Abstract
Objectives: To identify the regulated genes or the spliced genes of diethylnitorsamine (NDEA) in ATT-myc mice versus control group. Methods: We analysed the 9 hybridizations on the MouseExon10ST array of NDEA treatments and control non- transgenic by application of a mixed model analysis of variance. Results: The 907 genes had regulated significantly between the groups and 916 genes had regulated with a significant exon-group interaction among of them 150 genes had regulated with both gene and possible splicing differences (p<0.01). The 7,618 genes had tested for the alternative gene up-regulation and splicing and compared to the gene-classifications. The genes functions, pathways and gene-classifications in the current study had presented in the contingency table analysis of the set of the regulated genes and alternatively spliced that regulated significantly in the ATT-myc mice treated by diethylnitorsamine versus control non-transgenic. The GOMolFn of gene-classification had 321 groups that had significantly regulated in the set of the regulated genes or differentially spliced. While the GOProcess of gene-classification had 330 groups that had significantly regulated in the set of differentially regulated genes or spliced. Additionally, the CELlLoc of gene-classification had 70 groups that had significantly regulated in the set of differentially regulated genes spliced. Finally, the Pathway gene-classification had 8 groups that had significantly regulated in the set of differentially regulated genes or spliced (p<0.01) in diethylnitorsamine when compared to control group. Conclusion: we summarized the toxicogenomics induced by diethylnitrosamine in early liver carcinogenesis in ATT-myc transgenic mice of liver cancer. Doi: 10.28991/SciMedJ-2021-0302-6 Full Text: PDF
Highlights
To shorten the validation stage time or with higher-state analysis, it is critical to validate the transgenic model by testing the carcinogen such as diethylnitrosamine and comparing the date result with previously published dates of the same compound in old and classical tests [9, 11, 12]
The current study explored the function of liver genome at early carcinogenesis induced by NDEA in att-myc mouse model of hepatocellular carcinoma
In terms of gene groups regulated in GOProcess of the GOMolFn, GOProcess, CELlLoc, and Pathway classes, it was discovered that the collection of regulated genes and alternatively spliced genes was significantly regulated in groups of the GOMolFn, GOProcess, CELlLoc, and Pathway classes of NDEA treatment in ATT-myc transgenic model of liver cancer as well as similar study recorded earlier the molecular effect of NDEA in rat hepatocarcinogenesis [20]
Summary
100,000 or more new substances, medications, and vaccines are introduced to our population each year, and the FDA and other safety organizations must allow their use for at least 18 months [1]. To protect more people and solve health issues, we need to reduce the time it takes for some vaccines and medicines to be approved in disasters, pandemics, and exotic diseases like corona. Several experiments and techniques are used to determine the carcinogenicity of chemicals or drugs, which started with two years of testing and has progressed to more sophisticated technology such as microarray, exon array, and models that replicate human tumor genes. The differences between these tests are time consuming during the procedure of each test, and the accuracy of the data results from these projects is questionable. To shorten the validation stage time or with higher-state analysis, it is critical to validate the transgenic model by testing the carcinogen such as diethylnitrosamine and comparing the date result with previously published dates of the same compound in old and classical tests [9, 11, 12]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
