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HER2+ Breast Cancer Escalation and De-Escalation Trial Design: Potential Role of Intrinsic Subtyping
SIMPLE SUMMARY: Classical clinical research has been developed according to immunohistochemical breast cancer subtypes, instead of designing trials specifically for each molecular subtype. Efforts in de-escalating treatment should focus on identifying a subgroup of HER2 oncogene addicted tumours tha...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8833556/ https://www.ncbi.nlm.nih.gov/pubmed/35158778 http://dx.doi.org/10.3390/cancers14030512 |
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author | Bueno Muiño, Coralia Martín, Miguel del Monte-Millán, María García-Saénz, José Ángel López-Tarruella, Sara |
author_facet | Bueno Muiño, Coralia Martín, Miguel del Monte-Millán, María García-Saénz, José Ángel López-Tarruella, Sara |
author_sort | Bueno Muiño, Coralia |
collection | PubMed |
description | SIMPLE SUMMARY: Classical clinical research has been developed according to immunohistochemical breast cancer subtypes, instead of designing trials specifically for each molecular subtype. Efforts in de-escalating treatment should focus on identifying a subgroup of HER2 oncogene addicted tumours that are especially sensitive to anti-HER2 therapies and, thus, spare unnecessary treatments. A prognostic assay that integrates molecular tumour features with clinical and pathologic variables and accurately defines a group of HER2 addicted tumours remains the best candidate among these strategies. ABSTRACT: Long-term outcomes in breast cancer patients differ based on the molecular subtype, with HER2-E being the most aggressive one. Advances in clinical practice have dramatically shifted HER2+ breast cancer prognosis. Risk adapted strategies to individualize therapies are necessary. De-escalation approaches have been encouraged based on the risks of clinical-pathological factors. Molecular gene subtyping could further accurately define HER2 addicted tumours that are sensitive to anti-HER2 therapies, thus sparing unnecessary treatments. The transition from immunochemistry to molecular profiling in HER2+ breast cancer is discussed. |
format | Online Article Text |
id | pubmed-8833556 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-88335562022-02-12 HER2+ Breast Cancer Escalation and De-Escalation Trial Design: Potential Role of Intrinsic Subtyping Bueno Muiño, Coralia Martín, Miguel del Monte-Millán, María García-Saénz, José Ángel López-Tarruella, Sara Cancers (Basel) Review SIMPLE SUMMARY: Classical clinical research has been developed according to immunohistochemical breast cancer subtypes, instead of designing trials specifically for each molecular subtype. Efforts in de-escalating treatment should focus on identifying a subgroup of HER2 oncogene addicted tumours that are especially sensitive to anti-HER2 therapies and, thus, spare unnecessary treatments. A prognostic assay that integrates molecular tumour features with clinical and pathologic variables and accurately defines a group of HER2 addicted tumours remains the best candidate among these strategies. ABSTRACT: Long-term outcomes in breast cancer patients differ based on the molecular subtype, with HER2-E being the most aggressive one. Advances in clinical practice have dramatically shifted HER2+ breast cancer prognosis. Risk adapted strategies to individualize therapies are necessary. De-escalation approaches have been encouraged based on the risks of clinical-pathological factors. Molecular gene subtyping could further accurately define HER2 addicted tumours that are sensitive to anti-HER2 therapies, thus sparing unnecessary treatments. The transition from immunochemistry to molecular profiling in HER2+ breast cancer is discussed. MDPI 2022-01-20 /pmc/articles/PMC8833556/ /pubmed/35158778 http://dx.doi.org/10.3390/cancers14030512 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Bueno Muiño, Coralia Martín, Miguel del Monte-Millán, María García-Saénz, José Ángel López-Tarruella, Sara HER2+ Breast Cancer Escalation and De-Escalation Trial Design: Potential Role of Intrinsic Subtyping |
title | HER2+ Breast Cancer Escalation and De-Escalation Trial Design: Potential Role of Intrinsic Subtyping |
title_full | HER2+ Breast Cancer Escalation and De-Escalation Trial Design: Potential Role of Intrinsic Subtyping |
title_fullStr | HER2+ Breast Cancer Escalation and De-Escalation Trial Design: Potential Role of Intrinsic Subtyping |
title_full_unstemmed | HER2+ Breast Cancer Escalation and De-Escalation Trial Design: Potential Role of Intrinsic Subtyping |
title_short | HER2+ Breast Cancer Escalation and De-Escalation Trial Design: Potential Role of Intrinsic Subtyping |
title_sort | her2+ breast cancer escalation and de-escalation trial design: potential role of intrinsic subtyping |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8833556/ https://www.ncbi.nlm.nih.gov/pubmed/35158778 http://dx.doi.org/10.3390/cancers14030512 |
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