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Viruses 2011, 3(6), 886-900;

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

Department of Medicine, Division of Molecular Oncology, Washington University School of Medicine, Campus Box 8069, 660 S. Euclid Ave., St. Louis, MO 63110, USA
Author to whom correspondence should be addressed.
Received: 27 April 2011 / Revised: 7 June 2011 / Accepted: 9 June 2011 / Published: 21 June 2011
(This article belongs to the Special Issue Recent Developments in HTLV Research)
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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.
Keywords: HTLV-1; tax; NFκB; mouse models; ATLL therapy HTLV-1; tax; NFκB; mouse models; ATLL therapy
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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Rauch, D.A.; Ratner, L. Targeting HTLV-1 Activation of NFκB in Mouse Models and ATLL Patients. Viruses 2011, 3, 886-900.

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