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Tumor growth accelerated by chemotherapy-induced senescent cells is suppressed by treatment with IL-12 producing cellular vaccines
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SYSNO ASEP 0473062 Druh ASEP J - Článek v odborném periodiku Zařazení RIV J - Článek v odborném periodiku Poddruh J Článek ve WOS Název Tumor growth accelerated by chemotherapy-induced senescent cells is suppressed by treatment with IL-12 producing cellular vaccines Tvůrce(i) Šímová, Jana (UMG-J) RID
Sapega, Olena (UMG-J)
Imrichová, Terezie (UMG-J)
Štěpánek, Ivan (UMG-J) RID
Kyjacová, Lenka (UMG-J)
Mikyšková, Romana (UMG-J) RID
Indrová, Marie (UMG-J) RID
Bieblová, Jana (UMG-J)
Bubeník, Jan (UMG-J)
Bártek, Jiří (UMG-J) RID
Hodný, Zdeněk (UMG-J) RID
Reiniš, Milan (UMG-J) RIDCelkový počet autorů 12 Zdroj.dok. OncoTarget. - : Impact Journals LLC - ISSN 1949-2553
Roč. 7, č. 34 (2016), s. 54952-54964Poč.str. 13 Jazyk dok. eng - angličtina Země vyd. US - Spojené státy americké Klíč. slova cellular senescence ; cancer chemotherapy ; docetaxel ; IL-12 ; cell therapy Vědní obor RIV EB - Genetika a molekulární biologie CEP NT14461 GA MZd - Ministerstvo zdravotnictví Institucionální podpora UMG-J - RVO:68378050 UT WOS 000385435000069 DOI 10.18632/oncotarget.10712 Anotace Standard-of-care chemo-or radio-therapy can induce, besides tumor cell death, also tumor cell senescence. While senescence is considered to be a principal barrier against tumorigenesis, senescent cells can survive in the organism for protracted periods of time and they can promote tumor development. Based on this emerging concept, we hypothesized that elimination of such potentially cancer-promoting senescent cells could offer a therapeutic benefit. To assess this possibility, here we first show that tumor growth of proliferating mouse TC-1 HPV-16-associated cancer cells in syngeneic mice becomes accelerated by co-administration of TC-1 or TRAMP-C2 prostate cancer cells made senescent by pre-treatment with the anti-cancer drug docetaxel, or lethally irradiated. Phenotypic analyses of tumor-explanted cells indicated that the observed acceleration of tumor growth was attributable to a protumorigenic environment created by the co-injected senescent and proliferating cancer cells rather than to escape of the docetaxel-treated cells from senescence. Notably, accelerated tumor growth was effectively inhibited by cell immunotherapy using irradiated TC-1 cells engineered to produce interleukin IL-12. Collectively, our data document that immunotherapy, such as the IL-12 treatment, can provide an effective strategy for elimination of the detrimental effects caused by bystander senescent tumor cells in vivo. Pracoviště Ústav molekulární genetiky Kontakt Nikol Škňouřilová, nikol.sknourilova@img.cas.cz, Tel.: 241 063 217 Rok sběru 2017
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