Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA128165 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We performed a microRNA (miRNA) microarray on 10 metastatic RCC tumors and compared differential miRNA expresison to 19 primary clear cell renal cell carcinomas (ccRCC). We found there were 65 significantly dysregulated miRNAs; 9 miRNAs were significantly upregulated and 56 miRNAs were significantly downregulated in metastatic RCC when compared to primary clear cell renal cell carcinoma. miRNA microarray was performed on 10 metastatic RCC tumors
2012-08-13 | E-GEOD-39440 | biostudies-arrayexpress
Project description:The understanding of metastatic spread is limited and molecular mechanisms causing particular characteristics of metastasis are largely unknown. This comprises the extremely varying dormancy periods of tumor cells in the secondary organ after metastatic spread, represented by the disease-free survival (DFS) of the patients, or differing numbers of metastases in different patients. Knowing the molecular fundamentals of these phenomena would support the individual prediction of patients´ outcome and facilitate the decision for an appropriate monitoring and therapy regime. In a first study (PMID 19391132) we analyzed the transcriptome-wide expression profiles of 20 pulmonary metastases of renal cell carcinoma (Met1-9, Met11-18, Met20, Met23, Met25) to identify expression patterns associated with the dormancy period and the number of metastases per patient. Pre-processed and analyzed data for this study are available in GEO Series GSE14378. In this second study, we validated the DFS-associated expression pattern from the first study on four further metastases and also included primary ccRCC with different DFS. For this, the microarray data of all metastases and primary tumors were pre-processed together. The aim of this second study was to identify those genes, which are differentially expressed in metastases developed after different dormancy periods and which are already deregulated in primary tumors. Genes differentially expressed in synchronously vs. metachronously metastases might contribute functionally to the dormancy period. Genes already deregulated in primary ccRCC might be suitable for prognostic purposes. metastases manifested synchronously or metachronously (DFS less than or equal to 9 months compared with DFS greater than or equal to 60 months); primary ccRCC which developed synchronous or metachronous metastases (DFS less than or equal to 6 months compared with DFS greater than or equal to 45 months)
2010-07-30 | E-GEOD-22541 | biostudies-arrayexpress
Project description:We performed a microRNA (miRNA) microarray on 10 metastatic RCC tumors and compared differential miRNA expresison to 19 primary clear cell renal cell carcinomas (ccRCC). We found there were 65 significantly dysregulated miRNAs; 9 miRNAs were significantly upregulated and 56 miRNAs were significantly downregulated in metastatic RCC when compared to primary clear cell renal cell carcinoma.
2012-08-14 | GSE39440 | GEO
Project description:The proteome of clinical tissue samples diagnosed with clear cell renal cell carcinoma (ccRCC) and papillary renal cell carcinoma (pRCC) were evaluated analyzed along with the dataset identifier PXD022018 to establish a potential discriminative biomarker panel of proteins for these tumors subtypes.
2021-12-15 | PXD023296 | Pride
Project description:The understanding of metastatic spread is limited and molecular mechanisms causing particular characteristics of metastasis are largely unknown. This comprises the extremely varying dormancy periods of tumor cells in the secondary organ after metastatic spread, represented by the disease-free survival (DFS) of the patients, or differing numbers of metastases in different patients. Knowing the molecular fundamentals of these phenomena would support the individual prediction of patients´ outcome and facilitate the decision for an appropriate monitoring and therapy regime. In a first study (PMID 19391132) we analyzed the transcriptome-wide expression profiles of 20 pulmonary metastases of renal cell carcinoma (Met1-9, Met11-18, Met20, Met23, Met25) to identify expression patterns associated with the dormancy period and the number of metastases per patient. Pre-processed and analyzed data for this study are available in GEO Series GSE14378. In this second study, we validated the DFS-associated expression pattern from the first study on four further metastases and also included primary ccRCC with different DFS. For this, the microarray data of all metastases and primary tumors were pre-processed together. The aim of this second study was to identify those genes, which are differentially expressed in metastases developed after different dormancy periods and which are already deregulated in primary tumors. Genes differentially expressed in synchronously vs. metachronously metastases might contribute functionally to the dormancy period. Genes already deregulated in primary ccRCC might be suitable for prognostic purposes.
2010-06-25 | GSE22541 | GEO
Project description:Renal cell carcinoma (RCC) exhibits some unusual features and genes commonly mutated in cancer are rarely mutated in clear-cell RCC (ccRCC), the most common type. The most prevalent genetic alteration in ccRCC is the inactivation of the tumor suppressor gene VHL. Using whole-genome and exome sequencing we discovered BAP1 as a novel tumor suppressor in ccRCC that shows little overlap with mutations in PBRM1, another recent tumor suppressor. Whereas VHL was mutated in 81% of the patients (142/176), PBRM1 was lost in 58% and BAP1 in 15% of the patients analyzed. All these tumor suppressor genes are located in chromosome 3p, which is partially or completely lost in most ccRCC patients. However, BAP1 but not PBRM1 loss was associated with higher Fuhrman grade and, therefore, poorer outcome. Xenograft tumors (tumorgrafts) implanted orthotopically in mice retained >92% of mutations and exhibited similar DNA copy number alterations to corresponding primary tumors. Thus, after inactivation of VHL, the acquisition of a mutation in BAP1 or PBRM1 defines a different program that might alter the fate of the patient. Our results establish the foundation for an integrated pathological and molecular genetic classification of about 70% of ccRCC patients, paving the way for subtype-specific treatments exploiting genetic vulnerabilities. The genomic DNA of clear-cell renal cell carcinoma (ccRCC) primary tumors, tumors growing in immunodeficient mice (tumorgrafts), and normal samples were labeled and hybridized to Affymetrix SNP arrays 6.0.
2012-06-09 | E-GEOD-25540 | biostudies-arrayexpress
Project description:BRCA1-associated protein 1 (BAP1) is a member of the ubiquitin C‑terminal hydrolase family of deubiquitinating enzymes and is implicated in transcriptional regulation. The BAP1 gene is mutated in about 10% of patients with clear cell renal cell carcinoma (ccRCC), the most common form of renal cancer, suggesting that BAP1 may be a tumor suppressor. However, whether BAP1 influences the progression of ccRCC tumors expressing WT BAP1 is unclear. Here, we assessed the expression and function of BAP1 using human ccRCC specimens and cell lines.
2019-04-18 | PXD012288 | Pride
Project description:Clear cell renal cell carcinoma (ccRCC) is a highly immune infiltrated cancer, but how the tumor immune microenvironment (TIME) evolves during disease progression is unknown. Insights into heterogeneity within primary ccRCC raise questions about potential heterogeneity between primary and paired metastatic tumors. This information may improve understanding of immune evasion leading to metastatic disease and response to immunotherapy. In this study, we characterize and compare the TIME of primary ccRCC with paired asynchronous metastases. We demonstrate higher infiltration of immunosuppressive cells in the TIME of primary ccRCC compared with metastatic sites. Further studies are necessary to determine the prognostic and therapeutic significance of these findings. Understanding the heterogeneity of the tumor immune microenvironment in RCC, both intratumorally and between metastatic sites, has important clinical implications for selecting appropriate therapies and developing predictive biomarkers. Future research should focus on elucidating the impact of these findings on immunotherapeutic responses and patient outcomes in ccRCC.
2024-09-27 | GSE278174 | GEO
Project description:Renal cell carcinoma (RCC) exhibits some unusual features and genes commonly mutated in cancer are rarely mutated in clear-cell RCC (ccRCC), the most common type. The most prevalent genetic alteration in ccRCC is the inactivation of the tumor suppressor gene VHL. Using whole-genome and exome sequencing we discovered BAP1 as a novel tumor suppressor in ccRCC that shows little overlap with mutations in PBRM1, another recent tumor suppressor. Whereas VHL was mutated in 81% of the patients (142/176), PBRM1 was lost in 58% and BAP1 in 15% of the patients analyzed. All these tumor suppressor genes are located in chromosome 3p, which is partially or completely lost in most ccRCC patients. However, BAP1 but not PBRM1 loss was associated with higher Fuhrman grade and, therefore, poorer outcome. Xenograft tumors (tumorgrafts) implanted orthotopically in mice exhibited similar gene expression profiling to corresponding primary tumors. Gene expression profiling of tumors and tumorgrafts displayed different signatures for BAP1- and PBRM1-deficient samples. Thus, after inactivation of VHL, the acquisition of a mutation in BAP1 or PBRM1 defines a different program that might alter the fate of the patient. Our results establish the foundation for an integrated pathological and molecular genetic classification of about 70% of ccRCC patients, paving the way for subtype-specific treatments exploiting genetic vulnerabilities. The RNA of clear-cell renal cell carcinoma (ccRCC) primary tumors, tumors growing in immunodeficient mice (tumorgrafts), and normal kidney cortices were labeled and hybridized to Affymetrix Human Genome U133 Plus 2.0 arrays.
2012-06-09 | E-GEOD-36895 | biostudies-arrayexpress
Project description:SETD2, a H3K36 trimethyltransferase, is frequently mutated in human cancers with the highest prevalence (13%) in clear cell renal cell carcinoma (ccRCC). Genomic profiling of primary ccRCC tumors reveals a positive correlation between SETD2 mutations and metastasis. However, whether and how SETD2-loss promotes metastasis remains unclear. Here, we detected SETD2 mutations in 24 of 51 (47%) metastatic ccRCC tumors. Using SETD2-mutant metastatic ccRCC patient-derived cell line and xenograft models, we showed that H3K36me3 restoration greatly reduced distant metastases of ccRCC in mice. An integrated ATAC-seq, ChIP-seq, and transcriptome analysis concluded a tumor suppressor model in which loss of SETD2-mediated H3K36me3 activates enhancers to drive oncogenic transcription through dysregulating histone chaperone recruitment, enhancing histone exchange, and expanding chromatin accessibility. Furthermore, we uncovered mechanism-based therapeutic strategies for SETD2-deficient cancer through inhibition of histone chaperones. Overall, SETD2-loss creates a permissive epigenetic landscape for cooperating oncogenic drivers to amplify transcriptional output, providing unique therapeutic opportunities.
2021-11-15 | GSE146538 | GEO