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An oncogenic Kras expression signature identified by cross-species

ABSTRACT: Mouse lung cancers were generated using the KrasLA model, in which a latent mutated Kras2 allele (resulting in the amino acid substitution G12D) is sporadically activated through spontaneous homologous recombination. These mice develop lung adenomas with full penetrance; over time, the tumors acquire morphologic characteristics reminiscent of those of human adenocarcinoma, such as nuclear atypia and a high mitotic index. KrasLA2 mice on a 129svJae background were crossed with wild type C57B/6J mice to obtain F1 progeny. The initial report of this mouse model described two alleles, KrasLA1 and KrasLA2. All expression profiles in this study were generated using the KrasLA2 mice. We call the model KrasLA throughout for simplicity. Mice bearing the KrasLA latent allele were allowed to develop to 5-6 month of age and sacrificed by cervical dislocation. Lungs were removed and placed in RNAlaterTM solution (Ambion). Individual tumors large enough to be easily dissected (3mm-8mm) were removed and cut into 2 pieces. One piece was placed in formalin to be used for histological analysis while the other piece was stored at -80 for RNA/DNA extraction.

ORGANISM(S): Mus musculus

PROVIDER: GSE49200 | GEO | 2013/08/01

SECONDARY ACCESSION(S): PRJNA213295

REPOSITORIES: GEO

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An oncogenic Kras expression signature identified by cross-species

Project description:Mouse lung cancers were generated using the KrasLA model, in which a latent mutated Kras2 allele (resulting in the amino acid substitution G12D) is sporadically activated through spontaneous homologous recombination. These mice develop lung adenomas with full penetrance; over time, the tumors acquire morphologic characteristics reminiscent of those of human adenocarcinoma, such as nuclear atypia and a high mitotic index. KrasLA2 mice on a 129svJae background were crossed with wild type C57B/6J mice to obtain F1 progeny. The initial report of this mouse model described two alleles, KrasLA1 and KrasLA2. All expression profiles in this study were generated using the KrasLA2 mice. We call the model KrasLA throughout for simplicity. Mice bearing the KrasLA latent allele were allowed to develop to 5-6 month of age and sacrificed by cervical dislocation. Lungs were removed and placed in RNAlaterTM solution (Ambion). Individual tumors large enough to be easily dissected (3mm-8mm) were removed and cut into 2 pieces. One piece was placed in formalin to be used for histological analysis while the other piece was stored at -80 for RNA/DNA extraction. Gene expression profiling was perfomed on lung tumors derived from KrasLA mouse (n = 31) and normal mouse lung samples (n = 19).

2013-08-01 | E-GEOD-49200 | biostudies-arrayexpress

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Project description:Gene expression was evaluated in 9 appendix samples removed from patients who went to the operating room with the diagnosis of acute appendicitis and 4 samples removed for non-inflammatory reasons. A circumferential piece of tissue was obtained at the distal aspect of each specimen. The tissue was flash frozen at -80 degrees for later processing. Frozen specimens were homogenized into TriReagent and RNA was isolated according to the manufacturer's instruction. RNA was processed and hybridized to Affymetrix microarray. Keywords: Disease state analysis

2008-04-22 | GSE9579 | GEO

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Project description:Social stress mouse models were used to simulate human post-traumatic stress disorder (PTSD). C57B/6 mice exposed to SJL aggressor mice exhibited behaviors accepted as PTSD-in-mouse phenotype: 'frozen' motion, aggressor’s barrier avoidance, startled jumping, and retarded locomotion. Transcripts in hippocampus, amygdala, medial prefrontal cortex, ventral striatum (nucleus acumbens), septal region, corpus striatum, hemi-brain, blood, spleen and heart of stressed and control C57B/6 mice were analyzed using Agilent’s mouse genome-wide arrays.

2015-04-20 | GSE45035 | GEO

Gene expression under normoxia/hypoxia in mouse embryonic fibroblasts with mutations in the CH1 domains of p300 and CBP

Project description:The CH1 (TAZ) domain of the transcriptional coactivators p300 and CBP has been reported to interact with the transcription factor HIF-1alpha and this interaction is thought to be critical for HIF-1alpha target gene expression in response to hypoxia. To determine the requirement for the CH1 domain in hypoxia-responsive gene expression, primary mouse embryonic fibroblasts (MEFs) were generated from e14.5 C57B/6x129/Sv F2 embryos that were either wildtype or bore deletion mutations in the CH1 protein binding domains of both alleles of p300 and one allele of CBP (tri_CH1). Subconfluent MEFs were treated with 21% oxygen (normoxia) or 0.1% oxygen (hypoxia) with 5% carbon dioxide at 37 C in a humid chamber for 6hrs. At the start of treatment, medium was removed and replaced with medium (DMEM+10% FBS+pen-strep+ l-glu) that had been preequilibrated overnight in normoxia or hypoxia as appropriate. Immediately after treatment, cells were lysed in Trizol for RNA extraction. Keywords: genetic modification, dose response

2005-10-24 | GSE3195 | GEO

Removed

Project description:Removed

| PRJEB28844 | ENA

miRNA profiles of lung tissues from Mtb H37Rv infected C57B/6 mice and uninfected controls

Project description:The C57B/6 mice were infected with Mtb H37Rv (CFU=200) for 28 days, and the miRNA expression profile from lung tissues were analyzed with deep sequencing.

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PROTOMAP analysis of Human Cartoid Plaques

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