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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...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
OAE Publishing Inc.
2022
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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. |
format | Online Article Text |
id | pubmed-9511797 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | OAE Publishing Inc. |
record_format | MEDLINE/PubMed |
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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