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: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>
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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: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.
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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.
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Project description:Approximately 70% of clear cell renal cell carcinoma are characterised by the biallelic inactivation of VHL on chromosome 3p. ELOC-mutated renal cell carcinoma with biallelic ELOC inactivation on chromosome 8q are considered a novel subtype of renal cancer possessing a morphological overlap with ccRCC; however, the frequency and consequences of ELOC alterations in wtVHL and mutVHL is unclear. In this study, we characterise 123 renal tumours with clear cell morphology with known VHL mutation status to assess morphological and molecular consequences of ELOC inactivation. Using Oncoscan and whole exome sequencing we identify 18 ELOC deleted RCC, three of which contain ELOC mutations resulting in the biallelic inactivation of ELOC. Biallelic ELOC and biallelic VHL aberrations were mutually exclusive, although two ELOC-mutated RCC showed monoallelic VHL alterations. Using High Ambiguity Driven Biomolecular Docking we report a novel ELOC variant containing a duplication event disrupting ELOC-pVHL interaction alongside the frequently seen Y79C alteration. Using HRM mass spectrometry we show RCC with biallelic ELOC alterations have significantly reduced ELOC expression but similar CAIX and VEGFA expression when compared to classical ccRCC with VHL inactivation. These data demonstrate that RCC with ELOC and VHL alterations have comparable downstream effects with similar pathways to ccRCC tumourigenesis indicating that both entities are closely related.
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Project description:Circadian disruption enhances cancer risk, and many tumors exhibit disordered circadian gene expression. We show rhythmic gene expression is unexpectedly robust in clear cell renal cell carcinoma (ccRCC). Furthermore, the clock gene BMAL1 is higher in ccRCC than in healthy kidneys, unlike in other tumor types. BMAL1 is closely related to ARNT and we show that BMAL1-HIF2α regulates a subset of HIF2α target genes in ccRCC cells. Depletion of BMAL1 reprograms HIF2α chromatin association and target gene expression and reduces ccRCC growth in culture and in xenografts. Analysis of pre-existing data reveals higher BMAL1 in patient-derived xenografts that are sensitive to growth suppression by HIF2α antagonists. We show that increasing BMAL1 sensitizes ccRCC-derived 786O cells to growth inhibition by PT2399. Together, these findings indicate that an alternate HIF2α heterodimer containing the circadian partner BMAL1 contributes to HIF2α activity, growth, and sensitivity to HIF2α antagonist drugs in ccRCC cells.
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