[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"doc-seo-333857-105":3,"detail-sidebar-cat-0-en-105":81,"doc-detail-333857-en":130},{"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":74,"head_meta":76,"extra_data":78,"updated_unix":80},105,"en","estrogen-regulated-genes-compel-apoptosis-in-breast-cancer-cells-whilst-stimulate-antitumor-activity-in-peritumoral-immune-cells-in-a-janus-faced-manner","Estrogen Regulated Genes Compel Apoptosis in Breast Cancer Cells, Whilst Stimulate Antitumor Activity in Peritumoral Immune Cells in a Janus-Faced Manner","","Background: Breast cancer incidence and mortality are increasing worldwide among both premenopausal and postmenopausal women, implying serious shortcomings in prevention and therapy. Purpose: The study argues that heightened estrogen signaling may support prevention and treatment rather than inhibition. Results: BRCA1/2-mutated breast and breast cancer cells show impaired liganded ER signaling linked to genomic instability; receptor and HER2 expression patterns reflect compensatory repair and endocrine response or nonresponse. Conclusions: Breast cancer cell behavior may enable supportive, non-genotoxic therapeutic strategies.",{"@graph":14,"@context":73},[15,34,56],{"@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/estrogen-regulated-genes-compel-apoptosis-in-breast-cancer-cells-whilst-stimulate-antitumor-activity-in-peritumoral-immune-cells-in-a-janus-faced-manner/333857/",4,{"url":32,"name":10,"@type":35,"image":36,"author":41,"headline":10,"publisher":44,"fileFormat":47,"inLanguage":8,"description":12,"dateModified":48,"datePublished":49,"encodingFormat":47,"isAccessibleForFree":50,"interactionStatistic":51},"DigitalDocument",{"url":37,"@type":38,"width":39,"height":40},"https://docshare.wps.com/thumbnails/estrogen-regulated-genes-compel-apoptosis-in-breast-cancer-cells-whilst-stimulate-antitumor-activity-in-peritumoral-immune-cells-in-a-janus-faced-manner/333857.png","ImageObject",300,407,{"name":42,"@type":43},"Miles","Person",{"url":19,"name":45,"@type":46},"DocShare","Organization","application/pdf","2026-10-29","2026-09-21",true,{"@type":52,"interactionType":53,"userInteractionCount":55},"InteractionCounter",{"@type":54},"ViewAction",6,{"@type":57,"mainEntity":58},"FAQPage",[59,65,69],{"name":60,"@type":61,"acceptedAnswer":62},"What is the study’s main purpose regarding estrogen signaling in breast cancer therapy?","Question",{"text":63,"@type":64},"It presents the role of increasing estrogen signaling in prevention and therapy, emphasizing support rather than estrogen inhibition.","Answer",{"name":66,"@type":61,"acceptedAnswer":67},"How do breast cancer cells with germline BRCA1/2 mutations relate to estrogen receptor signaling?",{"text":68,"@type":64},"They show similarly defective liganded estrogen receptor (ER) signaling, indicating ER signaling’s role in genomic instability and cancer initiation.",{"name":70,"@type":61,"acceptedAnswer":71},"How does ER and HER2 expression differ between endocrine-responsive and non-responsive breast tumors?",{"text":72,"@type":64},"ER-overexpression supports estrogen signaling and DNA repair, while in ER-negative tumors HER2 overexpression promotes unliganded ER activation; non-responsive tumors rely on HER2 compensation to offset hormonal ER inhibition.","https://schema.org",{"og:url":32,"og:type":75,"og:title":10,"og:site_name":45,"og:description":12},"article",{"robots":77,"canonical":32},"index,follow",{"doc_id":79,"site_id":7},333857,1790012897,{"code":4,"msg":82,"data":83},"success",[84,88,92,96,101,105,110,114,119,122,126],{"id":22,"doc_module":4,"doc_module_name":25,"category_name":85,"show_sort_weight":86,"slug":87},"Story & Novel",90,"story-novel",{"id":26,"doc_module":4,"doc_module_name":25,"category_name":89,"show_sort_weight":90,"slug":91},"Literature",80,"literature",{"id":33,"doc_module":4,"doc_module_name":25,"category_name":93,"show_sort_weight":94,"slug":95},"Exam",70,"exam",{"id":97,"doc_module":4,"doc_module_name":25,"category_name":98,"show_sort_weight":99,"slug":100},5,"Comic",60,"comic",{"id":55,"doc_module":4,"doc_module_name":25,"category_name":102,"show_sort_weight":103,"slug":104},"Technology",50,"technology",{"id":106,"doc_module":4,"doc_module_name":25,"category_name":107,"show_sort_weight":108,"slug":109},7,"Healthcare",40,"healthcare",{"id":111,"doc_module":4,"doc_module_name":25,"category_name":29,"show_sort_weight":112,"slug":113},8,30,"research-report",{"id":115,"doc_module":4,"doc_module_name":25,"category_name":116,"show_sort_weight":117,"slug":118},9,"Religion & Spirituality",20,"religion-spirituality",{"id":117,"doc_module":4,"doc_module_name":25,"category_name":120,"show_sort_weight":117,"slug":121},"World Cup","world-cup",{"id":123,"doc_module":4,"doc_module_name":25,"category_name":124,"show_sort_weight":123,"slug":125},10,"Lifestyle","lifestyle",{"id":127,"doc_module":4,"doc_module_name":25,"category_name":128,"show_sort_weight":97,"slug":129},19,"General","general",{"code":4,"msg":82,"data":131},{"doc_id":79,"user_id":132,"nickname":42,"user_avatar":133,"doc_module":4,"category_id":111,"category_name":29,"doc_title":10,"doc_description":12,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":55,"is_deleted":4,"is_public":22,"is_downloadable":22,"audit_status":22,"page_count":139,"language":140,"language_code":8,"site_id":7,"html_lang":8,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":12,"update_tm":144,"read_time":145,"preview_page_count":4},13056703019404,"https://ap-avatar.wpscdn.com/davatar_29158cc5080c5b710cf443261637dec0","Review  \nEstrogen Regulated Genes Compel Apoptosis in Breast Cancer Cells, Whilst Stimulate Antitumor Activity in Peritumoral Immune Cells in a Janus-Faced Manner  \nZsuzsanna Suba   \nCitation: Suba, Z. Estrogen Regulated Genes Compel Apoptosis in Breast Cancer Cells, Whilst Stimulate Antitumor Activity in Peritumoral Immune Cells in a Janus-Faced Manner. Curr. Oncol. 2024, 31, 4885–4907. [https://doi.org/](https://doi.org/)[ ](https://doi.org/)[10.3390/curroncol31090362](10.3390/curroncol31090362)  \nReceived: 13 July 2024  \nRevised: 15 August 2024  \nAccepted: 22 August 2024  \nPublished: 24 August 2024  \nCopyright: © 2024 by the author. 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/)) .  \nDepartment of Molecular Pathology, National Institute of Oncology, Ráth György Str. 7-9, H-1122 Budapest, Hungary; [subazdr@gmail.com](subazdr@gmail.com); Tel.: +36-1-224-86-00; Fax.: +36-1-224-86-20  \nAbstract: Background: Breast cancer incidence and mortality exhibit a rising trend globally among both premenopausal and postmenopausal women, suggesting that there are serious errors in our preventive and therapeutic measures. Purpose: Providing a series of valuable, but misunderstood inventions highlighting the role of increasing estrogen signaling in prevention and therapy of breast cancer instead of its inhibition. Results: 1. Breast cells and breast cancer cells with germline BRCA1/2 mutations similarly show defects in liganded estrogen receptor (ER) signaling, demonstrating its role in genomic instability and cancer initiation. 2. In breast tumors, the increased expression of special receptor family maybe an effort for self-directed improvement of genomic defects, while the weakness or loss of receptors indicates a defect requiring medical repair. 3. ER overexpression in breast cancer cells is capable of strengthening estrogen signaling and DNA repair, while in ER negative tumors, HER2 overexpression tries to upregulate unliganded ER activation and genome stabilization. 4. ERpositive breast cancers responsive to endocrine therapy may show a compensatory ER overexpression resulting in a transient tumor response. Breast cancers non-responsive to antiestrogen treatment exhibit HER2-overexpression for compensating the complete inhibition of hormonal ER activation.  \n5. In breast tumors, somatic mutations serve upregulation of ER activation via liganded or unliganded pathway helping genome stabilization and apoptotic death. 6. The mutual communication between breast cancer and its inflammatory environment is a wonderful partnership among cells fighting for genome stabilization and apoptotic death of tumor. 7. In breast cancers, there is no resistance to genotoxic or immune blocker therapies, but rather, the nonresponsive tumor cells exhaust all compensatory possibilities against therapeutic damages. Conclusions: Understanding the behavior and ambition of breast cancer cells may achieve a turn in therapy via applying supportive care instead of genotoxic measures.  \nKeywords: antiestrogen; breast cancer; cancer therapy; DNA damage; DNA repair; endocrine disruptor; estrogen receptor; growth factor receptor; immune reaction; mutation  \n1. Introduction  \nBreast cancer constitutes a major public health problem globally, as it is the most commonly diagnosed cancer in the world. The recent global cancer burden data estimate that there were nearly 2.3 million diagnosed breast cancer cases in 2020 and this disease is the leading cause of cancer mortality worldwide among women [1] . The therapy of breast cancer is a great challenge even today, illuminating that there are serious shortcomings in our preventive and therapeutic measures.  \nBreast cancer incidence and mortality exhibit a ris","cbCairz5qnXdol93","https://ap.wps.com/l/cbCairz5qnXdol93","pdf",2462238,23,"English","# Abstract\n## 1. Introduction\n## 2. Background and global burden of breast cancer","[{\"question\":\"What is the study’s main purpose regarding estrogen signaling in breast cancer therapy?\",\"answer\":\"It presents the role of increasing estrogen signaling in prevention and therapy, emphasizing support rather than estrogen inhibition.\"},{\"question\":\"How do breast cancer cells with germline BRCA1/2 mutations relate to estrogen receptor signaling?\",\"answer\":\"They show similarly defective liganded estrogen receptor (ER) signaling, indicating ER signaling’s role in genomic instability and cancer initiation.\"},{\"question\":\"How does ER and HER2 expression differ between endocrine-responsive and non-responsive breast tumors?\",\"answer\":\"ER-overexpression supports estrogen signaling and DNA repair, while in ER-negative tumors HER2 overexpression promotes unliganded ER activation; non-responsive tumors rely on HER2 compensation to offset hormonal ER inhibition.\"}]","Estrogen Regulated Genes Compel Apoptosis in Breast Cancer Cells, Whilst Stimulate Antitumor Activity in Peritumoral Immune Cells in a Janus-Faced Manner | PDF",1790004346,58]