- Resistance of novel mouse strains different in MHC class I and the NK…
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Resistance of novel mouse strains different in MHC class I and the NKC domain to the development of experimental tumors

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    SYSNO ASEP0472126
    Document TypeJ - Journal Article
    R&D Document TypeJournal Article
    Subsidiary JČlánek ve WOS
    TitleResistance of novel mouse strains different in MHC class I and the NKC domain to the development of experimental tumors
    Author(s) Fišerová, A. (CZ)
    Richter, J. (CZ)
    Čapková, K. (CZ)
    Bieblová, Jana (UMG-J)
    Mikyšková, Romana (UMG-J) RID
    Reiniš, Milan (UMG-J) RID
    Indrová, Marie (UMG-J) RID
    Number of authors7
    Source TitleInternational Journal of Oncology. - : Spandidos Publications - ISSN 1019-6439
    Roč. 49, č. 2 (2016), s. 763-772
    Number of pages10 s.
    Languageeng - English
    CountryGR - Greece
    Keywordsnovel mouse strains ; NKC domain ; TC-1/A9 ; B16F10 ; MCB8 ; colorectal cancer ; cancer development
    Subject RIVEB - Genetics ; Molecular Biology
    R&D ProjectsGA14-10100S GA ČR - Czech Science Foundation (CSF)
    LM2011032 GA MŠMT - Ministry of Education, Youth and Sports (MEYS)
    ED1.1.00/02.0109 GA MŠMT - Ministry of Education, Youth and Sports (MEYS)
    Institutional supportUMG-J - RVO:68378050
    UT WOS000378263600034
    DOI https://doi.org/10.3892/ijo.2016.3561
    AnnotationTo elucidate the immunological mechanisms critical for tumor progression, we bred novel mouse strains, different in the NKC and H-2D domains. We used inbreeding to generate hybrids of Balb/c and C57BL/6 of stable H-2Db+d-NK1.1neg and H-2Db-d+NK1.1high phenotypes. We analyzed the growth of three established MHC class I-deficient tumor cell lines: TC-1/A9 tumor (HPV-associated) and B16F10 melanoma, both syngeneic to C57BL/6, and the MCB8 (3-methycholanthreneinduced tumor) syngeneic to Balb/c. Furthermore, we induced colorectal carcinoma by azoxymethane-DSS treatment to test the susceptibility to chemically-induced primary cancer. We found that the novel strains spontaneously regressed the tumor transplants syngeneic to both Balb/c (MCB8) and C57BL/6 (B16F10 and TC-1/A9) mice. The H2-Db+d-NK1.1neg, but not the H2-Db-d+NK1.1high strain was also highly resistant to chemically-induced colorectal cancer in comparison to the parental mice. The immune changes during TC-1/A9 cancer development involved an increase of the NK cell distribution in the peripheral blood and spleen along with higher expression of NKG2D activation antigen; this was in correlation with the time-dependent rise of cytotoxic activity in comparison to C57BL/6 mice. The TC-1/A9 cancer regression was accompanied by higher proportion of B cells in the spleen and B220(+)/CD86(+) activated antigen-presenting B cells distributed in the lymphoid organs, as well as in the periphery. The changes in the T-cell population were represented mainly by the prevalence of T helper cells reflected by grown CD4/CD8 ratio, most prominent in the b+d-NK1.1neg strain. The results of the present study imply usefulness of the two novel mouse strains as an experimental model for further studies of tumor resistance mechanisms.
    WorkplaceInstitute of Molecular Genetics
    ContactNikol Škňouřilová, nikol.sknourilova@img.cas.cz, Tel.: 241 063 217
    Year of Publishing2017
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