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Viruses 2011, 3(6), 886-900; doi:10.3390/v3060886
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Targeting HTLV-1 Activation of NFκB in Mouse Models and ATLL Patients

 and
*
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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Abstract

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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