Blocking cancer-fibroblast mutualism inhibits proliferation of endocrine therapy resistant breast cancer
In early-stage estrogen receptor-positive (ER + ) breast cancer, resistance to endocrine therapy (ET) and CDK4/6 inhibitors (CDK4/6i) often involve a shift away from estrogen-driven proliferation. The nature and source of compensatory growth signals driving cancer proliferation remain unknown but re...
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| Published in | Molecular systems biology Vol. 21; no. 7; pp. 825 - 855 |
|---|---|
| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
02.07.2025
Springer Nature |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1744-4292 1744-4292 |
| DOI | 10.1038/s44320-025-00104-6 |
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| Abstract | In early-stage estrogen receptor-positive (ER + ) breast cancer, resistance to endocrine therapy (ET) and CDK4/6 inhibitors (CDK4/6i) often involve a shift away from estrogen-driven proliferation. The nature and source of compensatory growth signals driving cancer proliferation remain unknown but represent direct therapeutic targets of resistant cells. By analyzing single-cell RNA-sequencing data from serial biopsies of patient tumors, we elucidated compensatory growth signaling pathways activated in ET + CDK4/6i-resistant cancer cells, along with the intercellular growth signal communications within the tumor microenvironment. In most patient tumors, resistant cancer cells increased ERBB growth pathway activity during treatment, only partially through ERBB receptor upregulation. Concurrently, fibroblasts within the tumor increased ERBB ligand communication with cancer cells, as they differentiated to a proliferative and mesenchymal phenotype in response to TGF
β
signals from cancer cells. In vitro model systems demonstrated molecularly how therapy induces a mutualistic cycle of crosstalk between cancer cells and fibroblasts, fostering a growth factor-rich tumor microenvironment circumventing estrogen reliance. We show that ERBB inhibition can break this cancer-fibroblasts mutualism, targeting an acquired sensitivity of resistant cancer cells.
Synopsis
Serial single-cell RNA sequencing of estrogen receptor-positive (ER + ) breast tumors from multiple patient cohorts, combined with experimental analyses, uncovers molecular mechanisms of compensatory growth signaling that drive proliferation in endocrine +/- CDK4/6 inhibitor-resistant cancer cells.
A shift to ERBB growth factor mediated proliferation away from estrogen signaling is observed in resistant cancer cells in most tumors during treatment, partially facilitated by ERBB receptor upregulation.
Fibroblasts are stimulated by cancer cells exposed to endocrine therapy to differentiate and secrete ERBB ligands, which in turn crosstalk with ERBB receptors on cancer cells to drive growth.
Mutualistic cancer-fibroblast crosstalk mechanisms, identified from patient samples, were verified across in vitro model systems, showing that ERBB growth factor-enrichment bypasses estrogen dependence.
This cancer-fibroblast communication is blocked by pan-ERBB inhibitors, targeting an acquired sensitivity to overcome endocrine resistance.
Serial single-cell RNA sequencing of estrogen receptor-positive (ER + ) breast tumors from multiple patient cohorts, combined with experimental analyses, uncovers molecular mechanisms of compensatory growth signaling that drives proliferation in endocrine +/- CDK4/6 inhibitor-resistant cancer cells. |
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| AbstractList | In early-stage estrogen receptor-positive (ER + ) breast cancer, resistance to endocrine therapy (ET) and CDK4/6 inhibitors (CDK4/6i) often involve a shift away from estrogen-driven proliferation. The nature and source of compensatory growth signals driving cancer proliferation remain unknown but represent direct therapeutic targets of resistant cells. By analyzing single-cell RNA-sequencing data from serial biopsies of patient tumors, we elucidated compensatory growth signaling pathways activated in ET + CDK4/6i-resistant cancer cells, along with the intercellular growth signal communications within the tumor microenvironment. In most patient tumors, resistant cancer cells increased ERBB growth pathway activity during treatment, only partially through ERBB receptor upregulation. Concurrently, fibroblasts within the tumor increased ERBB ligand communication with cancer cells, as they differentiated to a proliferative and mesenchymal phenotype in response to TGF $$\beta$$ β signals from cancer cells. In vitro model systems demonstrated molecularly how therapy induces a mutualistic cycle of crosstalk between cancer cells and fibroblasts, fostering a growth factor-rich tumor microenvironment circumventing estrogen reliance. We show that ERBB inhibition can break this cancer-fibroblasts mutualism, targeting an acquired sensitivity of resistant cancer cells. In early-stage estrogen receptor-positive (ER + ) breast cancer, resistance to endocrine therapy (ET) and CDK4/6 inhibitors (CDK4/6i) often involve a shift away from estrogen-driven proliferation. The nature and source of compensatory growth signals driving cancer proliferation remain unknown but represent direct therapeutic targets of resistant cells. By analyzing single-cell RNA-sequencing data from serial biopsies of patient tumors, we elucidated compensatory growth signaling pathways activated in ET + CDK4/6i-resistant cancer cells, along with the intercellular growth signal communications within the tumor microenvironment. In most patient tumors, resistant cancer cells increased ERBB growth pathway activity during treatment, only partially through ERBB receptor upregulation. Concurrently, fibroblasts within the tumor increased ERBB ligand communication with cancer cells, as they differentiated to a proliferative and mesenchymal phenotype in response to TGF \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\beta$$\end{document} β signals from cancer cells. In vitro model systems demonstrated molecularly how therapy induces a mutualistic cycle of crosstalk between cancer cells and fibroblasts, fostering a growth factor-rich tumor microenvironment circumventing estrogen reliance. We show that ERBB inhibition can break this cancer-fibroblasts mutualism, targeting an acquired sensitivity of resistant cancer cells. Serial single-cell RNA sequencing of estrogen receptor-positive (ER + ) breast tumors from multiple patient cohorts, combined with experimental analyses, uncovers molecular mechanisms of compensatory growth signaling that drive proliferation in endocrine +/- CDK4/6 inhibitor-resistant cancer cells. A shift to ERBB growth factor mediated proliferation away from estrogen signaling is observed in resistant cancer cells in most tumors during treatment, partially facilitated by ERBB receptor upregulation. Fibroblasts are stimulated by cancer cells exposed to endocrine therapy to differentiate and secrete ERBB ligands, which in turn crosstalk with ERBB receptors on cancer cells to drive growth. Mutualistic cancer-fibroblast crosstalk mechanisms, identified from patient samples, were verified across in vitro model systems, showing that ERBB growth factor-enrichment bypasses estrogen dependence. This cancer-fibroblast communication is blocked by pan-ERBB inhibitors, targeting an acquired sensitivity to overcome endocrine resistance. Serial single-cell RNA sequencing of estrogen receptor-positive (ER + ) breast tumors from multiple patient cohorts, combined with experimental analyses, uncovers molecular mechanisms of compensatory growth signaling that drives proliferation in endocrine +/- CDK4/6 inhibitor-resistant cancer cells. In early-stage estrogen receptor-positive (ER + ) breast cancer, resistance to endocrine therapy (ET) and CDK4/6 inhibitors (CDK4/6i) often involve a shift away from estrogen-driven proliferation. The nature and source of compensatory growth signals driving cancer proliferation remain unknown but represent direct therapeutic targets of resistant cells. By analyzing single-cell RNA-sequencing data from serial biopsies of patient tumors, we elucidated compensatory growth signaling pathways activated in ET + CDK4/6i-resistant cancer cells, along with the intercellular growth signal communications within the tumor microenvironment. In most patient tumors, resistant cancer cells increased ERBB growth pathway activity during treatment, only partially through ERBB receptor upregulation. Concurrently, fibroblasts within the tumor increased ERBB ligand communication with cancer cells, as they differentiated to a proliferative and mesenchymal phenotype in response to TGF β signals from cancer cells. In vitro model systems demonstrated molecularly how therapy induces a mutualistic cycle of crosstalk between cancer cells and fibroblasts, fostering a growth factor-rich tumor microenvironment circumventing estrogen reliance. We show that ERBB inhibition can break this cancer-fibroblasts mutualism, targeting an acquired sensitivity of resistant cancer cells.In early-stage estrogen receptor-positive (ER + ) breast cancer, resistance to endocrine therapy (ET) and CDK4/6 inhibitors (CDK4/6i) often involve a shift away from estrogen-driven proliferation. The nature and source of compensatory growth signals driving cancer proliferation remain unknown but represent direct therapeutic targets of resistant cells. By analyzing single-cell RNA-sequencing data from serial biopsies of patient tumors, we elucidated compensatory growth signaling pathways activated in ET + CDK4/6i-resistant cancer cells, along with the intercellular growth signal communications within the tumor microenvironment. In most patient tumors, resistant cancer cells increased ERBB growth pathway activity during treatment, only partially through ERBB receptor upregulation. Concurrently, fibroblasts within the tumor increased ERBB ligand communication with cancer cells, as they differentiated to a proliferative and mesenchymal phenotype in response to TGF β signals from cancer cells. In vitro model systems demonstrated molecularly how therapy induces a mutualistic cycle of crosstalk between cancer cells and fibroblasts, fostering a growth factor-rich tumor microenvironment circumventing estrogen reliance. We show that ERBB inhibition can break this cancer-fibroblasts mutualism, targeting an acquired sensitivity of resistant cancer cells. In early-stage estrogen receptor-positive (ER + ) breast cancer, resistance to endocrine therapy (ET) and CDK4/6 inhibitors (CDK4/6i) often involve a shift away from estrogen-driven proliferation. The nature and source of compensatory growth signals driving cancer proliferation remain unknown but represent direct therapeutic targets of resistant cells. By analyzing single-cell RNA-sequencing data from serial biopsies of patient tumors, we elucidated compensatory growth signaling pathways activated in ET + CDK4/6i-resistant cancer cells, along with the intercellular growth signal communications within the tumor microenvironment. In most patient tumors, resistant cancer cells increased ERBB growth pathway activity during treatment, only partially through ERBB receptor upregulation. Concurrently, fibroblasts within the tumor increased ERBB ligand communication with cancer cells, as they differentiated to a proliferative and mesenchymal phenotype in response to TGF signals from cancer cells. In vitro model systems demonstrated molecularly how therapy induces a mutualistic cycle of crosstalk between cancer cells and fibroblasts, fostering a growth factor-rich tumor microenvironment circumventing estrogen reliance. We show that ERBB inhibition can break this cancer-fibroblasts mutualism, targeting an acquired sensitivity of resistant cancer cells. In early-stage estrogen receptor-positive (ER + ) breast cancer, resistance to endocrine therapy (ET) and CDK4/6 inhibitors (CDK4/6i) often involve a shift away from estrogen-driven proliferation. The nature and source of compensatory growth signals driving cancer proliferation remain unknown but represent direct therapeutic targets of resistant cells. By analyzing single-cell RNA-sequencing data from serial biopsies of patient tumors, we elucidated compensatory growth signaling pathways activated in ET + CDK4/6i-resistant cancer cells, along with the intercellular growth signal communications within the tumor microenvironment. In most patient tumors, resistant cancer cells increased ERBB growth pathway activity during treatment, only partially through ERBB receptor upregulation. Concurrently, fibroblasts within the tumor increased ERBB ligand communication with cancer cells, as they differentiated to a proliferative and mesenchymal phenotype in response to TGF β signals from cancer cells. In vitro model systems demonstrated molecularly how therapy induces a mutualistic cycle of crosstalk between cancer cells and fibroblasts, fostering a growth factor-rich tumor microenvironment circumventing estrogen reliance. We show that ERBB inhibition can break this cancer-fibroblasts mutualism, targeting an acquired sensitivity of resistant cancer cells. Synopsis Serial single-cell RNA sequencing of estrogen receptor-positive (ER + ) breast tumors from multiple patient cohorts, combined with experimental analyses, uncovers molecular mechanisms of compensatory growth signaling that drive proliferation in endocrine +/- CDK4/6 inhibitor-resistant cancer cells. A shift to ERBB growth factor mediated proliferation away from estrogen signaling is observed in resistant cancer cells in most tumors during treatment, partially facilitated by ERBB receptor upregulation. Fibroblasts are stimulated by cancer cells exposed to endocrine therapy to differentiate and secrete ERBB ligands, which in turn crosstalk with ERBB receptors on cancer cells to drive growth. Mutualistic cancer-fibroblast crosstalk mechanisms, identified from patient samples, were verified across in vitro model systems, showing that ERBB growth factor-enrichment bypasses estrogen dependence. This cancer-fibroblast communication is blocked by pan-ERBB inhibitors, targeting an acquired sensitivity to overcome endocrine resistance. Serial single-cell RNA sequencing of estrogen receptor-positive (ER + ) breast tumors from multiple patient cohorts, combined with experimental analyses, uncovers molecular mechanisms of compensatory growth signaling that drives proliferation in endocrine +/- CDK4/6 inhibitor-resistant cancer cells. Abstract In early-stage estrogen receptor-positive (ER + ) breast cancer, resistance to endocrine therapy (ET) and CDK4/6 inhibitors (CDK4/6i) often involve a shift away from estrogen-driven proliferation. The nature and source of compensatory growth signals driving cancer proliferation remain unknown but represent direct therapeutic targets of resistant cells. By analyzing single-cell RNA-sequencing data from serial biopsies of patient tumors, we elucidated compensatory growth signaling pathways activated in ET + CDK4/6i-resistant cancer cells, along with the intercellular growth signal communications within the tumor microenvironment. In most patient tumors, resistant cancer cells increased ERBB growth pathway activity during treatment, only partially through ERBB receptor upregulation. Concurrently, fibroblasts within the tumor increased ERBB ligand communication with cancer cells, as they differentiated to a proliferative and mesenchymal phenotype in response to TGF $$\beta$$ β signals from cancer cells. In vitro model systems demonstrated molecularly how therapy induces a mutualistic cycle of crosstalk between cancer cells and fibroblasts, fostering a growth factor-rich tumor microenvironment circumventing estrogen reliance. We show that ERBB inhibition can break this cancer-fibroblasts mutualism, targeting an acquired sensitivity of resistant cancer cells. |
| Author | Adler, Frederick R Khan, Qamar J Bild, Andrea H Farmaki, Elena Chang, Jeffrey T Karimi, Kimya L Nath, Aritro Cosgrove, Patrick A Medina, Eric F Chen, Jinfeng Chi, Feng Grolmusz, Vince K Griffiths, Jason I |
| Author_xml | – sequence: 1 givenname: Jason I orcidid: 0000-0002-1667-8233 surname: Griffiths fullname: Griffiths, Jason I email: jasonigriff@gmail.com, jgriffiths@coh.org organization: Department of Medical Oncology & Therapeutics, City of Hope National Medical Center, Department of Mathematics, University of Utah 155 South 1400 East – sequence: 2 givenname: Feng surname: Chi fullname: Chi, Feng organization: Department of Medical Oncology & Therapeutics, City of Hope National Medical Center – sequence: 3 givenname: Elena surname: Farmaki fullname: Farmaki, Elena organization: Department of Medical Oncology & Therapeutics, City of Hope National Medical Center – sequence: 4 givenname: Eric F surname: Medina fullname: Medina, Eric F organization: Department of Medical Oncology & Therapeutics, City of Hope National Medical Center – sequence: 5 givenname: Patrick A orcidid: 0000-0001-7784-7785 surname: Cosgrove fullname: Cosgrove, Patrick A organization: Department of Medical Oncology & Therapeutics, City of Hope National Medical Center – sequence: 6 givenname: Kimya L orcidid: 0000-0003-0070-2224 surname: Karimi fullname: Karimi, Kimya L organization: Department of Medical Oncology & Therapeutics, City of Hope National Medical Center – sequence: 7 givenname: Jinfeng surname: Chen fullname: Chen, Jinfeng organization: Department of Medical Oncology & Therapeutics, City of Hope National Medical Center – sequence: 8 givenname: Vince K orcidid: 0000-0002-5677-895X surname: Grolmusz fullname: Grolmusz, Vince K organization: Department of Medical Oncology & Therapeutics, City of Hope National Medical Center – sequence: 9 givenname: Frederick R surname: Adler fullname: Adler, Frederick R organization: Department of Mathematics, University of Utah 155 South 1400 East, School of Biological Sciences, University of Utah 257 South 1400 East – sequence: 10 givenname: Qamar J surname: Khan fullname: Khan, Qamar J organization: Division of Medical Oncology, Department of Internal Medicine, The University of Kansas Medical Center – sequence: 11 givenname: Aritro surname: Nath fullname: Nath, Aritro organization: Department of Medical Oncology & Therapeutics, City of Hope National Medical Center – sequence: 12 givenname: Jeffrey T orcidid: 0000-0002-4578-5636 surname: Chang fullname: Chang, Jeffrey T organization: Department of Integrative Biology and Pharmacology, School of Medicine, School of Biomedical Informatics, UT Health Science Center at Houston – sequence: 13 givenname: Andrea H orcidid: 0000-0003-4850-0453 surname: Bild fullname: Bild, Andrea H email: abild@coh.org organization: Department of Medical Oncology & Therapeutics, City of Hope National Medical Center |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/40341770$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1016/j.celrep.2018.10.047 10.1038/nbt.4314 10.1016/j.ccell.2020.06.005 10.1038/s41590-018-0276-y 10.1002/lsm.1900080106 10.1016/j.semcancer.2013.12.008 10.1038/nrc1477 10.17504/protocols.io.t3aeqie 10.3389/fimmu.2022.1026954 10.1038/cddis.2017.42 10.1093/bioinformatics/btr260 10.1074/jbc.M111.226563 10.1186/s13059-018-1593-z 10.1038/nm.1951 10.3390/cancers12103029 10.4049/jimmunol.0802703 10.1172/JCI30740 10.3390/cancers14163906 10.1007/s10549-012-2289-9 10.3390/cancers9050052 10.3389/fonc.2019.00718 10.1038/s41467-018-08188-5 10.18637/jss.v067.i01 10.1016/S0140-6736(05)66544-0 10.1186/1471-2105-14-7 10.1038/nmeth.3137 10.1038/s43018-021-00215-7 10.18637/jss.v082.i13 10.1038/s41467-017-02554-5 10.1038/s41698-017-0017-y 10.1093/bib/bbab039 10.1038/s41467-020-14766-3 10.1038/s41467-023-39242-6 10.1016/j.ccell.2020.03.009 10.1158/1055-9965.EPI-18-0863 10.1016/j.isci.2019.07.034 10.1056/NEJM199811263392207 10.1186/s12943-015-0291-7 10.1038/ncomms8866 10.3390/cancers11020189 10.1038/s41388-021-01719-3 10.1038/s41392-021-00641-0 10.1042/CS20220472 10.1038/sdata.2017.166 10.1200/JCO.20.03639 10.1093/jnci/djx131 10.3390/cancers14153570 10.1530/JME-15-0310 10.2307/2530044 10.1200/JCO.2020.38.15_suppl.505 10.1073/pnas.1910420116 10.1038/mt.2008.6 10.1056/NEJMoa2203690 10.3390/biom10121666 10.1186/s12935-020-01337-1 10.1038/srep05853 10.1038/s41467-025-56279-x 10.1186/s13058-022-01510-6 10.1016/0169-5347(94)90088-4 10.1016/j.bioorg.2017.02.011 10.15252/embj.2019104063 10.1042/BST20160387 10.5061/dryad.03n60 10.3389/fendo.2019.00245 10.1111/jvs.12123 10.2353/ajpath.2010.090802 10.1200/JCO.20.02514 10.1074/jbc.M113.451336 10.3390/ijms21176400 10.1038/s41576-020-00292-x 10.3390/cancers12051232 10.1093/bioinformatics/btt656 10.18632/oncotarget.12207 10.1016/S1470-2045(20)30642-2 10.1038/s41598-019-53549-9 10.1016/j.tree.2008.10.008 10.1186/bcr42 10.3390/ijms21062011 |
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| Keywords | Cancer-fibroblast-mutualism TME-communication ERBB Signaling Endocrine Resistance |
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| References | CR Henderson (104_CR31) 1982; 38 MM Mueller (104_CR56) 2004; 4 K Weber (104_CR76) 2008; 16 JI Griffiths (104_CR23) 2021; 2 MA Schumacher (104_CR69) 2017; 8 S Almaraz Postigo (104_CR2) 2023; 137 X Liu (104_CR47) 2021; 22 S Loibl (104_CR48) 2021; 39 S Navid (104_CR57) 2020; 21 M Hafner (104_CR27) 2017; 4 GH Heppner (104_CR32) 2014; 28 QJ Khan (104_CR38) 2020; 38 D Bates (104_CR6) 2015; 67 H Masuda (104_CR50) 2012; 136 A Ootani (104_CR58) 2009; 15 X Ren (104_CR64) 2018; 19 A Calon (104_CR12) 2014; 25 S Chatterjee (104_CR14) 2019; 19 R Michalet (104_CR53) 2014; 25 AC Midgley (104_CR54) 2013; 288 VK Grolmusz (104_CR25) 2020; 20 A Papait (104_CR60) 2022; 14 MP Rogers (104_CR66) 2022; 14 A Jameera Begam (104_CR33) 2017; 71 S Modi (104_CR55) 2022; 387 Y Liao (104_CR45) 2014; 30 104_CR24 SP Hammarlund (104_CR28) 2019; 116 M Kretzschmar (104_CR39) 2000; 2 A Dominiak (104_CR16) 2020; 12 RC Ekyalongo (104_CR18) 2017; 1 104_CR26 UE Martinez-Outschoorn (104_CR49) 2019; 9 D Aran (104_CR3) 2019; 20 A Rani (104_CR63) 2019; 10 Z Zhang (104_CR82) 2020; 38 E Armingol (104_CR4) 2021; 22 JP Edwards (104_CR17) 2009; 182 S Hänzelmann (104_CR30) 2013; 14 MP Kumar (104_CR41) 2018; 25 F Wu (104_CR79) 2021; 6 H Zhao (104_CR83) 2016; 57 V Erba (104_CR20) 2019; 9 C Kerneur (104_CR36) 2022; 13 K Van den Berge (104_CR74) 2020; 11 EL Mayer (104_CR51) 2021; 22 S Biswas (104_CR10) 2007; 117 JA Ramilowski (104_CR62) 2015; 6 B Erdogan (104_CR21) 2017; 45 MD Bertness (104_CR9) 1994; 9 RA Glabman (104_CR22) 2022; 14 X Shi (104_CR71) 2020; 10 PF Christopoulos (104_CR15) 2015; 14 MF Santolla (104_CR68) 2020; 12 104_CR37 W Zhang (104_CR81) 2016; 7 M Piezzo (104_CR61) 2020; 21 104_CR70 S Meran (104_CR52) 2011; 286 D Risso (104_CR65) 2018; 9 KH Kensler (104_CR35) 2019; 28 GM LaMuraglia (104_CR43) 1988; 8 104_CR73 A Kuznetsova (104_CR42) 2017; 82 B Rozeboom (104_CR67) 2019; 9 M Berdiel-Acer (104_CR8) 2021; 40 104_CR1 M Krzywinski (104_CR40) 2014; 11 A Liberzon (104_CR46) 2011; 27 104_CR7 104_CR5 RML Simpson (104_CR72) 2010; 176 SRD Johnston (104_CR34) 2020; 38 F Wu (104_CR78) 2019; 10 R Emond (104_CR19) 2023; 14 104_CR84 AM Castellaro (104_CR13) 2019; 11 CK Osborne (104_CR59) 1998; 339 SZ Wu (104_CR80) 2020; 39 E Lee (104_CR44) 2014; 4 AC Watt (104_CR75) 2022; 24 BM Bolker (104_CR11) 2009; 24 AB Hanker (104_CR29) 2020; 37 P Wee (104_CR77) 2017; 9 |
| References_xml | – volume: 25 start-page: 1458 year: 2018 ident: 104_CR41 publication-title: Cell Rep doi: 10.1016/j.celrep.2018.10.047 – ident: 104_CR7 doi: 10.1038/nbt.4314 – volume: 38 start-page: 279 year: 2020 ident: 104_CR82 publication-title: Cancer Cell doi: 10.1016/j.ccell.2020.06.005 – volume: 20 start-page: 163 year: 2019 ident: 104_CR3 publication-title: Nat Immunol doi: 10.1038/s41590-018-0276-y – volume: 8 start-page: 18 year: 1988 ident: 104_CR43 publication-title: Lasers Surg Med doi: 10.1002/lsm.1900080106 – volume: 25 start-page: 15 year: 2014 ident: 104_CR12 publication-title: Semin Cancer Biol doi: 10.1016/j.semcancer.2013.12.008 – volume: 4 start-page: 839 year: 2004 ident: 104_CR56 publication-title: Nat Rev Cancer doi: 10.1038/nrc1477 – ident: 104_CR70 doi: 10.17504/protocols.io.t3aeqie – volume: 13 start-page: 1026954 year: 2022 ident: 104_CR36 publication-title: Front Immunol doi: 10.3389/fimmu.2022.1026954 – volume: 8 year: 2017 ident: 104_CR69 publication-title: Cell Death Dis doi: 10.1038/cddis.2017.42 – volume: 27 start-page: 1739 year: 2011 ident: 104_CR46 publication-title: Bioinformatics doi: 10.1093/bioinformatics/btr260 – ident: 104_CR37 – volume: 286 start-page: 17618 year: 2011 ident: 104_CR52 publication-title: J Biol Chem doi: 10.1074/jbc.M111.226563 – volume: 19 year: 2018 ident: 104_CR64 publication-title: Genome Biol doi: 10.1186/s13059-018-1593-z – volume: 15 start-page: 701 year: 2009 ident: 104_CR58 publication-title: Nat Med doi: 10.1038/nm.1951 – volume: 12 start-page: 3029 year: 2020 ident: 104_CR68 publication-title: Cancers doi: 10.3390/cancers12103029 – volume: 182 start-page: 1929 year: 2009 ident: 104_CR17 publication-title: J Immunol doi: 10.4049/jimmunol.0802703 – volume: 117 start-page: 1305 year: 2007 ident: 104_CR10 publication-title: J Clin Investig doi: 10.1172/JCI30740 – volume: 14 start-page: 3906 year: 2022 ident: 104_CR22 publication-title: Cancers doi: 10.3390/cancers14163906 – volume: 136 start-page: 331 year: 2012 ident: 104_CR50 publication-title: Breast Cancer Res Treat doi: 10.1007/s10549-012-2289-9 – volume: 9 start-page: 52 year: 2017 ident: 104_CR77 publication-title: Cancers doi: 10.3390/cancers9050052 – volume: 9 start-page: 718 year: 2019 ident: 104_CR49 publication-title: Front Oncol doi: 10.3389/fonc.2019.00718 – volume: 10 year: 2019 ident: 104_CR78 publication-title: Nat Commun doi: 10.1038/s41467-018-08188-5 – volume: 67 start-page: 1 year: 2015 ident: 104_CR6 publication-title: J Stat Softw doi: 10.18637/jss.v067.i01 – ident: 104_CR1 doi: 10.1016/S0140-6736(05)66544-0 – volume: 14 year: 2013 ident: 104_CR30 publication-title: BMC Bioinforma doi: 10.1186/1471-2105-14-7 – volume: 11 start-page: 977 year: 2014 ident: 104_CR40 publication-title: Nat Methods doi: 10.1038/nmeth.3137 – volume: 2 start-page: 658 year: 2021 ident: 104_CR23 publication-title: Nat Cancer doi: 10.1038/s43018-021-00215-7 – volume: 82 start-page: 1 year: 2017 ident: 104_CR42 publication-title: J Stat Softw doi: 10.18637/jss.v082.i13 – volume: 9 year: 2018 ident: 104_CR65 publication-title: Nat Commun doi: 10.1038/s41467-017-02554-5 – volume: 1 year: 2017 ident: 104_CR18 publication-title: NPJ Precis Oncol doi: 10.1038/s41698-017-0017-y – volume: 22 start-page: bbab039 year: 2021 ident: 104_CR47 publication-title: Brief Bioinform doi: 10.1093/bib/bbab039 – volume: 11 year: 2020 ident: 104_CR74 publication-title: Nat Commun doi: 10.1038/s41467-020-14766-3 – volume: 14 year: 2023 ident: 104_CR19 publication-title: Nat Commun doi: 10.1038/s41467-023-39242-6 – volume: 37 start-page: 496 year: 2020 ident: 104_CR29 publication-title: Cancer Cell doi: 10.1016/j.ccell.2020.03.009 – volume: 28 start-page: 798 year: 2019 ident: 104_CR35 publication-title: Cancer Epidemiol Biomark Prev doi: 10.1158/1055-9965.EPI-18-0863 – volume: 19 start-page: 388 year: 2019 ident: 104_CR14 publication-title: iScience doi: 10.1016/j.isci.2019.07.034 – volume: 339 start-page: 1609 year: 1998 ident: 104_CR59 publication-title: New Engl J Med doi: 10.1056/NEJM199811263392207 – volume: 14 year: 2015 ident: 104_CR15 publication-title: Mol Cancer doi: 10.1186/s12943-015-0291-7 – volume: 6 year: 2015 ident: 104_CR62 publication-title: Nat Commun doi: 10.1038/ncomms8866 – volume: 11 start-page: 189 year: 2019 ident: 104_CR13 publication-title: Cancers doi: 10.3390/cancers11020189 – volume: 40 start-page: 2651 year: 2021 ident: 104_CR8 publication-title: Oncogene doi: 10.1038/s41388-021-01719-3 – volume: 6 start-page: 218 year: 2021 ident: 104_CR79 publication-title: Signal Transduct Target Ther doi: 10.1038/s41392-021-00641-0 – volume: 137 start-page: 1 year: 2023 ident: 104_CR2 publication-title: Clin Sci doi: 10.1042/CS20220472 – volume: 4 year: 2017 ident: 104_CR27 publication-title: Sci Data doi: 10.1038/sdata.2017.166 – volume: 39 start-page: 1518 year: 2021 ident: 104_CR48 publication-title: J Clin Oncol doi: 10.1200/JCO.20.03639 – ident: 104_CR5 doi: 10.1093/jnci/djx131 – volume: 14 start-page: 3570 year: 2022 ident: 104_CR60 publication-title: Cancers doi: 10.3390/cancers14153570 – volume: 57 start-page: R19 year: 2016 ident: 104_CR83 publication-title: J Mol Endocrinol doi: 10.1530/JME-15-0310 – volume: 38 start-page: 623 year: 1982 ident: 104_CR31 publication-title: Biometrics doi: 10.2307/2530044 – volume: 38 start-page: 505 year: 2020 ident: 104_CR38 publication-title: J Clin Oncol doi: 10.1200/JCO.2020.38.15_suppl.505 – volume: 116 start-page: 15760 year: 2019 ident: 104_CR28 publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.1910420116 – volume: 9 start-page: 2821 year: 2019 ident: 104_CR67 publication-title: Am J Cancer Res – volume: 16 start-page: 698 year: 2008 ident: 104_CR76 publication-title: Mol Ther doi: 10.1038/mt.2008.6 – volume: 387 start-page: 9 year: 2022 ident: 104_CR55 publication-title: New Engl J Med doi: 10.1056/NEJMoa2203690 – volume: 10 start-page: 1666 year: 2020 ident: 104_CR71 publication-title: Biomolecules doi: 10.3390/biom10121666 – volume: 14 start-page: e29354 year: 2022 ident: 104_CR66 publication-title: Cureus – volume: 20 year: 2020 ident: 104_CR25 publication-title: Cancer Cell Int doi: 10.1186/s12935-020-01337-1 – volume: 4 year: 2014 ident: 104_CR44 publication-title: Sci Rep doi: 10.1038/srep05853 – ident: 104_CR24 doi: 10.1038/s41467-025-56279-x – volume: 24 year: 2022 ident: 104_CR75 publication-title: Breast Cancer Res doi: 10.1186/s13058-022-01510-6 – volume: 9 start-page: 191 year: 1994 ident: 104_CR9 publication-title: Trends Ecol Evol doi: 10.1016/0169-5347(94)90088-4 – volume: 71 start-page: 257 year: 2017 ident: 104_CR33 publication-title: Bioorg Chem doi: 10.1016/j.bioorg.2017.02.011 – volume: 39 year: 2020 ident: 104_CR80 publication-title: EMBO J doi: 10.15252/embj.2019104063 – volume: 45 start-page: 229 year: 2017 ident: 104_CR21 publication-title: Biochem Soc Trans doi: 10.1042/BST20160387 – ident: 104_CR26 doi: 10.5061/dryad.03n60 – volume: 28 start-page: 780 year: 2014 ident: 104_CR32 publication-title: Oncology – volume: 10 start-page: 245 year: 2019 ident: 104_CR63 publication-title: Front Endocrinol doi: 10.3389/fendo.2019.00245 – ident: 104_CR73 – volume: 25 start-page: 609 year: 2014 ident: 104_CR53 publication-title: J Vegetation Sci doi: 10.1111/jvs.12123 – volume: 176 start-page: 1215 year: 2010 ident: 104_CR72 publication-title: Am J Pathol doi: 10.2353/ajpath.2010.090802 – ident: 104_CR84 – volume: 38 start-page: 3987 year: 2020 ident: 104_CR34 publication-title: J Clin Oncol doi: 10.1200/JCO.20.02514 – volume: 288 start-page: 14824 year: 2013 ident: 104_CR54 publication-title: J Biol Chem doi: 10.1074/jbc.M113.451336 – volume: 21 start-page: 6400 year: 2020 ident: 104_CR61 publication-title: Int J Mol Sci doi: 10.3390/ijms21176400 – volume: 22 start-page: 71 year: 2021 ident: 104_CR4 publication-title: Nat Rev Genet doi: 10.1038/s41576-020-00292-x – volume: 12 start-page: 1232 year: 2020 ident: 104_CR16 publication-title: Cancers doi: 10.3390/cancers12051232 – volume: 30 start-page: 923 year: 2014 ident: 104_CR45 publication-title: Bioinformatics doi: 10.1093/bioinformatics/btt656 – volume: 7 start-page: 75366 year: 2016 ident: 104_CR81 publication-title: Oncotarget doi: 10.18632/oncotarget.12207 – volume: 22 start-page: 212 year: 2021 ident: 104_CR51 publication-title: Lancet Oncol doi: 10.1016/S1470-2045(20)30642-2 – volume: 9 year: 2019 ident: 104_CR20 publication-title: Sci Rep doi: 10.1038/s41598-019-53549-9 – volume: 24 start-page: 127 year: 2009 ident: 104_CR11 publication-title: Trends Ecol Evol doi: 10.1016/j.tree.2008.10.008 – volume: 2 start-page: 107 year: 2000 ident: 104_CR39 publication-title: Breast Cancer Res doi: 10.1186/bcr42 – volume: 21 start-page: 2011 year: 2020 ident: 104_CR57 publication-title: Int J Mol Sci doi: 10.3390/ijms21062011 |
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| Snippet | In early-stage estrogen receptor-positive (ER + ) breast cancer, resistance to endocrine therapy (ET) and CDK4/6 inhibitors (CDK4/6i) often involve a shift... In early-stage estrogen receptor-positive (ER + ) breast cancer, resistance to endocrine therapy (ET) and CDK4/6 inhibitors (CDK4/6i) often involve a shift... Abstract In early-stage estrogen receptor-positive (ER + ) breast cancer, resistance to endocrine therapy (ET) and CDK4/6 inhibitors (CDK4/6i) often involve a... |
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| SubjectTerms | Antineoplastic Agents, Hormonal - pharmacology Biomedical and Life Sciences Breast Neoplasms - drug therapy Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology Cancer-Associated Fibroblasts - drug effects Cancer-Associated Fibroblasts - metabolism Cancer-Associated Fibroblasts - pathology Cancer-fibroblast-mutualism Cell Line, Tumor Cell Proliferation - drug effects Cyclin-Dependent Kinase 4 - antagonists & inhibitors Cyclin-Dependent Kinase 6 - antagonists & inhibitors Drug Resistance, Neoplasm - drug effects EMBO03 EMBO09 Endocrine Resistance ErbB Receptors - metabolism ERBB Signaling Female Fibroblasts - drug effects Fibroblasts - metabolism Gene Expression Regulation, Neoplastic - drug effects Humans Life Sciences Protein Kinase Inhibitors - pharmacology Signal Transduction - drug effects Systems Biology TME-communication Tumor Microenvironment - drug effects |
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| Title | Blocking cancer-fibroblast mutualism inhibits proliferation of endocrine therapy resistant breast cancer |
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