Characterization of differential gene expression in adrenocortical tumors harbouring β-catenin (CTNNB1) mutations.
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE28476 | GEO | 2011/04/09
SECONDARY ACCESSION(S): PRJNA139317
REPOSITORIES: GEO
Similar Datasets
Project description:Mutations of β-catenin gene (CTNNB1) are frequent in adrenocortical adenomas (AA) and carcinomas (ACC). However, the target genes of CTNNB1 have not yet been identified in adrenocortical tumors. Our objective was to identify genes de-regulated in adrenocortical tumors harbouring CTNNB1 genetic alterations. We compared gene expression profiles of AA with (n: 3) and without (n: 4) CTNNB1 mutations using Affymetrix arrays.
2011-04-09 | E-GEOD-28476 | biostudies-arrayexpress
Project description:Micro-RNA sequencing of adrenocortical tumors and normal adrenal samples. miRNA sequencing of 45 adrenocortical carcinomas (ACC), 30 adrenocortical adenomas (ACA) and 3 normal adrenal samples.
2014-04-29 | E-GEOD-49279 | biostudies-arrayexpress
Project description:Transcription factor 21 (TCF21) directly binds and regulates SF1 in tumor and normal adrenocortical cells, and both are involved in the development and steroidogenesis of the adrenal cortex. TCF21 is a tumor suppressor gene and its expression is reduced in malignant tumors. In adrenocortical tumors, it is less expressed in adrenocortical carcinomas (ACC) than in adrenocortical adenomas (ACA) and normal tissue. However, a comprehensive analysis to identify TCF21 targets have not yet been conducted in any type of cancer. In this study, we performed Chromatin Immunoprecipitation and Sequencing (ChIP-Seq) in adrenocortical carcinoma cell line (NCI-H295R) overexpressing TCF21, with the aim of identifying TCF21 new targets. The five most frequently identified sequences corresponded to the PRDM7, CNTNAP2, CACNA1B, PTPRN2 and KCNE1B genes. Validation experiments showed that, in NCI-H295R cells, TCF21 regulates gene expression positively in PRDM7 and negatively in CACNA1B. Recently, it was observed that the N-type calcium channel v2.2 (Cav2.2) encoded by CACNA1B gene is important in Angiotensin II signal transduction for corticosteroid biosynthesis in NCI-H295R adrenocortical carcinoma cells. Indeed, TCF21 inhibits CACNA1B and Cav2.2 expression in NCI-H295R. In addition, in a cohort of 55 adult patients with adrenocortical tumor, CACNA1B expression was higher in ACC than ACA, and was related to poor disease-free survival in ACC patients. These results suggest a mechanism of steroidogenesis control by TCF21 in adrenocortical tumor cells, in addition to the control observed through SF1 inhibition. Importantly, steroid production could impair tumor immunogenicity, contributing to the immune resistance described in adrenal cancer.
2022-06-30 | GSE179308 | GEO
Project description:We used the H295R cell line, human adrenocortical cells, harboring a heterozygous CTNNB1 (beta-catenin) gene mutation affecting the GSK3 beta-phosphorylation site (S45P) and leading to constitutive transcriptional activity of beta-catenin-LEF/TCF. Whole-transcript gene expression was analyzed in three stable clones of H295R cells expressing a doxycycline-inducible shRNA targeting CTNNB1 mRNA and in a control clone, without or with doxycycline for 5 days.
2015-08-03 | E-MTAB-3330 | biostudies-arrayexpress
Project description:Background: Adrenal myelolipoma (AML) is a relatively common and invariably benign tumor composed of adipose tissue and hematopoietic elements. Due to the variable proportion of fat and hematopoietic elements, it is sometimes challenging to differentiate AML from adrenocortical carcinoma (ACC). MicroRNAs have been identified as promising biomarkers in many tumors, including adrenocortical neoplasms, but the microRNA expression of adrenal myelolipoma has not been investigated, yet. Aims: To perform a large scale microRNA expression profiling in adrenal myelolipoma, benign and malignant adrenocortical tumors to identify potential microRNA biomarkers. Methods: Next-generation sequencing (NGS) on 30 formalin-fixed paraffin-embedded archived tissue samples (discovery cohort: 10 adrenocortical adenoma (ACA), 10 ACC and 10 myelolipoma) was performed by Illumina MiSeq. Significantly differentially expressed microRNAs were validated by real-time RT-qPCR in an independent validation cohort comprised of 10 ACA, 10 myelolipoma and 9 ACC samples. Results: We have found relative overexpression of miR- 451a, miR-486-5p, miR-363-3p and miR-150-5p in myelolipoma compared to the other two tumor groups by NGS. For ACC, we have found up-regulation of miR-184, miR-483-5p, miR-431-5p and miR-183-5p compared to myelolipoma and ACA. Validation by RT-qPCR, confirmed significant overexpression of miR-451a, miR-486-5p and miR-150-5p in myelolipomas relative to ACA and ACC, whereas significant overexpression of miR-184 and miR-183-5p was confirmed in ACC relative to the other 2 groups. The overexpression of miR-483-5p has not turned out to be significant in ACC relative to myelolipomas in the validation cohort. Conclusions: Overexpressed miR-451a, miR-486-5p and miR-150-5p might be potential tissue markers of adrenal myelolipoma. The lack of significance in the expression of miR-483-5p between ACC and myelolipoma is remarkable, as miR-483-5p has been considered to be the best marker of adrenal malignancy to date.
2018-04-07 | GSE112804 | 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:Genome wide DNA methylation profiling of normal adrenocortical tissue, adrenocortical adenomas and adrenocortical carcinomas. The Illumina Infinium 27k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles. Samples included 6 normal adrenocortical tissue samples, 27 adenomas and 15 carcinomas.
2012-09-01 | GSE36353 | GEO
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.
2015-11-25 | GSE75415 | GEO
Project description:We performed miRNA expression profiling in a series of adrenocortical carcinomas, adrenocortical adenomas and normal adreno cortex using a microarray approach. Significant differentially expressed miRNAs among groups were identified using SAM analysis.
2011-06-01 | GSE22816 | GEO