• Login
    View Item 
    •   Home
    • The Manchester Institute Cancer Research UK
    • All Paterson Institute for Cancer Research
    • View Item
    •   Home
    • The Manchester Institute Cancer Research UK
    • All Paterson Institute for Cancer Research
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Browse

    All of ChristieCommunitiesTitleAuthorsIssue DateSubmit DateSubjectsThis CollectionTitleAuthorsIssue DateSubmit DateSubjects

    My Account

    LoginRegister

    Local Links

    The Christie WebsiteChristie Library and Knowledge Service

    Statistics

    Display statistics

    Resistance to endocrine therapy: are breast cancer stem cells the culprits?

    • CSV
    • RefMan
    • EndNote
    • BibTex
    • RefWorks
    Authors
    O'Brien, Ciara S
    Howell, Sacha J
    Farnie, Gillian
    Clarke, Robert B
    Affiliation
    Breast Biology Group, School of Cancer and Imaging Sciences, Paterson Institute for Cancer Research, University of Manchester, Manchester, UK.
    Issue Date
    2009-03
    
    Metadata
    Show full item record
    Abstract
    From a developmental point of view, tumors can be seen as aberrant versions of their tissue of origin. For example, tumors often partially retain differentiation markers of their tissue of origin and there is evidence that they contain cancer stem cells (CSCs) that drive tumorigenesis. In this review, we summarise current evidence that breast CSCs may partly explain endocrine resistance in breast cancer. In normal breast, the stem cells are known to possess a basal phenotype and to be mainly ERalpha-. If the hierarchy in breast cancer reflects this, the breast CSC may be endocrine resistant because it expresses very little ERalpha and can only respond to treatment by virtue of paracrine influences of neighboring, differentiated ERalpha+ tumor cells. Normal breast epithelial stem cells are highly dependent on the EGFR and other growth factor receptors and it may be that the observed increased growth factor receptor expression in endocrine-resistant breast cancers reflects an increased proportion of CSCs selected by endocrine therapies. There is evidence from a number of studies that breast CSCs are ERalpha- and EGFR+/HER2+, which would support this view. CSCs also express mesenchymal genes which are suppressed by ERalpha expression, further indicating the mutual exclusion between ERalpha+ cells and the CSCs. As we learn more about CSCs, differentiation and the expression and functional activity of the ERalpha in these cells in diverse breast tumor sub-types, it is hoped that our understanding will lead to new modalities to overcome the problem of endocrine resistance in the clinic.
    Citation
    Resistance to endocrine therapy: are breast cancer stem cells the culprits? 2009, 14 (1):45-54 J Mammary Gland Biol Neoplasia
    Journal
    Journal of Mammary Gland Biology and Neoplasia
    URI
    http://hdl.handle.net/10541/69760
    DOI
    10.1007/s10911-009-9115-y
    PubMed ID
    19252972
    Type
    Article
    Language
    en
    ISSN
    1573-7039
    ae974a485f413a2113503eed53cd6c53
    10.1007/s10911-009-9115-y
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research
    Breast Biology

    entitlement

    Related articles

    • Breast cancer stem cells and their role in resistance to endocrine therapy.
    • Authors: O'Brien CS, Farnie G, Howell SJ, Clarke RB
    • Issue date: 2011 Apr
    • Basal/HER2 breast carcinomas: integrating molecular taxonomy with cancer stem cell dynamics to predict primary resistance to trastuzumab (Herceptin).
    • Authors: Martin-Castillo B, Oliveras-Ferraros C, Vazquez-Martin A, Cufí S, Moreno JM, Corominas-Faja B, Urruticoechea A, Martín ÁG, López-Bonet E, Menendez JA
    • Issue date: 2013 Jan 15
    • YB-1 interplays with ERα to regulate the stemness and differentiation of ER-positive breast cancer stem cells.
    • Authors: Yang F, Chen S, He S, Huo Q, Hu Y, Xie N
    • Issue date: 2020
    • Lapatinib restores hormone sensitivity with differential effects on estrogen receptor signaling in cell models of human epidermal growth factor receptor 2-negative breast cancer with acquired endocrine resistance.
    • Authors: Leary AF, Drury S, Detre S, Pancholi S, Lykkesfeldt AE, Martin LA, Dowsett M, Johnston SR
    • Issue date: 2010 Mar 1
    • Antiestrogen Therapy Increases Plasticity and Cancer Stemness of Prolactin-Induced ERα(+) Mammary Carcinomas.
    • Authors: Shea MP, O'Leary KA, Fakhraldeen SA, Goffin V, Friedl A, Wisinski KB, Alexander CM, Schuler LA
    • Issue date: 2018 Apr 1
    DSpace software (copyright © 2002 - 2023)  DuraSpace
    Quick Guide | Contact Us
    Open Repository is a service operated by 
    Atmire NV
     

    Export search results

    The export option will allow you to export the current search results of the entered query to a file. Different formats are available for download. To export the items, click on the button corresponding with the preferred download format.

    By default, clicking on the export buttons will result in a download of the allowed maximum amount of items.

    To select a subset of the search results, click "Selective Export" button and make a selection of the items you want to export. The amount of items that can be exported at once is similarly restricted as the full export.

    After making a selection, click one of the export format buttons. The amount of items that will be exported is indicated in the bubble next to export format.