Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA315971 | ENA |
REPOSITORIES: ENA
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Project description:The goal of this study was to determine genes affected by expressing KRAS mutation (G12V) in NCI-H1703 cells This data was used in Meng Wang et. al. Cancer Research 2016 to determine the alterations of gene expression profiling associated with expression of KRAS mutation (G12V). The experiment uses a pBABE-Puro vector encoding KRAS G12V and a corresponding empty vector control.
2016-03-23 | E-GEOD-79486 | biostudies-arrayexpress
Project description:The goal of this study was to determine genes affected by expressing KRAS mutation (G12V) in NCI-H1703 cells This data was used in Meng Wang et. al. Cancer Research 2016 to determine the alterations of gene expression profiling associated with expression of KRAS mutation (G12V).
2016-03-23 | GSE79486 | GEO
Project description:Purpose: The uncommonness of gallbladder cancer in the developed world has contributed to the generally poor understanding of the disease. The development of new and effective treatment has been and continues to be a major public health imperative. Methods: We report mutational and copy number analysis of 44 predominantly early-staged gallbladder tumors and 5-gallbladder cancer cell lines by a combination of directed and whole exome sequencing at an average coverage of 100X and above. Using gallbladder cancer cell lines and xenograft mouse models we performed phospho-proteome array profiling, followed by an in-depth functional characterization. Results: We describe recurrent activating ERBB2 somatic mutation in 6 of 44 gallbladder primary tumors with an overall mutation frequency of 13%, along with KRAS activating mutations in 3 of 44 samples. Consistent with whole exome findings, a phospho-proteomic array profile of 49-tyrosine kinase revealed constitutive phosphorylation of ERBB2 and EGFR that were found to heterodimerize. We demonstrate that treatment with ERBB2-specific, EGFR-specific shRNA or with covalent EGFR family inhibitor BIBW-2992 inhibits transformation, survival, migration, invasion, and tumor forming characteristics of gallbladder cancer cells harboring wild type or KRAS (G13D) but not KRAS (G12V) mutation. Furthermore, we show in vivo reduction in tumor size is paralleled by a reduction in the amounts of phospho-ERK in KRAS (G13D) but not in KRAS (G12V) xenografts, validating the in vitro findings Conclusion: Findings from this study implicate ERBB2 as an important therapeutic target in early stage gallbladder cancer. We also present the first evidence that the presence of KRAS (G12V), but not KRAS (G13D) mutation, may preclude gallbladder cancer patients to respond to anti-EGFR treatment, similar to the clinical algorithm commonly practiced to opt for anti-EGFR treatment in colorectal cancer.
2018-12-29 | E-MTAB-6619 | biostudies-arrayexpress
Project description:To explore the distinct mechanism of KRAS G12V and G12D mutation. We used microarray to explore the distinct differences in gene expression profiles of H838 KRAS mutation isogenic cell lines
2020-05-21 | GSE119146 | GEO
Project description:A Cartes d'Identite des Tumeurs (CIT) project from the French National League Against Cancer (http://cit.ligue-cancer.net ) : 165 lung adenocarcinomas without prior chemotherapy, hybridized on Illumina SNP HumanCNV370 and Affymetrix HGU133Plus2 arrays. Project leader : Prof. Pierre FOURET (pierre.fouret@igr.fr). Note: Bronchiolo-alveolarComponent : a non invasive tumor component shown in well differentiated tumor cells. EGFR Gene Mutation Status: Gene mutation status of epidermal growth factor receptor (erythroblastic leukemia viral (v; -erb-b) ; oncogene homolog, avian) ; HGNC:3236 ; Approved Symbol:EGFR; Chromosome:7p12 ; UniProt ; ID:P00533 ; OMIMID:131550 ; EntrezGeneID:1956 ; ; RefSeq:NM_201283 ; M=mutated ; WT=non mutated=wild type. KRAS Gene Mutation Status: Gene mutation status of v-Ki-ras2 Kirsten rat ; sarcoma viral oncogene homolog ; HGNC:6407 ; Approved Symbol:KRAS ; Chromosome:12p12.1 ; UniProtID:P01116; OMIM ID:190070 ; EntrezGeneID:3845 ; ;RefSeq:NM_033360 ; M=yes=mutated ; WT=non mutated.
2012-10-19 | E-MTAB-923 | biostudies-arrayexpress
Project description:Activating mutants of RAS are commonly found in many human cancers, but to date selective targeting of RAS in the clinic has been limited to KRAS(G12C) through covalent inhibitors. Here, we have developed a monobody, termed 12VC1, that recognizes the active state of both KRAS(G12V) and KRAS(G12C) up to 400-times more tightly than wild-type KRAS. Affinity purification were performed on PATU8902 and H358 cell lines that contain KRAS(G12V) and KRAS(G12C), respectively, but not from growth factor stimulated HEK293T cells containing only wild-type RAS. The mass spectrometric data was acquired in data dependent mode to show the clear enrichment of KRAS in the 2 cell lines that carry the mutated RAS. In addition, a targeted analysis was performed for the peptide carrying the G12V mutation as well as the wild type KRAS peptide to further verify enrichment of only the KRAS mutant.
2020-12-07 | MSV000086569 | MassIVE
Project description:Gene expression profiles were collected from HEK-HT cells expressing H-Ras with Ras-activating (G12V), Raf-activating (G12V,T35S), RalGEF-activating (G12V,E37G), or PI3K-activating (G12V,Y40C) mutations. Keywords: Comparison of Ras pathway components. THX=control; 12V=G12V mutation; 35S=G12V,T35S mutation; 37G=G12V,E37G mutation; 40C=G12V,Y40C mutation. 5 replicates of each. Total of 25 samples.
2009-02-21 | E-GEOD-14934 | biostudies-arrayexpress
Project description:We established human colorectal tumor organoids from benign adenoma, primary colorectal cancer or metastasized colorectal cancer. The gene signature of tumor organoids associated with their tumor progression status. We also generated genome-edited organoids from human intestinal organoids recapitulating adenoma-carcinoma sequence. Gene expression signature of the genome engineered organoids were similar to that of adenoma organoids. This result indicated multiple (up to five) genetic mutations were insufficient for gene expression reprogramming of colorectal cancer. We used microarrays to detail the global program of gene expression in human colorectal tumor organoids and artificially mutation introduced organoids. To assess the expression profiling of genome-engineered organoids, we prepared total-RNA from cultured adenoma, carcinoma and genome-engineered organoids. We produced two types of genome-engineered organoids using the CRISPR/Cas9 or lentivirus vector system. Each engineered gene and engineered methods are described as a single alphabet and method name, respectively, in the sample characteristics field. The abbreviations for the engineered genes are as follows. 1) Genome-engineered organoids with CRISPR/Cas9 A = APC deletion; K = KRAS G12V knock in; S = Smad4 deletion; T = TP53 deletion; P = PIK3CA E545K knock in. 2) Genome-engineered organoids with Lent virus vector B = CTNNB1 S33Y overexpression; K = KRAS G12V overexpression; S = Smad4 shRNA overexpression; T = TP53 shRNA overexpression; P = PIK3CA E545K overexpression.
2015-01-18 | E-GEOD-57965 | biostudies-arrayexpress
Project description:To identify the mechanisms driving resistance upon KrasG12V ablation, we established lung cancer cell lines that carried loxP sequences flanking the exon 1 of Kras containing the G12V mutation (Kras +/loxG12Vlox), and lacked Trp53 alleles (Trp53 -/-). Tumor cells were infected with Adeno-Cre particles to excise the floxed sequences and individual cells that survived were expanded for further analysis.
2023-03-05 | GSE204754 | GEO
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
2010-09-25 | GSE24338 | GEO