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Minimal residual disease in EGFR-mutant non-small-cell lung cancer

Targeted therapy with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) is an effective treatment for EGFR-mutant non-small-cell lung cancer (NSCLC), however most patients invariably relapse after a period of minimal residual disease (MRD). This mini-review explores the mecha...

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Autores principales: Bain, Nathan T., Wang, Yang, Arulananda, Surein
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9533094/
https://www.ncbi.nlm.nih.gov/pubmed/36212398
http://dx.doi.org/10.3389/fonc.2022.1002714
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author Bain, Nathan T.
Wang, Yang
Arulananda, Surein
author_facet Bain, Nathan T.
Wang, Yang
Arulananda, Surein
author_sort Bain, Nathan T.
collection PubMed
description Targeted therapy with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) is an effective treatment for EGFR-mutant non-small-cell lung cancer (NSCLC), however most patients invariably relapse after a period of minimal residual disease (MRD). This mini-review explores the mechanistic pathways leading to tumour dormancy, cellular senescence and epigenetic changes involving YAP/TEAD activation. We describe the various approaches of utilising TKIs in combination with agents to intensify initial depth of response, enhance apoptosis and target senescence-like dormancy. This mini-review will also highlight the potential novel therapies under development targeting MRD to improve outcomes for patients with EGFR-mutant NSCLC.
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spelling pubmed-95330942022-10-06 Minimal residual disease in EGFR-mutant non-small-cell lung cancer Bain, Nathan T. Wang, Yang Arulananda, Surein Front Oncol Oncology Targeted therapy with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) is an effective treatment for EGFR-mutant non-small-cell lung cancer (NSCLC), however most patients invariably relapse after a period of minimal residual disease (MRD). This mini-review explores the mechanistic pathways leading to tumour dormancy, cellular senescence and epigenetic changes involving YAP/TEAD activation. We describe the various approaches of utilising TKIs in combination with agents to intensify initial depth of response, enhance apoptosis and target senescence-like dormancy. This mini-review will also highlight the potential novel therapies under development targeting MRD to improve outcomes for patients with EGFR-mutant NSCLC. Frontiers Media S.A. 2022-09-21 /pmc/articles/PMC9533094/ /pubmed/36212398 http://dx.doi.org/10.3389/fonc.2022.1002714 Text en Copyright © 2022 Bain, Wang and Arulananda https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Oncology
Bain, Nathan T.
Wang, Yang
Arulananda, Surein
Minimal residual disease in EGFR-mutant non-small-cell lung cancer
title Minimal residual disease in EGFR-mutant non-small-cell lung cancer
title_full Minimal residual disease in EGFR-mutant non-small-cell lung cancer
title_fullStr Minimal residual disease in EGFR-mutant non-small-cell lung cancer
title_full_unstemmed Minimal residual disease in EGFR-mutant non-small-cell lung cancer
title_short Minimal residual disease in EGFR-mutant non-small-cell lung cancer
title_sort minimal residual disease in egfr-mutant non-small-cell lung cancer
topic Oncology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9533094/
https://www.ncbi.nlm.nih.gov/pubmed/36212398
http://dx.doi.org/10.3389/fonc.2022.1002714
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