Viruses 2011, 3(6), 886-900; doi:10.3390/v3060886
Review

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

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Received: 27 April 2011; in revised form: 7 June 2011 / Accepted: 9 June 2011 / Published: 21 June 2011
(This article belongs to the Special Issue Recent Developments in HTLV Research)
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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
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MDPI and ACS Style

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

AMA Style

Rauch DA, Ratner L. Targeting HTLV-1 Activation of NFκB in Mouse Models and ATLL Patients. Viruses. 2011; 3(6):886-900.

Chicago/Turabian Style

Rauch, Daniel A.; Ratner, Lee. 2011. "Targeting HTLV-1 Activation of NFκB in Mouse Models and ATLL Patients." Viruses 3, no. 6: 886-900.


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