NSCLC metastasis: K-ras/p53 mutant and syngeneic mouse models
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ABSTRACT:
PROVIDER: PRJNA111451 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series:; GSE14449: Gene expression profiles of spontaneous metastasis in a K-ras/p53 mutant mouse model; GSE14458: Gene expression profiles of 344SQ lung adenocarcinoma cells with high metastatic potential (syngeneic mouse model) Experiment Overall Design: Refer to individual Series
2009-11-23 | E-GEOD-14459 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below.
2009-11-10 | GSE14459 | GEO
Project description:The biologic basis for NSCLC metastasis is not well understood. Here we addressed this deficiency by transcriptionally profiling tumors from a genetic mouse model of human lung adenocarcinoma that develops metastatic disease owing to the expression of K-rasG12D and p53R172H. We identified 2,209 genes that were differentially expressed in distant metastases relative to matched lung tumors. Mining of publicly available data bases revealed this expression signature in a subset of NSCLC patients who had a poorer prognosis than those without the signature. Primary lung adenocarcinomas and metastases from p53R172H∆g/+ K-rasLA1/+ mice or syngeneic tumors were isolated, carefully dissected to remove the adjacent tissue, snap-frozen in liquid nitrogen and stored at -80° until use. Part of each dissected tumor was histologically evaluated by a board-certified pathologist. Synthesis of cRNA and hybridization to Mouse Expression Array 430A 2.0 chips were performed. Two-sided t-paired tests using log-transformed expression values determined significant differences between primary tumors and metastasis.
2009-04-14 | E-GEOD-14449 | biostudies-arrayexpress
Project description:The cell line-derived xenografts and patient derived xenografts have limited use in cancer immunotherapy evaluation because an immune compromised host is required for xenotransplantation. Syngeneic mouse models are derived by transplanting established mouse cell lines or tumor tissues to strain matched mouse hosts, which are better suited to study the interplay between immune and tumor cells. We investigated the differences as well as similarities of a panel of ten mouse syngeneic models to features of human tumors by proteomics, which will provide valuable information to assist experimental biologists in model selection.
2019-12-03 | PXD011885 | Pride
Project description:Salivary tumors isolated from MMTV-ras transgenic mice expressing wild-type p53, no p53 or p53R172H gain-of-funcion mutant were subjected to genome-wide gene expression profiling to assess the effect of the different p53 status on tumor gene expression. A total of 12 spontaneous salivary tumors from MMTV-ras/p53+/+, MMTV-ras/p53-/- or MMTV-ras/p53R172H/R172H mice (4 tumors per genotype) were analyzed using Affymetric GeneChip for gene expression profiling. The multi-class comparison function of Significance Analysis of Microarray (SAM) with an FDR of 1% was used to identify genes that are differentially regulated across the three genotypic groups.
2014-08-15 | E-GEOD-59452 | biostudies-arrayexpress
Project description:As a critical cellular stress sensor, p53 mediates a variety of defensive processes including cell-cycle arrest, apoptosis, and senescence to prevent propagation of hyperproliferative cells or cells with a damaged genome, hence the formation of neoplasia. Transactivation of downstream genes plays an important while sometimes controversial role in regulating these cellular processes. To evaluate the dependence on transcriptional activation in p53’s activities, we generated genetically-modified mouse lines carrying mutations in the transactivation domains (TADs) of p53. These transactivatio-deficient mutants serve as unique reagents to probe the dependence on robust transactivation in p53-mediated cellular functions, as well as the underneath mechanisms. To identify genes differentially regulated by these p53 mutants, we performed gene expression profiling analysis on mouse embryonic fibroblast cells (MEFs) from these mice in the context of oncogenic Ras-induced premature cellular senescence. Mouse embryonic fibroblasts (MEFs) with different p53 genotypes were infected with retroviral H-Ras V12, which induces premature cellular senescence in p53 wild-type MEFs but not in p53 null MEFs. 5 genotypic groups of MEFs were used in the study: (i) p53L25Q/W26S, or "25,26", in which the first TAD (transactivation domain) of p53 is disrupted by the mutation, 5 biological samples; (ii) p53W53Q/F54S, or "53,54", in which the second TAD of p53 is disrupted by the mutation, 3 biological samples; (iii) p53L25Q/W26S/W53Q/F54S, or "QM", in which both TADs or p53 are disrupted, 3 biological samples; (iv) p53 wild-type, or "WT", 6 biological samples; (v) p53 null, or "Null", 6 biological samples.
2011-05-13 | E-GEOD-27901 | biostudies-arrayexpress
Project description:Salivary tumors isolated from MMTV-ras transgenic mice expressing wild-type p53, no p53 or p53R172H gain-of-funcion mutant were subjected to genome-wide gene expression profiling to assess the effect of the different p53 status on tumor gene expression.
2014-08-15 | GSE59452 | GEO
Project description:The p53 gain of function p53R172H promotes accelerated tumor growth and progression to carcinoma. To identify gene expression changes associated with the oncogenic function of mutant p53 we compared the expression profiles of oral tumors induced by activation of oncogenic K-ras and p53 gain- or loss-of-function mutations Oral tumors were induced by activation of endogenous oncogenic K-rasG12D and p53 loss- or gain-of-function mutations (p53R172H)
2012-03-31 | GSE28203 | GEO
Project description:Addition of liver-specific Keap1 deletion to mice harboring mutant K-ras and p53 accelerated cholangiocarcinoma formation, with hallmarks of Nrf2 activation.
2021-09-27 | GSE138101 | GEO
Project description:The p53 gain of function p53R172H promotes accelerated tumor growth and progression to carcinoma. To identify gene expression changes associated with the oncogenic function of mutant p53 we compared the expression profiles of oral tumors induced by activation of oncogenic K-ras and p53 gain- or loss-of-function mutations Oral tumors were induced by activation of endogenous oncogenic K-rasG12D and p53 loss- or gain-of-function mutations (p53R172H) Oral tumors from mice carrying the p53R172H mutation or deletion of p53 were collected for gene expression analysis
2012-03-30 | E-GEOD-28203 | biostudies-arrayexpress