The relationship between serum vascular endothelial growth factor A and microsatellite instability in colorectal cancer

Aim  It has been suggested that colorectal neoplasms with or without microsatellite instability (MSI) can stimulate angiogenesis in different ways. The vascular endothelial growth factor (VEGF) system is essential for the angiogenetic process and the growth of malignant tumours. The aim of this stud...

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Veröffentlicht in:Colorectal disease 2011-09, Vol.13 (9), p.984-988
Hauptverfasser: Hansen, T. F., Jensen, L. H., Spindler, K.-L. G., Lindebjerg, J., Brandslund, I., Jakobsen, A.
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container_end_page 988
container_issue 9
container_start_page 984
container_title Colorectal disease
container_volume 13
creator Hansen, T. F.
Jensen, L. H.
Spindler, K.-L. G.
Lindebjerg, J.
Brandslund, I.
Jakobsen, A.
description Aim  It has been suggested that colorectal neoplasms with or without microsatellite instability (MSI) can stimulate angiogenesis in different ways. The vascular endothelial growth factor (VEGF) system is essential for the angiogenetic process and the growth of malignant tumours. The aim of this study was to analyse the relationship between serum VEGF‐A and the MSI status of patients with colorectal cancer (CRC). Method  In the study, 249 patients with CRC were divided into a test cohort of 83 patients and a validation cohort of 166. MSI was determined using immunohistochemistry. Tumours lacking protein expression of any of the four mismatch repair genes (MLH1, PMS2, MSH2 or MSH6) were labelled as high MSI. The rest were considered to be microsatellite stable (MSS). The serum VEGF‐A analyses were performed by ELISA. Results  The tumours of 15 patients in the test cohort and 27 in the validation cohort were classified as MSI. In the test cohort, patients with an MSI tumour had a significantly higher median serum VEGF‐A concentration [617 pg/ml (95% CI 445–863)], compared with patients with an MSS tumour, [317 pg/ml (95% CI 224–386)], P = 0.01. A similar relationship was confirmed in the validation cohort, P = 0.04. Conclusion  This study provides some evidence to suggest that patients with an MSI tumour have higher serum VEGF‐A levels than patients with an MSS tumour. If further validated, these findings could be of importance when considering the effects of anti‐VEGF‐A treatment.
doi_str_mv 10.1111/j.1463-1318.2010.02357.x
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F. ; Jensen, L. H. ; Spindler, K.-L. G. ; Lindebjerg, J. ; Brandslund, I. ; Jakobsen, A.</creator><creatorcontrib>Hansen, T. F. ; Jensen, L. H. ; Spindler, K.-L. G. ; Lindebjerg, J. ; Brandslund, I. ; Jakobsen, A.</creatorcontrib><description>Aim  It has been suggested that colorectal neoplasms with or without microsatellite instability (MSI) can stimulate angiogenesis in different ways. The vascular endothelial growth factor (VEGF) system is essential for the angiogenetic process and the growth of malignant tumours. The aim of this study was to analyse the relationship between serum VEGF‐A and the MSI status of patients with colorectal cancer (CRC). Method  In the study, 249 patients with CRC were divided into a test cohort of 83 patients and a validation cohort of 166. MSI was determined using immunohistochemistry. Tumours lacking protein expression of any of the four mismatch repair genes (MLH1, PMS2, MSH2 or MSH6) were labelled as high MSI. The rest were considered to be microsatellite stable (MSS). The serum VEGF‐A analyses were performed by ELISA. Results  The tumours of 15 patients in the test cohort and 27 in the validation cohort were classified as MSI. In the test cohort, patients with an MSI tumour had a significantly higher median serum VEGF‐A concentration [617 pg/ml (95% CI 445–863)], compared with patients with an MSS tumour, [317 pg/ml (95% CI 224–386)], P = 0.01. A similar relationship was confirmed in the validation cohort, P = 0.04. Conclusion  This study provides some evidence to suggest that patients with an MSI tumour have higher serum VEGF‐A levels than patients with an MSS tumour. If further validated, these findings could be of importance when considering the effects of anti‐VEGF‐A treatment.</description><identifier>ISSN: 1462-8910</identifier><identifier>EISSN: 1463-1318</identifier><identifier>DOI: 10.1111/j.1463-1318.2010.02357.x</identifier><identifier>PMID: 20594200</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adaptor Proteins, Signal Transducing - genetics ; Adenocarcinoma - blood ; Adenocarcinoma - genetics ; Adenocarcinoma - pathology ; Adenosine Triphosphatases - genetics ; Adult ; Aged ; Aged, 80 and over ; Colorectal neoplasms ; Colorectal Neoplasms - blood ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - pathology ; DNA Repair Enzymes - genetics ; DNA-Binding Proteins - genetics ; Female ; Humans ; Male ; Microsatellite Instability ; Middle Aged ; Mismatch Repair Endonuclease PMS2 ; MutL Protein Homolog 1 ; MutS Homolog 2 Protein - genetics ; Nuclear Proteins - genetics ; vascular endothelial growth factor A ; Vascular Endothelial Growth Factor A - blood</subject><ispartof>Colorectal disease, 2011-09, Vol.13 (9), p.984-988</ispartof><rights>2011 The Authors. Colorectal Disease © 2011 The Association of Coloproctology of Great Britain and Ireland</rights><rights>2011 The Authors. Colorectal Disease © 2011 The Association of Coloproctology of Great Britain and Ireland.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3587-420572638d7ffec1d1b81941787c11f6e23d609b631e37febc2425efcbfc53863</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1463-1318.2010.02357.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1463-1318.2010.02357.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20594200$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hansen, T. F.</creatorcontrib><creatorcontrib>Jensen, L. H.</creatorcontrib><creatorcontrib>Spindler, K.-L. G.</creatorcontrib><creatorcontrib>Lindebjerg, J.</creatorcontrib><creatorcontrib>Brandslund, I.</creatorcontrib><creatorcontrib>Jakobsen, A.</creatorcontrib><title>The relationship between serum vascular endothelial growth factor A and microsatellite instability in colorectal cancer</title><title>Colorectal disease</title><addtitle>Colorectal Dis</addtitle><description>Aim  It has been suggested that colorectal neoplasms with or without microsatellite instability (MSI) can stimulate angiogenesis in different ways. The vascular endothelial growth factor (VEGF) system is essential for the angiogenetic process and the growth of malignant tumours. The aim of this study was to analyse the relationship between serum VEGF‐A and the MSI status of patients with colorectal cancer (CRC). Method  In the study, 249 patients with CRC were divided into a test cohort of 83 patients and a validation cohort of 166. MSI was determined using immunohistochemistry. Tumours lacking protein expression of any of the four mismatch repair genes (MLH1, PMS2, MSH2 or MSH6) were labelled as high MSI. The rest were considered to be microsatellite stable (MSS). The serum VEGF‐A analyses were performed by ELISA. Results  The tumours of 15 patients in the test cohort and 27 in the validation cohort were classified as MSI. In the test cohort, patients with an MSI tumour had a significantly higher median serum VEGF‐A concentration [617 pg/ml (95% CI 445–863)], compared with patients with an MSS tumour, [317 pg/ml (95% CI 224–386)], P = 0.01. A similar relationship was confirmed in the validation cohort, P = 0.04. Conclusion  This study provides some evidence to suggest that patients with an MSI tumour have higher serum VEGF‐A levels than patients with an MSS tumour. If further validated, these findings could be of importance when considering the effects of anti‐VEGF‐A treatment.</description><subject>Adaptor Proteins, Signal Transducing - genetics</subject><subject>Adenocarcinoma - blood</subject><subject>Adenocarcinoma - genetics</subject><subject>Adenocarcinoma - pathology</subject><subject>Adenosine Triphosphatases - genetics</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Colorectal neoplasms</subject><subject>Colorectal Neoplasms - blood</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - pathology</subject><subject>DNA Repair Enzymes - genetics</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Female</subject><subject>Humans</subject><subject>Male</subject><subject>Microsatellite Instability</subject><subject>Middle Aged</subject><subject>Mismatch Repair Endonuclease PMS2</subject><subject>MutL Protein Homolog 1</subject><subject>MutS Homolog 2 Protein - genetics</subject><subject>Nuclear Proteins - genetics</subject><subject>vascular endothelial growth factor A</subject><subject>Vascular Endothelial Growth Factor A - blood</subject><issn>1462-8910</issn><issn>1463-1318</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9UU1vEzEQtRAV_YC_gHzjtMEfu2vnglQCpJUKRVVRpV4sr3eWOHjXwfaS5N_jbdrMZZ5m3jyN3kMIUzKjuT6uZ7SseUE5lTNG8pQwXonZ7hU6Oy5eP2FWyDklp-g8xjUhtBZUvkGnjFTzkhFyhrb3K8ABnE7WD3FlN7iBtAUYcIQw9vifjmZ0OmAYWp9W4Kx2-Hfw27TCnTbJB3yJ9dDi3prgo07gnE2A7RCTbmzG-4yx8c4HMCkfGz0YCG_RSaddhHfP_QL9-vb1fnFV3NwurxeXN4XhlRRFfrISrOayFV0Hhra0kXReUiGFobSrgfG2JvOm5hS46KAxrGQVdKbpTMVlzS_Qh4PuJvi_I8SkehtNflIP4MeopCxLxqWoMvP9M3NsemjVJtheh7168SoTPh0IW-tgf9xToqZM1FpN1qvJejVlop4yUTu1uP1yPcEsUBwEbEywOwro8EfVgotKPfxYqmr5c_H57vFOfef_AYegkRI</recordid><startdate>201109</startdate><enddate>201109</enddate><creator>Hansen, T. 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F.</creatorcontrib><creatorcontrib>Jensen, L. H.</creatorcontrib><creatorcontrib>Spindler, K.-L. G.</creatorcontrib><creatorcontrib>Lindebjerg, J.</creatorcontrib><creatorcontrib>Brandslund, I.</creatorcontrib><creatorcontrib>Jakobsen, A.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Colorectal disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hansen, T. F.</au><au>Jensen, L. H.</au><au>Spindler, K.-L. G.</au><au>Lindebjerg, J.</au><au>Brandslund, I.</au><au>Jakobsen, A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The relationship between serum vascular endothelial growth factor A and microsatellite instability in colorectal cancer</atitle><jtitle>Colorectal disease</jtitle><addtitle>Colorectal Dis</addtitle><date>2011-09</date><risdate>2011</risdate><volume>13</volume><issue>9</issue><spage>984</spage><epage>988</epage><pages>984-988</pages><issn>1462-8910</issn><eissn>1463-1318</eissn><abstract>Aim  It has been suggested that colorectal neoplasms with or without microsatellite instability (MSI) can stimulate angiogenesis in different ways. The vascular endothelial growth factor (VEGF) system is essential for the angiogenetic process and the growth of malignant tumours. The aim of this study was to analyse the relationship between serum VEGF‐A and the MSI status of patients with colorectal cancer (CRC). Method  In the study, 249 patients with CRC were divided into a test cohort of 83 patients and a validation cohort of 166. MSI was determined using immunohistochemistry. Tumours lacking protein expression of any of the four mismatch repair genes (MLH1, PMS2, MSH2 or MSH6) were labelled as high MSI. The rest were considered to be microsatellite stable (MSS). The serum VEGF‐A analyses were performed by ELISA. Results  The tumours of 15 patients in the test cohort and 27 in the validation cohort were classified as MSI. In the test cohort, patients with an MSI tumour had a significantly higher median serum VEGF‐A concentration [617 pg/ml (95% CI 445–863)], compared with patients with an MSS tumour, [317 pg/ml (95% CI 224–386)], P = 0.01. A similar relationship was confirmed in the validation cohort, P = 0.04. Conclusion  This study provides some evidence to suggest that patients with an MSI tumour have higher serum VEGF‐A levels than patients with an MSS tumour. If further validated, these findings could be of importance when considering the effects of anti‐VEGF‐A treatment.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>20594200</pmid><doi>10.1111/j.1463-1318.2010.02357.x</doi><tpages>5</tpages></addata></record>
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subjects Adaptor Proteins, Signal Transducing - genetics
Adenocarcinoma - blood
Adenocarcinoma - genetics
Adenocarcinoma - pathology
Adenosine Triphosphatases - genetics
Adult
Aged
Aged, 80 and over
Colorectal neoplasms
Colorectal Neoplasms - blood
Colorectal Neoplasms - genetics
Colorectal Neoplasms - pathology
DNA Repair Enzymes - genetics
DNA-Binding Proteins - genetics
Female
Humans
Male
Microsatellite Instability
Middle Aged
Mismatch Repair Endonuclease PMS2
MutL Protein Homolog 1
MutS Homolog 2 Protein - genetics
Nuclear Proteins - genetics
vascular endothelial growth factor A
Vascular Endothelial Growth Factor A - blood
title The relationship between serum vascular endothelial growth factor A and microsatellite instability in colorectal cancer
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