Inhibiting tumor necrosis factor-alpha diminishes desmoplasia and inflammation to overcome chemoresistance in pancreatic ductal adenocarcinoma
Pancreatic ductal adenocarcinoma (PDAC) is one of the most common cancer death reasons. Anti-tumor necrosis factor-alpha (TNF-α) antibodies have shown promising effects in PDAC pre-clinical models. However, the prognostic values of TNF-α, underlying mechanisms by which anti-TNF-α treatments inhibit...
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| creator | Zhao, Xianda Fan, Wei Xu, Zhigao Chen, Honglei He, Yuyu Yang, Gui Yang, Gang Hu, Hanning Tang, Shihui Wang, Ping Zhang, Zheng Xu, Peipei Yu, Mingxia |
| description | Pancreatic ductal adenocarcinoma (PDAC) is one of the most common cancer death reasons. Anti-tumor necrosis factor-alpha (TNF-α) antibodies have shown promising effects in PDAC pre-clinical models. However, the prognostic values of TNF-α, underlying mechanisms by which anti-TNF-α treatments inhibit PDAC, and potential synergistic effects of anti-TNF-α treatments with chemotherapy are still unclear.
To identify the targeting values of TNF-α in PDAC, we measured TNF-α expression in different stages of PDAC initiation and evaluated its prognostic significance in a pancreatic cancer cohort. We found that TNF-α expression elevated in PDAC initiation process, and high expression of TNF-α was an independent prognostic marker of poor survival. We further evaluated anti-tumor effects of anti-TNF-α treatments in PDAC. Anti-TNF-α treatments resulted in decreased cell viability in both PDAC tumor cells and pancreatic satellite cells in similar dose in vitro. In vivo, anti-TNF-α treatments showed effects in reducing desmoplasia and the tumor promoting inflammatory microenvironment in PDAC. Combination of anti-TNF-α treatments with chemotherapy partly overcame chemoresistance of PDAC tumor cells and prolonged the survival of PDAC mouse model.
In conclusion, our findings indicated that TNF-α in PDAC can be a prognostic and therapeutic target. Inhibition of TNF-α synergized with chemotherapy in PDAC resulted in better pre-clinical responses via killing tumor cells as well as diminishing desmoplasia and inflammation in PDAC tumor stroma. |
| doi_str_mv | 10.18632/oncotarget.13212 |
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To identify the targeting values of TNF-α in PDAC, we measured TNF-α expression in different stages of PDAC initiation and evaluated its prognostic significance in a pancreatic cancer cohort. We found that TNF-α expression elevated in PDAC initiation process, and high expression of TNF-α was an independent prognostic marker of poor survival. We further evaluated anti-tumor effects of anti-TNF-α treatments in PDAC. Anti-TNF-α treatments resulted in decreased cell viability in both PDAC tumor cells and pancreatic satellite cells in similar dose in vitro. In vivo, anti-TNF-α treatments showed effects in reducing desmoplasia and the tumor promoting inflammatory microenvironment in PDAC. Combination of anti-TNF-α treatments with chemotherapy partly overcame chemoresistance of PDAC tumor cells and prolonged the survival of PDAC mouse model.
In conclusion, our findings indicated that TNF-α in PDAC can be a prognostic and therapeutic target. Inhibition of TNF-α synergized with chemotherapy in PDAC resulted in better pre-clinical responses via killing tumor cells as well as diminishing desmoplasia and inflammation in PDAC tumor stroma.</description><identifier>ISSN: 1949-2553</identifier><identifier>EISSN: 1949-2553</identifier><identifier>DOI: 10.18632/oncotarget.13212</identifier><identifier>PMID: 27835602</identifier><language>eng</language><publisher>United States: Impact Journals LLC</publisher><subject>Animals ; Anti-Inflammatory Agents - pharmacology ; Antibody-Dependent Cell Cytotoxicity - drug effects ; Antineoplastic Combined Chemotherapy Protocols - pharmacology ; Carcinoma, Pancreatic Ductal - drug therapy ; Carcinoma, Pancreatic Ductal - metabolism ; Carcinoma, Pancreatic Ductal - mortality ; Carcinoma, Pancreatic Ductal - pathology ; Cell Line, Tumor ; Cell Survival - drug effects ; Complement Activation - drug effects ; Deoxycytidine - analogs & derivatives ; Deoxycytidine - pharmacology ; Drug Resistance, Neoplasm - drug effects ; Drug Synergism ; Etanercept - pharmacology ; Female ; Humans ; Infliximab - pharmacology ; Kaplan-Meier Estimate ; Male ; Mice, Inbred BALB C ; Mice, Nude ; Middle Aged ; Paclitaxel - pharmacology ; Pancreatic Neoplasms - drug therapy ; Pancreatic Neoplasms - metabolism ; Pancreatic Neoplasms - mortality ; Pancreatic Neoplasms - pathology ; Pancreatic Stellate Cells - drug effects ; Pancreatic Stellate Cells - metabolism ; Pancreatic Stellate Cells - pathology ; Proportional Hazards Models ; Research Paper ; Stromal Cells - drug effects ; Stromal Cells - metabolism ; Stromal Cells - pathology ; Time Factors ; Tumor Microenvironment ; Tumor Necrosis Factor-alpha - antagonists & inhibitors ; Tumor Necrosis Factor-alpha - metabolism ; Xenograft Model Antitumor Assays</subject><ispartof>Oncotarget, 2016-12, Vol.7 (49), p.81110-81122</ispartof><rights>Copyright: © 2016 Zhao et al. 2016</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c356t-9c488e1e4ba986d264df01864f66af7c78539c6d8e54da81e384bf20faf404243</citedby><cites>FETCH-LOGICAL-c356t-9c488e1e4ba986d264df01864f66af7c78539c6d8e54da81e384bf20faf404243</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/PMC5348380/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5348380/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27835602$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhao, Xianda</creatorcontrib><creatorcontrib>Fan, Wei</creatorcontrib><creatorcontrib>Xu, Zhigao</creatorcontrib><creatorcontrib>Chen, Honglei</creatorcontrib><creatorcontrib>He, Yuyu</creatorcontrib><creatorcontrib>Yang, Gui</creatorcontrib><creatorcontrib>Yang, Gang</creatorcontrib><creatorcontrib>Hu, Hanning</creatorcontrib><creatorcontrib>Tang, Shihui</creatorcontrib><creatorcontrib>Wang, Ping</creatorcontrib><creatorcontrib>Zhang, Zheng</creatorcontrib><creatorcontrib>Xu, Peipei</creatorcontrib><creatorcontrib>Yu, Mingxia</creatorcontrib><title>Inhibiting tumor necrosis factor-alpha diminishes desmoplasia and inflammation to overcome chemoresistance in pancreatic ductal adenocarcinoma</title><title>Oncotarget</title><addtitle>Oncotarget</addtitle><description>Pancreatic ductal adenocarcinoma (PDAC) is one of the most common cancer death reasons. Anti-tumor necrosis factor-alpha (TNF-α) antibodies have shown promising effects in PDAC pre-clinical models. However, the prognostic values of TNF-α, underlying mechanisms by which anti-TNF-α treatments inhibit PDAC, and potential synergistic effects of anti-TNF-α treatments with chemotherapy are still unclear.
To identify the targeting values of TNF-α in PDAC, we measured TNF-α expression in different stages of PDAC initiation and evaluated its prognostic significance in a pancreatic cancer cohort. We found that TNF-α expression elevated in PDAC initiation process, and high expression of TNF-α was an independent prognostic marker of poor survival. We further evaluated anti-tumor effects of anti-TNF-α treatments in PDAC. Anti-TNF-α treatments resulted in decreased cell viability in both PDAC tumor cells and pancreatic satellite cells in similar dose in vitro. In vivo, anti-TNF-α treatments showed effects in reducing desmoplasia and the tumor promoting inflammatory microenvironment in PDAC. Combination of anti-TNF-α treatments with chemotherapy partly overcame chemoresistance of PDAC tumor cells and prolonged the survival of PDAC mouse model.
In conclusion, our findings indicated that TNF-α in PDAC can be a prognostic and therapeutic target. Inhibition of TNF-α synergized with chemotherapy in PDAC resulted in better pre-clinical responses via killing tumor cells as well as diminishing desmoplasia and inflammation in PDAC tumor stroma.</description><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Antibody-Dependent Cell Cytotoxicity - drug effects</subject><subject>Antineoplastic Combined Chemotherapy Protocols - pharmacology</subject><subject>Carcinoma, Pancreatic Ductal - drug therapy</subject><subject>Carcinoma, Pancreatic Ductal - metabolism</subject><subject>Carcinoma, Pancreatic Ductal - mortality</subject><subject>Carcinoma, Pancreatic Ductal - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cell Survival - drug effects</subject><subject>Complement Activation - drug effects</subject><subject>Deoxycytidine - analogs & derivatives</subject><subject>Deoxycytidine - pharmacology</subject><subject>Drug Resistance, Neoplasm - drug effects</subject><subject>Drug Synergism</subject><subject>Etanercept - pharmacology</subject><subject>Female</subject><subject>Humans</subject><subject>Infliximab - pharmacology</subject><subject>Kaplan-Meier Estimate</subject><subject>Male</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Middle Aged</subject><subject>Paclitaxel - pharmacology</subject><subject>Pancreatic Neoplasms - drug therapy</subject><subject>Pancreatic Neoplasms - metabolism</subject><subject>Pancreatic Neoplasms - mortality</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Pancreatic Stellate Cells - drug effects</subject><subject>Pancreatic Stellate Cells - metabolism</subject><subject>Pancreatic Stellate Cells - pathology</subject><subject>Proportional Hazards Models</subject><subject>Research Paper</subject><subject>Stromal Cells - drug effects</subject><subject>Stromal Cells - metabolism</subject><subject>Stromal Cells - pathology</subject><subject>Time Factors</subject><subject>Tumor Microenvironment</subject><subject>Tumor Necrosis Factor-alpha - antagonists & inhibitors</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1949-2553</issn><issn>1949-2553</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkc9qFTEUhwex2NL2AbqRLN1Mzb-Zm9kIUqwWCm7sOpybnNyJTJIxyRR8CZ_Z2NZas8mBfOfL4fy67oLRS6ZGwd-naFKFfMB6yQRn_FV3wiY59XwYxOsX9XF3Xsp32s4gd4pPb7pjvlNiGCk_6X7dxNnvffXxQOoWUiYRTU7FF-LA1JR7WNYZiPXBR19mLMRiCWldoHggEC3x0S0QAlSfIqmJpHvMJgUkZsYmxOaqEA02kKytyNhQQ-xmKiwELMZkIBsfU4Cz7sjBUvD86T7t7q4_fbv60t9-_Xxz9fG2N23u2k9GKoUM5R4mNVo-Suto24p04whuZ3ZqEJMZrcJBWlAMhZJ7x6kDJ6nkUpx2Hx6967YPaA3GmmHRa_YB8k-dwOv_X6Kf9SHd60FIJRRtgndPgpx-bFiqDr4YXBaImLaimRITY7SxDWWP6J-9lozu-RtG9UOU-l-U-iHK1vP25XzPHX-DE78BbBqirA</recordid><startdate>20161206</startdate><enddate>20161206</enddate><creator>Zhao, Xianda</creator><creator>Fan, Wei</creator><creator>Xu, Zhigao</creator><creator>Chen, Honglei</creator><creator>He, Yuyu</creator><creator>Yang, Gui</creator><creator>Yang, Gang</creator><creator>Hu, Hanning</creator><creator>Tang, Shihui</creator><creator>Wang, Ping</creator><creator>Zhang, Zheng</creator><creator>Xu, Peipei</creator><creator>Yu, Mingxia</creator><general>Impact Journals LLC</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20161206</creationdate><title>Inhibiting tumor necrosis factor-alpha diminishes desmoplasia and inflammation to overcome chemoresistance in pancreatic ductal adenocarcinoma</title><author>Zhao, Xianda ; Fan, Wei ; Xu, Zhigao ; Chen, Honglei ; He, Yuyu ; Yang, Gui ; Yang, Gang ; Hu, Hanning ; Tang, Shihui ; Wang, Ping ; Zhang, Zheng ; Xu, Peipei ; Yu, Mingxia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c356t-9c488e1e4ba986d264df01864f66af7c78539c6d8e54da81e384bf20faf404243</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Antibody-Dependent Cell Cytotoxicity - drug effects</topic><topic>Antineoplastic Combined Chemotherapy Protocols - pharmacology</topic><topic>Carcinoma, Pancreatic Ductal - drug therapy</topic><topic>Carcinoma, Pancreatic Ductal - metabolism</topic><topic>Carcinoma, Pancreatic Ductal - mortality</topic><topic>Carcinoma, Pancreatic Ductal - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cell Survival - drug effects</topic><topic>Complement Activation - drug effects</topic><topic>Deoxycytidine - analogs & derivatives</topic><topic>Deoxycytidine - pharmacology</topic><topic>Drug Resistance, Neoplasm - drug effects</topic><topic>Drug Synergism</topic><topic>Etanercept - pharmacology</topic><topic>Female</topic><topic>Humans</topic><topic>Infliximab - pharmacology</topic><topic>Kaplan-Meier Estimate</topic><topic>Male</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Middle Aged</topic><topic>Paclitaxel - pharmacology</topic><topic>Pancreatic Neoplasms - drug therapy</topic><topic>Pancreatic Neoplasms - metabolism</topic><topic>Pancreatic Neoplasms - mortality</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Pancreatic Stellate Cells - drug effects</topic><topic>Pancreatic Stellate Cells - metabolism</topic><topic>Pancreatic Stellate Cells - pathology</topic><topic>Proportional Hazards Models</topic><topic>Research Paper</topic><topic>Stromal Cells - drug effects</topic><topic>Stromal Cells - metabolism</topic><topic>Stromal Cells - pathology</topic><topic>Time Factors</topic><topic>Tumor Microenvironment</topic><topic>Tumor Necrosis Factor-alpha - antagonists & inhibitors</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>online_resources</toplevel><creatorcontrib>Zhao, Xianda</creatorcontrib><creatorcontrib>Fan, Wei</creatorcontrib><creatorcontrib>Xu, Zhigao</creatorcontrib><creatorcontrib>Chen, Honglei</creatorcontrib><creatorcontrib>He, Yuyu</creatorcontrib><creatorcontrib>Yang, Gui</creatorcontrib><creatorcontrib>Yang, Gang</creatorcontrib><creatorcontrib>Hu, Hanning</creatorcontrib><creatorcontrib>Tang, Shihui</creatorcontrib><creatorcontrib>Wang, Ping</creatorcontrib><creatorcontrib>Zhang, Zheng</creatorcontrib><creatorcontrib>Xu, Peipei</creatorcontrib><creatorcontrib>Yu, Mingxia</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncotarget</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhao, Xianda</au><au>Fan, Wei</au><au>Xu, Zhigao</au><au>Chen, Honglei</au><au>He, Yuyu</au><au>Yang, Gui</au><au>Yang, Gang</au><au>Hu, Hanning</au><au>Tang, Shihui</au><au>Wang, Ping</au><au>Zhang, Zheng</au><au>Xu, Peipei</au><au>Yu, Mingxia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibiting tumor necrosis factor-alpha diminishes desmoplasia and inflammation to overcome chemoresistance in pancreatic ductal adenocarcinoma</atitle><jtitle>Oncotarget</jtitle><addtitle>Oncotarget</addtitle><date>2016-12-06</date><risdate>2016</risdate><volume>7</volume><issue>49</issue><spage>81110</spage><epage>81122</epage><pages>81110-81122</pages><issn>1949-2553</issn><eissn>1949-2553</eissn><abstract>Pancreatic ductal adenocarcinoma (PDAC) is one of the most common cancer death reasons. Anti-tumor necrosis factor-alpha (TNF-α) antibodies have shown promising effects in PDAC pre-clinical models. However, the prognostic values of TNF-α, underlying mechanisms by which anti-TNF-α treatments inhibit PDAC, and potential synergistic effects of anti-TNF-α treatments with chemotherapy are still unclear.
To identify the targeting values of TNF-α in PDAC, we measured TNF-α expression in different stages of PDAC initiation and evaluated its prognostic significance in a pancreatic cancer cohort. We found that TNF-α expression elevated in PDAC initiation process, and high expression of TNF-α was an independent prognostic marker of poor survival. We further evaluated anti-tumor effects of anti-TNF-α treatments in PDAC. Anti-TNF-α treatments resulted in decreased cell viability in both PDAC tumor cells and pancreatic satellite cells in similar dose in vitro. In vivo, anti-TNF-α treatments showed effects in reducing desmoplasia and the tumor promoting inflammatory microenvironment in PDAC. Combination of anti-TNF-α treatments with chemotherapy partly overcame chemoresistance of PDAC tumor cells and prolonged the survival of PDAC mouse model.
In conclusion, our findings indicated that TNF-α in PDAC can be a prognostic and therapeutic target. Inhibition of TNF-α synergized with chemotherapy in PDAC resulted in better pre-clinical responses via killing tumor cells as well as diminishing desmoplasia and inflammation in PDAC tumor stroma.</abstract><cop>United States</cop><pub>Impact Journals LLC</pub><pmid>27835602</pmid><doi>10.18632/oncotarget.13212</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Anti-Inflammatory Agents - pharmacology Antibody-Dependent Cell Cytotoxicity - drug effects Antineoplastic Combined Chemotherapy Protocols - pharmacology Carcinoma, Pancreatic Ductal - drug therapy Carcinoma, Pancreatic Ductal - metabolism Carcinoma, Pancreatic Ductal - mortality Carcinoma, Pancreatic Ductal - pathology Cell Line, Tumor Cell Survival - drug effects Complement Activation - drug effects Deoxycytidine - analogs & derivatives Deoxycytidine - pharmacology Drug Resistance, Neoplasm - drug effects Drug Synergism Etanercept - pharmacology Female Humans Infliximab - pharmacology Kaplan-Meier Estimate Male Mice, Inbred BALB C Mice, Nude Middle Aged Paclitaxel - pharmacology Pancreatic Neoplasms - drug therapy Pancreatic Neoplasms - metabolism Pancreatic Neoplasms - mortality Pancreatic Neoplasms - pathology Pancreatic Stellate Cells - drug effects Pancreatic Stellate Cells - metabolism Pancreatic Stellate Cells - pathology Proportional Hazards Models Research Paper Stromal Cells - drug effects Stromal Cells - metabolism Stromal Cells - pathology Time Factors Tumor Microenvironment Tumor Necrosis Factor-alpha - antagonists & inhibitors Tumor Necrosis Factor-alpha - metabolism Xenograft Model Antitumor Assays |
| title | Inhibiting tumor necrosis factor-alpha diminishes desmoplasia and inflammation to overcome chemoresistance in pancreatic ductal adenocarcinoma |
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