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Aberrant calcium signalling downstream of mutations in TP53 and the PI3K/AKT pathway genes promotes disease progression and therapy resistance in triple negative breast cancer

Triple-negative breast cancer (TNBC) is characterized as an aggressive form of breast cancer (BC) associated with poor patient outcomes. For the majority of patients, there is a lack of approved targeted therapies. Therefore, chemotherapy remains a key treatment option for these patients, but signif...

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Autores principales: Eustace, Alex J., Lee, Min Jie, Colley, Grace, Roban, Jack, Downing, Tim, Buchanan, Paul J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: OAE Publishing Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9511797/
https://www.ncbi.nlm.nih.gov/pubmed/36176752
http://dx.doi.org/10.20517/cdr.2022.41
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author Eustace, Alex J.
Lee, Min Jie
Colley, Grace
Roban, Jack
Downing, Tim
Buchanan, Paul J.
author_facet Eustace, Alex J.
Lee, Min Jie
Colley, Grace
Roban, Jack
Downing, Tim
Buchanan, Paul J.
author_sort Eustace, Alex J.
collection PubMed
description Triple-negative breast cancer (TNBC) is characterized as an aggressive form of breast cancer (BC) associated with poor patient outcomes. For the majority of patients, there is a lack of approved targeted therapies. Therefore, chemotherapy remains a key treatment option for these patients, but significant issues around acquired resistance limit its efficacy. Thus, TNBC has an unmet need for new targeted personalized medicine approaches. Calcium (Ca(2+)) is a ubiquitous second messenger that is known to control a range of key cellular processes by mediating signalling transduction and gene transcription. Changes in Ca(2+) through altered calcium channel expression or activity are known to promote tumorigenesis and treatment resistance in a range of cancers including BC. Emerging evidence shows that this is mediated by Ca(2+) modulation, supporting the function of tumour suppressor genes (TSGs) and oncogenes. This review provides insight into the underlying alterations in calcium signalling and how it plays a key role in promoting disease progression and therapy resistance in TNBC which harbours mutations in tumour protein p53 (TP53) and the PI3K/AKT pathway.
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spelling pubmed-95117972022-09-28 Aberrant calcium signalling downstream of mutations in TP53 and the PI3K/AKT pathway genes promotes disease progression and therapy resistance in triple negative breast cancer Eustace, Alex J. Lee, Min Jie Colley, Grace Roban, Jack Downing, Tim Buchanan, Paul J. Cancer Drug Resist Review Triple-negative breast cancer (TNBC) is characterized as an aggressive form of breast cancer (BC) associated with poor patient outcomes. For the majority of patients, there is a lack of approved targeted therapies. Therefore, chemotherapy remains a key treatment option for these patients, but significant issues around acquired resistance limit its efficacy. Thus, TNBC has an unmet need for new targeted personalized medicine approaches. Calcium (Ca(2+)) is a ubiquitous second messenger that is known to control a range of key cellular processes by mediating signalling transduction and gene transcription. Changes in Ca(2+) through altered calcium channel expression or activity are known to promote tumorigenesis and treatment resistance in a range of cancers including BC. Emerging evidence shows that this is mediated by Ca(2+) modulation, supporting the function of tumour suppressor genes (TSGs) and oncogenes. This review provides insight into the underlying alterations in calcium signalling and how it plays a key role in promoting disease progression and therapy resistance in TNBC which harbours mutations in tumour protein p53 (TP53) and the PI3K/AKT pathway. OAE Publishing Inc. 2022-06-21 /pmc/articles/PMC9511797/ /pubmed/36176752 http://dx.doi.org/10.20517/cdr.2022.41 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 Review
Eustace, Alex J.
Lee, Min Jie
Colley, Grace
Roban, Jack
Downing, Tim
Buchanan, Paul J.
Aberrant calcium signalling downstream of mutations in TP53 and the PI3K/AKT pathway genes promotes disease progression and therapy resistance in triple negative breast cancer
title Aberrant calcium signalling downstream of mutations in TP53 and the PI3K/AKT pathway genes promotes disease progression and therapy resistance in triple negative breast cancer
title_full Aberrant calcium signalling downstream of mutations in TP53 and the PI3K/AKT pathway genes promotes disease progression and therapy resistance in triple negative breast cancer
title_fullStr Aberrant calcium signalling downstream of mutations in TP53 and the PI3K/AKT pathway genes promotes disease progression and therapy resistance in triple negative breast cancer
title_full_unstemmed Aberrant calcium signalling downstream of mutations in TP53 and the PI3K/AKT pathway genes promotes disease progression and therapy resistance in triple negative breast cancer
title_short Aberrant calcium signalling downstream of mutations in TP53 and the PI3K/AKT pathway genes promotes disease progression and therapy resistance in triple negative breast cancer
title_sort aberrant calcium signalling downstream of mutations in tp53 and the pi3k/akt pathway genes promotes disease progression and therapy resistance in triple negative breast cancer
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9511797/
https://www.ncbi.nlm.nih.gov/pubmed/36176752
http://dx.doi.org/10.20517/cdr.2022.41
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