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.
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.
Project description:We studied the miRNA expression profile of a series of childhood adrenocortical tumors (ACT) and age-matched normal adrenal samples
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.
Project description:We studied the miRNA expression profile of a series of childhood adrenocortical tumors (ACT) and age-matched normal adrenal samples 25 ACT - 5 normal
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.
Project description:Human samples of 33 adrenocortical carcinomas, 22 adrenocortical adenomas, and 10 normal adrenal cortex samples, each from a different patient, had mRNA assays performed using Affymetrix HG_U133_plus_2 arrays, with 54675 probe-sets. We note that the same array data is in GEO series GSE33371, where we assayed the cancer samples for Beta-catenin staining or mutation, and make new comparisons based on those assays. Keywords: disease state analysis
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.
Project description:Human samples of 33 adrenocortical carcinomas, 22 adrenocortical adenomas, and 10 normal adrenal cortex samples, each from a different patient, had mRNA assays performed using Affymetrix HG_U133_plus_2 arrays, with 54675 probe-sets. Experiment Overall Design: Two supplementary files are attached below. The Adrenocortical_logs.xls file shows the log-transformed probe-set values and the results of a statistical analysis for each probe-set. The Readme file describes the columns of this log file.
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.