
<ArticleTitle>The contribution of<prot> NF-kappa B</prot> activity to spontaneous proliferation and resistance to apoptosis in human T-cell leukemia virus type 1 Tax-induced tumors.</ArticleTitle>
<AbstractText>Human T-cell leukemia virus type I is the etiologic agent of adult T-cell leukemia/lymphoma. The <prot><prot>Tax</prot> protein</prot> of this virus is thought to contribute to cellular transformation and tumor development. In this report, we have used a Tax transgenic mouse model of tumorigenesis to study the contribution of nuclear factor <prot>(NF)-kappa B</prot> activity to spontaneous tumor cell proliferation and resistance to apoptosis. We have demonstrated elevated expression levels of <prot>NF-kappa B</prot>--inducible cytokines, including <prot>interleukin (<prot>IL</prot>)-6</prot>, <prot>IL-10</prot>, <prot>IL-15</prot>, and <prot>interferon (<prot>IFN</prot>)-gamma</prot>, in freshly isolated primary tumors from <prot>Tax</prot> transgenic mice. Inhibitors of <prot>NF-kappa B</prot> activity, sodium salicylate and cyclopentenone prostaglandins (prostaglandin A(1) and 15-deoxy-Delta(12,14)-prostaglandin J(2)), blocked spontaneous proliferation of Tax transgenic mouse spleen cells. In addition, <prot>Tax</prot>-induced tumor cells, which are resistant to irradiation-induced apoptosis, became sensitive to apoptosis in the presence of sodium salicylate and prostaglandins. These results strongly suggest that <prot>Tax</prot>-mediated induction of <prot>NF-kappa B</prot> activity contributes to tumorigenesis in vivo. (Blood. 2001;98:1200-1208)</AbstractText>
