Iodine-125 induces apoptosis via regulating p53, microvessel density, and vascular endothelial growth factor in colorectal cancer
Iodine interstitial brachytherapy has been widely reported for treating colorectal cancer (CRC). However, the inhibitory molecular mechanism of iodine-125 (I-125) on CRC has not been reported. To illustrate the inhibitory mechanism of iodine-125 (I-125) on CRC, we established the animal models of CR...
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| Veröffentlicht in: | World journal of surgical oncology 2014-07, Vol.12 (1), p.222-222, Article 222 |
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| creator | Ma, Zhenhuan Yang, Yong Yang, Guokai Wan, Jia Li, Guojian Lu, Ping Du, Lingjuan |
| description | Iodine interstitial brachytherapy has been widely reported for treating colorectal cancer (CRC). However, the inhibitory molecular mechanism of iodine-125 (I-125) on CRC has not been reported.
To illustrate the inhibitory mechanism of iodine-125 (I-125) on CRC, we established the animal models of CRC via the injection of HCT-8 cells into nude mice. Subsequently, the I-125 granules were implanted into the tumor of the animal model at different dosages. Proliferating cell nuclear antigen and terminal transferase dUTP nick end labeling were used to detect the apoptosis of the tumor cells. Immunohistochemistry SP staining was used to measure the expression of p53 protein. The protein levels were examined with western blot and ELISA. Meanwhile, microvessel density (MVD) was counted by endothelial cells immunostained by anti-CD34 antibody.
The results showed that I-125 protests against CRC via increasing the protein level of p53 and decreasing the level of vascular endothelial growth factor (VEGF), leading to the decrease of MVD in CRC (P |
| doi_str_mv | 10.1186/1477-7819-12-222 |
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To illustrate the inhibitory mechanism of iodine-125 (I-125) on CRC, we established the animal models of CRC via the injection of HCT-8 cells into nude mice. Subsequently, the I-125 granules were implanted into the tumor of the animal model at different dosages. Proliferating cell nuclear antigen and terminal transferase dUTP nick end labeling were used to detect the apoptosis of the tumor cells. Immunohistochemistry SP staining was used to measure the expression of p53 protein. The protein levels were examined with western blot and ELISA. Meanwhile, microvessel density (MVD) was counted by endothelial cells immunostained by anti-CD34 antibody.
The results showed that I-125 protests against CRC via increasing the protein level of p53 and decreasing the level of vascular endothelial growth factor (VEGF), leading to the decrease of MVD in CRC (P <0.0001). An effective inhibition dosage of I-125 ranged from 0.4 to 0.8 mCi.
The inhibitory mechanisms of iodine on CRC acted through an increase in the level of p53 and a decrease in the level of VEGF, resulting in a decrease of MVD.</description><identifier>ISSN: 1477-7819</identifier><identifier>EISSN: 1477-7819</identifier><identifier>DOI: 10.1186/1477-7819-12-222</identifier><identifier>PMID: 25033896</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Analysis ; Animals ; Antigens ; Apoptosis ; Biomarkers, Tumor - metabolism ; Blotting, Western ; Brachytherapy ; Cancer ; Care and treatment ; Cell Proliferation ; Colorectal cancer ; Colorectal Neoplasms - metabolism ; Colorectal Neoplasms - pathology ; Colorectal Neoplasms - radiotherapy ; Flow Cytometry ; Humans ; Immunohistochemistry ; Iodine Radioisotopes - therapeutic use ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Microvessels - metabolism ; Microvessels - pathology ; Neovascularization, Pathologic ; Physiological aspects ; Radiation therapy ; Seeds ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53 - metabolism ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor A - metabolism ; Xenograft Model Antitumor Assays</subject><ispartof>World journal of surgical oncology, 2014-07, Vol.12 (1), p.222-222, Article 222</ispartof><rights>COPYRIGHT 2014 BioMed Central Ltd.</rights><rights>2014 Ma et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.</rights><rights>Copyright © 2014 Ma et al.; licensee BioMed Central Ltd. 2014 Ma et al.; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b615t-31fc4c911fcb1225f6c0a23b95d401b45f12141a4e1dc2539f709d290f9a6983</citedby><cites>FETCH-LOGICAL-b615t-31fc4c911fcb1225f6c0a23b95d401b45f12141a4e1dc2539f709d290f9a6983</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4304198/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4304198/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25033896$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ma, Zhenhuan</creatorcontrib><creatorcontrib>Yang, Yong</creatorcontrib><creatorcontrib>Yang, Guokai</creatorcontrib><creatorcontrib>Wan, Jia</creatorcontrib><creatorcontrib>Li, Guojian</creatorcontrib><creatorcontrib>Lu, Ping</creatorcontrib><creatorcontrib>Du, Lingjuan</creatorcontrib><title>Iodine-125 induces apoptosis via regulating p53, microvessel density, and vascular endothelial growth factor in colorectal cancer</title><title>World journal of surgical oncology</title><addtitle>World J Surg Oncol</addtitle><description>Iodine interstitial brachytherapy has been widely reported for treating colorectal cancer (CRC). However, the inhibitory molecular mechanism of iodine-125 (I-125) on CRC has not been reported.
To illustrate the inhibitory mechanism of iodine-125 (I-125) on CRC, we established the animal models of CRC via the injection of HCT-8 cells into nude mice. Subsequently, the I-125 granules were implanted into the tumor of the animal model at different dosages. Proliferating cell nuclear antigen and terminal transferase dUTP nick end labeling were used to detect the apoptosis of the tumor cells. Immunohistochemistry SP staining was used to measure the expression of p53 protein. The protein levels were examined with western blot and ELISA. Meanwhile, microvessel density (MVD) was counted by endothelial cells immunostained by anti-CD34 antibody.
The results showed that I-125 protests against CRC via increasing the protein level of p53 and decreasing the level of vascular endothelial growth factor (VEGF), leading to the decrease of MVD in CRC (P <0.0001). An effective inhibition dosage of I-125 ranged from 0.4 to 0.8 mCi.
The inhibitory mechanisms of iodine on CRC acted through an increase in the level of p53 and a decrease in the level of VEGF, resulting in a decrease of MVD.</description><subject>Analysis</subject><subject>Animals</subject><subject>Antigens</subject><subject>Apoptosis</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Blotting, Western</subject><subject>Brachytherapy</subject><subject>Cancer</subject><subject>Care and treatment</subject><subject>Cell Proliferation</subject><subject>Colorectal cancer</subject><subject>Colorectal Neoplasms - metabolism</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Colorectal Neoplasms - radiotherapy</subject><subject>Flow Cytometry</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Iodine Radioisotopes - therapeutic use</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Microvessels - metabolism</subject><subject>Microvessels - pathology</subject><subject>Neovascularization, Pathologic</subject><subject>Physiological aspects</subject><subject>Radiation therapy</subject><subject>Seeds</subject><subject>Tumor Cells, Cultured</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1477-7819</issn><issn>1477-7819</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNqNks9rFDEUxwdRbK3ePUlAEA-dmh-TzOQilMUfhYKX3kMm82Y3JZusSWZLj_7nZty67koFyeGF9z7vm_C-r6peE3xBSCc-kKZt67Yjsia0ppQ-qU73qacH95PqRUq3GFPGOHtenVCOGeukOK1-XIXBeij9HFk_TAYS0puwySHZhLZWowjLyels_RJtODtHa2ti2EJK4NAAPtl8f460H9BWJ1PIiMAPIa_AWe3QMoa7vEKjNjnE8gIywYUIJpea0d5AfFk9G7VL8OohnlU3nz_dLL7W19--XC0ur-teEJ5rRkbTGElK6AmlfBQGa8p6yYcGk77hI6GkIboBMhjKmRxbLAcq8Si1kB07qz7uZDdTv4bBgM9RO7WJdq3jvQraquOKtyu1DFvVMNyQXwKLnUBvwz8EjismrNXsgJodUISqYlBRef_wjRi-T5CyWttkwDntIUxJEcEb0ZKWd_-BspYLKRtZ0Ld_obdhir6Mc6Y46xgR9A-11A6U9WMo_zSzqLosAxNiXopCXTxClTNAsT54GG3JHzW8O2hYgXZ5lYKbsg0-HYN4B5YFSinCuB8ewWre58fG9ebQtX3D7wVmPwFzYu9m</recordid><startdate>20140717</startdate><enddate>20140717</enddate><creator>Ma, Zhenhuan</creator><creator>Yang, Yong</creator><creator>Yang, Guokai</creator><creator>Wan, Jia</creator><creator>Li, Guojian</creator><creator>Lu, Ping</creator><creator>Du, Lingjuan</creator><general>BioMed Central Ltd</general><general>BioMed Central</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>7QL</scope><scope>7QO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7TO</scope><scope>H94</scope><scope>5PM</scope></search><sort><creationdate>20140717</creationdate><title>Iodine-125 induces apoptosis via regulating p53, microvessel density, and vascular endothelial growth factor in colorectal cancer</title><author>Ma, Zhenhuan ; Yang, Yong ; Yang, Guokai ; Wan, Jia ; Li, Guojian ; Lu, Ping ; Du, Lingjuan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b615t-31fc4c911fcb1225f6c0a23b95d401b45f12141a4e1dc2539f709d290f9a6983</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Analysis</topic><topic>Animals</topic><topic>Antigens</topic><topic>Apoptosis</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Blotting, Western</topic><topic>Brachytherapy</topic><topic>Cancer</topic><topic>Care and treatment</topic><topic>Cell Proliferation</topic><topic>Colorectal cancer</topic><topic>Colorectal Neoplasms - metabolism</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Colorectal Neoplasms - radiotherapy</topic><topic>Flow Cytometry</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Iodine Radioisotopes - therapeutic use</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Microvessels - metabolism</topic><topic>Microvessels - pathology</topic><topic>Neovascularization, Pathologic</topic><topic>Physiological aspects</topic><topic>Radiation therapy</topic><topic>Seeds</topic><topic>Tumor Cells, Cultured</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><topic>Vascular endothelial growth factor</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ma, Zhenhuan</creatorcontrib><creatorcontrib>Yang, Yong</creatorcontrib><creatorcontrib>Yang, Guokai</creatorcontrib><creatorcontrib>Wan, Jia</creatorcontrib><creatorcontrib>Li, Guojian</creatorcontrib><creatorcontrib>Lu, Ping</creatorcontrib><creatorcontrib>Du, Lingjuan</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</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 Essentials</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</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>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content 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>MEDLINE - Academic</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>World journal of surgical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ma, Zhenhuan</au><au>Yang, Yong</au><au>Yang, Guokai</au><au>Wan, Jia</au><au>Li, Guojian</au><au>Lu, Ping</au><au>Du, Lingjuan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Iodine-125 induces apoptosis via regulating p53, microvessel density, and vascular endothelial growth factor in colorectal cancer</atitle><jtitle>World journal of surgical oncology</jtitle><addtitle>World J Surg Oncol</addtitle><date>2014-07-17</date><risdate>2014</risdate><volume>12</volume><issue>1</issue><spage>222</spage><epage>222</epage><pages>222-222</pages><artnum>222</artnum><issn>1477-7819</issn><eissn>1477-7819</eissn><abstract>Iodine interstitial brachytherapy has been widely reported for treating colorectal cancer (CRC). However, the inhibitory molecular mechanism of iodine-125 (I-125) on CRC has not been reported.
To illustrate the inhibitory mechanism of iodine-125 (I-125) on CRC, we established the animal models of CRC via the injection of HCT-8 cells into nude mice. Subsequently, the I-125 granules were implanted into the tumor of the animal model at different dosages. Proliferating cell nuclear antigen and terminal transferase dUTP nick end labeling were used to detect the apoptosis of the tumor cells. Immunohistochemistry SP staining was used to measure the expression of p53 protein. The protein levels were examined with western blot and ELISA. Meanwhile, microvessel density (MVD) was counted by endothelial cells immunostained by anti-CD34 antibody.
The results showed that I-125 protests against CRC via increasing the protein level of p53 and decreasing the level of vascular endothelial growth factor (VEGF), leading to the decrease of MVD in CRC (P <0.0001). An effective inhibition dosage of I-125 ranged from 0.4 to 0.8 mCi.
The inhibitory mechanisms of iodine on CRC acted through an increase in the level of p53 and a decrease in the level of VEGF, resulting in a decrease of MVD.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>25033896</pmid><doi>10.1186/1477-7819-12-222</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Analysis Animals Antigens Apoptosis Biomarkers, Tumor - metabolism Blotting, Western Brachytherapy Cancer Care and treatment Cell Proliferation Colorectal cancer Colorectal Neoplasms - metabolism Colorectal Neoplasms - pathology Colorectal Neoplasms - radiotherapy Flow Cytometry Humans Immunohistochemistry Iodine Radioisotopes - therapeutic use Male Mice Mice, Inbred BALB C Mice, Nude Microvessels - metabolism Microvessels - pathology Neovascularization, Pathologic Physiological aspects Radiation therapy Seeds Tumor Cells, Cultured Tumor Suppressor Protein p53 - metabolism Vascular endothelial growth factor Vascular Endothelial Growth Factor A - metabolism Xenograft Model Antitumor Assays |
| title | Iodine-125 induces apoptosis via regulating p53, microvessel density, and vascular endothelial growth factor in colorectal cancer |
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