Mechanisms of endocrine resistance in hormone receptor-positive breast cancer Journal Article
| Authors: | Marra, A.; Trapani, D.; Ferraro, E.; Curigliano, G. |
| Editors: | Al Jarroudi, O.; El Bairi, K.; Curigliano, G. |
| Article Title: | Mechanisms of endocrine resistance in hormone receptor-positive breast cancer |
| Abstract: | Hormone receptor-positive (HR+) breast cancer (BC) accounts for approximately 70% of all breast invasive tumors. Endocrine therapy (ET) represents the standard treatment for HR + BC. Most patients, however, eventually develop resistance to ET, which limits their effectiveness and poses a major challenge for the management of HR + BC. Several mechanisms that contribute to ET resistance have been described. One of the most common mechanisms is the upregulation of alternative signaling pathways that can bypass estrogen dependency, such as activation of the PI3K/Akt/mTOR as well as mitogen-activated protein kinase (MAPK) and the insulin-like growth factor 1 receptor (IGF-1R) pathways. Another common mechanism of endocrine resistance is the acquisition of activating mutations of ESR1, which encodes for the estrogen receptor, that lead to structural changes of the receptor, prevent the binding to anti-estrogen drugs and result in constitutive activation of the receptor, even in the absence of estrogens. Epigenetic changes, such as DNA methylation and histone modifications, can also contribute to ET resistance by altering the expression of genes that are involved in estrogen signaling. Understanding the mechanisms of resistance to ET is crucial for the development of new therapies that can overcome resistance and improve outcomes for patients with HR + BC. © The Author(s), under exclusive license to Springer Nature Switzerland AG 2023. |
| Keywords: | signal transduction; mitogen activated protein kinase; protein kinase b; protein expression; unclassified drug; gene mutation; genetics; histone deacetylase inhibitor; cancer growth; drug efficacy; monotherapy; drug targeting; breast cancer; aromatase inhibitor; estrogen; estrogens; drug resistance; protein tyrosine kinase; breast neoplasms; phosphatidylinositol 3 kinase; cancer resistance; exemestane; cancer hormone therapy; breast tumor; mammalian target of rapamycin; vorinostat; tamoxifen; receptors, estrogen; estrogen receptor; trastuzumab; estradiol; metastatic breast cancer; cyclin dependent kinase inhibitor; cell cycle regulation; bioinformatics; breast carcinogenesis; drug sensitivity; everolimus; fulvestrant; neratinib; entinostat; phosphatidylinositol 3-kinases; estrogen receptor alpha; dna methyltransferase inhibitor; selective estrogen receptor modulator; akt signaling; high throughput sequencing; combination drug therapy; mapk signaling; advanced breast cancer; estrogen receptor positive breast cancer; luminal a breast cancer; humans; human; female; palbociclib; hormone receptor positive breast cancer; alpelisib; abemaciclib; ribociclib; luminal b breast cancer; esr1 gene; selective estrogen receptor degrader; capivasertib; hormone receptor-positive, her2-negative breast cancer; patritumab deruxtecan; elacestrant; proteolysis targeting chimera; azd 9496; giredestrant; hormone receptor blocking agent; selective estrogen receptor covalent antagonist |
| Journal Title: | Cancer Treatment and Research |
| Volume: | 188 |
| ISSN: | 0927-3042 |
| Publisher: | Springer |
| Date Published: | 2023-01-01 |
| Start Page: | 219 |
| End Page: | 235 |
| Language: | English |
| DOI: | 10.1007/978-3-031-33602-7_9 |
| PROVIDER: | scopus |
| PUBMED: | 38175348 |
| DOI/URL: | |
| Notes: | This book chapter is part of the book Cancer Treatment and Research: Innovative Concepts (978-3-031-33601-0) -- Source: Scopus |
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