The importance of KRAS mutations and EGF61A>G polymorphism to the effect of cetuximab and irinotecan in metastatic colorectal cancer
The effect of anti-epidermal growth factor receptor (EGFR) antibodies (mAb) in metastatic colorectal cancer seems limited to KRAS wild-type (wt) tumours, but still a major fraction of KRASwt patients are nonresponders and supplementary selection criteria are needed. We investigated methodological as...
Gespeichert in:
| Veröffentlicht in: | Annals of oncology 2009-05, Vol.20 (5), p.879-884 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 884 |
|---|---|
| container_issue | 5 |
| container_start_page | 879 |
| container_title | Annals of oncology |
| container_volume | 20 |
| creator | Garm Spindler, K. -L. Pallisgaard, N. Rasmussen, A.A. Lindebjerg, J. Andersen, R.F. Crüger, D. Jakobsen, A. |
| description | The effect of anti-epidermal growth factor receptor (EGFR) antibodies (mAb) in metastatic colorectal cancer seems limited to KRAS wild-type (wt) tumours, but still a major fraction of KRASwt patients are nonresponders and supplementary selection criteria are needed. We investigated methodological aspects of KRAS testing and the predictive and prognostic value of KRAS status combined with three EGFR-related gene polymorphisms [single-nucleotide polymorphisms (SNPs)] in patients treated with cetuximab and irinotecan.
The study included 71 patients referred to third-line cetuximab–irinotecan. Blood samples were analysed for SNPs. KRAS analysis was carried out by sequencing analysis and quantitative PCR (DxS kit) in primary tumour and distant metastases.
There was a clear correlation between KRAS status in primary tumours and metastasis. The DxS kit presented the highest sensitivity. Response was confined to KRASwt patients (40% response rate versus 0%, P < 0.1-3), which translated into a significant difference in PFS. The EGF61A>G polymorphism showed relation to clinical outcome. A combined biomarker analysis showed a 19% progression rate in KRASwt-EGF61 homozygote patients and 60% in the EGF61A/G patients (P = 0.006) and a significant increase in overall survival (17.1 versus 5.9 months, log-rank, P = 0.002).
The combined biomarker analysis maybe an attractive approach to selection of patients for third-line treatment including anti-EGFR mAbs. |
| doi_str_mv | 10.1093/annonc/mdn712 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_196664013</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><oup_id>10.1093/annonc/mdn712</oup_id><els_id>S0923753419408119</els_id><sourcerecordid>1702341231</sourcerecordid><originalsourceid>FETCH-LOGICAL-c436t-bc0b906e34cc2d15e3a8c484ac52b3bd4fc7339e171a179dd26d832a3b6691693</originalsourceid><addsrcrecordid>eNqFkcFr1zAcxYMo7uf06FWCIHipS5o0bS7Cj7Hfb7LBRCfKLiFNUpbZJjVJZbv7h5uuZZ6Gp1w-77289wXgNUYfMOLkSDrnnToatKtx-QRscMV40SCKn4IN4iUp6orQA_AixhuEEOMlfw4OMMc1r2izAX8urw20w-hDkk4Z6Dt49mX7FQ5Tksl6F6F0Gp7sdwxvP-7h6Pu7wYfx2sYBJg9TVpuuMyrNSmXSdGsH2d6LbLDOJ6Okg9bBwSQZZ08Fle99yBLZQzWHhpfgWSf7aF6t7yH4tju5PD4tzi_2n46354WihKWiVajliBlClSo1rgyRjaINlaoqW9Jq2qmaEG5wjWXup3XJdENKSVrGOGacHIK3i-8Y_K_JxCRu_BRcjhSYM8YowiRDxQKp4GMMphNjyJ3CncBIzJOLZXKxTJ75N6vp1A5G_6PXjTPwbgVkVLLvQu5s4wNXYpqDS5S59wvnp_G_mesfbUzm9gGW4adgNakrcfrjSnyvdpju8JX4nPl64U1e97c1QURlTZ5e2_kQQnv7SNJfdvi83w</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>196664013</pqid></control><display><type>article</type><title>The importance of KRAS mutations and EGF61A>G polymorphism to the effect of cetuximab and irinotecan in metastatic colorectal cancer</title><source>MEDLINE</source><source>Alma/SFX Local Collection</source><source>EZB Electronic Journals Library</source><creator>Garm Spindler, K. -L. ; Pallisgaard, N. ; Rasmussen, A.A. ; Lindebjerg, J. ; Andersen, R.F. ; Crüger, D. ; Jakobsen, A.</creator><creatorcontrib>Garm Spindler, K. -L. ; Pallisgaard, N. ; Rasmussen, A.A. ; Lindebjerg, J. ; Andersen, R.F. ; Crüger, D. ; Jakobsen, A.</creatorcontrib><description>The effect of anti-epidermal growth factor receptor (EGFR) antibodies (mAb) in metastatic colorectal cancer seems limited to KRAS wild-type (wt) tumours, but still a major fraction of KRASwt patients are nonresponders and supplementary selection criteria are needed. We investigated methodological aspects of KRAS testing and the predictive and prognostic value of KRAS status combined with three EGFR-related gene polymorphisms [single-nucleotide polymorphisms (SNPs)] in patients treated with cetuximab and irinotecan.
The study included 71 patients referred to third-line cetuximab–irinotecan. Blood samples were analysed for SNPs. KRAS analysis was carried out by sequencing analysis and quantitative PCR (DxS kit) in primary tumour and distant metastases.
There was a clear correlation between KRAS status in primary tumours and metastasis. The DxS kit presented the highest sensitivity. Response was confined to KRASwt patients (40% response rate versus 0%, P < 0.1-3), which translated into a significant difference in PFS. The EGF61A>G polymorphism showed relation to clinical outcome. A combined biomarker analysis showed a 19% progression rate in KRASwt-EGF61 homozygote patients and 60% in the EGF61A/G patients (P = 0.006) and a significant increase in overall survival (17.1 versus 5.9 months, log-rank, P = 0.002).
The combined biomarker analysis maybe an attractive approach to selection of patients for third-line treatment including anti-EGFR mAbs.</description><identifier>ISSN: 0923-7534</identifier><identifier>EISSN: 1569-8041</identifier><identifier>DOI: 10.1093/annonc/mdn712</identifier><identifier>PMID: 19179548</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Adult ; Aged ; Antibodies, Monoclonal - administration & dosage ; Antibodies, Monoclonal, Humanized ; Antineoplastic agents ; Antineoplastic Combined Chemotherapy Protocols - adverse effects ; Antineoplastic Combined Chemotherapy Protocols - therapeutic use ; Biological and medical sciences ; Biomarkers, Tumor - genetics ; Camptothecin - administration & dosage ; Camptothecin - analogs & derivatives ; Cetuximab ; cetuximab–irinotecan ; Colorectal Neoplasms - drug therapy ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - mortality ; Colorectal Neoplasms - pathology ; Disease-Free Survival ; DNA Mutational Analysis ; EGF61A>G ; Epidermal Growth Factor - genetics ; ErbB Receptors - antagonists & inhibitors ; ErbB Receptors - genetics ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene Expression Regulation, Neoplastic ; gene polymorphisms ; Humans ; Irinotecan ; Kaplan-Meier Estimate ; KRAS ; Male ; mCRC ; Medical sciences ; Middle Aged ; Mutation ; Neoplasm Metastasis ; Patient Selection ; Pharmacology. Drug treatments ; Polymorphism, Single Nucleotide ; Proportional Hazards Models ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins p21(ras) ; ras Proteins - genetics ; Retrospective Studies ; Risk Assessment ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Time Factors ; Treatment Outcome ; Tumors</subject><ispartof>Annals of oncology, 2009-05, Vol.20 (5), p.879-884</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 2009</rights><rights>2009 INIST-CNRS</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</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c436t-bc0b906e34cc2d15e3a8c484ac52b3bd4fc7339e171a179dd26d832a3b6691693</citedby><cites>FETCH-LOGICAL-c436t-bc0b906e34cc2d15e3a8c484ac52b3bd4fc7339e171a179dd26d832a3b6691693</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=21464020$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19179548$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Garm Spindler, K. -L.</creatorcontrib><creatorcontrib>Pallisgaard, N.</creatorcontrib><creatorcontrib>Rasmussen, A.A.</creatorcontrib><creatorcontrib>Lindebjerg, J.</creatorcontrib><creatorcontrib>Andersen, R.F.</creatorcontrib><creatorcontrib>Crüger, D.</creatorcontrib><creatorcontrib>Jakobsen, A.</creatorcontrib><title>The importance of KRAS mutations and EGF61A>G polymorphism to the effect of cetuximab and irinotecan in metastatic colorectal cancer</title><title>Annals of oncology</title><addtitle>Ann Oncol</addtitle><description>The effect of anti-epidermal growth factor receptor (EGFR) antibodies (mAb) in metastatic colorectal cancer seems limited to KRAS wild-type (wt) tumours, but still a major fraction of KRASwt patients are nonresponders and supplementary selection criteria are needed. We investigated methodological aspects of KRAS testing and the predictive and prognostic value of KRAS status combined with three EGFR-related gene polymorphisms [single-nucleotide polymorphisms (SNPs)] in patients treated with cetuximab and irinotecan.
The study included 71 patients referred to third-line cetuximab–irinotecan. Blood samples were analysed for SNPs. KRAS analysis was carried out by sequencing analysis and quantitative PCR (DxS kit) in primary tumour and distant metastases.
There was a clear correlation between KRAS status in primary tumours and metastasis. The DxS kit presented the highest sensitivity. Response was confined to KRASwt patients (40% response rate versus 0%, P < 0.1-3), which translated into a significant difference in PFS. The EGF61A>G polymorphism showed relation to clinical outcome. A combined biomarker analysis showed a 19% progression rate in KRASwt-EGF61 homozygote patients and 60% in the EGF61A/G patients (P = 0.006) and a significant increase in overall survival (17.1 versus 5.9 months, log-rank, P = 0.002).
The combined biomarker analysis maybe an attractive approach to selection of patients for third-line treatment including anti-EGFR mAbs.</description><subject>Adult</subject><subject>Aged</subject><subject>Antibodies, Monoclonal - administration & dosage</subject><subject>Antibodies, Monoclonal, Humanized</subject><subject>Antineoplastic agents</subject><subject>Antineoplastic Combined Chemotherapy Protocols - adverse effects</subject><subject>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Camptothecin - administration & dosage</subject><subject>Camptothecin - analogs & derivatives</subject><subject>Cetuximab</subject><subject>cetuximab–irinotecan</subject><subject>Colorectal Neoplasms - drug therapy</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - mortality</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Disease-Free Survival</subject><subject>DNA Mutational Analysis</subject><subject>EGF61A>G</subject><subject>Epidermal Growth Factor - genetics</subject><subject>ErbB Receptors - antagonists & inhibitors</subject><subject>ErbB Receptors - genetics</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>gene polymorphisms</subject><subject>Humans</subject><subject>Irinotecan</subject><subject>Kaplan-Meier Estimate</subject><subject>KRAS</subject><subject>Male</subject><subject>mCRC</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Mutation</subject><subject>Neoplasm Metastasis</subject><subject>Patient Selection</subject><subject>Pharmacology. Drug treatments</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Proportional Hazards Models</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogene Proteins p21(ras)</subject><subject>ras Proteins - genetics</subject><subject>Retrospective Studies</subject><subject>Risk Assessment</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Time Factors</subject><subject>Treatment Outcome</subject><subject>Tumors</subject><issn>0923-7534</issn><issn>1569-8041</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcFr1zAcxYMo7uf06FWCIHipS5o0bS7Cj7Hfb7LBRCfKLiFNUpbZJjVJZbv7h5uuZZ6Gp1w-77289wXgNUYfMOLkSDrnnToatKtx-QRscMV40SCKn4IN4iUp6orQA_AixhuEEOMlfw4OMMc1r2izAX8urw20w-hDkk4Z6Dt49mX7FQ5Tksl6F6F0Gp7sdwxvP-7h6Pu7wYfx2sYBJg9TVpuuMyrNSmXSdGsH2d6LbLDOJ6Okg9bBwSQZZ08Fle99yBLZQzWHhpfgWSf7aF6t7yH4tju5PD4tzi_2n46354WihKWiVajliBlClSo1rgyRjaINlaoqW9Jq2qmaEG5wjWXup3XJdENKSVrGOGacHIK3i-8Y_K_JxCRu_BRcjhSYM8YowiRDxQKp4GMMphNjyJ3CncBIzJOLZXKxTJ75N6vp1A5G_6PXjTPwbgVkVLLvQu5s4wNXYpqDS5S59wvnp_G_mesfbUzm9gGW4adgNakrcfrjSnyvdpju8JX4nPl64U1e97c1QURlTZ5e2_kQQnv7SNJfdvi83w</recordid><startdate>20090501</startdate><enddate>20090501</enddate><creator>Garm Spindler, K. -L.</creator><creator>Pallisgaard, N.</creator><creator>Rasmussen, A.A.</creator><creator>Lindebjerg, J.</creator><creator>Andersen, R.F.</creator><creator>Crüger, D.</creator><creator>Jakobsen, A.</creator><general>Elsevier Ltd</general><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</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>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>H94</scope><scope>K9.</scope></search><sort><creationdate>20090501</creationdate><title>The importance of KRAS mutations and EGF61A>G polymorphism to the effect of cetuximab and irinotecan in metastatic colorectal cancer</title><author>Garm Spindler, K. -L. ; Pallisgaard, N. ; Rasmussen, A.A. ; Lindebjerg, J. ; Andersen, R.F. ; Crüger, D. ; Jakobsen, A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c436t-bc0b906e34cc2d15e3a8c484ac52b3bd4fc7339e171a179dd26d832a3b6691693</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Antibodies, Monoclonal - administration & dosage</topic><topic>Antibodies, Monoclonal, Humanized</topic><topic>Antineoplastic agents</topic><topic>Antineoplastic Combined Chemotherapy Protocols - adverse effects</topic><topic>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Camptothecin - administration & dosage</topic><topic>Camptothecin - analogs & derivatives</topic><topic>Cetuximab</topic><topic>cetuximab–irinotecan</topic><topic>Colorectal Neoplasms - drug therapy</topic><topic>Colorectal Neoplasms - genetics</topic><topic>Colorectal Neoplasms - mortality</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Disease-Free Survival</topic><topic>DNA Mutational Analysis</topic><topic>EGF61A>G</topic><topic>Epidermal Growth Factor - genetics</topic><topic>ErbB Receptors - antagonists & inhibitors</topic><topic>ErbB Receptors - genetics</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>gene polymorphisms</topic><topic>Humans</topic><topic>Irinotecan</topic><topic>Kaplan-Meier Estimate</topic><topic>KRAS</topic><topic>Male</topic><topic>mCRC</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Mutation</topic><topic>Neoplasm Metastasis</topic><topic>Patient Selection</topic><topic>Pharmacology. Drug treatments</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Proportional Hazards Models</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Proto-Oncogene Proteins p21(ras)</topic><topic>ras Proteins - genetics</topic><topic>Retrospective Studies</topic><topic>Risk Assessment</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Time Factors</topic><topic>Treatment Outcome</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Garm Spindler, K. -L.</creatorcontrib><creatorcontrib>Pallisgaard, N.</creatorcontrib><creatorcontrib>Rasmussen, A.A.</creatorcontrib><creatorcontrib>Lindebjerg, J.</creatorcontrib><creatorcontrib>Andersen, R.F.</creatorcontrib><creatorcontrib>Crüger, D.</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>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><jtitle>Annals of oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Garm Spindler, K. -L.</au><au>Pallisgaard, N.</au><au>Rasmussen, A.A.</au><au>Lindebjerg, J.</au><au>Andersen, R.F.</au><au>Crüger, D.</au><au>Jakobsen, A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The importance of KRAS mutations and EGF61A>G polymorphism to the effect of cetuximab and irinotecan in metastatic colorectal cancer</atitle><jtitle>Annals of oncology</jtitle><addtitle>Ann Oncol</addtitle><date>2009-05-01</date><risdate>2009</risdate><volume>20</volume><issue>5</issue><spage>879</spage><epage>884</epage><pages>879-884</pages><issn>0923-7534</issn><eissn>1569-8041</eissn><abstract>The effect of anti-epidermal growth factor receptor (EGFR) antibodies (mAb) in metastatic colorectal cancer seems limited to KRAS wild-type (wt) tumours, but still a major fraction of KRASwt patients are nonresponders and supplementary selection criteria are needed. We investigated methodological aspects of KRAS testing and the predictive and prognostic value of KRAS status combined with three EGFR-related gene polymorphisms [single-nucleotide polymorphisms (SNPs)] in patients treated with cetuximab and irinotecan.
The study included 71 patients referred to third-line cetuximab–irinotecan. Blood samples were analysed for SNPs. KRAS analysis was carried out by sequencing analysis and quantitative PCR (DxS kit) in primary tumour and distant metastases.
There was a clear correlation between KRAS status in primary tumours and metastasis. The DxS kit presented the highest sensitivity. Response was confined to KRASwt patients (40% response rate versus 0%, P < 0.1-3), which translated into a significant difference in PFS. The EGF61A>G polymorphism showed relation to clinical outcome. A combined biomarker analysis showed a 19% progression rate in KRASwt-EGF61 homozygote patients and 60% in the EGF61A/G patients (P = 0.006) and a significant increase in overall survival (17.1 versus 5.9 months, log-rank, P = 0.002).
The combined biomarker analysis maybe an attractive approach to selection of patients for third-line treatment including anti-EGFR mAbs.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>19179548</pmid><doi>10.1093/annonc/mdn712</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0923-7534 |
| ispartof | Annals of oncology, 2009-05, Vol.20 (5), p.879-884 |
| issn | 0923-7534 1569-8041 |
| language | eng |
| recordid | cdi_proquest_journals_196664013 |
| source | MEDLINE; Alma/SFX Local Collection; EZB Electronic Journals Library |
| subjects | Adult Aged Antibodies, Monoclonal - administration & dosage Antibodies, Monoclonal, Humanized Antineoplastic agents Antineoplastic Combined Chemotherapy Protocols - adverse effects Antineoplastic Combined Chemotherapy Protocols - therapeutic use Biological and medical sciences Biomarkers, Tumor - genetics Camptothecin - administration & dosage Camptothecin - analogs & derivatives Cetuximab cetuximab–irinotecan Colorectal Neoplasms - drug therapy Colorectal Neoplasms - genetics Colorectal Neoplasms - mortality Colorectal Neoplasms - pathology Disease-Free Survival DNA Mutational Analysis EGF61A>G Epidermal Growth Factor - genetics ErbB Receptors - antagonists & inhibitors ErbB Receptors - genetics Female Gastroenterology. Liver. Pancreas. Abdomen Gene Expression Regulation, Neoplastic gene polymorphisms Humans Irinotecan Kaplan-Meier Estimate KRAS Male mCRC Medical sciences Middle Aged Mutation Neoplasm Metastasis Patient Selection Pharmacology. Drug treatments Polymorphism, Single Nucleotide Proportional Hazards Models Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins p21(ras) ras Proteins - genetics Retrospective Studies Risk Assessment Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Time Factors Treatment Outcome Tumors |
| title | The importance of KRAS mutations and EGF61A>G polymorphism to the effect of cetuximab and irinotecan in metastatic colorectal cancer |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-11T18%3A25%3A20IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20importance%20of%20KRAS%20mutations%20and%20EGF61A%3EG%20polymorphism%20to%20the%20effect%20of%20cetuximab%20and%20irinotecan%20in%20metastatic%20colorectal%20cancer&rft.jtitle=Annals%20of%20oncology&rft.au=Garm%20Spindler,%20K.%20-L.&rft.date=2009-05-01&rft.volume=20&rft.issue=5&rft.spage=879&rft.epage=884&rft.pages=879-884&rft.issn=0923-7534&rft.eissn=1569-8041&rft_id=info:doi/10.1093/annonc/mdn712&rft_dat=%3Cproquest_cross%3E1702341231%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=196664013&rft_id=info:pmid/19179548&rft_oup_id=10.1093/annonc/mdn712&rft_els_id=S0923753419408119&rfr_iscdi=true |