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Modeling therapy resistance via the EGFR signaling pathway
Mutations in KRAS are often associated with resistance to EGFR‐targeting antibody therapy. Using comprehensive systems analyses, GNB5 has been identified as a potential target to overcome therapy resistance targeting the EGFR signaling pathways, whereby the AKT signaling pathway (PI3K) rather than t...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6850018/ https://www.ncbi.nlm.nih.gov/pubmed/30892828 http://dx.doi.org/10.1111/febs.14809 |
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author | Plattner, Christina Hackl, Hubert |
author_facet | Plattner, Christina Hackl, Hubert |
author_sort | Plattner, Christina |
collection | PubMed |
description | Mutations in KRAS are often associated with resistance to EGFR‐targeting antibody therapy. Using comprehensive systems analyses, GNB5 has been identified as a potential target to overcome therapy resistance targeting the EGFR signaling pathways, whereby the AKT signaling pathway (PI3K) rather than the ERK signaling pathway (RAS) might be dominantly affected. Personalized mathematical modeling and simulations of this signaling pathway/network and respective perturbations are of great utility to customize therapy for patients. [Image: see text] |
format | Online Article Text |
id | pubmed-6850018 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-68500182019-11-15 Modeling therapy resistance via the EGFR signaling pathway Plattner, Christina Hackl, Hubert FEBS J Commentary Mutations in KRAS are often associated with resistance to EGFR‐targeting antibody therapy. Using comprehensive systems analyses, GNB5 has been identified as a potential target to overcome therapy resistance targeting the EGFR signaling pathways, whereby the AKT signaling pathway (PI3K) rather than the ERK signaling pathway (RAS) might be dominantly affected. Personalized mathematical modeling and simulations of this signaling pathway/network and respective perturbations are of great utility to customize therapy for patients. [Image: see text] John Wiley and Sons Inc. 2019-03-20 2019-04 /pmc/articles/PMC6850018/ /pubmed/30892828 http://dx.doi.org/10.1111/febs.14809 Text en © 2019 The Authors. The FEBS Journal published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Commentary Plattner, Christina Hackl, Hubert Modeling therapy resistance via the EGFR signaling pathway |
title | Modeling therapy resistance via the EGFR signaling pathway |
title_full | Modeling therapy resistance via the EGFR signaling pathway |
title_fullStr | Modeling therapy resistance via the EGFR signaling pathway |
title_full_unstemmed | Modeling therapy resistance via the EGFR signaling pathway |
title_short | Modeling therapy resistance via the EGFR signaling pathway |
title_sort | modeling therapy resistance via the egfr signaling pathway |
topic | Commentary |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6850018/ https://www.ncbi.nlm.nih.gov/pubmed/30892828 http://dx.doi.org/10.1111/febs.14809 |
work_keys_str_mv | AT plattnerchristina modelingtherapyresistanceviatheegfrsignalingpathway AT hacklhubert modelingtherapyresistanceviatheegfrsignalingpathway |