ADAPTeR Study: TCRseq data from ccRCC patients
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ABSTRACT:
PROVIDER: EGAS00001005639 | EGA |
REPOSITORIES: EGA
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Project description:To identify a therapeutic candidate target molecule for ccRCC, we analyzed the microRNA (miRNA) expression signatures in ccRCC clinical specimens.
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Project description:To identify a therapeutic candidate target molecule for ccRCC, we analyzed the microRNA (miRNA) expression signatures in ccRCC clinical specimens. 9 matched pair (normal tissue and ccRCC tissue) plus 7 ccRCC tissue were analyzed for miRNA-microarray
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Project description:This is a supplementary study to the CPTAC CCRCC Discovery Study - Proteome. Unlabeled, digested peptide material from individual tissue samples (ccRCC and NAT) was spiked with index Retention Time (iRT) peptides (Biognosys) and subjected to data-independent acquisition (DIA) analysis.
Kidney cancer is among the 10 most common cancers in both men and women and each year there are approximately 60,000 new cases with over 14,000 deaths (<a href="https://seer.cancer.gov/statfacts/html/kidrp.html" target="_blank">NCI, Surveillance, Epidemiology and End Results (SEER) Program</a>). Several histological and molecular subtypes have been identified and clear cell renal cell carcinoma (CCRCC) is the most prevalent (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5936048/" target="_blank">Hsieh el al., 2017 Nat Rev Dis Primers</a>). To advance the proteogenomic understanding of CCRCC, the CPTAC program has investigated 110 tumors (CPTAC discovery cohort) and subjected these samples to global proteome and phosphoproteome analysis. An optimized workflow for mass spectrometry of tissues using isobaric tags (TMT (tandem mass tags)-10) was used (<a href="https://www.nature.com/articles/s41596-018-0006-9" target="_blank">Mertins et al., Nature Protocols 2018</a>). Proteome and phosphoproteome data from the CCRCC tumors is available below along with peptide spectrum analyses (PSMs) and protein summary reports from the CPTAC common data analysis pipeline (CDAP).
Clinical data is provided. Additional attributes along with genotypes will be available as cohort characterization proceeds.
Genomic data will be available from the NCI Genomic Data Commons.
<em>Note: Sample-wise assessment of genomic profiles in this cohort identified seven tumor samples with molecular aberrations atypical for ccRCC. While these seven non-ccRCC samples (C3L-00359-01, C3N-00313-03, C3N-00435-05, C3N-00492-04, C3N-00832-01, C3N-01175-01, C3N-01180-01) and their corresponding NATs (C3N-00435-06, C3N-00492-05, C3N-01175-05) were excluded from the ccRCC cohort in all downstream analyses, the non-ccRCC samples served as useful controls to highlight ccRCC-specific features. These seven samples were therefore annotated as non-ccRCC samples.</em>
<ul><li>Dataset imported into MassIVE from <a href="https://pdc.cancer.gov/pdc/study/PDC000200" target="_blank">https://pdc.cancer.gov/pdc/study/PDC000200</a> on 10/04/23</li></ul>
2023-10-04 | MSV000093041 | MassIVE
Project description:We have sampled several tumour regions from nine clear cell renal cell carcinoma (ccRCC) patients to investigate intra-tumour heterogeneity.
2014-01-06 | GSE53000 | GEO
Project description:Presently, there is a deficiency of effective therapies designed to target clear cell renal cell carcinoma (ccRCC), with poor prognosis resulting in patients with advanced disease. Additionally, there is a lack of molecular factors which can be remedially targeted resulting in tumor specific inhibition, and therefore current therapeutic approaches often produce adverse side effects in patients. We identified that Stearoyl-CoA desaturase 1 (SCD1) was consistently overexpressed in patient ccRCC samples, and further investigation of SCD1 as a potential molecular target for ccRCC intervention utilizing a SCD1 inhibitor (A939572) resulted in tumor specific growth inhibition and induction of cell death. In order to understand the mechanism by which the SCD1 inhibitor mediated its anti-tumor effects, we performed gene array analysis and compared expression patterns between treated and untreated samples. Four established ccRCC cell lines purchased from ATCC were treated with DMSO control versus A939572 over a 24 hour time period. RNA from each group was isolated and sent of for gene array anaylsis. Gene expression data from each individual treatment group was normalized to its respective DMSO contol, and resulting expression patterns associated with drug exposure was compared between the four cell lines.
2012-10-11 | E-GEOD-41485 | biostudies-arrayexpress
Project description:Presently, there is a deficiency of effective therapies designed to target clear cell renal cell carcinoma (ccRCC), with poor prognosis resulting in patients with advanced disease. Additionally, there is a lack of molecular factors which can be remedially targeted resulting in tumor specific inhibition, and therefore current therapeutic approaches often produce adverse side effects in patients. We identified that Stearoyl-CoA desaturase 1 (SCD1) was consistently overexpressed in patient ccRCC samples, and further investigation of SCD1 as a potential molecular target for ccRCC intervention utilizing a SCD1 inhibitor (A939572) resulted in tumor specific growth inhibition and induction of cell death. In order to understand the mechanism by which the SCD1 inhibitor mediated its anti-tumor effects, we performed gene array analysis and compared expression patterns between treated and untreated samples.
2012-10-11 | GSE41485 | GEO
Project description:We have sampled several tumour regions from nine clear cell renal cell carcinoma (ccRCC) patients to investigate intra-tumour heterogeneity. We selected 56 tumour samples and 6 normal samples from the 9 patients for expression analysis using microarray data. All samples were fresh frozen upon extraction.
2014-01-06 | E-GEOD-53000 | 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 | GSE146537 | GEO
Project description:Based on multiple public databases, we investigated the expression level of BGN in ccRCC, its clinical significance, and its association with immune cells. Real-time fluorescence quantitative PCR was employed to validate BGN expression in tumor and adjacent normal tissues. Differential gene analysis, GO-KEGG analysis, and GSEA analysis were performed by RNA sequencing to elucidate the underlying signaling pathways. BGN knockdown cells were generated through lentiviral transfection to examine the impact of BGN on ccRCC. Cell proliferation, migration, and invasion were assessed using CCK8, colony formation, wound healing, Transwell migration, and invasion assays, respectively. Results: Our findings from database analysis and polymerase chain reaction (PCR) revealed a significant upregulation of BGN expression in kidney cancer tissues compared to normal tissues. Further analysis demonstrated a correlation between high BGN expression and ccRCC progression and immune infiltration. In vitro experiments confirmed that BGN silencing effectively inhibited cell proliferation, migration, and invasion of ccRCC. Mechanistically, these effects may be mediated through the MAPK signaling pathway. Conclusion: BGN potentially plays a pivotal role in the progression and metastasis of ccRCC, possibly acting through the MAPK signaling pathway. Therefore, BGN holds promise as a potential therapeutic target for ccRCC.
2024-09-01 | GSE264075 | GEO
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.
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