Journal article : Review
Role of PI3K/Akt/mTOR pathway in mediating endocrine resistance: concept to clinic
- Abstract:
- The majority of breast cancers express the estrogen receptor (ER) and for this group of patients, endocrine therapy is the cornerstone of systemic treatment. However, drug resistance is common and a focus for breast cancer preclinical and clinical research. Over the past 2 decades, the PI3K/Akt/mTOR axis has emerged as an important driver of treatment failure, and inhibitors of mTOR and PI3K are now licensed for the treatment of women with advanced ER-positive breast cancer who have relapsed on first-line hormonal therapy. This review presents the preclinical and clinical data that led to this new treatment paradigm and discusses future directions.
- Publication status:
- Published
- Peer review status:
- Peer reviewed
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(Preview, Version of record, pdf, 2.1MB, Terms of use)
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- Publisher copy:
- 10.37349/etat.2022.00078
Authors
+ National Institute for Health and Care Research
More from this funder
- Funder identifier:
- https://ror.org/0187kwz08
- Grant:
- ACF-2020-13-009
- Publisher:
- Open Exploration Publishing
- Journal:
- Exploration of Targeted Anti-tumor Therapy More from this journal
- Volume:
- 3
- Issue:
- 2
- Pages:
- 172-199
- Publication date:
- 2022-04-24
- Acceptance date:
- 2022-02-11
- DOI:
- EISSN:
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2692-3114
- Pmid:
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36046843
- Language:
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English
- Keywords:
- Subtype:
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Review
- Pubs id:
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1260526
- Local pid:
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pubs:1260526
- Deposit date:
-
2024-10-19
- ARK identifier:
Terms of use
- Copyright holder:
- Skolariki et al.
- Copyright date:
- 2022
- Rights statement:
- Copyright: © The Author(s) 2022. This is an Open Access article 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.
- Licence:
- CC Attribution (CC BY)
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