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Mus musculus

ABSTRACT: Differential Gene Expression in Mouse Bone Marrow in Response to Dibenzo[def,p]chrysene by RNA-Seq

PROVIDER: PRJNA293553 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2180050.fastq.gz	Fastqsanger.gz
	SRR2180051.fastq.gz	Fastqsanger.gz
	SRR2180052.fastq.gz	Fastqsanger.gz
	SRR2180053.fastq.gz	Fastqsanger.gz
	SRR2180054.fastq.gz	Fastqsanger.gz

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Project description:Alterations of DNA methlation in oral cavity of mice induced by dibenzo[def,p]chrysene

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Project description:Despite advances in treatment modalities, 5-year survival of OSCC has remained at ~50% for the past decades, mostly due to the high risk of developing secondary primary tumors. Early detection of OSCC represents one of the most promising approaches to improving survival. In this study, we examined the alterations of DNA methylation in early stage of oral carcinogenesis in mice induced by carcinogen dibenzo[def,p]chrysene. We identified 30 differentially methylated sites and canonical pathways that may be served as potential biomarkers for early detection of OSCC.

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Project description:Differential expression of mouse Grem1+ Vs. Grem1- bone-marrow cells

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Project description:Comparison of C57Bl/KalwRij mouse bone marrow to C57BL6 mouse bone marrow

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Transcriptional Response of Male MutaTMMouse Spleen to Dibenzo[def,p]chrysene Exposure

Project description:Dibenzo[def,p]chrysene (DBC) is the most carcinogenic polycyclic aromatic hydrocarbon (PAH) examined to date. We investigated the immunotoxicity of DBC, manifested as spleen atrophy following acute exposure of adult Muta™Mouse males by oral gavage. Mice were exposed to 0, 2.0, 6.2, or 20.0 mg DBC /kg-bw per day, for three days. Genotoxic endpoints (DBC-DNA adducts and lacZ mutant frequency in spleen and bone marrow, and red blood cell micronucleus frequency) and global gene expression changes were measured. All of the genotoxicity measures increased in a dose-dependent manner in both tissues. Gene expression analysis showed that DBC activates p53 signalling pathways related to cellular growth and proliferation, which was evident even at the low dose. Strikingly, the expression profiles of DBC exposed mouse spleens were highly inversely correlated with the expression profiles of the only published toxicogenomics dataset of enlarged mouse spleen. This analysis suggested a central role for Bnip3l, a pro-apoptotic protein involved in negative regulation of erythroid maturation. RT-PCR confirmed expression changes in several genes related to apoptosis, iron metabolism, and aryl hydrocarbon receptor signalling that are regulated in the opposite direction during spleen atrophy versus benzo[a]pyrene-mediated splenomegaly. In addition, benchmark dose modeling of toxicogenomics data yielded toxicity estimates that are very close to traditional toxicity endpoints. This work illustrates the power of toxicogenomics to reveal rich mechanistic information of immunotoxic compounds and its ability to provide information that is quantitatively similar to that derived from standard toxicity methods in health risk assessment.

2015-11-18 | GSE72334 | GEO

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