Resistance is futile: overcoming resistance to targeted therapies in lung adenocarcinoma
Abstract The advent of genomics has led to the identification of specific “driver” mutations in oncogenic kinases, and the development of targeted small molecule inhibitors to block their tumor-driving functions. These specific inhibitors have been a clinical success, and often significantly prolong...
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Format: | Article |
Language: | English |
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Nature Portfolio
2017-03-01
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Series: | npj Precision Oncology |
Online Access: | https://doi.org/10.1038/s41698-017-0007-0 |
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author | Dana S. Neel Trever G. Bivona |
author_facet | Dana S. Neel Trever G. Bivona |
author_sort | Dana S. Neel |
collection | DOAJ |
description | Abstract The advent of genomics has led to the identification of specific “driver” mutations in oncogenic kinases, and the development of targeted small molecule inhibitors to block their tumor-driving functions. These specific inhibitors have been a clinical success, and often significantly prolong the lives of individuals with cancer. Inevitably, however, the treated tumors recur as resistance to these targeted therapies develops. Here, we review the major mechanisms by which a cancer cell can evade targeted therapy, focusing on mechanisms of resistance to kinase inhibitors in lung cancer. We discuss the promising concept of rational upfront polytherapy in lung cancer, which involves concurrently targeting multiple proteins in critical signaling pathways in a cancer cell to prevent or delay resistance. |
first_indexed | 2024-03-09T09:01:46Z |
format | Article |
id | doaj.art-0533102711904302b1f2fc1f1df3168a |
institution | Directory Open Access Journal |
issn | 2397-768X |
language | English |
last_indexed | 2024-03-09T09:01:46Z |
publishDate | 2017-03-01 |
publisher | Nature Portfolio |
record_format | Article |
series | npj Precision Oncology |
spelling | doaj.art-0533102711904302b1f2fc1f1df3168a2023-12-02T11:16:51ZengNature Portfolionpj Precision Oncology2397-768X2017-03-01111610.1038/s41698-017-0007-0Resistance is futile: overcoming resistance to targeted therapies in lung adenocarcinomaDana S. Neel0Trever G. Bivona1Department of Medicine, University of California at San FranciscoDepartment of Medicine, University of California at San FranciscoAbstract The advent of genomics has led to the identification of specific “driver” mutations in oncogenic kinases, and the development of targeted small molecule inhibitors to block their tumor-driving functions. These specific inhibitors have been a clinical success, and often significantly prolong the lives of individuals with cancer. Inevitably, however, the treated tumors recur as resistance to these targeted therapies develops. Here, we review the major mechanisms by which a cancer cell can evade targeted therapy, focusing on mechanisms of resistance to kinase inhibitors in lung cancer. We discuss the promising concept of rational upfront polytherapy in lung cancer, which involves concurrently targeting multiple proteins in critical signaling pathways in a cancer cell to prevent or delay resistance.https://doi.org/10.1038/s41698-017-0007-0 |
spellingShingle | Dana S. Neel Trever G. Bivona Resistance is futile: overcoming resistance to targeted therapies in lung adenocarcinoma npj Precision Oncology |
title | Resistance is futile: overcoming resistance to targeted therapies in lung adenocarcinoma |
title_full | Resistance is futile: overcoming resistance to targeted therapies in lung adenocarcinoma |
title_fullStr | Resistance is futile: overcoming resistance to targeted therapies in lung adenocarcinoma |
title_full_unstemmed | Resistance is futile: overcoming resistance to targeted therapies in lung adenocarcinoma |
title_short | Resistance is futile: overcoming resistance to targeted therapies in lung adenocarcinoma |
title_sort | resistance is futile overcoming resistance to targeted therapies in lung adenocarcinoma |
url | https://doi.org/10.1038/s41698-017-0007-0 |
work_keys_str_mv | AT danasneel resistanceisfutileovercomingresistancetotargetedtherapiesinlungadenocarcinoma AT trevergbivona resistanceisfutileovercomingresistancetotargetedtherapiesinlungadenocarcinoma |