Peritumoral adipose tissue as a source of inflammatory and angiogenic factors in colorectal cancer
Purpose Obesity is a risk factor for the development of human colorectal cancer (CC). The aim of this work is to report the inflammatory and angiogenic scenario in lean (BMI 30 kg/m 2 ) patients with and without CC and to assess the role of peritumoral adipose tissue in CC-induced inflammation. Mat...
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Veröffentlicht in: | International journal of colorectal disease 2016-02, Vol.31 (2), p.365-375 |
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creator | Amor, S. Iglesias-de la Cruz, M. C. Ferrero, E. García-Villar, O. Barrios, V. Fernandez, N. Monge, L. García-Villalón, A. L. Granado, M. |
description | Purpose
Obesity is a risk factor for the development of human colorectal cancer (CC). The aim of this work is to report the inflammatory and angiogenic scenario in lean (BMI 30 kg/m
2
) patients with and without CC and to assess the role of peritumoral adipose tissue in CC-induced inflammation.
Material and methods
Patients were divided in four experimental groups: obese patients with CC (OB-CC), lean patients with CC (LEAN-CC), obese patients without CC (OB), and lean patients without CC (LEAN).
Results
Plasma levels of pro-inflammatory cytokines (interleukin (IL)-6, IL-4, IL-8) and granulocyte-macrophage colony-stimulating factor (GM-CSF) were increased in OB-CC patients. Peritumoral adipose tissue (TF) explants and cultured mature adipocytes secreted higher amounts of nitrites and nitrates than did control and non-tumoral (NTF) adipose tissue both alone and in response to lipopolysaccharide (LPS). Nitrite and nitrate secretion was also increased in TF explants from OB-CC patients compared with that from LEAN-CC patients. Gene expression of adiponectin, tumor necrosis factor alpha (TNF-α), insulin-like growth factor type I (IGF-I), cyclooxygenase-2 (COX-2), and peroxisome proliferator-activated receptor γ (PPAR-γ) was increased in TF explants from CC patients. LPS increased the gene expression of IL-6, IL-10, TNF-α, vascular endothelial growth factor (VEGF), and COX-2 in OB and in TF explants from OB-CC patients. COX-2 and PPAR-γ inhibition further increased LPS-induced release of nitrites and nitrates in TF explants and adipocytes from OB-CC patients.
Conclusions
In conclusion, OB-CC patients have increased plasma levels of pro-inflammatory and angiogenic factors. TF from OB-CC patients shows an increased secretion of inflammatory markers compared with both TF from LEAN-CC and non-tumoral adipose tissue (AT) through a COX-2- and PPAR-γ-independent mechanism. |
doi_str_mv | 10.1007/s00384-015-2420-6 |
format | Article |
fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_1793907241</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A714489845</galeid><sourcerecordid>A714489845</sourcerecordid><originalsourceid>FETCH-LOGICAL-c509t-1158b31c79a665979e596063e5256a62596ad99a4536f56f4e3297bb3063c4123</originalsourceid><addsrcrecordid>eNp1kU2LFDEQhoMo7jj6A7xIwIuXXvPdneOyrB-woAc9h-p09ZCluzMm3Yf999Yw6ydKCKEqz1tU1cvYSykupRDt2yqE7kwjpG2UUaJxj9hOGq0aqZx6zHZCtr6R3nYX7Fmtd4Ji15qn7EI547Xs3I71n7GkdZtzgYnDkI65Il9TrRtyqBx4zVuJyPPI0zJOMM-w5nLPYRnoHlI-4JIiHyFSuhLDY55ywbhSvQhLxPKcPRlhqvji4d2zr-9uvlx_aG4_vf94fXXbRCv82khpu17L2HpwzvrWo_VOOI1WWQdOUQSD92CsdqN1o0GtfNv3mphopNJ79uZc91jytw3rGuZUI04TLJi3GmgZ2otWGUno67_QOxpzoe6Icsq1ktb4izrAhIHGz2uBeCoarlppTOc7ambPLv9B0RlwTjEvOCbK_yGQZ0EsudaCYziWNEO5D1KEk6_h7GsgX8PJ1-BI8-qh4a2fcfip-GEkAeoMVPpaDlh-m-i_Vb8DjrqqYg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1762671143</pqid></control><display><type>article</type><title>Peritumoral adipose tissue as a source of inflammatory and angiogenic factors in colorectal cancer</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Amor, S. ; Iglesias-de la Cruz, M. C. ; Ferrero, E. ; García-Villar, O. ; Barrios, V. ; Fernandez, N. ; Monge, L. ; García-Villalón, A. L. ; Granado, M.</creator><creatorcontrib>Amor, S. ; Iglesias-de la Cruz, M. C. ; Ferrero, E. ; García-Villar, O. ; Barrios, V. ; Fernandez, N. ; Monge, L. ; García-Villalón, A. L. ; Granado, M.</creatorcontrib><description>Purpose
Obesity is a risk factor for the development of human colorectal cancer (CC). The aim of this work is to report the inflammatory and angiogenic scenario in lean (BMI < 25 kg/m
2
) and obese (BMI > 30 kg/m
2
) patients with and without CC and to assess the role of peritumoral adipose tissue in CC-induced inflammation.
Material and methods
Patients were divided in four experimental groups: obese patients with CC (OB-CC), lean patients with CC (LEAN-CC), obese patients without CC (OB), and lean patients without CC (LEAN).
Results
Plasma levels of pro-inflammatory cytokines (interleukin (IL)-6, IL-4, IL-8) and granulocyte-macrophage colony-stimulating factor (GM-CSF) were increased in OB-CC patients. Peritumoral adipose tissue (TF) explants and cultured mature adipocytes secreted higher amounts of nitrites and nitrates than did control and non-tumoral (NTF) adipose tissue both alone and in response to lipopolysaccharide (LPS). Nitrite and nitrate secretion was also increased in TF explants from OB-CC patients compared with that from LEAN-CC patients. Gene expression of adiponectin, tumor necrosis factor alpha (TNF-α), insulin-like growth factor type I (IGF-I), cyclooxygenase-2 (COX-2), and peroxisome proliferator-activated receptor γ (PPAR-γ) was increased in TF explants from CC patients. LPS increased the gene expression of IL-6, IL-10, TNF-α, vascular endothelial growth factor (VEGF), and COX-2 in OB and in TF explants from OB-CC patients. COX-2 and PPAR-γ inhibition further increased LPS-induced release of nitrites and nitrates in TF explants and adipocytes from OB-CC patients.
Conclusions
In conclusion, OB-CC patients have increased plasma levels of pro-inflammatory and angiogenic factors. TF from OB-CC patients shows an increased secretion of inflammatory markers compared with both TF from LEAN-CC and non-tumoral adipose tissue (AT) through a COX-2- and PPAR-γ-independent mechanism.</description><identifier>ISSN: 0179-1958</identifier><identifier>EISSN: 1432-1262</identifier><identifier>DOI: 10.1007/s00384-015-2420-6</identifier><identifier>PMID: 26493186</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Adipocytes - metabolism ; Adiponectin - genetics ; Adipose Tissue - metabolism ; Adipose Tissue - secretion ; Adipose tissues ; Body fat ; Body Mass Index ; Colorectal cancer ; Colorectal Neoplasms - metabolism ; Colorectal Neoplasms - pathology ; Cyclooxygenase 2 Inhibitors - metabolism ; Cytokines - blood ; Cytokines - genetics ; Cytokines - metabolism ; Development and progression ; Gastroenterology ; Gene Expression ; Granulocyte-Macrophage Progenitor Cells - metabolism ; Hepatology ; Humans ; Inflammation - metabolism ; Insulin-Like Growth Factor I - genetics ; Interleukins ; Internal Medicine ; Macrophage colony stimulating factor ; Medicine ; Medicine & Public Health ; Neovascularization, Pathologic ; Nitrates ; Nitrates - metabolism ; Nitrites - metabolism ; Obesity - metabolism ; Original Article ; PPAR gamma - genetics ; Proctology ; Risk factors ; Surgery ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor A - blood ; Vascular Endothelial Growth Factor A - genetics</subject><ispartof>International journal of colorectal disease, 2016-02, Vol.31 (2), p.365-375</ispartof><rights>Springer-Verlag Berlin Heidelberg 2015</rights><rights>COPYRIGHT 2016 Springer</rights><rights>Springer-Verlag Berlin Heidelberg 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c509t-1158b31c79a665979e596063e5256a62596ad99a4536f56f4e3297bb3063c4123</citedby><cites>FETCH-LOGICAL-c509t-1158b31c79a665979e596063e5256a62596ad99a4536f56f4e3297bb3063c4123</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00384-015-2420-6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00384-015-2420-6$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26493186$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Amor, S.</creatorcontrib><creatorcontrib>Iglesias-de la Cruz, M. C.</creatorcontrib><creatorcontrib>Ferrero, E.</creatorcontrib><creatorcontrib>García-Villar, O.</creatorcontrib><creatorcontrib>Barrios, V.</creatorcontrib><creatorcontrib>Fernandez, N.</creatorcontrib><creatorcontrib>Monge, L.</creatorcontrib><creatorcontrib>García-Villalón, A. L.</creatorcontrib><creatorcontrib>Granado, M.</creatorcontrib><title>Peritumoral adipose tissue as a source of inflammatory and angiogenic factors in colorectal cancer</title><title>International journal of colorectal disease</title><addtitle>Int J Colorectal Dis</addtitle><addtitle>Int J Colorectal Dis</addtitle><description>Purpose
Obesity is a risk factor for the development of human colorectal cancer (CC). The aim of this work is to report the inflammatory and angiogenic scenario in lean (BMI < 25 kg/m
2
) and obese (BMI > 30 kg/m
2
) patients with and without CC and to assess the role of peritumoral adipose tissue in CC-induced inflammation.
Material and methods
Patients were divided in four experimental groups: obese patients with CC (OB-CC), lean patients with CC (LEAN-CC), obese patients without CC (OB), and lean patients without CC (LEAN).
Results
Plasma levels of pro-inflammatory cytokines (interleukin (IL)-6, IL-4, IL-8) and granulocyte-macrophage colony-stimulating factor (GM-CSF) were increased in OB-CC patients. Peritumoral adipose tissue (TF) explants and cultured mature adipocytes secreted higher amounts of nitrites and nitrates than did control and non-tumoral (NTF) adipose tissue both alone and in response to lipopolysaccharide (LPS). Nitrite and nitrate secretion was also increased in TF explants from OB-CC patients compared with that from LEAN-CC patients. Gene expression of adiponectin, tumor necrosis factor alpha (TNF-α), insulin-like growth factor type I (IGF-I), cyclooxygenase-2 (COX-2), and peroxisome proliferator-activated receptor γ (PPAR-γ) was increased in TF explants from CC patients. LPS increased the gene expression of IL-6, IL-10, TNF-α, vascular endothelial growth factor (VEGF), and COX-2 in OB and in TF explants from OB-CC patients. COX-2 and PPAR-γ inhibition further increased LPS-induced release of nitrites and nitrates in TF explants and adipocytes from OB-CC patients.
Conclusions
In conclusion, OB-CC patients have increased plasma levels of pro-inflammatory and angiogenic factors. TF from OB-CC patients shows an increased secretion of inflammatory markers compared with both TF from LEAN-CC and non-tumoral adipose tissue (AT) through a COX-2- and PPAR-γ-independent mechanism.</description><subject>Adipocytes - metabolism</subject><subject>Adiponectin - genetics</subject><subject>Adipose Tissue - metabolism</subject><subject>Adipose Tissue - secretion</subject><subject>Adipose tissues</subject><subject>Body fat</subject><subject>Body Mass Index</subject><subject>Colorectal cancer</subject><subject>Colorectal Neoplasms - metabolism</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Cyclooxygenase 2 Inhibitors - metabolism</subject><subject>Cytokines - blood</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Development and progression</subject><subject>Gastroenterology</subject><subject>Gene Expression</subject><subject>Granulocyte-Macrophage Progenitor Cells - metabolism</subject><subject>Hepatology</subject><subject>Humans</subject><subject>Inflammation - metabolism</subject><subject>Insulin-Like Growth Factor I - genetics</subject><subject>Interleukins</subject><subject>Internal Medicine</subject><subject>Macrophage colony stimulating factor</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Neovascularization, Pathologic</subject><subject>Nitrates</subject><subject>Nitrates - metabolism</subject><subject>Nitrites - metabolism</subject><subject>Obesity - metabolism</subject><subject>Original Article</subject><subject>PPAR gamma - genetics</subject><subject>Proctology</subject><subject>Risk factors</subject><subject>Surgery</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - blood</subject><subject>Vascular Endothelial Growth Factor A - genetics</subject><issn>0179-1958</issn><issn>1432-1262</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kU2LFDEQhoMo7jj6A7xIwIuXXvPdneOyrB-woAc9h-p09ZCluzMm3Yf999Yw6ydKCKEqz1tU1cvYSykupRDt2yqE7kwjpG2UUaJxj9hOGq0aqZx6zHZCtr6R3nYX7Fmtd4Ji15qn7EI547Xs3I71n7GkdZtzgYnDkI65Il9TrRtyqBx4zVuJyPPI0zJOMM-w5nLPYRnoHlI-4JIiHyFSuhLDY55ywbhSvQhLxPKcPRlhqvji4d2zr-9uvlx_aG4_vf94fXXbRCv82khpu17L2HpwzvrWo_VOOI1WWQdOUQSD92CsdqN1o0GtfNv3mphopNJ79uZc91jytw3rGuZUI04TLJi3GmgZ2otWGUno67_QOxpzoe6Icsq1ktb4izrAhIHGz2uBeCoarlppTOc7ambPLv9B0RlwTjEvOCbK_yGQZ0EsudaCYziWNEO5D1KEk6_h7GsgX8PJ1-BI8-qh4a2fcfip-GEkAeoMVPpaDlh-m-i_Vb8DjrqqYg</recordid><startdate>20160201</startdate><enddate>20160201</enddate><creator>Amor, S.</creator><creator>Iglesias-de la Cruz, M. C.</creator><creator>Ferrero, E.</creator><creator>García-Villar, O.</creator><creator>Barrios, V.</creator><creator>Fernandez, N.</creator><creator>Monge, L.</creator><creator>García-Villalón, A. L.</creator><creator>Granado, M.</creator><general>Springer Berlin Heidelberg</general><general>Springer</general><general>Springer Nature B.V</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>7T5</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>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope></search><sort><creationdate>20160201</creationdate><title>Peritumoral adipose tissue as a source of inflammatory and angiogenic factors in colorectal cancer</title><author>Amor, S. ; Iglesias-de la Cruz, M. C. ; Ferrero, E. ; García-Villar, O. ; Barrios, V. ; Fernandez, N. ; Monge, L. ; García-Villalón, A. L. ; Granado, M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c509t-1158b31c79a665979e596063e5256a62596ad99a4536f56f4e3297bb3063c4123</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adipocytes - metabolism</topic><topic>Adiponectin - genetics</topic><topic>Adipose Tissue - metabolism</topic><topic>Adipose Tissue - secretion</topic><topic>Adipose tissues</topic><topic>Body fat</topic><topic>Body Mass Index</topic><topic>Colorectal cancer</topic><topic>Colorectal Neoplasms - metabolism</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Cyclooxygenase 2 Inhibitors - metabolism</topic><topic>Cytokines - blood</topic><topic>Cytokines - genetics</topic><topic>Cytokines - metabolism</topic><topic>Development and progression</topic><topic>Gastroenterology</topic><topic>Gene Expression</topic><topic>Granulocyte-Macrophage Progenitor Cells - metabolism</topic><topic>Hepatology</topic><topic>Humans</topic><topic>Inflammation - metabolism</topic><topic>Insulin-Like Growth Factor I - genetics</topic><topic>Interleukins</topic><topic>Internal Medicine</topic><topic>Macrophage colony stimulating factor</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Neovascularization, Pathologic</topic><topic>Nitrates</topic><topic>Nitrates - metabolism</topic><topic>Nitrites - metabolism</topic><topic>Obesity - metabolism</topic><topic>Original Article</topic><topic>PPAR gamma - genetics</topic><topic>Proctology</topic><topic>Risk factors</topic><topic>Surgery</topic><topic>Vascular endothelial growth factor</topic><topic>Vascular Endothelial Growth Factor A - blood</topic><topic>Vascular Endothelial Growth Factor A - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Amor, S.</creatorcontrib><creatorcontrib>Iglesias-de la Cruz, M. C.</creatorcontrib><creatorcontrib>Ferrero, E.</creatorcontrib><creatorcontrib>García-Villar, O.</creatorcontrib><creatorcontrib>Barrios, V.</creatorcontrib><creatorcontrib>Fernandez, N.</creatorcontrib><creatorcontrib>Monge, L.</creatorcontrib><creatorcontrib>García-Villalón, A. L.</creatorcontrib><creatorcontrib>Granado, M.</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>Immunology Abstracts</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>AIDS and Cancer Research Abstracts</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>MEDLINE - Academic</collection><jtitle>International journal of colorectal disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Amor, S.</au><au>Iglesias-de la Cruz, M. C.</au><au>Ferrero, E.</au><au>García-Villar, O.</au><au>Barrios, V.</au><au>Fernandez, N.</au><au>Monge, L.</au><au>García-Villalón, A. L.</au><au>Granado, M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Peritumoral adipose tissue as a source of inflammatory and angiogenic factors in colorectal cancer</atitle><jtitle>International journal of colorectal disease</jtitle><stitle>Int J Colorectal Dis</stitle><addtitle>Int J Colorectal Dis</addtitle><date>2016-02-01</date><risdate>2016</risdate><volume>31</volume><issue>2</issue><spage>365</spage><epage>375</epage><pages>365-375</pages><issn>0179-1958</issn><eissn>1432-1262</eissn><abstract>Purpose
Obesity is a risk factor for the development of human colorectal cancer (CC). The aim of this work is to report the inflammatory and angiogenic scenario in lean (BMI < 25 kg/m
2
) and obese (BMI > 30 kg/m
2
) patients with and without CC and to assess the role of peritumoral adipose tissue in CC-induced inflammation.
Material and methods
Patients were divided in four experimental groups: obese patients with CC (OB-CC), lean patients with CC (LEAN-CC), obese patients without CC (OB), and lean patients without CC (LEAN).
Results
Plasma levels of pro-inflammatory cytokines (interleukin (IL)-6, IL-4, IL-8) and granulocyte-macrophage colony-stimulating factor (GM-CSF) were increased in OB-CC patients. Peritumoral adipose tissue (TF) explants and cultured mature adipocytes secreted higher amounts of nitrites and nitrates than did control and non-tumoral (NTF) adipose tissue both alone and in response to lipopolysaccharide (LPS). Nitrite and nitrate secretion was also increased in TF explants from OB-CC patients compared with that from LEAN-CC patients. Gene expression of adiponectin, tumor necrosis factor alpha (TNF-α), insulin-like growth factor type I (IGF-I), cyclooxygenase-2 (COX-2), and peroxisome proliferator-activated receptor γ (PPAR-γ) was increased in TF explants from CC patients. LPS increased the gene expression of IL-6, IL-10, TNF-α, vascular endothelial growth factor (VEGF), and COX-2 in OB and in TF explants from OB-CC patients. COX-2 and PPAR-γ inhibition further increased LPS-induced release of nitrites and nitrates in TF explants and adipocytes from OB-CC patients.
Conclusions
In conclusion, OB-CC patients have increased plasma levels of pro-inflammatory and angiogenic factors. TF from OB-CC patients shows an increased secretion of inflammatory markers compared with both TF from LEAN-CC and non-tumoral adipose tissue (AT) through a COX-2- and PPAR-γ-independent mechanism.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>26493186</pmid><doi>10.1007/s00384-015-2420-6</doi><tpages>11</tpages></addata></record> |
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source | MEDLINE; SpringerLink Journals - AutoHoldings |
subjects | Adipocytes - metabolism Adiponectin - genetics Adipose Tissue - metabolism Adipose Tissue - secretion Adipose tissues Body fat Body Mass Index Colorectal cancer Colorectal Neoplasms - metabolism Colorectal Neoplasms - pathology Cyclooxygenase 2 Inhibitors - metabolism Cytokines - blood Cytokines - genetics Cytokines - metabolism Development and progression Gastroenterology Gene Expression Granulocyte-Macrophage Progenitor Cells - metabolism Hepatology Humans Inflammation - metabolism Insulin-Like Growth Factor I - genetics Interleukins Internal Medicine Macrophage colony stimulating factor Medicine Medicine & Public Health Neovascularization, Pathologic Nitrates Nitrates - metabolism Nitrites - metabolism Obesity - metabolism Original Article PPAR gamma - genetics Proctology Risk factors Surgery Vascular endothelial growth factor Vascular Endothelial Growth Factor A - blood Vascular Endothelial Growth Factor A - genetics |
title | Peritumoral adipose tissue as a source of inflammatory and angiogenic factors in colorectal cancer |
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