ERRα Expression in Bone Metastases Leads to an Exacerbated Antitumor Immune Response
Bone is the most common metastatic site for breast cancer. Although the estrogen-related receptor alpha (ERRα) has been implicated in breast cancer cell dissemination to the bone from the primary tumor, its role after tumor cell anchorage in the bone microenvironment remains elusive. Here, we reveal...
Gespeichert in:
| Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 2020-07, Vol.80 (13), p.2914-2926 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 2926 |
|---|---|
| container_issue | 13 |
| container_start_page | 2914 |
| container_title | Cancer research (Chicago, Ill.) |
| container_volume | 80 |
| creator | Bouchet, Mathilde Lainé, Alexandra Boyault, Cyril Proponnet-Guerault, Mathilde Meugnier, Emmanuelle Bouazza, Lamia Kan, Casina W S Geraci, Sandra El-Moghrabi, Soumaya Hernandez-Vargas, Hector Benetollo, Claire Yoshiko, Yuji Duterque-Coquillaud, Martine Clézardin, Philippe Marie, Julien C Bonnelye, Edith |
| description | Bone is the most common metastatic site for breast cancer. Although the estrogen-related receptor alpha (ERRα) has been implicated in breast cancer cell dissemination to the bone from the primary tumor, its role after tumor cell anchorage in the bone microenvironment remains elusive. Here, we reveal that ERRα inhibits the progression of bone metastases of breast cancer cells by increasing the immune activity of the bone microenvironment. Overexpression of ERRα in breast cancer bone metastases induced expression of chemokines CCL17 and CCL20 and repressed production of TGFβ3. Subsequently, CD8
T lymphocytes recruited to bone metastases escaped TGFβ signaling control and were endowed with exacerbated cytotoxic features, resulting in significant reduction in metastases. The clinical relevance of our findings in mice was confirmed in over 240 patients with breast cancer. Thus, this study reveals that ERRα regulates immune properties in the bone microenvironment that contributes to decreasing metastatic growth. SIGNIFICANCE: This study places ERRα at the interplay between the immune response and bone metastases of breast cancer, highlighting a potential target for intervention in advanced disease. |
| doi_str_mv | 10.1158/0008-5472.CAN-19-3584 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2398629455</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2398629455</sourcerecordid><originalsourceid>FETCH-LOGICAL-c286t-43b935b1b062dd7f062fb4842764f83f307a196494de335999deb1d31d12c96a3</originalsourceid><addsrcrecordid>eNo9kNtKAzEQhoMotlYfQcmlN1uTzWGTy1qqFqpCsdchu5mFle7BZBf0sXwRn8ks1sLAz8D3z8CH0DUlc0qFuiOEqETwLJ0vFy8J1QkTip-gKRVMJRnn4hRNj8wEXYTwHldBiThHE5YyKXkmp2i32m5_vvHqs_MQQtU2uGrwfdsAfobehjgQ8AasC7hvsW0iaQvwue3B4UXTV_1Qtx6v63qInS2Erm0CXKKz0u4DXB1yhnYPq7flU7J5fVwvF5ukSJXsE85yzUROcyJT57IyRplzxdNM8lKxkpHMUi255g4YE1prBzl1jDqaFlpaNkO3f3c7334MEHpTV6GA_d420A7BpEwrmWouRETFH1r4NgQPpel8VVv_ZSgxo1Ez2jKjLRONGqrNaDT2bg4vhrwGd2z9K2S_XTRxSg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2398629455</pqid></control><display><type>article</type><title>ERRα Expression in Bone Metastases Leads to an Exacerbated Antitumor Immune Response</title><source>MEDLINE</source><source>American Association for Cancer Research</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><creator>Bouchet, Mathilde ; Lainé, Alexandra ; Boyault, Cyril ; Proponnet-Guerault, Mathilde ; Meugnier, Emmanuelle ; Bouazza, Lamia ; Kan, Casina W S ; Geraci, Sandra ; El-Moghrabi, Soumaya ; Hernandez-Vargas, Hector ; Benetollo, Claire ; Yoshiko, Yuji ; Duterque-Coquillaud, Martine ; Clézardin, Philippe ; Marie, Julien C ; Bonnelye, Edith</creator><creatorcontrib>Bouchet, Mathilde ; Lainé, Alexandra ; Boyault, Cyril ; Proponnet-Guerault, Mathilde ; Meugnier, Emmanuelle ; Bouazza, Lamia ; Kan, Casina W S ; Geraci, Sandra ; El-Moghrabi, Soumaya ; Hernandez-Vargas, Hector ; Benetollo, Claire ; Yoshiko, Yuji ; Duterque-Coquillaud, Martine ; Clézardin, Philippe ; Marie, Julien C ; Bonnelye, Edith</creatorcontrib><description>Bone is the most common metastatic site for breast cancer. Although the estrogen-related receptor alpha (ERRα) has been implicated in breast cancer cell dissemination to the bone from the primary tumor, its role after tumor cell anchorage in the bone microenvironment remains elusive. Here, we reveal that ERRα inhibits the progression of bone metastases of breast cancer cells by increasing the immune activity of the bone microenvironment. Overexpression of ERRα in breast cancer bone metastases induced expression of chemokines CCL17 and CCL20 and repressed production of TGFβ3. Subsequently, CD8
T lymphocytes recruited to bone metastases escaped TGFβ signaling control and were endowed with exacerbated cytotoxic features, resulting in significant reduction in metastases. The clinical relevance of our findings in mice was confirmed in over 240 patients with breast cancer. Thus, this study reveals that ERRα regulates immune properties in the bone microenvironment that contributes to decreasing metastatic growth. SIGNIFICANCE: This study places ERRα at the interplay between the immune response and bone metastases of breast cancer, highlighting a potential target for intervention in advanced disease.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>DOI: 10.1158/0008-5472.CAN-19-3584</identifier><identifier>PMID: 32366476</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Apoptosis ; Biomarkers, Tumor - genetics ; Biomarkers, Tumor - metabolism ; Bone Neoplasms - immunology ; Bone Neoplasms - metabolism ; Bone Neoplasms - prevention & control ; Bone Neoplasms - secondary ; Breast Neoplasms - immunology ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Breast Neoplasms - prevention & control ; Cell Proliferation ; Chemokine CCL17 - genetics ; Chemokine CCL17 - metabolism ; Chemokine CCL20 - genetics ; Chemokine CCL20 - metabolism ; ERRalpha Estrogen-Related Receptor ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Prognosis ; Receptors, Estrogen - genetics ; Receptors, Estrogen - metabolism ; Signal Transduction ; T-Lymphocytes - immunology ; Transforming Growth Factor beta3 - genetics ; Transforming Growth Factor beta3 - metabolism ; Tumor Cells, Cultured ; Tumor Microenvironment - immunology ; Xenograft Model Antitumor Assays</subject><ispartof>Cancer research (Chicago, Ill.), 2020-07, Vol.80 (13), p.2914-2926</ispartof><rights>2020 American Association for Cancer Research.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c286t-43b935b1b062dd7f062fb4842764f83f307a196494de335999deb1d31d12c96a3</citedby><cites>FETCH-LOGICAL-c286t-43b935b1b062dd7f062fb4842764f83f307a196494de335999deb1d31d12c96a3</cites><orcidid>0000-0002-4658-6655 ; 0000-0003-0149-4463 ; 0000-0001-6713-7923 ; 0000-0002-3298-5970 ; 0000-0003-0537-4506 ; 0000-0002-8367-6115 ; 0000-0003-2574-1246</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3343,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32366476$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bouchet, Mathilde</creatorcontrib><creatorcontrib>Lainé, Alexandra</creatorcontrib><creatorcontrib>Boyault, Cyril</creatorcontrib><creatorcontrib>Proponnet-Guerault, Mathilde</creatorcontrib><creatorcontrib>Meugnier, Emmanuelle</creatorcontrib><creatorcontrib>Bouazza, Lamia</creatorcontrib><creatorcontrib>Kan, Casina W S</creatorcontrib><creatorcontrib>Geraci, Sandra</creatorcontrib><creatorcontrib>El-Moghrabi, Soumaya</creatorcontrib><creatorcontrib>Hernandez-Vargas, Hector</creatorcontrib><creatorcontrib>Benetollo, Claire</creatorcontrib><creatorcontrib>Yoshiko, Yuji</creatorcontrib><creatorcontrib>Duterque-Coquillaud, Martine</creatorcontrib><creatorcontrib>Clézardin, Philippe</creatorcontrib><creatorcontrib>Marie, Julien C</creatorcontrib><creatorcontrib>Bonnelye, Edith</creatorcontrib><title>ERRα Expression in Bone Metastases Leads to an Exacerbated Antitumor Immune Response</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>Bone is the most common metastatic site for breast cancer. Although the estrogen-related receptor alpha (ERRα) has been implicated in breast cancer cell dissemination to the bone from the primary tumor, its role after tumor cell anchorage in the bone microenvironment remains elusive. Here, we reveal that ERRα inhibits the progression of bone metastases of breast cancer cells by increasing the immune activity of the bone microenvironment. Overexpression of ERRα in breast cancer bone metastases induced expression of chemokines CCL17 and CCL20 and repressed production of TGFβ3. Subsequently, CD8
T lymphocytes recruited to bone metastases escaped TGFβ signaling control and were endowed with exacerbated cytotoxic features, resulting in significant reduction in metastases. The clinical relevance of our findings in mice was confirmed in over 240 patients with breast cancer. Thus, this study reveals that ERRα regulates immune properties in the bone microenvironment that contributes to decreasing metastatic growth. SIGNIFICANCE: This study places ERRα at the interplay between the immune response and bone metastases of breast cancer, highlighting a potential target for intervention in advanced disease.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Bone Neoplasms - immunology</subject><subject>Bone Neoplasms - metabolism</subject><subject>Bone Neoplasms - prevention & control</subject><subject>Bone Neoplasms - secondary</subject><subject>Breast Neoplasms - immunology</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Breast Neoplasms - prevention & control</subject><subject>Cell Proliferation</subject><subject>Chemokine CCL17 - genetics</subject><subject>Chemokine CCL17 - metabolism</subject><subject>Chemokine CCL20 - genetics</subject><subject>Chemokine CCL20 - metabolism</subject><subject>ERRalpha Estrogen-Related Receptor</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Prognosis</subject><subject>Receptors, Estrogen - genetics</subject><subject>Receptors, Estrogen - metabolism</subject><subject>Signal Transduction</subject><subject>T-Lymphocytes - immunology</subject><subject>Transforming Growth Factor beta3 - genetics</subject><subject>Transforming Growth Factor beta3 - metabolism</subject><subject>Tumor Cells, Cultured</subject><subject>Tumor Microenvironment - immunology</subject><subject>Xenograft Model Antitumor Assays</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kNtKAzEQhoMotlYfQcmlN1uTzWGTy1qqFqpCsdchu5mFle7BZBf0sXwRn8ks1sLAz8D3z8CH0DUlc0qFuiOEqETwLJ0vFy8J1QkTip-gKRVMJRnn4hRNj8wEXYTwHldBiThHE5YyKXkmp2i32m5_vvHqs_MQQtU2uGrwfdsAfobehjgQ8AasC7hvsW0iaQvwue3B4UXTV_1Qtx6v63qInS2Erm0CXKKz0u4DXB1yhnYPq7flU7J5fVwvF5ukSJXsE85yzUROcyJT57IyRplzxdNM8lKxkpHMUi255g4YE1prBzl1jDqaFlpaNkO3f3c7334MEHpTV6GA_d420A7BpEwrmWouRETFH1r4NgQPpel8VVv_ZSgxo1Ez2jKjLRONGqrNaDT2bg4vhrwGd2z9K2S_XTRxSg</recordid><startdate>20200701</startdate><enddate>20200701</enddate><creator>Bouchet, Mathilde</creator><creator>Lainé, Alexandra</creator><creator>Boyault, Cyril</creator><creator>Proponnet-Guerault, Mathilde</creator><creator>Meugnier, Emmanuelle</creator><creator>Bouazza, Lamia</creator><creator>Kan, Casina W S</creator><creator>Geraci, Sandra</creator><creator>El-Moghrabi, Soumaya</creator><creator>Hernandez-Vargas, Hector</creator><creator>Benetollo, Claire</creator><creator>Yoshiko, Yuji</creator><creator>Duterque-Coquillaud, Martine</creator><creator>Clézardin, Philippe</creator><creator>Marie, Julien C</creator><creator>Bonnelye, Edith</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-4658-6655</orcidid><orcidid>https://orcid.org/0000-0003-0149-4463</orcidid><orcidid>https://orcid.org/0000-0001-6713-7923</orcidid><orcidid>https://orcid.org/0000-0002-3298-5970</orcidid><orcidid>https://orcid.org/0000-0003-0537-4506</orcidid><orcidid>https://orcid.org/0000-0002-8367-6115</orcidid><orcidid>https://orcid.org/0000-0003-2574-1246</orcidid></search><sort><creationdate>20200701</creationdate><title>ERRα Expression in Bone Metastases Leads to an Exacerbated Antitumor Immune Response</title><author>Bouchet, Mathilde ; Lainé, Alexandra ; Boyault, Cyril ; Proponnet-Guerault, Mathilde ; Meugnier, Emmanuelle ; Bouazza, Lamia ; Kan, Casina W S ; Geraci, Sandra ; El-Moghrabi, Soumaya ; Hernandez-Vargas, Hector ; Benetollo, Claire ; Yoshiko, Yuji ; Duterque-Coquillaud, Martine ; Clézardin, Philippe ; Marie, Julien C ; Bonnelye, Edith</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c286t-43b935b1b062dd7f062fb4842764f83f307a196494de335999deb1d31d12c96a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Bone Neoplasms - immunology</topic><topic>Bone Neoplasms - metabolism</topic><topic>Bone Neoplasms - prevention & control</topic><topic>Bone Neoplasms - secondary</topic><topic>Breast Neoplasms - immunology</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Breast Neoplasms - prevention & control</topic><topic>Cell Proliferation</topic><topic>Chemokine CCL17 - genetics</topic><topic>Chemokine CCL17 - metabolism</topic><topic>Chemokine CCL20 - genetics</topic><topic>Chemokine CCL20 - metabolism</topic><topic>ERRalpha Estrogen-Related Receptor</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Prognosis</topic><topic>Receptors, Estrogen - genetics</topic><topic>Receptors, Estrogen - metabolism</topic><topic>Signal Transduction</topic><topic>T-Lymphocytes - immunology</topic><topic>Transforming Growth Factor beta3 - genetics</topic><topic>Transforming Growth Factor beta3 - metabolism</topic><topic>Tumor Cells, Cultured</topic><topic>Tumor Microenvironment - immunology</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bouchet, Mathilde</creatorcontrib><creatorcontrib>Lainé, Alexandra</creatorcontrib><creatorcontrib>Boyault, Cyril</creatorcontrib><creatorcontrib>Proponnet-Guerault, Mathilde</creatorcontrib><creatorcontrib>Meugnier, Emmanuelle</creatorcontrib><creatorcontrib>Bouazza, Lamia</creatorcontrib><creatorcontrib>Kan, Casina W S</creatorcontrib><creatorcontrib>Geraci, Sandra</creatorcontrib><creatorcontrib>El-Moghrabi, Soumaya</creatorcontrib><creatorcontrib>Hernandez-Vargas, Hector</creatorcontrib><creatorcontrib>Benetollo, Claire</creatorcontrib><creatorcontrib>Yoshiko, Yuji</creatorcontrib><creatorcontrib>Duterque-Coquillaud, Martine</creatorcontrib><creatorcontrib>Clézardin, Philippe</creatorcontrib><creatorcontrib>Marie, Julien C</creatorcontrib><creatorcontrib>Bonnelye, Edith</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bouchet, Mathilde</au><au>Lainé, Alexandra</au><au>Boyault, Cyril</au><au>Proponnet-Guerault, Mathilde</au><au>Meugnier, Emmanuelle</au><au>Bouazza, Lamia</au><au>Kan, Casina W S</au><au>Geraci, Sandra</au><au>El-Moghrabi, Soumaya</au><au>Hernandez-Vargas, Hector</au><au>Benetollo, Claire</au><au>Yoshiko, Yuji</au><au>Duterque-Coquillaud, Martine</au><au>Clézardin, Philippe</au><au>Marie, Julien C</au><au>Bonnelye, Edith</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ERRα Expression in Bone Metastases Leads to an Exacerbated Antitumor Immune Response</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>2020-07-01</date><risdate>2020</risdate><volume>80</volume><issue>13</issue><spage>2914</spage><epage>2926</epage><pages>2914-2926</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><abstract>Bone is the most common metastatic site for breast cancer. Although the estrogen-related receptor alpha (ERRα) has been implicated in breast cancer cell dissemination to the bone from the primary tumor, its role after tumor cell anchorage in the bone microenvironment remains elusive. Here, we reveal that ERRα inhibits the progression of bone metastases of breast cancer cells by increasing the immune activity of the bone microenvironment. Overexpression of ERRα in breast cancer bone metastases induced expression of chemokines CCL17 and CCL20 and repressed production of TGFβ3. Subsequently, CD8
T lymphocytes recruited to bone metastases escaped TGFβ signaling control and were endowed with exacerbated cytotoxic features, resulting in significant reduction in metastases. The clinical relevance of our findings in mice was confirmed in over 240 patients with breast cancer. Thus, this study reveals that ERRα regulates immune properties in the bone microenvironment that contributes to decreasing metastatic growth. SIGNIFICANCE: This study places ERRα at the interplay between the immune response and bone metastases of breast cancer, highlighting a potential target for intervention in advanced disease.</abstract><cop>United States</cop><pmid>32366476</pmid><doi>10.1158/0008-5472.CAN-19-3584</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-4658-6655</orcidid><orcidid>https://orcid.org/0000-0003-0149-4463</orcidid><orcidid>https://orcid.org/0000-0001-6713-7923</orcidid><orcidid>https://orcid.org/0000-0002-3298-5970</orcidid><orcidid>https://orcid.org/0000-0003-0537-4506</orcidid><orcidid>https://orcid.org/0000-0002-8367-6115</orcidid><orcidid>https://orcid.org/0000-0003-2574-1246</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0008-5472 |
| ispartof | Cancer research (Chicago, Ill.), 2020-07, Vol.80 (13), p.2914-2926 |
| issn | 0008-5472 1538-7445 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2398629455 |
| source | MEDLINE; American Association for Cancer Research; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Animals Apoptosis Biomarkers, Tumor - genetics Biomarkers, Tumor - metabolism Bone Neoplasms - immunology Bone Neoplasms - metabolism Bone Neoplasms - prevention & control Bone Neoplasms - secondary Breast Neoplasms - immunology Breast Neoplasms - metabolism Breast Neoplasms - pathology Breast Neoplasms - prevention & control Cell Proliferation Chemokine CCL17 - genetics Chemokine CCL17 - metabolism Chemokine CCL20 - genetics Chemokine CCL20 - metabolism ERRalpha Estrogen-Related Receptor Female Gene Expression Regulation, Neoplastic Humans Mice Mice, Inbred BALB C Mice, Nude Prognosis Receptors, Estrogen - genetics Receptors, Estrogen - metabolism Signal Transduction T-Lymphocytes - immunology Transforming Growth Factor beta3 - genetics Transforming Growth Factor beta3 - metabolism Tumor Cells, Cultured Tumor Microenvironment - immunology Xenograft Model Antitumor Assays |
| title | ERRα Expression in Bone Metastases Leads to an Exacerbated Antitumor Immune Response |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-02T22%3A03%3A38IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=ERR%CE%B1%20Expression%20in%20Bone%20Metastases%20Leads%20to%20an%20Exacerbated%20Antitumor%20Immune%20Response&rft.jtitle=Cancer%20research%20(Chicago,%20Ill.)&rft.au=Bouchet,%20Mathilde&rft.date=2020-07-01&rft.volume=80&rft.issue=13&rft.spage=2914&rft.epage=2926&rft.pages=2914-2926&rft.issn=0008-5472&rft.eissn=1538-7445&rft_id=info:doi/10.1158/0008-5472.CAN-19-3584&rft_dat=%3Cproquest_cross%3E2398629455%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2398629455&rft_id=info:pmid/32366476&rfr_iscdi=true |