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Toll-Like Receptor 4 Activation in Cancer Progression and Therapy

Cancer immunotherapy has been the focus of intense research since the late 19th century when Coley observed that bacterial components can contribute to cancer regression by eliciting an antitumor immune response. Successful activation and maturation of tumor-specific immune cells is now known to be...

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Detalles Bibliográficos
Autores principales: Oblak, Alja, Jerala, Roman
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3216292/
https://www.ncbi.nlm.nih.gov/pubmed/22110526
http://dx.doi.org/10.1155/2011/609579
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author Oblak, Alja
Jerala, Roman
author_facet Oblak, Alja
Jerala, Roman
author_sort Oblak, Alja
collection PubMed
description Cancer immunotherapy has been the focus of intense research since the late 19th century when Coley observed that bacterial components can contribute to cancer regression by eliciting an antitumor immune response. Successful activation and maturation of tumor-specific immune cells is now known to be mediated by bacterial endotoxin, which activates Toll-like receptor 4 (TLR4). TLR4 is expressed on a variety of immune as well as tumor cells, but its activation can have opposing effects. While TLR4 activation can promote antitumor immunity, it can also result in increased tumor growth and immunosuppression. Nevertheless, TLR4 engagement by endotoxin as well as by endogenous ligands represents notable contribution to the outcome of different cancer treatments, such as radiation or chemotherapy. Further research of the role and mechanisms of TLR4 activation in cancer may provide novel antitumor vaccine adjuvants as well as TLR4 inhibitors that could prevent inflammation-induced carcinogenesis.
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spelling pubmed-32162922011-11-22 Toll-Like Receptor 4 Activation in Cancer Progression and Therapy Oblak, Alja Jerala, Roman Clin Dev Immunol Review Article Cancer immunotherapy has been the focus of intense research since the late 19th century when Coley observed that bacterial components can contribute to cancer regression by eliciting an antitumor immune response. Successful activation and maturation of tumor-specific immune cells is now known to be mediated by bacterial endotoxin, which activates Toll-like receptor 4 (TLR4). TLR4 is expressed on a variety of immune as well as tumor cells, but its activation can have opposing effects. While TLR4 activation can promote antitumor immunity, it can also result in increased tumor growth and immunosuppression. Nevertheless, TLR4 engagement by endotoxin as well as by endogenous ligands represents notable contribution to the outcome of different cancer treatments, such as radiation or chemotherapy. Further research of the role and mechanisms of TLR4 activation in cancer may provide novel antitumor vaccine adjuvants as well as TLR4 inhibitors that could prevent inflammation-induced carcinogenesis. Hindawi Publishing Corporation 2011 2011-11-03 /pmc/articles/PMC3216292/ /pubmed/22110526 http://dx.doi.org/10.1155/2011/609579 Text en Copyright © 2011 A. Oblak and R. Jerala. https://creativecommons.org/licenses/by/3.0/ 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.
spellingShingle Review Article
Oblak, Alja
Jerala, Roman
Toll-Like Receptor 4 Activation in Cancer Progression and Therapy
title Toll-Like Receptor 4 Activation in Cancer Progression and Therapy
title_full Toll-Like Receptor 4 Activation in Cancer Progression and Therapy
title_fullStr Toll-Like Receptor 4 Activation in Cancer Progression and Therapy
title_full_unstemmed Toll-Like Receptor 4 Activation in Cancer Progression and Therapy
title_short Toll-Like Receptor 4 Activation in Cancer Progression and Therapy
title_sort toll-like receptor 4 activation in cancer progression and therapy
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3216292/
https://www.ncbi.nlm.nih.gov/pubmed/22110526
http://dx.doi.org/10.1155/2011/609579
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