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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 ASEP 0472126 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Resistance 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) RIDNumber of authors 7 Source Title International Journal of Oncology. - : Spandidos Publications - ISSN 1019-6439
Roč. 49, č. 2 (2016), s. 763-772Number of pages 10 s. Language eng - English Country GR - Greece Keywords novel mouse strains ; NKC domain ; TC-1/A9 ; B16F10 ; MCB8 ; colorectal cancer ; cancer development Subject RIV EB - Genetics ; Molecular Biology R&D Projects GA14-10100S 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 support UMG-J - RVO:68378050 UT WOS 000378263600034 DOI https://doi.org/10.3892/ijo.2016.3561 Annotation To 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. Workplace Institute of Molecular Genetics Contact Nikol Škňouřilová, nikol.sknourilova@img.cas.cz, Tel.: 241 063 217 Year of Publishing 2017
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