Gene expression analysis of metastatic adrenocortical tumors
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PROVIDER: PRJNA600262 | ENA |
REPOSITORIES: ENA
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Project description:microRNA expression analysis of metastatic adrenocortical tumors
| PRJNA600261 | ENA
Project description:Background: Adrenocortical carcinoma (ACC) is a rare, often-aggressive neoplasm of the adrenal cortex, with a 14.5-month median overall survival. We asked whether tumors from patients with advanced or metastatic ACC would offer clues as to putative genes that might have critical roles in disease progression or in more aggressive disease biology. Methods: We conducted comprehensive genomic and expression analyses of 43 ACCs. Results: Copy number gains and losses matched that previously reported. We identified a median mutation rate of 3.38 per megabase (Mb), somewhat higher than in a previous study possibly related to the more advanced disease. The mutational signature was characterized by a predominance of C>T, C>A and T>C transitions. As in previously reports, only cancer genes TP53 (26%) and beta-catenin (CTNNB1, 14%) were mutated in more than 10% of samples. The TCGA-identified putative cancer genes MEN1 and PRKAR1A were found in low frequency – 4.7% and 2.3%, respectively. Most of the mutations were in genes not implicated in the etiology or maintenance of cancer. Specifically, amongst the 38 genes that were mutated in more than 9% of samples, only four were represented in Tier 1 of the 576 COSMIC Cancer Gene Census (CCGC). Thus, 82% of genes found to have mutations likely have no role in the etiology or biology of ACC; while the role of the other 18%, if any, remains to be proven. Finally, the transcript length for the 38 most frequently mutated genes in ACC is statistically longer than the average of all coding genes, raising the question of whether transcript length in part determined mutation probability. Conclusions: We conclude that the mutational and expression profiles of advanced and metastatic tumors is very similar to those from newly diagnosed patients –with very little in the way of genomic aberration to explain it. Our data and that in the previous analyses finds the rate of mutations in ACCs lower than that in other cancers and suggests an epigenetic basis for the disease should be the focus of future studies. The Affymetrix PrimeView platform was used for the gene expression profiling.
2020-09-25 | GSE143383 | GEO
Project description:Background: Adrenocortical carcinoma (ACC) is a rare, often-aggressive neoplasm of the adrenal cortex, with a 14.5-month median overall survival. We asked whether tumors from patients with advanced or metastatic ACC would offer clues as to putative genes that might have critical roles in disease progression or in more aggressive disease biology. Methods: We conducted comprehensive genomic and expression analyses, including microRNA profiling, of 33 ACCs and 6 normal adrenals. Results: Copy number gains and losses matched that previously reported. We identified a median mutation rate of 3.38 per megabase (Mb), somewhat higher than in a previous study possibly related to the more advanced disease. The mutational signature was characterized by a predominance of C>T, C>A and T>C transitions. As in previously reports, only cancer genes TP53 (26%) and beta-catenin (CTNNB1, 14%) were mutated in more than 10% of samples. The TCGA-identified putative cancer genes MEN1 and PRKAR1A were found in low frequency – 4.7% and 2.3%, respectively. Most of the mutations were in genes not implicated in the etiology or maintenance of cancer. Specifically, amongst the 38 genes that were mutated in more than 9% of samples, only four were represented in Tier 1 of the 576 COSMIC Cancer Gene Census (CCGC). Thus, 82% of genes found to have mutations likely have no role in the etiology or biology of ACC; while the role of the other 18%, if any, remains to be proven. Finally, the transcript length for the 38 most frequently mutated genes in ACC is statistically longer than the average of all coding genes, raising the question of whether transcript length in part determined mutation probability. Conclusions: We conclude that the mutational and expression profiles of advanced and metastatic tumors is very similar to those from newly diagnosed patients –with very little in the way of genomic aberration to explain it. Our data and that in the previous analyses finds the rate of mutations in ACCs lower than that in other cancers and suggests an epigenetic basis for the disease should be the focus of future studies. The Exiqon miRCURY LNA microRNA array v.11.0 platform was used for the microRNA profiling.
2020-09-25 | GSE143385 | 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:<p>We have analyzed 33 human metastatic adrenocortical tumors from 14 patients with advanced metastases and performed whole exome sequencing to identify novel signatures in these tumors. We observed tumor heterogeneity in these tumors coming from the same metastatic tissue site across different patients while the different metastatic tumor sites coming from the same patient are more homogenous in nature.</p>
| phs001658 | dbGaP
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.
2011-04-09 | GSE28476 | 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 have compared the microsomal protein fractions from benign and malignant adrenocortical tumors. Protein extracts were trypsinized, peptides separated by HiRIEF (high resolution isoelectric focusing) and analysed by LC-MS.
2014-02-11 | PXD000604 | Pride
Project description:Human benign adrenocortical tumors miRNome
| PRJEB25822 | ENA