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Drugging the addict: non‐oncogene addiction as a target for cancer therapy

Historically, cancers have been treated with chemotherapeutics aimed to have profound effects on tumor cells with only limited effects on normal tissue. This approach was followed by the development of small‐molecule inhibitors that can target oncogenic pathways critical for the survival of tumor ce...

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Detalles Bibliográficos
Autores principales: Nagel, Remco, Semenova, Ekaterina A, Berns, Anton
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5090709/
https://www.ncbi.nlm.nih.gov/pubmed/27702988
http://dx.doi.org/10.15252/embr.201643030
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author Nagel, Remco
Semenova, Ekaterina A
Berns, Anton
author_facet Nagel, Remco
Semenova, Ekaterina A
Berns, Anton
author_sort Nagel, Remco
collection PubMed
description Historically, cancers have been treated with chemotherapeutics aimed to have profound effects on tumor cells with only limited effects on normal tissue. This approach was followed by the development of small‐molecule inhibitors that can target oncogenic pathways critical for the survival of tumor cells. The clinical targeting of these so‐called oncogene addictions, however, is in many instances hampered by the outgrowth of resistant clones. More recently, the proper functioning of non‐mutated genes has been shown to enhance the survival of many cancers, a phenomenon called non‐oncogene addiction. In the current review, we will focus on the distinct non‐oncogenic addictions found in cancer cells, including synthetic lethal interactions, the underlying stress phenotypes, and arising therapeutic opportunities.
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spelling pubmed-50907092016-12-12 Drugging the addict: non‐oncogene addiction as a target for cancer therapy Nagel, Remco Semenova, Ekaterina A Berns, Anton EMBO Rep Reviews Historically, cancers have been treated with chemotherapeutics aimed to have profound effects on tumor cells with only limited effects on normal tissue. This approach was followed by the development of small‐molecule inhibitors that can target oncogenic pathways critical for the survival of tumor cells. The clinical targeting of these so‐called oncogene addictions, however, is in many instances hampered by the outgrowth of resistant clones. More recently, the proper functioning of non‐mutated genes has been shown to enhance the survival of many cancers, a phenomenon called non‐oncogene addiction. In the current review, we will focus on the distinct non‐oncogenic addictions found in cancer cells, including synthetic lethal interactions, the underlying stress phenotypes, and arising therapeutic opportunities. John Wiley and Sons Inc. 2016-10-04 2016-11 /pmc/articles/PMC5090709/ /pubmed/27702988 http://dx.doi.org/10.15252/embr.201643030 Text en © 2016 The Authors. Published under the terms of the CC BY NC ND 4.0 license This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs 4.0 (http://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Reviews
Nagel, Remco
Semenova, Ekaterina A
Berns, Anton
Drugging the addict: non‐oncogene addiction as a target for cancer therapy
title Drugging the addict: non‐oncogene addiction as a target for cancer therapy
title_full Drugging the addict: non‐oncogene addiction as a target for cancer therapy
title_fullStr Drugging the addict: non‐oncogene addiction as a target for cancer therapy
title_full_unstemmed Drugging the addict: non‐oncogene addiction as a target for cancer therapy
title_short Drugging the addict: non‐oncogene addiction as a target for cancer therapy
title_sort drugging the addict: non‐oncogene addiction as a target for cancer therapy
topic Reviews
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5090709/
https://www.ncbi.nlm.nih.gov/pubmed/27702988
http://dx.doi.org/10.15252/embr.201643030
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