Raf kinase inhibitor protein (RKIP) deficiency decreases latency of tumorigenesis and increases metastasis in a murine genetic model of prostate cancer
BACKGROUND Raf kinase inhibitor protein (RKIP) has been shown to act as a metastasis suppressor gene in multiple models of cancer. Loss of RKIP expression promotes invasion and metastasis in cell transplantation animal models. However, it is unknown if RKIP expression can impact the progression of c...
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| Veröffentlicht in: | The Prostate 2015-02, Vol.75 (3), p.292-302 |
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| creator | Escara-Wilke, June Keller, Jill M. Ignatoski, Kathleen M. Woods Dai, Jinlu Shelley, Gregory Mizokami, Atsushi Zhang, Jian Yeung, Miranda L Yeung, Kam C. Keller, Evan T. |
| description | BACKGROUND
Raf kinase inhibitor protein (RKIP) has been shown to act as a metastasis suppressor gene in multiple models of cancer. Loss of RKIP expression promotes invasion and metastasis in cell transplantation animal models. However, it is unknown if RKIP expression can impact the progression of cancer in an autochthonous model of cancer. The goal of this study was to determine if loss of RKIP expression in a genetic mouse model of prostate cancer (PCa) impacts metastasis.
METHODS
Endogenous RKIP expression was measured in the primary tumors and metastases of transgenic adenocarcinoma of the mouse prostate (TRAMP+) mice. RKIP knockout mice (RKIP−/−) were crossbred with (TRAMP+) mice to create RKIP−/−TRAMP+ mice. Mice were euthanized at 10, 20, and 30 weeks for evaluation of primary and metastatic tumor development. To determine if loss of RKIP alone promotes metastasis, RKIP was knocked down in the low metastatic LNCaP prostate cancer cell line.
RESULTS
Endogenous RKIP expression decreased in TRAMP+ mice as tumors progressed. Primary tumors developed earlier in RKIP−/−TRAMP+ compared to TRAMP+ mice. At 30 weeks of age, distant metastases were identified only the RKIP−/−TRAMP+ mice. While prostate epithelial cell proliferation rates were higher at 10 and 20 weeks in RKIP−/−TRAMP+ compared to TRAMP+ mice, by 30 weeks there was no difference. Apoptosis rates in both groups were similar at all timepoints. Decreased RKIP expression did not impact the metastatic rate of LNCaP in an orthotopic PCa model.
CONCLUSIONS
These results demonstrate that loss of RKIP decreases latency of tumor development and promotes distant metastasis in the TRAMP mouse model in the context of a pro‐metastatic background; but loss of RKIP alone is insufficient to promote metastasis. These findings suggest that in addition to its known metastasis suppressor activity, RKIP may promote tumor progression through enhancing tumor initiation. Prostate 75:292–302, 2015. © 2014 Wiley Periodicals, Inc. |
| doi_str_mv | 10.1002/pros.22915 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1660393405</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1652398022</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4355-e5e5880f17349011b1c66d23be2d578a6ffb9eab938d05da9681f5f90c4dfb973</originalsourceid><addsrcrecordid>eNqNkd9qFDEUh4Modq3e-AAS8KYKU_N3Mrm0xa7FxZZV8TJkMieadiZTkxl0n8TXNdvt9sILEQIJOd_5wi8HoeeUHFNC2JubNOZjxjSVD9CCEq0qQoR8iBaEKVIJytUBepLzFSEFJ-wxOmCSM6UFXaDfa-vxdYg2Aw7xe2jDNCZcjBOEiI_WH84vX-EOfHABotuUo0tQ4Ix7O93ejB5P8zCm8A0i5JCxjV1R7bEBJpvLKoUitHiYU4iAt_AUHB7GDvqtYxtiKkrsbHSQnqJH3vYZnt3th-jL2bvPp--r1cXy_PTtqnKCS1mBBNk0xFPFhSaUttTVdcd4C6yTqrG1960G22redER2VtcN9dJr4kRXKoofoqOdt7z_Y4Y8mSFkB31vI4xzNrSuCddcEPkfqGRcN4Sxgr78C70a5xRLkEIJIXktNC_U6x3lSvacwJubFAabNoYSs52s2X6KuZ1sgV_cKed2gO4e3Y-yAHQH_Aw9bP6hMpfri097abXrCXmCX_c9Nl2bWnElzdePS7NeNSf87ESZJf8DTMy-tw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1644536493</pqid></control><display><type>article</type><title>Raf kinase inhibitor protein (RKIP) deficiency decreases latency of tumorigenesis and increases metastasis in a murine genetic model of prostate cancer</title><source>MEDLINE</source><source>Wiley Online Library All Journals</source><creator>Escara-Wilke, June ; Keller, Jill M. ; Ignatoski, Kathleen M. Woods ; Dai, Jinlu ; Shelley, Gregory ; Mizokami, Atsushi ; Zhang, Jian ; Yeung, Miranda L ; Yeung, Kam C. ; Keller, Evan T.</creator><creatorcontrib>Escara-Wilke, June ; Keller, Jill M. ; Ignatoski, Kathleen M. Woods ; Dai, Jinlu ; Shelley, Gregory ; Mizokami, Atsushi ; Zhang, Jian ; Yeung, Miranda L ; Yeung, Kam C. ; Keller, Evan T.</creatorcontrib><description>BACKGROUND
Raf kinase inhibitor protein (RKIP) has been shown to act as a metastasis suppressor gene in multiple models of cancer. Loss of RKIP expression promotes invasion and metastasis in cell transplantation animal models. However, it is unknown if RKIP expression can impact the progression of cancer in an autochthonous model of cancer. The goal of this study was to determine if loss of RKIP expression in a genetic mouse model of prostate cancer (PCa) impacts metastasis.
METHODS
Endogenous RKIP expression was measured in the primary tumors and metastases of transgenic adenocarcinoma of the mouse prostate (TRAMP+) mice. RKIP knockout mice (RKIP−/−) were crossbred with (TRAMP+) mice to create RKIP−/−TRAMP+ mice. Mice were euthanized at 10, 20, and 30 weeks for evaluation of primary and metastatic tumor development. To determine if loss of RKIP alone promotes metastasis, RKIP was knocked down in the low metastatic LNCaP prostate cancer cell line.
RESULTS
Endogenous RKIP expression decreased in TRAMP+ mice as tumors progressed. Primary tumors developed earlier in RKIP−/−TRAMP+ compared to TRAMP+ mice. At 30 weeks of age, distant metastases were identified only the RKIP−/−TRAMP+ mice. While prostate epithelial cell proliferation rates were higher at 10 and 20 weeks in RKIP−/−TRAMP+ compared to TRAMP+ mice, by 30 weeks there was no difference. Apoptosis rates in both groups were similar at all timepoints. Decreased RKIP expression did not impact the metastatic rate of LNCaP in an orthotopic PCa model.
CONCLUSIONS
These results demonstrate that loss of RKIP decreases latency of tumor development and promotes distant metastasis in the TRAMP mouse model in the context of a pro‐metastatic background; but loss of RKIP alone is insufficient to promote metastasis. These findings suggest that in addition to its known metastasis suppressor activity, RKIP may promote tumor progression through enhancing tumor initiation. Prostate 75:292–302, 2015. © 2014 Wiley Periodicals, Inc.</description><identifier>ISSN: 0270-4137</identifier><identifier>EISSN: 1097-0045</identifier><identifier>DOI: 10.1002/pros.22915</identifier><identifier>PMID: 25327941</identifier><identifier>CODEN: PRSTDS</identifier><language>eng</language><publisher>United States: Blackwell Publishing Ltd</publisher><subject>Adenocarcinoma - genetics ; Adenocarcinoma - pathology ; Animals ; Carcinogenesis - genetics ; Carcinogenesis - pathology ; Cell Line, Tumor ; Disease Models, Animal ; Disease Progression ; Humans ; LNCaP ; Male ; metastasis suppressor gene ; Mice ; Mice, Knockout ; Neoplasm Metastasis - genetics ; Neoplasm Metastasis - pathology ; Phosphatidylethanolamine Binding Protein - genetics ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - pathology ; TRAMP model</subject><ispartof>The Prostate, 2015-02, Vol.75 (3), p.292-302</ispartof><rights>2014 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4355-e5e5880f17349011b1c66d23be2d578a6ffb9eab938d05da9681f5f90c4dfb973</citedby><cites>FETCH-LOGICAL-c4355-e5e5880f17349011b1c66d23be2d578a6ffb9eab938d05da9681f5f90c4dfb973</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fpros.22915$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fpros.22915$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27923,27924,45573,45574</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25327941$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Escara-Wilke, June</creatorcontrib><creatorcontrib>Keller, Jill M.</creatorcontrib><creatorcontrib>Ignatoski, Kathleen M. Woods</creatorcontrib><creatorcontrib>Dai, Jinlu</creatorcontrib><creatorcontrib>Shelley, Gregory</creatorcontrib><creatorcontrib>Mizokami, Atsushi</creatorcontrib><creatorcontrib>Zhang, Jian</creatorcontrib><creatorcontrib>Yeung, Miranda L</creatorcontrib><creatorcontrib>Yeung, Kam C.</creatorcontrib><creatorcontrib>Keller, Evan T.</creatorcontrib><title>Raf kinase inhibitor protein (RKIP) deficiency decreases latency of tumorigenesis and increases metastasis in a murine genetic model of prostate cancer</title><title>The Prostate</title><addtitle>Prostate</addtitle><description>BACKGROUND
Raf kinase inhibitor protein (RKIP) has been shown to act as a metastasis suppressor gene in multiple models of cancer. Loss of RKIP expression promotes invasion and metastasis in cell transplantation animal models. However, it is unknown if RKIP expression can impact the progression of cancer in an autochthonous model of cancer. The goal of this study was to determine if loss of RKIP expression in a genetic mouse model of prostate cancer (PCa) impacts metastasis.
METHODS
Endogenous RKIP expression was measured in the primary tumors and metastases of transgenic adenocarcinoma of the mouse prostate (TRAMP+) mice. RKIP knockout mice (RKIP−/−) were crossbred with (TRAMP+) mice to create RKIP−/−TRAMP+ mice. Mice were euthanized at 10, 20, and 30 weeks for evaluation of primary and metastatic tumor development. To determine if loss of RKIP alone promotes metastasis, RKIP was knocked down in the low metastatic LNCaP prostate cancer cell line.
RESULTS
Endogenous RKIP expression decreased in TRAMP+ mice as tumors progressed. Primary tumors developed earlier in RKIP−/−TRAMP+ compared to TRAMP+ mice. At 30 weeks of age, distant metastases were identified only the RKIP−/−TRAMP+ mice. While prostate epithelial cell proliferation rates were higher at 10 and 20 weeks in RKIP−/−TRAMP+ compared to TRAMP+ mice, by 30 weeks there was no difference. Apoptosis rates in both groups were similar at all timepoints. Decreased RKIP expression did not impact the metastatic rate of LNCaP in an orthotopic PCa model.
CONCLUSIONS
These results demonstrate that loss of RKIP decreases latency of tumor development and promotes distant metastasis in the TRAMP mouse model in the context of a pro‐metastatic background; but loss of RKIP alone is insufficient to promote metastasis. These findings suggest that in addition to its known metastasis suppressor activity, RKIP may promote tumor progression through enhancing tumor initiation. Prostate 75:292–302, 2015. © 2014 Wiley Periodicals, Inc.</description><subject>Adenocarcinoma - genetics</subject><subject>Adenocarcinoma - pathology</subject><subject>Animals</subject><subject>Carcinogenesis - genetics</subject><subject>Carcinogenesis - pathology</subject><subject>Cell Line, Tumor</subject><subject>Disease Models, Animal</subject><subject>Disease Progression</subject><subject>Humans</subject><subject>LNCaP</subject><subject>Male</subject><subject>metastasis suppressor gene</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Neoplasm Metastasis - genetics</subject><subject>Neoplasm Metastasis - pathology</subject><subject>Phosphatidylethanolamine Binding Protein - genetics</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Prostatic Neoplasms - pathology</subject><subject>TRAMP model</subject><issn>0270-4137</issn><issn>1097-0045</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkd9qFDEUh4Modq3e-AAS8KYKU_N3Mrm0xa7FxZZV8TJkMieadiZTkxl0n8TXNdvt9sILEQIJOd_5wi8HoeeUHFNC2JubNOZjxjSVD9CCEq0qQoR8iBaEKVIJytUBepLzFSEFJ-wxOmCSM6UFXaDfa-vxdYg2Aw7xe2jDNCZcjBOEiI_WH84vX-EOfHABotuUo0tQ4Ix7O93ejB5P8zCm8A0i5JCxjV1R7bEBJpvLKoUitHiYU4iAt_AUHB7GDvqtYxtiKkrsbHSQnqJH3vYZnt3th-jL2bvPp--r1cXy_PTtqnKCS1mBBNk0xFPFhSaUttTVdcd4C6yTqrG1960G22redER2VtcN9dJr4kRXKoofoqOdt7z_Y4Y8mSFkB31vI4xzNrSuCddcEPkfqGRcN4Sxgr78C70a5xRLkEIJIXktNC_U6x3lSvacwJubFAabNoYSs52s2X6KuZ1sgV_cKed2gO4e3Y-yAHQH_Aw9bP6hMpfri097abXrCXmCX_c9Nl2bWnElzdePS7NeNSf87ESZJf8DTMy-tw</recordid><startdate>20150215</startdate><enddate>20150215</enddate><creator>Escara-Wilke, June</creator><creator>Keller, Jill M.</creator><creator>Ignatoski, Kathleen M. Woods</creator><creator>Dai, Jinlu</creator><creator>Shelley, Gregory</creator><creator>Mizokami, Atsushi</creator><creator>Zhang, Jian</creator><creator>Yeung, Miranda L</creator><creator>Yeung, Kam C.</creator><creator>Keller, Evan T.</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><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>7T5</scope><scope>7TO</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20150215</creationdate><title>Raf kinase inhibitor protein (RKIP) deficiency decreases latency of tumorigenesis and increases metastasis in a murine genetic model of prostate cancer</title><author>Escara-Wilke, June ; Keller, Jill M. ; Ignatoski, Kathleen M. Woods ; Dai, Jinlu ; Shelley, Gregory ; Mizokami, Atsushi ; Zhang, Jian ; Yeung, Miranda L ; Yeung, Kam C. ; Keller, Evan T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4355-e5e5880f17349011b1c66d23be2d578a6ffb9eab938d05da9681f5f90c4dfb973</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Adenocarcinoma - genetics</topic><topic>Adenocarcinoma - pathology</topic><topic>Animals</topic><topic>Carcinogenesis - genetics</topic><topic>Carcinogenesis - pathology</topic><topic>Cell Line, Tumor</topic><topic>Disease Models, Animal</topic><topic>Disease Progression</topic><topic>Humans</topic><topic>LNCaP</topic><topic>Male</topic><topic>metastasis suppressor gene</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Neoplasm Metastasis - genetics</topic><topic>Neoplasm Metastasis - pathology</topic><topic>Phosphatidylethanolamine Binding Protein - genetics</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Prostatic Neoplasms - pathology</topic><topic>TRAMP model</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Escara-Wilke, June</creatorcontrib><creatorcontrib>Keller, Jill M.</creatorcontrib><creatorcontrib>Ignatoski, Kathleen M. Woods</creatorcontrib><creatorcontrib>Dai, Jinlu</creatorcontrib><creatorcontrib>Shelley, Gregory</creatorcontrib><creatorcontrib>Mizokami, Atsushi</creatorcontrib><creatorcontrib>Zhang, Jian</creatorcontrib><creatorcontrib>Yeung, Miranda L</creatorcontrib><creatorcontrib>Yeung, Kam C.</creatorcontrib><creatorcontrib>Keller, Evan T.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Prostate</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Escara-Wilke, June</au><au>Keller, Jill M.</au><au>Ignatoski, Kathleen M. Woods</au><au>Dai, Jinlu</au><au>Shelley, Gregory</au><au>Mizokami, Atsushi</au><au>Zhang, Jian</au><au>Yeung, Miranda L</au><au>Yeung, Kam C.</au><au>Keller, Evan T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Raf kinase inhibitor protein (RKIP) deficiency decreases latency of tumorigenesis and increases metastasis in a murine genetic model of prostate cancer</atitle><jtitle>The Prostate</jtitle><addtitle>Prostate</addtitle><date>2015-02-15</date><risdate>2015</risdate><volume>75</volume><issue>3</issue><spage>292</spage><epage>302</epage><pages>292-302</pages><issn>0270-4137</issn><eissn>1097-0045</eissn><coden>PRSTDS</coden><abstract>BACKGROUND
Raf kinase inhibitor protein (RKIP) has been shown to act as a metastasis suppressor gene in multiple models of cancer. Loss of RKIP expression promotes invasion and metastasis in cell transplantation animal models. However, it is unknown if RKIP expression can impact the progression of cancer in an autochthonous model of cancer. The goal of this study was to determine if loss of RKIP expression in a genetic mouse model of prostate cancer (PCa) impacts metastasis.
METHODS
Endogenous RKIP expression was measured in the primary tumors and metastases of transgenic adenocarcinoma of the mouse prostate (TRAMP+) mice. RKIP knockout mice (RKIP−/−) were crossbred with (TRAMP+) mice to create RKIP−/−TRAMP+ mice. Mice were euthanized at 10, 20, and 30 weeks for evaluation of primary and metastatic tumor development. To determine if loss of RKIP alone promotes metastasis, RKIP was knocked down in the low metastatic LNCaP prostate cancer cell line.
RESULTS
Endogenous RKIP expression decreased in TRAMP+ mice as tumors progressed. Primary tumors developed earlier in RKIP−/−TRAMP+ compared to TRAMP+ mice. At 30 weeks of age, distant metastases were identified only the RKIP−/−TRAMP+ mice. While prostate epithelial cell proliferation rates were higher at 10 and 20 weeks in RKIP−/−TRAMP+ compared to TRAMP+ mice, by 30 weeks there was no difference. Apoptosis rates in both groups were similar at all timepoints. Decreased RKIP expression did not impact the metastatic rate of LNCaP in an orthotopic PCa model.
CONCLUSIONS
These results demonstrate that loss of RKIP decreases latency of tumor development and promotes distant metastasis in the TRAMP mouse model in the context of a pro‐metastatic background; but loss of RKIP alone is insufficient to promote metastasis. These findings suggest that in addition to its known metastasis suppressor activity, RKIP may promote tumor progression through enhancing tumor initiation. Prostate 75:292–302, 2015. © 2014 Wiley Periodicals, Inc.</abstract><cop>United States</cop><pub>Blackwell Publishing Ltd</pub><pmid>25327941</pmid><doi>10.1002/pros.22915</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenocarcinoma - genetics Adenocarcinoma - pathology Animals Carcinogenesis - genetics Carcinogenesis - pathology Cell Line, Tumor Disease Models, Animal Disease Progression Humans LNCaP Male metastasis suppressor gene Mice Mice, Knockout Neoplasm Metastasis - genetics Neoplasm Metastasis - pathology Phosphatidylethanolamine Binding Protein - genetics Prostatic Neoplasms - genetics Prostatic Neoplasms - pathology TRAMP model |
| title | Raf kinase inhibitor protein (RKIP) deficiency decreases latency of tumorigenesis and increases metastasis in a murine genetic model of prostate cancer |
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