FVB Cancer Mouse Genome
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR019100_1.fastq.gz | Fastqsanger.gz | |||
| ERR019100_2.fastq.gz | Fastqsanger.gz | |||
| ERR019101_1.fastq.gz | Fastqsanger.gz | |||
| ERR019101_2.fastq.gz | Fastqsanger.gz | |||
| ERR019102_1.fastq.gz | Fastqsanger.gz |
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Project description:Alterations in DNA copy number contribute to the development and progression of cancers and are common in epithelial tumors. We have used array Comparative Genomic Hybridization (aCGH) to visualize DNA copy number alterations across the genomes of lung tumors in the KrasLA2 model of lung cancer. Copy number gain involving the Kras locus, as focal amplification or whole chromosome gain, is the most common alteration in these tumors, and with a prevalence that increased significantly with increasing tumor size. Furthermore, Kras amplification was the only major genomic event among the smallest lung tumors, suggesting that this alteration occurs early during the development of mutant Kras driven lung cancers. Recurring gains and deletions of other chromosomes occur progressively more frequently among larger tumors. These results are in contrast to a previous aCGH analysis of lung tumors from KrasLA2 mice on a mixed genetic background, in which relatively few DNA copy alterations were observed regardless of tumor size. Our model features the KrasLA2 allele on the inbred FVB/N mouse strain, and in this genetic background there is a highly statistically significant increase in level of genomic instability with increasing tumor size. These data suggest that recurring DNA copy alterations are important for tumor progression in the KrasLA2 model of lung cancer, and that the requirement for these alterations may be dependent on the genetic background of the mouse strain.
2011-11-22 | GSE29230 | GEO
Project description:wild-type mouse (FVB strain) expression profiles of adult sciatic nerve and of cultured Schwann cell Keywords: other
2006-04-15 | GSE2530 | GEO
Project description:We sacrificed 6 (3 males, 3 females) FVB mice 8 weeks old and harvested their lungs. The dissected lungs lungs were assayed to RNA extraction (via trizol) in order to identify their transcriptomic signature.
2018-08-16 | GSE85115 | GEO
Project description:Analysis of glomerular gene expression levels was performed in 3- to 4-week-old FVB/N Cd151-/- mice and wild type controls. Identification of the glomerular gene expression profile at this early stage of disease progression in FVB/N Cd151-/- mice provides insight into the molecular mechanisms associated with glomerular disease development, including thickening and splitting of the glomerular basement membrane
2017-11-30 | GSE104624 | GEO
Project description:Alterations in DNA copy number contribute to the development and progression of cancers and are common in epithelial tumors. We have used array Comparative Genomic Hybridization (aCGH) to visualize DNA copy number alterations across the genomes of lung tumors in the KrasLA2 model of lung cancer. Copy number gain involving the Kras locus, as focal amplification or whole chromosome gain, is the most common alteration in these tumors, and with a prevalence that increased significantly with increasing tumor size. Furthermore, Kras amplification was the only major genomic event among the smallest lung tumors, suggesting that this alteration occurs early during the development of mutant Kras driven lung cancers. Recurring gains and deletions of other chromosomes occur progressively more frequently among larger tumors. These results are in contrast to a previous aCGH analysis of lung tumors from KrasLA2 mice on a mixed genetic background, in which relatively few DNA copy alterations were observed regardless of tumor size. Our model features the KrasLA2 allele on the inbred FVB/N mouse strain, and in this genetic background there is a highly statistically significant increase in level of genomic instability with increasing tumor size. These data suggest that recurring DNA copy alterations are important for tumor progression in the KrasLA2 model of lung cancer, and that the requirement for these alterations may be dependent on the genetic background of the mouse strain. The KrasLA2 allele, originally on a C57BL6/129svJae mixed background, was backcrossed into the FVB/N background for more than 10 generations in order to minimize the effect of genetic heterogeneity on lung tumor development. Mice were sacrificed at 6 months of age.
2011-11-22 | E-GEOD-29230 | biostudies-arrayexpress
Project description:FVB mice were engineered to express wild-type human cyclin E under control of the human surfactant C promoter (CEO mice; Ma et al, PNAS 2007). These mice develop spontaneous lung tumors, which were shown to be adenocarcinoma by histological analysis. Here we compare whole-genome RNA expression levels between the tumors and normal lung of 4 CEO mice as well as 4 nontransgenic animals. RNA was isolated from the lungs of 4 FVB mice and adjacent normal and tumor tissue from 4 FVB transgenes harboring human surfactant protein C- driven wild-type human cyclin E, all 7-11 months in age. These samples were divided into 3 groups of four, and 12 independent hybridizations were performed for analysis with Affymetrix GeneChip Mouse 430 2.0 arrays.
2013-04-04 | E-GEOD-45744 | biostudies-arrayexpress
Project description:Expression profiling comparing healthy kidneys of wild-type FVB mice and wild-type full congenic FVB-HIVAN1CAST mice HIV-1 transgenic mice on the FVB/NJ background (TgFVB) represent a validated model of HIV-associated nephropathy (HIVAN). A major susceptibility locus, HIVAN1, was previously mapped to chromosome 3A1-A3 in a cross between TgFVB and CAST/EiJ (CAST) strains, and introgression of a 51.9 Mb segment encompassing HIVAN1 from CAST into TgFVB results in accelerated development of nephropathy. We performed genome-wide expression profiling of whole kidneys from wild-type (without the HIV-1 transgene) full congenic FVB-HIVAN1CAST and FVB mouse strains, with the goal of identifying genes with differential renal expression in the HIVAN1 locus that may be associated with the development of nephropathy upon exposure to HIV-1. We only profiled healthy wild-type kidneys because the profound histopathological lesions of HIV-1 transgenic mice introduce many secondary gene expression changes that can confound interpretation of transcriptomic data.
2016-09-01 | GSE86269 | GEO
Project description:We injected 12 (6 males, 6 females) FVB mice 8 weeks old, with either saline or urethane. One week later we sacrificed and harvested their lungs. The dissected lungs were assayed to RNA extraction (via trizol). Moreover we cultured mouse tracheal epithelial cells. We compared all samples in order to identify each specific transcriptomic signature.
2019-06-28 | GSE94921 | GEO
Project description:BackgroundThe FVB/NJ mouse strain has its origins in a colony of outbred Swiss mice established in 1935 at the National Institutes of Health. Mice derived from this source were selectively bred for sensitivity to histamine diphosphate and the B strain of Friend leukemia virus. This led to the establishment of the FVB/N inbred strain, which was subsequently imported to the Jackson Laboratory and designated FVB/NJ. The FVB/NJ mouse has several distinct characteristics, such as large pronuclear morphology, vigorous reproductive performance, and consistently large litters that make it highly desirable for transgenic strain production and general purpose use.ResultsUsing next-generation sequencing technology, we have sequenced the genome of FVB/NJ to approximately 50-fold coverage, and have generated a comprehensive catalog of single nucleotide polymorphisms, small insertion/deletion polymorphisms, and structural variants, relative to the reference C57BL/6J genome. We have examined a previously identified quantitative trait locus for atherosclerosis susceptibility on chromosome 10 and identify several previously unknown candidate causal variants.ConclusionThe sequencing of the FVB/NJ genome and generation of this catalog has increased the number of known variant sites in FVB/NJ by a factor of four, and will help accelerate the identification of the precise molecular variants that are responsible for phenotypes observed in this widely used strain.
| S-EPMC3491372 | biostudies-literature