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Targeting HTLV-1 Activation of NFκB in Mouse Models and ATLL Patients

Author(s): Daniel A. Rauch | Lee Ratner

Journal: Viruses
ISSN 1999-4915

Volume: 3;
Issue: 6;
Start page: 886;
Date: 2011;
Original page

Keywords: HTLV-1 | tax | NFκB | mouse models | ATLL therapy

Of the millions of HTLV-1 infected carriers worldwide, 3–5% will develop an aggressive T-cell neoplasm that is highly refractory to conventional therapy. The virus carries the Tax oncogene which constitutively activates the NFκB pathway. This co-option of signaling through NFκB provides for the HTLV-1 infected cell an escape from cell cycle arrest and apoptosis, a steady source of growth factors, and a mechanism by which the virus can activate its own target cell. Therapies that target the NFκB pathway sensitize adult T-cell leukemia/lymphoma (ATLL) cells to apoptosis. A focus on translational interrogation of NFκB inhibitors in animal models and ATLL patients is needed to advance NFκB-targeted ATLL therapies to the bedside.
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