature of ACT, we determined the gene expression profiles of 24 pediatric tumors (five adenomas, 18 carcinomas, and one undetermined) and seven normal adrenal glands. Distinct patterns of gene expression, validated by quantitative real-time PCR and Western blot analysis, were identified that distinguish normal adrenal cortex from tumor. Differences in gene expression were also identified between adrenocortical adenomas and carcinomas. In addition, pediatric adrenocortical carcinomas were found to share similar patterns of gene expression when compared with those published for adult ACT. This study represents the first microarray analysis of childhood ACT. Our findings lay the groundwork for establishing gene expression profiles that may aid in the diagnosis and prognosis of pediatric ACT, and in the identification of signaling pathways that contribute to this disease. We used microarrays to explore the expression profiles differentially expressed in childhood adrenocortical tumors and in normal adrenal gland tissues. Pediatric adrenocortical adenoma and carcinoma patients were enrolled on the International Pediatric Adrenocortical Tumor Registry (IPACTR) and Bank protocol. Tumor specimens were harvested during surgery and snap frozen in liquid nitrogen to preserve tissue integrity. Data have been compiled for eight males and 15 females between 0 and 16 years of age. Table 1 (West et al, Cancer Research 67:601-608, 2007) summarizes the primary clinical information for each subject (excluding sample Unk1 with ACT of undetermined histology), including stage of the disease, tumor class, sex, age, relapse-free survival, and overall survival.
2015-11-25 | E-GEOD-75415 | biostudies-arrayexpress
Project description:Adrenocortical carcinoma (ACC) is an aggressive malignancy with high rates of recurrence following surgical resection. Long noncoding RNAs (lncRNAs) play an important role in cancer development. Pathogenesis of adrenal tumours has been characterised by mRNA, microRNA and methylation expression signatures but it is unknown if this extends to lncRNAs. We sought to describe lncRNA expression signatures in adrenocortical carcinoma (ACC), adrenal cortical adenoma (ACA) and normal adrenal cortex (NAC). RNA was extracted from freshly frozen tissue with confirmation of diagnosis by histopathology. Focused lncRNA and mRNA transcriptome analysis was performed using the ArrayStar Human LncRNA V3.0 microarray. Differentially expressed lncRNAs were validated using qRT-PCR.
2015-01-01 | GSE61359 | GEO
Project description:Cushing’s syndrome (CS) is a serious endocrine disorder that is rare in humans, but relatively common in dogs. In ~15-20% of cases, CS is caused by a cortisol-secreting adrenocortical tumor (csACT). To identify differentially expressed genes that can improve prognostic predictions after surgery and represent novel treatment targets, we performed RNA sequencing on csACTs (n=48) and normal adrenal cortices (NACs; n=10) of dogs. A gene was declared differentially expressed when the adjusted P-value was <0.05 and the log2 fold change was >2 or <-2. Between NACs and csACTs, 98 genes were differentially expressed. Based on the principal component analysis (PCA) the csACTs were separated in two groups, of which group 1 had significantly better survival after adrenalectomy (P=0.002) than group 2. Between csACT group 1 and group 2, 77 genes were differentially expressed. One of these, cytochrome P450 26B1 (CYP26B1), was significantly associated with survival in both our canine csACTs and in a publicly available dataset of 33 human cortisol-secreting adrenocortical carcinomas. In the validation cohort, CYP26B1 was also expressed significantly higher (P=0.012) in canine csACTs compared to NACs. In future studies it would be interesting to determine whether CYP26B1 inhibitors could inhibit csACT growth in both dogs and humans.
2022-02-11 | GSE196108 | 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