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Combating CHK1 resistance in triple negative breast cancer: EGFR inhibition as potential combinational therapy

Triple negative breast cancer (TNBC) is marked by a lack of expression of the Estrogen Receptor, Progesterone Receptor, and human epidermal growth factor receptor 2. Therefore, targeted therapies are being investigated based on the expression profiles of tumors. Due to the potential for acquired and...

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Detalles Bibliográficos
Autores principales: Stefanski, Casey D., Prosperi, Jenifer R.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: OAE Publishing Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8992589/
https://www.ncbi.nlm.nih.gov/pubmed/35582533
http://dx.doi.org/10.20517/cdr.2021.128
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author Stefanski, Casey D.
Prosperi, Jenifer R.
author_facet Stefanski, Casey D.
Prosperi, Jenifer R.
author_sort Stefanski, Casey D.
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description Triple negative breast cancer (TNBC) is marked by a lack of expression of the Estrogen Receptor, Progesterone Receptor, and human epidermal growth factor receptor 2. Therefore, targeted therapies are being investigated based on the expression profiles of tumors. Due to the potential for acquired and intrinsic resistance, there is a need for combination therapy to overcome resistance. In the article by Lee et al., the authors identify that, while prexasertib (a CHK1 inhibitor) lacks efficacy alone, combination with an EGFR inhibitor provides synergistic anti-tumor effects. Advances in targeted therapy for TNBC will benefit the clinical landscape for this disease, with this study initiating a new avenue of investigation.
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spelling pubmed-89925892022-05-16 Combating CHK1 resistance in triple negative breast cancer: EGFR inhibition as potential combinational therapy Stefanski, Casey D. Prosperi, Jenifer R. Cancer Drug Resist Commentary Triple negative breast cancer (TNBC) is marked by a lack of expression of the Estrogen Receptor, Progesterone Receptor, and human epidermal growth factor receptor 2. Therefore, targeted therapies are being investigated based on the expression profiles of tumors. Due to the potential for acquired and intrinsic resistance, there is a need for combination therapy to overcome resistance. In the article by Lee et al., the authors identify that, while prexasertib (a CHK1 inhibitor) lacks efficacy alone, combination with an EGFR inhibitor provides synergistic anti-tumor effects. Advances in targeted therapy for TNBC will benefit the clinical landscape for this disease, with this study initiating a new avenue of investigation. OAE Publishing Inc. 2022-03-08 /pmc/articles/PMC8992589/ /pubmed/35582533 http://dx.doi.org/10.20517/cdr.2021.128 Text en © The Author(s) 2022. https://creativecommons.org/licenses/by/4.0/© The Author(s) 2022. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Commentary
Stefanski, Casey D.
Prosperi, Jenifer R.
Combating CHK1 resistance in triple negative breast cancer: EGFR inhibition as potential combinational therapy
title Combating CHK1 resistance in triple negative breast cancer: EGFR inhibition as potential combinational therapy
title_full Combating CHK1 resistance in triple negative breast cancer: EGFR inhibition as potential combinational therapy
title_fullStr Combating CHK1 resistance in triple negative breast cancer: EGFR inhibition as potential combinational therapy
title_full_unstemmed Combating CHK1 resistance in triple negative breast cancer: EGFR inhibition as potential combinational therapy
title_short Combating CHK1 resistance in triple negative breast cancer: EGFR inhibition as potential combinational therapy
title_sort combating chk1 resistance in triple negative breast cancer: egfr inhibition as potential combinational therapy
topic Commentary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8992589/
https://www.ncbi.nlm.nih.gov/pubmed/35582533
http://dx.doi.org/10.20517/cdr.2021.128
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