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.

Original languageEnglish
Pages (from-to)886-900
Number of pages15
Issue number6
StatePublished - Jun 2011


  • ATLL therapy
  • HTLV-1
  • Mouse models
  • NFκB
  • TAX


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