Profiling of Primary and Metastatic ccRCC
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB32862 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR3349990.fastq.gz | Fastqsanger.gz | |||
| ERR3349991.fastq.gz | Fastqsanger.gz | |||
| ERR3349992.fastq.gz | Fastqsanger.gz | |||
| ERR3349993.fastq.gz | Fastqsanger.gz | |||
| ERR3349994.fastq.gz | Fastqsanger.gz |
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Project description:We have sampled several tumour regions from a single ccRCC patient after 6 weeks everolimus treatment, including both primary and metastatic site samples to investigate intra-tumour heterogeneity. We selected 8 samples from the primary tumour, and 2 samples from a chestwall metastatic site for expression analysis using microarray data. All samples were fresh frozen upon extraction.
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Project description:We have sampled several tumour regions from a single ccRCC patient after 6 weeks everolimus treatment, including both primary and metastatic site samples to investigate intra-tumour heterogeneity.
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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:A total of 3 metastatic and 3 non-metastatic ccRCC tissues were collected from patients. These tissues were flash frozen in liquid nitrogen immediately after surgery and subsequently stored at -80℃. All the resected nodules or metastatic masses were identified as renal tumor by pathologic examination. No patients received anticancer treatments before surgery in this study. We analyzed gene expression microarray data from our gene chip with 3 metastatic ccRCC tissues compared with 3 non-metastatic ccRCC tissues.
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Project description:Medulloblastoma, the most common malignant pediatric brain tumour, disseminates by shedding cells into the cerebrospinal fluid, which then re-implant to cover the surface of the brain and spinal cord. Metastases are a very poor prognostic sign at presentation and are usually lethal at recurrence. Mechanisms driving dissemination have been described in the bulk primary tumour, with the underlying assumption that primary tumour and metastases are biologically similar. Here we show that in both mouse and human medulloblastoma, multiple metastases from a single animal are extremely similar, but are genetically highly divergent from the primary tumour. Clonal genetic events in the metastases can be demonstrated in a restricted sub-clone of the primary tumour, suggesting that only rare cells within the primary tumour have the ability to metastasize. Failure to account for the bicompartmental nature of primary and metastatic medulloblastoma represents a major barrier to the development of effective targeted therapies. DNA methylation analysis of 15 pediatric medulloblastoma samples consisting of 6 primary-metastatic pairs and 4 normal cerebella samples profiled in Illumina Infinium HumanMethylation27 Beadchip v1.2
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2021-11-15 | GSE146540 | 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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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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