Change of gene expression of mutation of TP53 in LS174T cells
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PROVIDER: PRJNA511762 | ENA |
REPOSITORIES: ENA
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Project description:Change of gene expression of mutation on TP53 exon3 or exon10 by CRISPR-Cas9 system in LS174T cells
2018-12-26 | GSE124349 | GEO
Project description:Background: Gene expression profiling of breast carcinomas has increased our understanding of the heterogeneous biology of this disease and promises to impact clinical care. The aim of this study was to evaluate the prognostic value of gene expression-based classification along with established prognostic markers and mutation status of the TP53 gene, in a group of breast cancer patients with long-term (12-16 years) follow-up. Methods: The clinical and histopathological parameters of 200 breast cancer patients were studied for their effects on clinical outcome using univariate/multivariate Cox regression. The prognostic impact of mutations in the TP53 gene, identified using TTGE and sequencing, was also evaluated. Eighty of the samples were analyzed for gene expression using 42K cDNA microarrays and the patients were assigned to five previously defined molecular expression groups. The strength of the gene expression based classification versus standard markers was evaluated by adding this variable to the Cox regression model used to analyze all samples. Results: Both univariate and multivariate analysis showed that TP53 mutation status, tumor size and lymph node status were the strongest predictors of breast cancer survival for the whole group of patients. Analyses of the patients with gene expression data showed that TP53 mutation status, gene expression based classification, tumor size and lymph node status were significant predictors of survival. The TP53 mutation status showed strong association with the ?basal-like? and ?ERBB2+? gene expression subgroups, and tumors with mutation had a characteristic gene expression pattern. Conclusions: TP53 mutation status and gene-expression based groups are important survival markers of breast cancer, and these molecular markers may provide prognostic information that complements clinical variables. The study adds experience and knowledge to an ongoing characterization and classification of the disease. Experiment set consisting of 80 primary breast carcinomas collected at Ulleval University Hospital (ULL-samples), Oslo, Norway from 1990-94, and one normal sample from breast reduction surgery.
2012-09-18 | E-GEOD-40954 | biostudies-arrayexpress
Project description:Background: Gene expression profiling of breast carcinomas has increased our understanding of the heterogeneous biology of this disease and promises to impact clinical care. The aim of this study was to evaluate the prognostic value of gene expression-based classification along with established prognostic markers and mutation status of the TP53 gene, in a group of breast cancer patients with long-term (12-16 years) follow-up. Methods: The clinical and histopathological parameters of 200 breast cancer patients were studied for their effects on clinical outcome using univariate/multivariate Cox regression. The prognostic impact of mutations in the TP53 gene, identified using TTGE and sequencing, was also evaluated. Eighty of the samples were analyzed for gene expression using 42K cDNA microarrays and the patients were assigned to five previously defined molecular expression groups. The strength of the gene expression based classification versus standard markers was evaluated by adding this variable to the Cox regression model used to analyze all samples. Results: Both univariate and multivariate analysis showed that TP53 mutation status, tumor size and lymph node status were the strongest predictors of breast cancer survival for the whole group of patients. Analyses of the patients with gene expression data showed that TP53 mutation status, gene expression based classification, tumor size and lymph node status were significant predictors of survival. The TP53 mutation status showed strong association with the ?basal-like? and ?ERBB2+? gene expression subgroups, and tumors with mutation had a characteristic gene expression pattern. Conclusions: TP53 mutation status and gene-expression based groups are important survival markers of breast cancer, and these molecular markers may provide prognostic information that complements clinical variables. The study adds experience and knowledge to an ongoing characterization and classification of the disease.
2012-09-18 | GSE40954 | GEO
Project description:Background: Although TP53 gain-of-function (GOF) mutations promote cancer survival, its effect on EGFR-TKI efficacy remains unclear. We established EGFR-mutant lung cancer cell lines expressing various TP53 genotypes using CRISPR-Cas9 technology and found that TP53-GOF mutant cells develop an early resistance to EGFR-TKI osimertinib.The goal of this study is to elucidate the mechanisms underlying resistance to osimertinib treatment in TP53 GOF mutations through comprehensive gene analysis using RNA-seq with next-generation sequencing (NGS). Methods: Total RNA was isolated from PC-9 cells overexpressing TP53 R248Q mutation (PC9/p53R248Q: TP53 GOF mutation) and PC-9 cells overexpressing empty vector plasmid (PC9/p53EV: TP53 null) treated with DMSO or osimertinib for 24hours, using the RNeasy Micro Kit , in accordance with the manufacturer’s instructions. RNA samples were quantified by NanoDrop-2000 spectrophotometer, and the quality was confirmed with a 2200 TapeStation. rRNA was removed using MGI Easy rRNA Depletion Kit according to manufacturer's instructions followed by library construction using MGIEasy RNA Directional Library Prep Set (MGI). MGI DNBseq-G400 FAST was used to perform the amplicons deep sequencing following the standard operation protocol. The sequence format was 150bp pair read for all samples. All sequencing reads were trimmed low-quality bases and adapters with Trimmomatic (v.0.38) , and RNA sequencing reads were mapped to hg38 using HISAT2 software . Raw counts for each gene were estimated in each sample using RSEM version 1.3.0 and Bowtie 2. Calculation of the log fold-change (log FC) and p-value were performed using edgeR. Results: We explored the functions of specifically upregulated genes in TP53 GOF mutation after osimertinib treatment by KEGG pathway-enrichment analysis and found that the cytokine-cytokine receptor interaction was the most significantly altered pathway. Hallmark pathway analysis identified the TNF-α/NF-κB pathway was significantly enriched. Furthermore, TRRUST analysis showed enhanced activity of transcription factors especially RELA (p65) and NF-kB1. Conclusions: TP53 GOF mutaion induces osimertinib resistance by activating TNF-α/NF-κB pathway.
2023-05-25 | GSE232890 | GEO
Project description:Genome-wide copy number variation was measured in TP53 mutation negative ovarian tumours. Analysis described in "Driver mutations in TP53 are ubiquitous in high grade serous carcinoma of the ovary" (Ahmed et al., 2010)
2010-03-04 | GSE19416 | GEO
Project description:To screen the related miRNAs in the occurence and development of sebaceous gland carcinoma(SGC) of the eyelid , we have employed Human Agilient microarray expression profiling as a discovery platform to identify differentially expressed miRNAs for SGC and TP53 mtation related miRNAs. Human formalin-fixed paraffin-embedded (FFPE) SGC tissues and para-carcinoma sebaceous gland(SG) FFPE samples from SGC patients were screened using microarray assay. Human FFPE SGC tissues containing TP53 mutation and human FFPE SGC tissues without TP53 mutation were screened using microarray. The overlap of two sets of microarray differentially upregulated miRNAs were selected as our research object.
2021-09-01 | GSE182876 | GEO
Project description:To further development of our mRNA expression approach to ER stress, we have employed whole genome microarray expression profiling as a discovery platform to identify ER stress-responsible genes. LS174T cells were overexpressed with ER stress mediators, ATF6a or ATF6b. Genes responsible for each mediator were extracted and categorized by Gene Ontology. ATF6a and ATF6b were overexpressed in LS174T. Subsequently, cells were treated with 2 mM sodium butyrate, which induces LS174T cells to differentiate to mature goblet cells. Genes responsible for each mediator were extracted and categorized by Gene Ontology in GeneRanker program of Genomatix platform.
2015-08-05 | E-GEOD-49567 | biostudies-arrayexpress
Project description:Whole Exome sequencing of two patients with Cardiac angiosarcoma in Li-Fraumeni-like families discovers that a mutation in the pot1 gene is responsible for cardiac angiosarcoma in tp53-negative li-fraumeni-like families
2015-09-14 | E-MTAB-3858 | biostudies-arrayexpress
Project description:The goal of this experiment was to determine the expression signature in colon cancer LS174T cell line after selamectin treatment. The current study of selamectin is continuation of our previous work, PMID: 25143352.
2017-02-22 | GSE87873 | GEO
Project description:To further development of our mRNA expression approach to ER stress, we have employed whole genome microarray expression profiling as a discovery platform to identify ER stress-responsible genes. LS174T cells were overexpressed with ER stress mediators, ATF6a or ATF6b. Genes responsible for each mediator were extracted and categorized by Gene Ontology.
2015-08-05 | GSE49567 | GEO