Ontology highlight
ABSTRACT:
PROVIDER: PRJNA994866 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25278406_1.fastq.gz | Fastqsanger.gz | |||
| SRR25278406_2.fastq.gz | Fastqsanger.gz | |||
| SRR25278407_1.fastq.gz | Fastqsanger.gz | |||
| SRR25278407_2.fastq.gz | Fastqsanger.gz | |||
| SRR25278408_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 24 |
Similar Datasets
Project description:This project aimed to identify a specific target for chromosome 8p deletions. Using large-scale functional-genomic screening data of over 527 well-characterized cancer cell lines. We were able to identify the dependency of SLC25A28 (Mitoferrin-2, MFRN2), a mitochondrial iron transporter, in chromosome 8p deleted cancer cell lines. Interestingly, we found that SLC25A37 (Mitoferrin-1, MFRN1), the paralog of MFRN2, resides on chromosome 8p and is frequently deleted in liver cancer. We found a strong correlation between the cellular dependency on MFRN2 and the MFRN1 expression levels, possibly explaining why MFRN2 is a synthetic lethal target for 8p deletions. Our study discovered MFRN2 as a target for a therapeutic strategy in chromosome 8p deleted cancer specimens. Further, it revealed MFRN1 as a biomarker that predicts the response to MFRN2-directed therapy.
2024-06-03 | PXD044780 | Pride
Project description:Chromosome arm deletions are frequently observed in human cancers. Such large-scale aberrations may trigger phenotypes distinct from those that arise by loss of single genes. Using TALEN-based genomic engineering, we generated cell models with targeted 8p loss-of-heterozygosity (LOH) that mimics an 8p deletion commonly found in breast cancer patients. 8p LOH triggered up-regulation of the mevalonate pathway. The alterations in lipid metabolism led to increased metastatic potential and drug resistance of 8p-deleted cells that are in agreement with poorer survival rates of breast cancer patients harbouting 8p LOH. Our findings also suggest novel therapeutic strategies for treatment of 8p LOH tumors.
2015-05-21 | GSE68042 | GEO
Project description:Chromosome arm deletions are frequently observed in human cancers. Such large-scale aberrations may trigger phenotypes distinct from those that arise by loss of single genes. Using TALEN-based genomic engineering, we generated cell models with targeted 8p loss-of-heterozygosity (LOH) that mimics an 8p deletion commonly found in breast cancer patients. 8p LOH triggered up-regulation of the mevalonate pathway. The alterations in lipid metabolism led to increased metastatic potential and drug resistance of 8p-deleted cells that are in agreement with poorer survival rates of breast cancer patients harbouting 8p LOH. Our findings also suggest novel therapeutic strategies for treatment of 8p LOH tumors. RNASeq Analysis of two Wt 8p Cell clones vs two 8p LOH cell clones generated via TALEN Approach
2015-05-21 | E-GEOD-68042 | biostudies-arrayexpress
Project description:A large panel of 81 liver cancer cell models, designated as LIver cancer MOdel REpository (LIMORE) was constructed. These cell lines include 31 public cell lines and 50 new cell models establishend from Chinese liver cancer patients. Whole genome sequencing (WGS), exome sequencing (WES) and RNA sequencing (RNAseq) were performed to obtain the genetic information for these cell lines. These cell lines and associated data provide new models and also a rich resource for liver cancer.
2019-06-17 | GSE97098 | GEO
Project description:8p Loss of Heterozygosity triggers metastasis and drug resistance
| PRJNA281617 | ENA
Project description:Renal tumors with complex morphology require extensive workup for accurate classification. Chromosomal aberrations that define subtypes of renal epithelial neoplasms have been reported. We explored if whole-genome chromosome copy number and loss-of-heterozygosity analysis with single nucleotide polymorphism (SNP) arrays can be used to identify these aberrations. Keywords: Chromosome copy number and LOH analysis with SNP Genotyping Arrays
2008-01-24 | GSE9469 | GEO
Project description:Renal tumors with complex morphology require extensive workup for accurate classification. Chromosomal aberrations that define subtypes of renal epithelial neoplasms have been reported. We explored if whole-genome chromosome copy number and loss-of-heterozygosity analysis with single nucleotide polymorphism (SNP) arrays can be used to identify these aberrations in cases where morphology was unable to definitively classify these tumors. Keywords: Chromosome copy number and LOH analysis (virtual karyotyping) with SNP Genotyping Arrays Keywords: Genome variation profiling by SNP array
2008-11-01 | GSE11447 | GEO
Project description:Renal tumors with complex morphology require extensive workup for accurate classification. Chromosomal aberrations that define subtypes of renal epithelial neoplasms have been reported. We explored if whole-genome chromosome copy number and loss-of-heterozygosity analysis with single nucleotide polymorphism (SNP) arrays can be used to identify these aberrations. Experiment Overall Design: We analyzed 20 paraffin-embedded tissues representing conventional renal cell carcinoma (RCC), papillary RCC, chromophobe RCC, and oncocytoma with Affymetrix GeneChip 10K 2.0 Mapping arrays.
2008-04-10 | E-GEOD-9469 | biostudies-arrayexpress
Project description:Oncocytic variants of follicular thyroid carcinomas show a near-homozygous genome. Remarkably, homozygosity of chromosome 7 has never been observed which suggests that retention of heterozygosity is essential for cells. We hypothesized that cell survival genes are genetically imprinted on either of two copies of chromosome 7 which thwarts loss of heterozygosity at this chromosome in cancer cells. We identified 6 genes on chromosome 7 which demonstrated allele-specific expression. Subsequent knockdown of gene expression showed that CALCR, COPG2, GRB10, KLF14, MEST and PEG10 were essential for cancer cell survival resulting in reduced cell proliferation, G1-phase arrest and increased apoptosis. We propose that imprinted cell survival genes provide a genetic basis for retention of chromosome 7 heterozygosity in cancer cells.
2019-01-01 | GSE77804 | GEO
Project description:Purpose: In uveal melanoma (UM) research, several cell lines are used in preclinical studies. Because Mel285 and Mel290 do not harbour typical GNAQ or GNA11 hotspot mutations, we aimed at better classifying them and understanding if we could find genetic causes to explain their protein and mRNA expression profiles. Methods: We studied protein and mRNA expression in 14 UM cell lines and determined the presence of Single Nucleotide Variants and small Insertions and Deletions with next generation sequencing and copy number alterations (CNAs) with a single nucleotide polymorphism array. The lists of differentially expressed proteins and genes were merged, and shared lists were created, keeping only the terms with concordant mRNA and protein expression. Enrichment analysis and Gene Set Enrichment Analysis were performed on the shared lists. Results: Mel285 and Mel290 are distinct from the GNA-mutated cell lines and have downregulation of melanosome-related markers. Mel285 and Mel290 lack typical UM mutations but harbour putatively-deleterious variants in four genes each (Mel285: CTNNB1, PPP1R10, LIMCH1, APC; Mel290: ARID1A, PPP1R10, SPG11, RNF43). The upregulated terms in Mel285 and Mel290 did not point to a convincing alternative origin. Mel285 has several CNAs, among which loss of 1p, 3p, partial 3q, 6 and partial 8p, while Mel290 shows 1p loss and chromosome 6 loss. Conclusion: While Mel285 and Mel290 have some CNAs that resemble those in UM, multi-omics analyses show that they belong to a separate group compared to the other analysed UM cell lines. Therefore, they may not be representative models to test potential therapeutic targets for UM.
2024-07-16 | PXD051055 | Pride