ABSTRACT: The goal of the study is to define the impact of long-term administration of antioxidants on lung cancer progression. mTC and mTN cell lines were established from mice with KrasG12D/+ lung tumors 58 weeks post intranasal Cre-delivery. mTC cells comes from control mice, mTN cells come from NAC-treated mice. Mice were maintained on a mixed C57BL/6-129/Sv genetic background
Project description:The goal of the study is to define the impact of long-term administration of antioxidants on lung cancer progression. mTC and mTN cell lines were established from mice with KrasG12D/+ lung tumors 58 weeks post intranasal Cre-delivery. mTC cells comes from control mice, mTN cells come from NAC-treated mice. Mice were maintained on a mixed C57BL/6-129/Sv genetic background
Project description:This SuperSeries is composed of the following subset Series: GSE8549: Transcriptome of reloaded soleus muscle of 129/SV mice GSE8550: Transcriptome of soleus muscle of Tenascin-C deficient 129/SV mice GSE8551: Transcriptome of reloaded soleus muscle of Tenascin-C deficient 129/SV mice GSE8552: Transcriptome of soleus muscle of 129/SV mice Keywords: SuperSeries Refer to individual Series
Project description:Microarray expression data generated to compare the biological impact of KrasG12D allelic duplication in p53null mouse embryonic fibroblasts (MEFs). The RAS/MAPK-signalling pathway is frequently deregulated in non-small cell lung cancer (NSCLC), often through activating mutations in KRAS. Mouse models demonstrated that activation of a single endogenous mutant Kras allele is sufficient to promote lung tumour formation, but acquisition of other genetic alterations is required for malignant progression. Using a well-established lung cancer mouse model we recently demonstrated that advanced KrasG12D-driven spontaneous tumours frequently exhibit enhanced MAPK signalling and KrasG12D allelic enrichment (KrasG12D/Kraswild-type>1), implying that mutant Kras copy gains are positively selected during lung cancer progression. To compare the oncogenic impact of a single mutant allele versus additional mutant Kras copy gain, we carried out a comprehensive analysis of mutant Kras homozygous and heterozygous MEFs and lung cancer cells and show that these genotypes are phenotypically distinct. Title: Mutant Kras copy number defines metabolic reprogramming and therapeutic susceptibilities Authors: Emma M Kerr, Edoardo Gaude, Frances K Turrell, Christian Frezza and Carla P Martins For MEF generation, KrasLSL-G12D/+ ;p53Fx/Fx mixed background (C57Bl/6/129/Sv) animals were interbred and embryos collected at day E12.5 to overcome KrasLSL-G12D/G12D embryonic lethality and Cre-mediated recombination performed immediately after MEF generation. Cells were cultured in DMEM supplemented with 10% FBS, 2 mM L-Glutamine for one passage and then infected with adenovirus-Cre (5âÃâ107âplaque-forming units/1 x 106 cells). Recombination of LoxP sites was confirmed by PCR analysis. Three independent embryos per genotype were analysed using GPL6887 Illumina MouseWG-6 v2.0 expression beadchip.
Project description:In male Cyp2g1-null mice, the lateral nasal gland, one of the largest anterior glands in the nasal cavity, was found to be protected from acetaminophen toxicity. The goal of this study was to identify the genes that are involved in the mechanisms, especially those genes functional in drug metabolism, clearance and post-activation events. Lateral nasal gland from 2-3-month-old male mice were dissected from each strain of mouse (B6, 129/Sv and Cyp2g1-null). Both B6 and 129/Sv are used as control mice because the Cyp2g1-null mice are on the mixed genetic background. Glands from 10 mice of each strain were pooled for RNA preparaion for one chip. There are totally 9 chips including 2 for 129/Sv, four for B6 and 3 for Cyp2g1-null mice, respectively.