EGF61A>G polymorphism as predictive marker of clinical outcome to first-line capecitabine and oxaliplatin in metastatic colorectal cancer
The purpose of the present study was to investigate polymorphisms related to the metabolism of fluoropyrimidine and oxaliplatin, thymidylate synthase (TS) and excision repair cross-complementing gene 1 (ERCC1) 118, in metastatic colorectal cancer patients treated with capecitabine and oxaliplatin (X...
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| Veröffentlicht in: | Annals of oncology 2010-03, Vol.21 (3), p.535-539 |
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| creator | Spindler, K.-L. G. Andersen, R.F. Jensen, L.H. Ploen, J. Jakobsen, A. |
| description | The purpose of the present study was to investigate polymorphisms related to the metabolism of fluoropyrimidine and oxaliplatin, thymidylate synthase (TS) and excision repair cross-complementing gene 1 (ERCC1) 118, in metastatic colorectal cancer patients treated with capecitabine and oxaliplatin (XELOX). We also investigated the importance of the EGF61A>G polymorphism, which holds a functional influence on the tyrosine kinase receptor regulation.
We included 68 patients treated with first-line XELOX. Polymorphism analyses were carried out on pretreatment blood samples. Response was evaluated according to the RECIST. Survival analysis was described by the Kaplan–Meier method and log-rank testing.
The overall response rate was 38% and the median overall survival 19.4 months. A favorable outcome was seen in patients with the EGF61A/G genotype compared with the combined group of A/A and G/G, with response rates of 57% and 18%, respectively (P = 0.001). There was a significantly different progression-free survival (P = 0.018) in favor of the A/G group. The TS and ERCC1 genotypes failed to provide any significant impact on the outcome.
Polymorphism analysis of a simple blood sample is a feasible approach to biomarker analysis and the EGF61A>G polymorphism may influence the effect of first-line XELOX. Consequently, this marker deserves further investigation. |
| doi_str_mv | 10.1093/annonc/mdp336 |
| format | Article |
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We included 68 patients treated with first-line XELOX. Polymorphism analyses were carried out on pretreatment blood samples. Response was evaluated according to the RECIST. Survival analysis was described by the Kaplan–Meier method and log-rank testing.
The overall response rate was 38% and the median overall survival 19.4 months. A favorable outcome was seen in patients with the EGF61A/G genotype compared with the combined group of A/A and G/G, with response rates of 57% and 18%, respectively (P = 0.001). There was a significantly different progression-free survival (P = 0.018) in favor of the A/G group. The TS and ERCC1 genotypes failed to provide any significant impact on the outcome.
Polymorphism analysis of a simple blood sample is a feasible approach to biomarker analysis and the EGF61A>G polymorphism may influence the effect of first-line XELOX. Consequently, this marker deserves further investigation.</description><identifier>ISSN: 0923-7534</identifier><identifier>EISSN: 1569-8041</identifier><identifier>DOI: 10.1093/annonc/mdp336</identifier><identifier>PMID: 19850635</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Adenocarcinoma - drug therapy ; Adenocarcinoma - genetics ; Adenocarcinoma - pathology ; Adult ; Aged ; Antineoplastic agents ; Antineoplastic Combined Chemotherapy Protocols - therapeutic use ; Biological and medical sciences ; Capecitabine ; Colorectal Neoplasms - drug therapy ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - pathology ; Deoxycytidine - administration & dosage ; Deoxycytidine - analogs & derivatives ; DNA-Binding Proteins - genetics ; EGF61A>G ; Endonucleases - genetics ; Epidermal Growth Factor - genetics ; ERCC1 118 ; Feasibility Studies ; Female ; Fluorouracil - administration & dosage ; Fluorouracil - analogs & derivatives ; Gastroenterology. Liver. Pancreas. Abdomen ; gene polymorphisms ; Humans ; Male ; mCRC ; Medical sciences ; Middle Aged ; Neoplasm Staging ; Organoplatinum Compounds - administration & dosage ; Oxaliplatin ; Pharmacology. Drug treatments ; Polymorphism, Genetic - genetics ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Survival Rate ; Thymidylate Synthase - genetics ; Treatment Outcome ; Tumors ; XELOX</subject><ispartof>Annals of oncology, 2010-03, Vol.21 (3), p.535-539</ispartof><rights>2009 European Society for Medical Oncology</rights><rights>The Author 2009. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org 2010</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c546t-25978be5a74cf343a32e471329eef48d68f6653d93bb13a5a1e90c2489960fad3</citedby><cites>FETCH-LOGICAL-c546t-25978be5a74cf343a32e471329eef48d68f6653d93bb13a5a1e90c2489960fad3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22585931$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19850635$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Spindler, K.-L. G.</creatorcontrib><creatorcontrib>Andersen, R.F.</creatorcontrib><creatorcontrib>Jensen, L.H.</creatorcontrib><creatorcontrib>Ploen, J.</creatorcontrib><creatorcontrib>Jakobsen, A.</creatorcontrib><title>EGF61A>G polymorphism as predictive marker of clinical outcome to first-line capecitabine and oxaliplatin in metastatic colorectal cancer</title><title>Annals of oncology</title><addtitle>Ann Oncol</addtitle><description>The purpose of the present study was to investigate polymorphisms related to the metabolism of fluoropyrimidine and oxaliplatin, thymidylate synthase (TS) and excision repair cross-complementing gene 1 (ERCC1) 118, in metastatic colorectal cancer patients treated with capecitabine and oxaliplatin (XELOX). We also investigated the importance of the EGF61A>G polymorphism, which holds a functional influence on the tyrosine kinase receptor regulation.
We included 68 patients treated with first-line XELOX. Polymorphism analyses were carried out on pretreatment blood samples. Response was evaluated according to the RECIST. Survival analysis was described by the Kaplan–Meier method and log-rank testing.
The overall response rate was 38% and the median overall survival 19.4 months. A favorable outcome was seen in patients with the EGF61A/G genotype compared with the combined group of A/A and G/G, with response rates of 57% and 18%, respectively (P = 0.001). There was a significantly different progression-free survival (P = 0.018) in favor of the A/G group. The TS and ERCC1 genotypes failed to provide any significant impact on the outcome.
Polymorphism analysis of a simple blood sample is a feasible approach to biomarker analysis and the EGF61A>G polymorphism may influence the effect of first-line XELOX. Consequently, this marker deserves further investigation.</description><subject>Adenocarcinoma - drug therapy</subject><subject>Adenocarcinoma - genetics</subject><subject>Adenocarcinoma - pathology</subject><subject>Adult</subject><subject>Aged</subject><subject>Antineoplastic agents</subject><subject>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Capecitabine</subject><subject>Colorectal Neoplasms - drug therapy</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Deoxycytidine - administration & dosage</subject><subject>Deoxycytidine - analogs & derivatives</subject><subject>DNA-Binding Proteins - genetics</subject><subject>EGF61A>G</subject><subject>Endonucleases - genetics</subject><subject>Epidermal Growth Factor - genetics</subject><subject>ERCC1 118</subject><subject>Feasibility Studies</subject><subject>Female</subject><subject>Fluorouracil - administration & dosage</subject><subject>Fluorouracil - analogs & derivatives</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>gene polymorphisms</subject><subject>Humans</subject><subject>Male</subject><subject>mCRC</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Neoplasm Staging</subject><subject>Organoplatinum Compounds - administration & dosage</subject><subject>Oxaliplatin</subject><subject>Pharmacology. Drug treatments</subject><subject>Polymorphism, Genetic - genetics</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Survival Rate</subject><subject>Thymidylate Synthase - genetics</subject><subject>Treatment Outcome</subject><subject>Tumors</subject><subject>XELOX</subject><issn>0923-7534</issn><issn>1569-8041</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUFrFTEQx4Mo9vn06FVyEb2sTXY22c1FKLV9VQp6UCm9hGx2FqO7m22SLe1H8Fubxz7qSYRAGPLjP5nfEPKSs3ecKTg20-Qnezx2M4B8RDZcSFU0rOKPyYapEopaQHVEnsX4kzEmVamekiOuGsEkiA35fbY7l_zk_Y7OfrgffZh_uDhSE-kcsHM2uVukowm_MFDfUzu4yVkzUL8k60ekydPehZiK_IDUmhmtS6bdF2bqqL8zg5sHk9xE8xkxmZhyZan1gw9oU86yZrIYnpMnvRkivjjcW_Lt_Ozr6UVx-Xn38fTksrCikqkohaqbFoWpK9tDBQZKrGoOpULsq6aTTS-lgE5B23IwwnBUzJZVo5RkvelgS96suXPwNwvGpEcXLQ6DmdAvUdcAgoOSVSaLlbTBxxiw13Nw2cW95kzv5etVvl7lZ_7VIXlpR-z-0gfbGXh9AEzMEvuQB3fxgStL0QgFPHNvV84v8397Hv7oYsK7BzgvTMsaaqEvrq71p-9XwD5cf8mzbUm98pgV3zoMOlqH2X_n9tvQnXf_6PQHpRXB2g</recordid><startdate>20100301</startdate><enddate>20100301</enddate><creator>Spindler, K.-L. G.</creator><creator>Andersen, R.F.</creator><creator>Jensen, L.H.</creator><creator>Ploen, J.</creator><creator>Jakobsen, A.</creator><general>Elsevier Ltd</general><general>Oxford University Press</general><scope>6I.</scope><scope>AAFTH</scope><scope>BSCLL</scope><scope>IQODW</scope><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></search><sort><creationdate>20100301</creationdate><title>EGF61A>G polymorphism as predictive marker of clinical outcome to first-line capecitabine and oxaliplatin in metastatic colorectal cancer</title><author>Spindler, K.-L. G. ; Andersen, R.F. ; Jensen, L.H. ; Ploen, J. ; Jakobsen, A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c546t-25978be5a74cf343a32e471329eef48d68f6653d93bb13a5a1e90c2489960fad3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adenocarcinoma - drug therapy</topic><topic>Adenocarcinoma - genetics</topic><topic>Adenocarcinoma - pathology</topic><topic>Adult</topic><topic>Aged</topic><topic>Antineoplastic agents</topic><topic>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>Capecitabine</topic><topic>Colorectal Neoplasms - drug therapy</topic><topic>Colorectal Neoplasms - genetics</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Deoxycytidine - administration & dosage</topic><topic>Deoxycytidine - analogs & derivatives</topic><topic>DNA-Binding Proteins - genetics</topic><topic>EGF61A>G</topic><topic>Endonucleases - genetics</topic><topic>Epidermal Growth Factor - genetics</topic><topic>ERCC1 118</topic><topic>Feasibility Studies</topic><topic>Female</topic><topic>Fluorouracil - administration & dosage</topic><topic>Fluorouracil - analogs & derivatives</topic><topic>Gastroenterology. 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G.</creatorcontrib><creatorcontrib>Andersen, R.F.</creatorcontrib><creatorcontrib>Jensen, L.H.</creatorcontrib><creatorcontrib>Ploen, J.</creatorcontrib><creatorcontrib>Jakobsen, A.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Istex</collection><collection>Pascal-Francis</collection><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><jtitle>Annals of oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Spindler, K.-L. G.</au><au>Andersen, R.F.</au><au>Jensen, L.H.</au><au>Ploen, J.</au><au>Jakobsen, A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>EGF61A>G polymorphism as predictive marker of clinical outcome to first-line capecitabine and oxaliplatin in metastatic colorectal cancer</atitle><jtitle>Annals of oncology</jtitle><addtitle>Ann Oncol</addtitle><date>2010-03-01</date><risdate>2010</risdate><volume>21</volume><issue>3</issue><spage>535</spage><epage>539</epage><pages>535-539</pages><issn>0923-7534</issn><eissn>1569-8041</eissn><abstract>The purpose of the present study was to investigate polymorphisms related to the metabolism of fluoropyrimidine and oxaliplatin, thymidylate synthase (TS) and excision repair cross-complementing gene 1 (ERCC1) 118, in metastatic colorectal cancer patients treated with capecitabine and oxaliplatin (XELOX). We also investigated the importance of the EGF61A>G polymorphism, which holds a functional influence on the tyrosine kinase receptor regulation.
We included 68 patients treated with first-line XELOX. Polymorphism analyses were carried out on pretreatment blood samples. Response was evaluated according to the RECIST. Survival analysis was described by the Kaplan–Meier method and log-rank testing.
The overall response rate was 38% and the median overall survival 19.4 months. A favorable outcome was seen in patients with the EGF61A/G genotype compared with the combined group of A/A and G/G, with response rates of 57% and 18%, respectively (P = 0.001). There was a significantly different progression-free survival (P = 0.018) in favor of the A/G group. The TS and ERCC1 genotypes failed to provide any significant impact on the outcome.
Polymorphism analysis of a simple blood sample is a feasible approach to biomarker analysis and the EGF61A>G polymorphism may influence the effect of first-line XELOX. Consequently, this marker deserves further investigation.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>19850635</pmid><doi>10.1093/annonc/mdp336</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenocarcinoma - drug therapy Adenocarcinoma - genetics Adenocarcinoma - pathology Adult Aged Antineoplastic agents Antineoplastic Combined Chemotherapy Protocols - therapeutic use Biological and medical sciences Capecitabine Colorectal Neoplasms - drug therapy Colorectal Neoplasms - genetics Colorectal Neoplasms - pathology Deoxycytidine - administration & dosage Deoxycytidine - analogs & derivatives DNA-Binding Proteins - genetics EGF61A>G Endonucleases - genetics Epidermal Growth Factor - genetics ERCC1 118 Feasibility Studies Female Fluorouracil - administration & dosage Fluorouracil - analogs & derivatives Gastroenterology. Liver. Pancreas. Abdomen gene polymorphisms Humans Male mCRC Medical sciences Middle Aged Neoplasm Staging Organoplatinum Compounds - administration & dosage Oxaliplatin Pharmacology. Drug treatments Polymorphism, Genetic - genetics Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Survival Rate Thymidylate Synthase - genetics Treatment Outcome Tumors XELOX |
| title | EGF61A>G polymorphism as predictive marker of clinical outcome to first-line capecitabine and oxaliplatin in metastatic colorectal cancer |
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