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ChIP sequencing of BACH1 in mTC and mTN cells

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

ORGANISM(S): Mus musculus

PROVIDER: GSE128180 | GEO | 2019/07/02

REPOSITORIES: GEO

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RNA sequencing of mTC and mTN cells

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

2019-07-02 | GSE128153 | GEO

mTC and mTN cells

Project description:mTC and mTN cells

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ChIP sequencing of BACH1 in mTC and mTN cells

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RNA sequencing of mTC and mTN cells

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Mus musculus

Project description:Antioxidants Accelerate Lung Cancer Progression in Mice

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Glutaminase inhibition impairs CD8 T cell activation in STK11/Lkb1 deficient lung cancer

Project description:To characterize the impact of KRAS co-mutations KEAP1 and STK11/Lkb1 on the metabolic and immune microenvironment of lung adenocarcinoma in immune-intact models, we generated a cohort of genetically engineered mouse models (GEMMs) to reflect the diverse tumor suppressor landscape seen in patients. Mice carrying the KrasG12D allele (K)21 were crossed with Keap1flox/flox (KK)22 and/or Lkb1flox/flox (KKL, KL)23 mice and genetic recombination induced by intranasal inhalation of Ad5-CMV-Cre adenovirus. We interrogated the metabolites present in lung tumor nodules collected from cohorts of KK, KL and KKL mice.

2022-01-18 | ST002066 | MetabolomicsWorkbench

Comparison of KrasG12D/WT;p53Fx/Fx and KrasG12D/G12D;p53Fx/Fx MEFs

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.

2016-02-24 | E-GEOD-75871 | biostudies-arrayexpress

Blocking oncogenic Ras-induced β-catenin degradation and prosenescent inflammation redirects premature senescence to mesenchymal transformation (miRNA expression)

Project description:We constructed LSL-KrasG12D/+ and Spc-Cre;LSL-KrasG12D/+ mice to investigate the role of microRNA in the pathogenesis of lung cancer

2019-06-30 | GSE132096 | GEO

Gene expression in lung cells expressing MycER/KrasG12D from a transgenic mouse model of non-small cell lung cancer

Project description:A transgenic mouse model of Kras-driven lung adenocarcinoma, with reversible activation of Myc, was used to explore the effect of Myc activity on lipid metabolism in lung tumours. Gene expression analysis links lipid metabolism, transport and storage to Myc activity. Lung cells from adeno-cre infected R26LSL-CMER and LSL-KrasG12D; R26LSL-CMER mice were isolated 14 days post-treatment with (LSL-KrasG12D; R26LSL-CMER and R26LSL-CMER) or without (R26LSL-CMER only) tamoxifen. GFP positive cells were FACs sorted. To increase RNA yield, cells from two mice of the same genotype and treatment were combined. There were two biological replicates for each condition. Gene expression was compared between lung cells with inactive MycER and lung cells expressing active MycER plus or minus KRasG12D.

2020-08-10 | E-MTAB-9131 | biostudies-arrayexpress

Characterization of the genetic mouse model of non-small cells lung cancer p53R172HM-bM-^HM-^Fg/KrasG12D

Project description:Background: Non-small cell lung cancer (NSCLC) accounts for 81% of all cases of lung cancer and they are often fatal because 60% of the patients are diagnosed at an advanced stage. Besides the need for earlier diagnosis, there is a great need for additional effective therapies. In this work we investigated the feasibility of a lung cancer progression mouse model, mimicking features of human aggressive NSCLC cancer, as biological reservoir for potential therapeutic targets and biomarkers. Results:RNA-seq profiling was performed on total RNA extracted from lungs of 30 week-old p53R172HM-bM-^HM-^Fg/KrasG12D and wild type mice to detect fusion genes and gene/exon-level differential expression associated to the increase of tumor mass. Fusion events were not detected in p53R172HM-bM-^HM-^Fg/KrasG12D tumors. Differential expression at exon-level detected 33 genes with differential exon usage. The study provides a complete transcription overview of the p53R172HM-bM-^HM-^Fg/KrasG12D mouse NSCLC model Lung mRNA profiles of 30-week old wild type (WT) and p53R172HM-bM-^HM-^Fg/KrasG12D mice were generated by deep sequencing, in duplicate using Illumina HiSeq2000.

2013-09-25 | E-GEOD-51144 | biostudies-arrayexpress

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