[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"doc-seo-378367-105":3,"detail-sidebar-cat-0-en-105":79,"doc-detail-378367-en":129},{"code":4,"msg":5,"data":6},0,"ok",{"site_id":7,"language":8,"slug":9,"title":10,"keywords":11,"description":12,"schema_data":13,"social_meta":72,"head_meta":74,"extra_data":76,"updated_unix":78},105,"en","hormone-receptor-signaling-and-breast-cancer-resistance-to-anti-tumor-immunity","Hormone Receptor Signaling and Breast Cancer Resistance to Anti-Tumor Immunity","","Breast cancers comprise heterogeneous diseases with uneven responses to current therapies, with 70–80% expressing hormone receptors and benefiting from endocrine pathway targeting. Despite early promise, metastatic disease remains a major challenge, and relapses commonly follow limited immunotherapy success, particularly because only hormone-independent cases show clear benefit. This review analyzes hormone receptor signaling—especially estrogen receptor activity—and how its modulation shapes breast cancer sensitivity to anti-tumor immune effector mechanisms and enables immune escape.",{"@graph":14,"@context":71},[15,34,54],{"@type":16,"itemListElement":17},"BreadcrumbList",[18,23,27,31],{"item":19,"name":20,"@type":21,"position":22},"https://docshare.wps.com","Home","ListItem",1,{"item":24,"name":25,"@type":21,"position":26},"https://docshare.wps.com/document/","Document",2,{"item":28,"name":29,"@type":21,"position":30},"https://docshare.wps.com/document/research-report/","Research & Report",3,{"item":32,"name":10,"@type":21,"position":33},"https://docshare.wps.com/document/hormone-receptor-signaling-and-breast-cancer-resistance-to-anti-tumor-immunity/378367/",4,{"url":32,"name":10,"@type":35,"image":36,"author":41,"headline":10,"publisher":44,"fileFormat":47,"inLanguage":8,"description":12,"dateModified":48,"datePublished":48,"encodingFormat":47,"isAccessibleForFree":49,"interactionStatistic":50},"DigitalDocument",{"url":37,"@type":38,"width":39,"height":40},"https://docshare.wps.com/thumbnails/hormone-receptor-signaling-and-breast-cancer-resistance-to-anti-tumor-immunity/378367.png","ImageObject",300,407,{"name":42,"@type":43},"McGucket","Person",{"url":19,"name":45,"@type":46},"DocShare","Organization","application/pdf","2026-09-24",true,{"@type":51,"interactionType":52,"userInteractionCount":22},"InteractionCounter",{"@type":53},"ViewAction",{"@type":55,"mainEntity":56},"FAQPage",[57,63,67],{"name":58,"@type":59,"acceptedAnswer":60},"What fraction of breast cancers express hormone receptors and why does it matter?","Question",{"text":61,"@type":62},"About 70–80% of breast cancers express hormone receptors. 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Hormone Receptor Signaling and Breast Cancer Resistance to Anti-Tumor Immunity. Int. J. Mol. Sci. 2023, 24, 15048 . [https://doi.org/10.3390/](https://doi.org/10.3390/)[ ](https://doi.org/10.3390/)ijms242015048  \nAcademic Editor: Farzad Pakdel  \nReceived: 20 July 2023  \nRevised: 2 October 2023  \nAccepted: 10 October 2023  \nPublished: 10 October 2023  \nCopyright: © 2023 by the authors. 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://](https://)[ ](https://)[creativecommons.org/licenses/by/](creativecommons.org/licenses/by/)[ ](creativecommons.org/licenses/by/)[4.0/](4.0/)) .  \n1 CNRS UMR 5164, ImmunoConcEpT, Biological and Medical Sciences Department, University of Bordeaux, 33076 Bordeaux, France; [alexandra.moisand@u-bordeaux.fr](alexandra.moisand@u-bordeaux.fr) (A.M.); [mathilde.madery@u-bordeaux.fr](mathilde.madery@u-bordeaux.fr) (M.M.); [thomas.boyer@u-bordeaux.fr](thomas.boyer@u-bordeaux.fr) (T.B.); [charlotte.domblides@chu-bordeaux.fr](charlotte.domblides@chu-bordeaux.fr) (C.D.)  \n2 Cancer Biology Graduate Program, UB Grad 2.0, University of Bordeaux, 33076 Bordeaux, France  \n3 Department of Medical Oncology, University Hospital of Bordeaux, 33000 Bordeaux, France  \n* [Correspondence: blaye.celine@gmail.com](Correspondence: blaye.celine@gmail.com) (C.B.); [nicolas.larmonier@u-bordeaux.fr](nicolas.larmonier@u-bordeaux.fr) (N.L.)  \nAbstract: Breast cancers regroup many heterogeneous diseases unevenly responding to currently available therapies. Approximately 70–80% of breast cancers express hormone (estrogen or progesterone) receptors. Patients with these hormone-dependent breast malignancies benefit from therapies targeting endocrine pathways. Nevertheless, metastatic disease remains a major challenge despite available treatments, and relapses frequently ensue. By improving patient survival and quality of life, cancer immunotherapies have sparked considerable enthusiasm and hope in the last decade but have led to only limited success in breast cancers. In addition, only patients with hormone-independent breast cancers seem to benefit from these immune-based approaches. The present review examinesand discusses the current literature related to the role of hormone receptor signaling (specifically, an estrogen receptor) and the impact of its modulation on the sensitivity of breast cancer cells to the effector mechanisms of anti-tumor immune responses and on the capability of breast cancers to escape from protective anti-cancer immunity. Future research prospects related to the possibility of promoting the efficacy of immune-based interventions using hormone therapy agents are considered.  \nKeywords: hormone receptors; estrogen receptors; hormone signaling; breast cancers; cancer immunity; immunotherapies  \n1. Introduction  \nThe advent of immunotherapies over the last decade has constituted a major breakthrough in the treatment of cancer patients. However, although some patients with specific types of cancers, such as lung, bladder, colon, and liver malignancies, have benefited from such immune-based therapies, breast cancer (BC) patients have yet to experience comparable advantages. This relative absence of response to efficient immune-based interventions may be related to the multiple mechanisms of escape triggered by developing cancers. These mechanisms of resistance to immunotherapies can be “tumor-intrinsic”(the upregulation of ligands binding to inhibitory immune checkpoint receptors on effector immune cells and the impaired expression and presentation of neo-antigens, for instance) or“extrin","cbCais9RWp08e1Rt","https://ap.wps.com/l/cbCais9RWp08e1Rt","pdf",2285658,"English","# Introduction\n## Hormone receptor signaling and immune escape mechanisms\n## Modulation of estrogen receptor activity and tumor immunity","[{\"question\":\"What fraction of breast cancers express hormone receptors and why does it matter?\",\"answer\":\"About 70–80% of breast cancers express hormone receptors. These hormone-dependent malignancies can benefit from therapies that target endocrine pathways.\"},{\"question\":\"Why do immunotherapies show limited success in breast cancer?\",\"answer\":\"Limited response is linked to multiple resistance mechanisms triggered by developing tumors, including tumor-intrinsic and tumor-extrinsic escape pathways involving the tumor microenvironment.\"},{\"question\":\"How does hormone receptor signaling influence anti-tumor immunity?\",\"answer\":\"The review discusses how estrogen receptor signaling affects the sensitivity of breast cancer cells to anti-tumor immune effector mechanisms and their ability to escape protective anti-cancer immunity.\"}]","Hormone Receptor Signaling and Breast Cancer Resistance to Anti-Tumor Immunity | PDF",1790229661,48]