B7-H3 overexpression in pancreatic cancer promotes tumor progression
B7-H3, a member of the B7-family molecules, plays an important role in adaptive immune responses. In addition, B7-H3 is also expressed in several types of human cancers and is correlated with the poor outcome of cancer patients. However, its exact role in cancer is not known. In the present study, w...
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| Veröffentlicht in: | International journal of molecular medicine 2013-02, Vol.31 (2), p.283-291 |
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| creator | ZHAO, XIN LI, DE-CHUN ZHU, XIN-GUO GAN, WEN-JUAN LI, ZHI XIONG, FENG ZHANG, ZI-XIANG ZHANG, GUANG-BO ZHANG, XUE-GUANG ZHAO, HUA |
| description | B7-H3, a member of the B7-family molecules, plays an important role in adaptive immune responses. In addition, B7-H3 is also expressed in several types of human cancers and is correlated with the poor outcome of cancer patients. However, its exact role in cancer is not known. In the present study, we compared B7-H3 expression in normal pancreas and pancreatic cancer tissue specimens, and determined the effects of low B7-H3 expression on the human pancreatic cancer cell line Patu8988 using lentivirus-mediated RNA interference. B7-H3 expression in pancreatic specimens was determined by enzyme-linked immunosorbent assay (ELISA). A Patu8988 cell line with low B7-H3 expression was established by lentivirus-mediated RNA interference to investigate the effect of B7-H3 on cell proliferation, migration and invasion in vitro. By establishing subcutaneous transplantation tumor and orthotopic transplantation pancreatic cancer mouse models, the effect of B7-H3 on cell proliferation, migration and invasion was studied in vivo. B7-H3 in tissue samples was significantly higher in the pancreatic cancer group than in the normal pancreas group (mean ± SD, 193.6±9.352 vs. 87.74±7.433 ng/g; P |
| doi_str_mv | 10.3892/ijmm.2012.1212 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4042878</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1932350814</sourcerecordid><originalsourceid>FETCH-LOGICAL-c517t-18e3cc02e58afaf6dfb72e3bc9c135ed0a5c65ae662ed67acf807cd3327c8d973</originalsourceid><addsrcrecordid>eNpVkM9LwzAUx4Mobk6vHqXgxUtrfjRNehF0_oSBFwVvIUtfZ8fa1KQd-t-bujkUAnkhn_d9jw9CpwQnTOb0slrWdUIxoQmhhO6hMRE5iWmavu2HmmARM8GzETryfokx5WkuD9GIMpqGJj5GtzcifmSRXYODz9aB95VtoqqJWt0YB7qrTGRCCS5qna1tBz7q-tr-PBdb_hgdlHrl4WR7T9Dr_d3L9DGePT88Ta9nseFEdDGRwIzBFLjUpS6zopwLCmxuckMYhwJrbjKuIcsoFJnQppRYmIIxKowscsEm6GqT2_bzGgoDTef0SrWuqrX7UlZX6v9PU72rhV2rFKdUChkCzrcBzn704Du1tL1rws6K5IwyjiVJA5VsKOOs9w7K3QSC1WBdDdbVYF0N1kPD2d-9dviv5gBcbAAftBZVYf2OGaJiRmJMw5GMfQPqNY2g</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1932350814</pqid></control><display><type>article</type><title>B7-H3 overexpression in pancreatic cancer promotes tumor progression</title><source>Spandidos Publications Journals</source><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>ZHAO, XIN ; LI, DE-CHUN ; ZHU, XIN-GUO ; GAN, WEN-JUAN ; LI, ZHI ; XIONG, FENG ; ZHANG, ZI-XIANG ; ZHANG, GUANG-BO ; ZHANG, XUE-GUANG ; ZHAO, HUA</creator><creatorcontrib>ZHAO, XIN ; LI, DE-CHUN ; ZHU, XIN-GUO ; GAN, WEN-JUAN ; LI, ZHI ; XIONG, FENG ; ZHANG, ZI-XIANG ; ZHANG, GUANG-BO ; ZHANG, XUE-GUANG ; ZHAO, HUA</creatorcontrib><description>B7-H3, a member of the B7-family molecules, plays an important role in adaptive immune responses. In addition, B7-H3 is also expressed in several types of human cancers and is correlated with the poor outcome of cancer patients. However, its exact role in cancer is not known. In the present study, we compared B7-H3 expression in normal pancreas and pancreatic cancer tissue specimens, and determined the effects of low B7-H3 expression on the human pancreatic cancer cell line Patu8988 using lentivirus-mediated RNA interference. B7-H3 expression in pancreatic specimens was determined by enzyme-linked immunosorbent assay (ELISA). A Patu8988 cell line with low B7-H3 expression was established by lentivirus-mediated RNA interference to investigate the effect of B7-H3 on cell proliferation, migration and invasion in vitro. By establishing subcutaneous transplantation tumor and orthotopic transplantation pancreatic cancer mouse models, the effect of B7-H3 on cell proliferation, migration and invasion was studied in vivo. B7-H3 in tissue samples was significantly higher in the pancreatic cancer group than in the normal pancreas group (mean ± SD, 193.6±9.352 vs. 87.74±7.433 ng/g; P<0.0001). B7-H3 knockdown by RNA interference decreased cell migration and Transwell invasion up to 50% in vitro. No apparent impact was observed on cell proliferation in vitro. In the subcutaneous transplantation tumor mouse model, the tumor growth rate was reduced by the knockdown of B7-H3. In the orthotopic transplantation pancreatic cancer mouse model, the effect of inhibiting metastasis by knocking down B7-H3 was assessed in terms of the average postmortem abdominal visceral metastatic tumor weight. This demonstrated that inhibition of B7-H3 expression reduced pancreatic cancer metastasis in vivo. In conclusion, B7-H3 is aberrantly expressed in pancreatic cancer. In addition to modulating tumor immunity, B7-H3 may have a novel role in regulating pancreatic tumor progression.</description><identifier>ISSN: 1107-3756</identifier><identifier>EISSN: 1791-244X</identifier><identifier>DOI: 10.3892/ijmm.2012.1212</identifier><identifier>PMID: 23242015</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Animals ; B7 Antigens - analysis ; B7 Antigens - genetics ; B7-H3 ; Cancer therapies ; Cell growth ; Cell Line, Tumor ; Cell Proliferation ; Enzymes ; Gene Expression Regulation, Neoplastic ; Humans ; Infections ; invasiveness ; Laboratories ; Male ; Metastasis ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; migration ; Motility ; Neoplasm Invasiveness - genetics ; Neoplasm Invasiveness - pathology ; Pancreas - metabolism ; Pancreas - pathology ; Pancreatic cancer ; Pancreatic Neoplasms - genetics ; Pancreatic Neoplasms - pathology ; progression ; Proteins ; RNA interference ; Studies ; Surgery ; Tumors ; Up-Regulation</subject><ispartof>International journal of molecular medicine, 2013-02, Vol.31 (2), p.283-291</ispartof><rights>Copyright © 2013, Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2013</rights><rights>Copyright © 2013, Spandidos Publications 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c517t-18e3cc02e58afaf6dfb72e3bc9c135ed0a5c65ae662ed67acf807cd3327c8d973</citedby><cites>FETCH-LOGICAL-c517t-18e3cc02e58afaf6dfb72e3bc9c135ed0a5c65ae662ed67acf807cd3327c8d973</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,5556,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23242015$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>ZHAO, XIN</creatorcontrib><creatorcontrib>LI, DE-CHUN</creatorcontrib><creatorcontrib>ZHU, XIN-GUO</creatorcontrib><creatorcontrib>GAN, WEN-JUAN</creatorcontrib><creatorcontrib>LI, ZHI</creatorcontrib><creatorcontrib>XIONG, FENG</creatorcontrib><creatorcontrib>ZHANG, ZI-XIANG</creatorcontrib><creatorcontrib>ZHANG, GUANG-BO</creatorcontrib><creatorcontrib>ZHANG, XUE-GUANG</creatorcontrib><creatorcontrib>ZHAO, HUA</creatorcontrib><title>B7-H3 overexpression in pancreatic cancer promotes tumor progression</title><title>International journal of molecular medicine</title><addtitle>Int J Mol Med</addtitle><description>B7-H3, a member of the B7-family molecules, plays an important role in adaptive immune responses. In addition, B7-H3 is also expressed in several types of human cancers and is correlated with the poor outcome of cancer patients. However, its exact role in cancer is not known. In the present study, we compared B7-H3 expression in normal pancreas and pancreatic cancer tissue specimens, and determined the effects of low B7-H3 expression on the human pancreatic cancer cell line Patu8988 using lentivirus-mediated RNA interference. B7-H3 expression in pancreatic specimens was determined by enzyme-linked immunosorbent assay (ELISA). A Patu8988 cell line with low B7-H3 expression was established by lentivirus-mediated RNA interference to investigate the effect of B7-H3 on cell proliferation, migration and invasion in vitro. By establishing subcutaneous transplantation tumor and orthotopic transplantation pancreatic cancer mouse models, the effect of B7-H3 on cell proliferation, migration and invasion was studied in vivo. B7-H3 in tissue samples was significantly higher in the pancreatic cancer group than in the normal pancreas group (mean ± SD, 193.6±9.352 vs. 87.74±7.433 ng/g; P<0.0001). B7-H3 knockdown by RNA interference decreased cell migration and Transwell invasion up to 50% in vitro. No apparent impact was observed on cell proliferation in vitro. In the subcutaneous transplantation tumor mouse model, the tumor growth rate was reduced by the knockdown of B7-H3. In the orthotopic transplantation pancreatic cancer mouse model, the effect of inhibiting metastasis by knocking down B7-H3 was assessed in terms of the average postmortem abdominal visceral metastatic tumor weight. This demonstrated that inhibition of B7-H3 expression reduced pancreatic cancer metastasis in vivo. In conclusion, B7-H3 is aberrantly expressed in pancreatic cancer. In addition to modulating tumor immunity, B7-H3 may have a novel role in regulating pancreatic tumor progression.</description><subject>Animals</subject><subject>B7 Antigens - analysis</subject><subject>B7 Antigens - genetics</subject><subject>B7-H3</subject><subject>Cancer therapies</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Enzymes</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Infections</subject><subject>invasiveness</subject><subject>Laboratories</subject><subject>Male</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>migration</subject><subject>Motility</subject><subject>Neoplasm Invasiveness - genetics</subject><subject>Neoplasm Invasiveness - pathology</subject><subject>Pancreas - metabolism</subject><subject>Pancreas - pathology</subject><subject>Pancreatic cancer</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>progression</subject><subject>Proteins</subject><subject>RNA interference</subject><subject>Studies</subject><subject>Surgery</subject><subject>Tumors</subject><subject>Up-Regulation</subject><issn>1107-3756</issn><issn>1791-244X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpVkM9LwzAUx4Mobk6vHqXgxUtrfjRNehF0_oSBFwVvIUtfZ8fa1KQd-t-bujkUAnkhn_d9jw9CpwQnTOb0slrWdUIxoQmhhO6hMRE5iWmavu2HmmARM8GzETryfokx5WkuD9GIMpqGJj5GtzcifmSRXYODz9aB95VtoqqJWt0YB7qrTGRCCS5qna1tBz7q-tr-PBdb_hgdlHrl4WR7T9Dr_d3L9DGePT88Ta9nseFEdDGRwIzBFLjUpS6zopwLCmxuckMYhwJrbjKuIcsoFJnQppRYmIIxKowscsEm6GqT2_bzGgoDTef0SrWuqrX7UlZX6v9PU72rhV2rFKdUChkCzrcBzn704Du1tL1rws6K5IwyjiVJA5VsKOOs9w7K3QSC1WBdDdbVYF0N1kPD2d-9dviv5gBcbAAftBZVYf2OGaJiRmJMw5GMfQPqNY2g</recordid><startdate>20130201</startdate><enddate>20130201</enddate><creator>ZHAO, XIN</creator><creator>LI, DE-CHUN</creator><creator>ZHU, XIN-GUO</creator><creator>GAN, WEN-JUAN</creator><creator>LI, ZHI</creator><creator>XIONG, FENG</creator><creator>ZHANG, ZI-XIANG</creator><creator>ZHANG, GUANG-BO</creator><creator>ZHANG, XUE-GUANG</creator><creator>ZHAO, HUA</creator><general>D.A. Spandidos</general><general>Spandidos Publications UK Ltd</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>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>20130201</creationdate><title>B7-H3 overexpression in pancreatic cancer promotes tumor progression</title><author>ZHAO, XIN ; LI, DE-CHUN ; ZHU, XIN-GUO ; GAN, WEN-JUAN ; LI, ZHI ; XIONG, FENG ; ZHANG, ZI-XIANG ; ZHANG, GUANG-BO ; ZHANG, XUE-GUANG ; ZHAO, HUA</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c517t-18e3cc02e58afaf6dfb72e3bc9c135ed0a5c65ae662ed67acf807cd3327c8d973</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>B7 Antigens - analysis</topic><topic>B7 Antigens - genetics</topic><topic>B7-H3</topic><topic>Cancer therapies</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Enzymes</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Infections</topic><topic>invasiveness</topic><topic>Laboratories</topic><topic>Male</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>migration</topic><topic>Motility</topic><topic>Neoplasm Invasiveness - genetics</topic><topic>Neoplasm Invasiveness - pathology</topic><topic>Pancreas - metabolism</topic><topic>Pancreas - pathology</topic><topic>Pancreatic cancer</topic><topic>Pancreatic Neoplasms - genetics</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>progression</topic><topic>Proteins</topic><topic>RNA interference</topic><topic>Studies</topic><topic>Surgery</topic><topic>Tumors</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>ZHAO, XIN</creatorcontrib><creatorcontrib>LI, DE-CHUN</creatorcontrib><creatorcontrib>ZHU, XIN-GUO</creatorcontrib><creatorcontrib>GAN, WEN-JUAN</creatorcontrib><creatorcontrib>LI, ZHI</creatorcontrib><creatorcontrib>XIONG, FENG</creatorcontrib><creatorcontrib>ZHANG, ZI-XIANG</creatorcontrib><creatorcontrib>ZHANG, GUANG-BO</creatorcontrib><creatorcontrib>ZHANG, XUE-GUANG</creatorcontrib><creatorcontrib>ZHAO, HUA</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>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</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 China</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>ZHAO, XIN</au><au>LI, DE-CHUN</au><au>ZHU, XIN-GUO</au><au>GAN, WEN-JUAN</au><au>LI, ZHI</au><au>XIONG, FENG</au><au>ZHANG, ZI-XIANG</au><au>ZHANG, GUANG-BO</au><au>ZHANG, XUE-GUANG</au><au>ZHAO, HUA</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>B7-H3 overexpression in pancreatic cancer promotes tumor progression</atitle><jtitle>International journal of molecular medicine</jtitle><addtitle>Int J Mol Med</addtitle><date>2013-02-01</date><risdate>2013</risdate><volume>31</volume><issue>2</issue><spage>283</spage><epage>291</epage><pages>283-291</pages><issn>1107-3756</issn><eissn>1791-244X</eissn><abstract>B7-H3, a member of the B7-family molecules, plays an important role in adaptive immune responses. In addition, B7-H3 is also expressed in several types of human cancers and is correlated with the poor outcome of cancer patients. However, its exact role in cancer is not known. In the present study, we compared B7-H3 expression in normal pancreas and pancreatic cancer tissue specimens, and determined the effects of low B7-H3 expression on the human pancreatic cancer cell line Patu8988 using lentivirus-mediated RNA interference. B7-H3 expression in pancreatic specimens was determined by enzyme-linked immunosorbent assay (ELISA). A Patu8988 cell line with low B7-H3 expression was established by lentivirus-mediated RNA interference to investigate the effect of B7-H3 on cell proliferation, migration and invasion in vitro. By establishing subcutaneous transplantation tumor and orthotopic transplantation pancreatic cancer mouse models, the effect of B7-H3 on cell proliferation, migration and invasion was studied in vivo. B7-H3 in tissue samples was significantly higher in the pancreatic cancer group than in the normal pancreas group (mean ± SD, 193.6±9.352 vs. 87.74±7.433 ng/g; P<0.0001). B7-H3 knockdown by RNA interference decreased cell migration and Transwell invasion up to 50% in vitro. No apparent impact was observed on cell proliferation in vitro. In the subcutaneous transplantation tumor mouse model, the tumor growth rate was reduced by the knockdown of B7-H3. In the orthotopic transplantation pancreatic cancer mouse model, the effect of inhibiting metastasis by knocking down B7-H3 was assessed in terms of the average postmortem abdominal visceral metastatic tumor weight. This demonstrated that inhibition of B7-H3 expression reduced pancreatic cancer metastasis in vivo. In conclusion, B7-H3 is aberrantly expressed in pancreatic cancer. In addition to modulating tumor immunity, B7-H3 may have a novel role in regulating pancreatic tumor progression.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>23242015</pmid><doi>10.3892/ijmm.2012.1212</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals B7 Antigens - analysis B7 Antigens - genetics B7-H3 Cancer therapies Cell growth Cell Line, Tumor Cell Proliferation Enzymes Gene Expression Regulation, Neoplastic Humans Infections invasiveness Laboratories Male Metastasis Mice Mice, Inbred BALB C Mice, Nude migration Motility Neoplasm Invasiveness - genetics Neoplasm Invasiveness - pathology Pancreas - metabolism Pancreas - pathology Pancreatic cancer Pancreatic Neoplasms - genetics Pancreatic Neoplasms - pathology progression Proteins RNA interference Studies Surgery Tumors Up-Regulation |
| title | B7-H3 overexpression in pancreatic cancer promotes tumor progression |
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