TRIM37 Promotes Pancreatic Cancer Progression through Modulation of Cell Growth, Migration, Invasion, and Tumor Immune Microenvironment
TRIM37 dysregulation has been observed in several cancer types, implicating its possible role in tumorigenesis. However, the role of TRIM37 in pancreatic cancer progression remains unclear. In the present study, we observed that TRIM37 knockdown resulted in reduced proliferation, clonogenicity, migr...
Gespeichert in:
| Veröffentlicht in: | International journal of molecular sciences 2022-01, Vol.23 (3), p.1176 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | |
|---|---|
| container_issue | 3 |
| container_start_page | 1176 |
| container_title | International journal of molecular sciences |
| container_volume | 23 |
| creator | Do, Tuyen Thi Yeh, Chun-Chieh Wu, Guo-Wei Hsu, Chia-Chen Chang, Hung-Chih Chen, Hui-Chen |
| description | TRIM37 dysregulation has been observed in several cancer types, implicating its possible role in tumorigenesis. However, the role of TRIM37 in pancreatic cancer progression remains unclear. In the present study, we observed that TRIM37 knockdown resulted in reduced proliferation, clonogenicity, migration, and invasion ability of pancreatic cancer cells. Furthermore, an in vivo study using an orthotopic syngeneic animal model further confirmed that reduced expression of TRIM37 in cancer cells suppressed tumor growth in vivo. Moreover, in mice bearing TRIM37 knockdown pancreatic cancer cells, the proportion of CD11b
F4/80
MHCII
immunosuppressive macrophages was significantly reduced in tumor milieu, which might be due to the regulatory role of TRIM37 in cytokine production by pancreatic cancer cells. Collectively, these findings suggest a key role of TRIM37 in promoting pancreatic cancer progression. |
| doi_str_mv | 10.3390/ijms23031176 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8835669</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2629058524</sourcerecordid><originalsourceid>FETCH-LOGICAL-c412t-99d03676e862da4ccf82b22487f0a77f0c9d9970cd503cf3d3b8bfa0335d9aca3</originalsourceid><addsrcrecordid>eNpdkUFvGyEQhVHVqkmT3nqukHrpwW5ZZheWS6XIalNLsRJVzhlhYG2sBVLYddVfkL8d7KSRmws8MZ_eMPMQ-lCRLwCCfHVbnykQqCrOXqHTqqZ0Sgjjr4_0CXqX85YQCrQRb9EJNBUDIvgpul_-mi-A45sUfRxsxjcq6GTV4DSeFWnTvrRONmcXAx42KY7rDV5EM_YFKk-xwzPb9_gyxT_DZoIXbp0OlQmeh53KB6WCwcvRx4Tn3o_BFkqnaMPOpRi8DcM5etOpPtv3T_cZuv3xfTn7Ob26vpzPLq6muq7oMBXCEGCc2ZZRo2qtu5auKK1b3hHFy6GFEYITbRoCugMDq3bVKQLQGKG0gjP07dH3blx5a3RpnVQv75LzKv2VUTn5fyW4jVzHnWxbaBgTxeDzk0GKv0ebB-ld1mUBKtg4ZkkZFaRpG1oX9NMLdBvHFMp4e4qzMsfBcPJIlYXknGz3_JmKyH3C8jjhgn88HuAZ_hcpPAB4m6Q-</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2627667669</pqid></control><display><type>article</type><title>TRIM37 Promotes Pancreatic Cancer Progression through Modulation of Cell Growth, Migration, Invasion, and Tumor Immune Microenvironment</title><source>MDPI - Multidisciplinary Digital Publishing Institute</source><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Do, Tuyen Thi ; Yeh, Chun-Chieh ; Wu, Guo-Wei ; Hsu, Chia-Chen ; Chang, Hung-Chih ; Chen, Hui-Chen</creator><creatorcontrib>Do, Tuyen Thi ; Yeh, Chun-Chieh ; Wu, Guo-Wei ; Hsu, Chia-Chen ; Chang, Hung-Chih ; Chen, Hui-Chen</creatorcontrib><description>TRIM37 dysregulation has been observed in several cancer types, implicating its possible role in tumorigenesis. However, the role of TRIM37 in pancreatic cancer progression remains unclear. In the present study, we observed that TRIM37 knockdown resulted in reduced proliferation, clonogenicity, migration, and invasion ability of pancreatic cancer cells. Furthermore, an in vivo study using an orthotopic syngeneic animal model further confirmed that reduced expression of TRIM37 in cancer cells suppressed tumor growth in vivo. Moreover, in mice bearing TRIM37 knockdown pancreatic cancer cells, the proportion of CD11b
F4/80
MHCII
immunosuppressive macrophages was significantly reduced in tumor milieu, which might be due to the regulatory role of TRIM37 in cytokine production by pancreatic cancer cells. Collectively, these findings suggest a key role of TRIM37 in promoting pancreatic cancer progression.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms23031176</identifier><identifier>PMID: 35163097</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Animal models ; Animals ; Apoptosis ; Cancer therapies ; CD11b antigen ; Cell adhesion & migration ; Cell growth ; Cell Movement ; Cell Proliferation ; Chemokines ; Cloning ; Cytokines ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; In vivo methods and tests ; Localization ; Lung cancer ; Macrophages ; Mice ; Mice, Inbred C57BL ; Microenvironments ; Mutation ; Neoplasm Invasiveness ; Pancreatic cancer ; Pancreatic Neoplasms - genetics ; Pancreatic Neoplasms - metabolism ; Pancreatic Neoplasms - pathology ; Protein expression ; Proteins ; Regulation ; Tripartite Motif Proteins - genetics ; Tripartite Motif Proteins - metabolism ; Tumor Cells, Cultured ; Tumor Microenvironment ; Tumorigenesis ; Tumors ; Ubiquitin-Protein Ligases - genetics ; Ubiquitin-Protein Ligases - metabolism ; Wound healing ; Xenograft Model Antitumor Assays</subject><ispartof>International journal of molecular sciences, 2022-01, Vol.23 (3), p.1176</ispartof><rights>2022 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://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c412t-99d03676e862da4ccf82b22487f0a77f0c9d9970cd503cf3d3b8bfa0335d9aca3</citedby><cites>FETCH-LOGICAL-c412t-99d03676e862da4ccf82b22487f0a77f0c9d9970cd503cf3d3b8bfa0335d9aca3</cites><orcidid>0000-0001-9405-4170 ; 0000-0001-9751-5729 ; 0000-0001-6753-7564</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8835669/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8835669/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35163097$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Do, Tuyen Thi</creatorcontrib><creatorcontrib>Yeh, Chun-Chieh</creatorcontrib><creatorcontrib>Wu, Guo-Wei</creatorcontrib><creatorcontrib>Hsu, Chia-Chen</creatorcontrib><creatorcontrib>Chang, Hung-Chih</creatorcontrib><creatorcontrib>Chen, Hui-Chen</creatorcontrib><title>TRIM37 Promotes Pancreatic Cancer Progression through Modulation of Cell Growth, Migration, Invasion, and Tumor Immune Microenvironment</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>TRIM37 dysregulation has been observed in several cancer types, implicating its possible role in tumorigenesis. However, the role of TRIM37 in pancreatic cancer progression remains unclear. In the present study, we observed that TRIM37 knockdown resulted in reduced proliferation, clonogenicity, migration, and invasion ability of pancreatic cancer cells. Furthermore, an in vivo study using an orthotopic syngeneic animal model further confirmed that reduced expression of TRIM37 in cancer cells suppressed tumor growth in vivo. Moreover, in mice bearing TRIM37 knockdown pancreatic cancer cells, the proportion of CD11b
F4/80
MHCII
immunosuppressive macrophages was significantly reduced in tumor milieu, which might be due to the regulatory role of TRIM37 in cytokine production by pancreatic cancer cells. Collectively, these findings suggest a key role of TRIM37 in promoting pancreatic cancer progression.</description><subject>Animal models</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Cancer therapies</subject><subject>CD11b antigen</subject><subject>Cell adhesion & migration</subject><subject>Cell growth</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Chemokines</subject><subject>Cloning</subject><subject>Cytokines</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>In vivo methods and tests</subject><subject>Localization</subject><subject>Lung cancer</subject><subject>Macrophages</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Microenvironments</subject><subject>Mutation</subject><subject>Neoplasm Invasiveness</subject><subject>Pancreatic cancer</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Pancreatic Neoplasms - metabolism</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Regulation</subject><subject>Tripartite Motif Proteins - genetics</subject><subject>Tripartite Motif Proteins - metabolism</subject><subject>Tumor Cells, Cultured</subject><subject>Tumor Microenvironment</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><subject>Ubiquitin-Protein Ligases - genetics</subject><subject>Ubiquitin-Protein Ligases - metabolism</subject><subject>Wound healing</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkUFvGyEQhVHVqkmT3nqukHrpwW5ZZheWS6XIalNLsRJVzhlhYG2sBVLYddVfkL8d7KSRmws8MZ_eMPMQ-lCRLwCCfHVbnykQqCrOXqHTqqZ0Sgjjr4_0CXqX85YQCrQRb9EJNBUDIvgpul_-mi-A45sUfRxsxjcq6GTV4DSeFWnTvrRONmcXAx42KY7rDV5EM_YFKk-xwzPb9_gyxT_DZoIXbp0OlQmeh53KB6WCwcvRx4Tn3o_BFkqnaMPOpRi8DcM5etOpPtv3T_cZuv3xfTn7Ob26vpzPLq6muq7oMBXCEGCc2ZZRo2qtu5auKK1b3hHFy6GFEYITbRoCugMDq3bVKQLQGKG0gjP07dH3blx5a3RpnVQv75LzKv2VUTn5fyW4jVzHnWxbaBgTxeDzk0GKv0ebB-ld1mUBKtg4ZkkZFaRpG1oX9NMLdBvHFMp4e4qzMsfBcPJIlYXknGz3_JmKyH3C8jjhgn88HuAZ_hcpPAB4m6Q-</recordid><startdate>20220121</startdate><enddate>20220121</enddate><creator>Do, Tuyen Thi</creator><creator>Yeh, Chun-Chieh</creator><creator>Wu, Guo-Wei</creator><creator>Hsu, Chia-Chen</creator><creator>Chang, Hung-Chih</creator><creator>Chen, Hui-Chen</creator><general>MDPI AG</general><general>MDPI</general><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PIMPY</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-9405-4170</orcidid><orcidid>https://orcid.org/0000-0001-9751-5729</orcidid><orcidid>https://orcid.org/0000-0001-6753-7564</orcidid></search><sort><creationdate>20220121</creationdate><title>TRIM37 Promotes Pancreatic Cancer Progression through Modulation of Cell Growth, Migration, Invasion, and Tumor Immune Microenvironment</title><author>Do, Tuyen Thi ; Yeh, Chun-Chieh ; Wu, Guo-Wei ; Hsu, Chia-Chen ; Chang, Hung-Chih ; Chen, Hui-Chen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c412t-99d03676e862da4ccf82b22487f0a77f0c9d9970cd503cf3d3b8bfa0335d9aca3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Animal models</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Cancer therapies</topic><topic>CD11b antigen</topic><topic>Cell adhesion & migration</topic><topic>Cell growth</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Chemokines</topic><topic>Cloning</topic><topic>Cytokines</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>In vivo methods and tests</topic><topic>Localization</topic><topic>Lung cancer</topic><topic>Macrophages</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Microenvironments</topic><topic>Mutation</topic><topic>Neoplasm Invasiveness</topic><topic>Pancreatic cancer</topic><topic>Pancreatic Neoplasms - genetics</topic><topic>Pancreatic Neoplasms - metabolism</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>Regulation</topic><topic>Tripartite Motif Proteins - genetics</topic><topic>Tripartite Motif Proteins - metabolism</topic><topic>Tumor Cells, Cultured</topic><topic>Tumor Microenvironment</topic><topic>Tumorigenesis</topic><topic>Tumors</topic><topic>Ubiquitin-Protein Ligases - genetics</topic><topic>Ubiquitin-Protein Ligases - metabolism</topic><topic>Wound healing</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Do, Tuyen Thi</creatorcontrib><creatorcontrib>Yeh, Chun-Chieh</creatorcontrib><creatorcontrib>Wu, Guo-Wei</creatorcontrib><creatorcontrib>Hsu, Chia-Chen</creatorcontrib><creatorcontrib>Chang, Hung-Chih</creatorcontrib><creatorcontrib>Chen, Hui-Chen</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Do, Tuyen Thi</au><au>Yeh, Chun-Chieh</au><au>Wu, Guo-Wei</au><au>Hsu, Chia-Chen</au><au>Chang, Hung-Chih</au><au>Chen, Hui-Chen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TRIM37 Promotes Pancreatic Cancer Progression through Modulation of Cell Growth, Migration, Invasion, and Tumor Immune Microenvironment</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2022-01-21</date><risdate>2022</risdate><volume>23</volume><issue>3</issue><spage>1176</spage><pages>1176-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>TRIM37 dysregulation has been observed in several cancer types, implicating its possible role in tumorigenesis. However, the role of TRIM37 in pancreatic cancer progression remains unclear. In the present study, we observed that TRIM37 knockdown resulted in reduced proliferation, clonogenicity, migration, and invasion ability of pancreatic cancer cells. Furthermore, an in vivo study using an orthotopic syngeneic animal model further confirmed that reduced expression of TRIM37 in cancer cells suppressed tumor growth in vivo. Moreover, in mice bearing TRIM37 knockdown pancreatic cancer cells, the proportion of CD11b
F4/80
MHCII
immunosuppressive macrophages was significantly reduced in tumor milieu, which might be due to the regulatory role of TRIM37 in cytokine production by pancreatic cancer cells. Collectively, these findings suggest a key role of TRIM37 in promoting pancreatic cancer progression.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>35163097</pmid><doi>10.3390/ijms23031176</doi><orcidid>https://orcid.org/0000-0001-9405-4170</orcidid><orcidid>https://orcid.org/0000-0001-9751-5729</orcidid><orcidid>https://orcid.org/0000-0001-6753-7564</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1422-0067 |
| ispartof | International journal of molecular sciences, 2022-01, Vol.23 (3), p.1176 |
| issn | 1422-0067 1661-6596 1422-0067 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8835669 |
| source | MDPI - Multidisciplinary Digital Publishing Institute; MEDLINE; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Animal models Animals Apoptosis Cancer therapies CD11b antigen Cell adhesion & migration Cell growth Cell Movement Cell Proliferation Chemokines Cloning Cytokines Female Gene Expression Regulation, Neoplastic Humans In vivo methods and tests Localization Lung cancer Macrophages Mice Mice, Inbred C57BL Microenvironments Mutation Neoplasm Invasiveness Pancreatic cancer Pancreatic Neoplasms - genetics Pancreatic Neoplasms - metabolism Pancreatic Neoplasms - pathology Protein expression Proteins Regulation Tripartite Motif Proteins - genetics Tripartite Motif Proteins - metabolism Tumor Cells, Cultured Tumor Microenvironment Tumorigenesis Tumors Ubiquitin-Protein Ligases - genetics Ubiquitin-Protein Ligases - metabolism Wound healing Xenograft Model Antitumor Assays |
| title | TRIM37 Promotes Pancreatic Cancer Progression through Modulation of Cell Growth, Migration, Invasion, and Tumor Immune Microenvironment |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-19T00%3A28%3A57IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=TRIM37%20Promotes%20Pancreatic%20Cancer%20Progression%20through%20Modulation%20of%20Cell%20Growth,%20Migration,%20Invasion,%20and%20Tumor%20Immune%20Microenvironment&rft.jtitle=International%20journal%20of%20molecular%20sciences&rft.au=Do,%20Tuyen%20Thi&rft.date=2022-01-21&rft.volume=23&rft.issue=3&rft.spage=1176&rft.pages=1176-&rft.issn=1422-0067&rft.eissn=1422-0067&rft_id=info:doi/10.3390/ijms23031176&rft_dat=%3Cproquest_pubme%3E2629058524%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2627667669&rft_id=info:pmid/35163097&rfr_iscdi=true |