Targeting HTLV-1 Activation of NFκB in Mouse Models and ATLL Patients
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...
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Format: | Article |
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MDPI AG
2011-06-01
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Series: | Viruses |
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Online Access: | http://www.mdpi.com/1999-4915/3/6/886/ |
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author | Lee Ratner Daniel A. Rauch |
author_facet | Lee Ratner Daniel A. Rauch |
author_sort | Lee Ratner |
collection | DOAJ |
description | 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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format | Article |
id | doaj.art-447f38c1002d4a67b2dfa8307bc06ff2 |
institution | Directory Open Access Journal |
issn | 1999-4915 |
language | English |
last_indexed | 2024-04-12T03:15:15Z |
publishDate | 2011-06-01 |
publisher | MDPI AG |
record_format | Article |
series | Viruses |
spelling | doaj.art-447f38c1002d4a67b2dfa8307bc06ff22022-12-22T03:50:11ZengMDPI AGViruses1999-49152011-06-013688690010.3390/v3060886Targeting HTLV-1 Activation of NFκB in Mouse Models and ATLL PatientsLee RatnerDaniel A. RauchOf 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.http://www.mdpi.com/1999-4915/3/6/886/HTLV-1taxNFκBmouse modelsATLL therapy |
spellingShingle | Lee Ratner Daniel A. Rauch Targeting HTLV-1 Activation of NFκB in Mouse Models and ATLL Patients Viruses HTLV-1 tax NFκB mouse models ATLL therapy |
title | Targeting HTLV-1 Activation of NFκB in Mouse Models and ATLL Patients |
title_full | Targeting HTLV-1 Activation of NFκB in Mouse Models and ATLL Patients |
title_fullStr | Targeting HTLV-1 Activation of NFκB in Mouse Models and ATLL Patients |
title_full_unstemmed | Targeting HTLV-1 Activation of NFκB in Mouse Models and ATLL Patients |
title_short | Targeting HTLV-1 Activation of NFκB in Mouse Models and ATLL Patients |
title_sort | targeting htlv 1 activation of nfκb in mouse models and atll patients |
topic | HTLV-1 tax NFκB mouse models ATLL therapy |
url | http://www.mdpi.com/1999-4915/3/6/886/ |
work_keys_str_mv | AT leeratner targetinghtlv1activationofnfkbinmousemodelsandatllpatients AT danielarauch targetinghtlv1activationofnfkbinmousemodelsandatllpatients |