Beyond <it<KRAS</it< mutation status: influence of <it<KRAS</it< copy number status and microRNAs on clinical outcome to cetuximab in metastatic colorectal cancer patients

<p<Abstract</p< <p<Background</p< <p<<it<KRAS</it< mutation is a negative predictive factor for treatment with anti-epidermal growth factor receptor (EGFR) antibodies in metastatic colorectal cancer (mCRC). Novel predictive markers are required to further im...
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Autor*in:	Mekenkamp Leonie JM [verfasserIn] Tol Jolien [verfasserIn] Dijkstra Jeroen R [verfasserIn] de Krijger Inge [verfasserIn] Vink-Börger M [verfasserIn] van Vliet Shannon [verfasserIn] Teerenstra Steven [verfasserIn] Kamping Eveline [verfasserIn] Verwiel Eugène [verfasserIn] Koopman Miriam [verfasserIn] Meijer Gerrit A [verfasserIn] van Krieken J Han JM [verfasserIn] Kuiper Roland [verfasserIn] Punt Cornelis JA [verfasserIn] Nagtegaal Iris D [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2012

Übergeordnetes Werk:	In: BMC Cancer - BMC, 2003, 12(2012), 1, p 292
Übergeordnetes Werk:	volume:12 ; year:2012 ; number:1, p 292

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/1471-2407-12-292

Katalog-ID:	DOAJ050090364

Internformat


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100	0		\|a Mekenkamp Leonie JM \|e verfasserin \|4 aut
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264		1	\|c 2012
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520			\|a <p<Abstract</p< <p<Background</p< <p<<it<KRAS</it< mutation is a negative predictive factor for treatment with anti-epidermal growth factor receptor (EGFR) antibodies in metastatic colorectal cancer (mCRC). Novel predictive markers are required to further improve the selection of patients for this treatment. We assessed the influence of modification of <it<KRAS</it< by gene copy number aberration (CNA) and microRNAs (miRNAs) in correlation to clinical outcome in mCRC patients treated with cetuximab in combination with chemotherapy and bevacizumab.</p< <p<Methods</p< <p<Formalin-fixed paraffin-embedded primary tumour tissue was used from 34 mCRC patients in a phase III trial, who were selected based upon their good (n = 17) or poor (n = 17) progression-free survival (PFS) upon treatment with cetuximab in combination with capecitabine, oxaliplatin, and bevacizumab. Gene copy number at the <it<KRAS</it< locus was assessed using high resolution genome-wide array CGH and the expression levels of 17 miRNAs targeting <it<KRAS</it< were determined by real-time PCR.</p< <p<Results</p< <p<Copy number loss of the <it<KRAS</it< locus was observed in the tumour of 5 patients who were all good responders including patients with a <it<KRAS</it< mutation. Copy number gains in two wild-type <it<KRAS</it< tumours were associated with a poor PFS. In <it<KRAS</it< mutated tumours increased miR-200b and decreased miR-143 expression were associated with a good PFS. In wild-type <it<KRAS</it< patients, miRNA expression did not correlate with PFS in a multivariate model.</p< <p<Conclusions</p< <p<Our results indicate that the assessment of <it<KRAS</it< CNA and miRNAs targeting <it<KRAS</it< might further optimize the selection of mCRC eligible for anti-EGFR therapy.</p<
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700	0		\|a Vink-Börger M \|e verfasserin \|4 aut
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700	0		\|a Koopman Miriam \|e verfasserin \|4 aut
700	0		\|a Meijer Gerrit A \|e verfasserin \|4 aut
700	0		\|a van Krieken J Han JM \|e verfasserin \|4 aut
700	0		\|a Kuiper Roland \|e verfasserin \|4 aut
700	0		\|a Punt Cornelis JA \|e verfasserin \|4 aut
700	0		\|a Nagtegaal Iris D \|e verfasserin \|4 aut
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912			\|a GBV_ILN_4012
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Indexfelder

author_variant	m l j mlj t j tj d j r djr d k i dki v b m vbm v v s vvs t s ts k e ke v e ve k m km m g a mga v k j h j vkjhj k r kr p c j pcj n i d nid
matchkey_str	article:14712407:2012----::eodtrstuainttsnlecoikaicpnmesauadirraociiaotoeoeuia
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publishDate	2012
allfields	10.1186/1471-2407-12-292 doi (DE-627)DOAJ050090364 (DE-599)DOAJ0bf1a254f99f41f19d8735d421926b94 DE-627 ger DE-627 rakwb eng RC254-282 Mekenkamp Leonie JM verfasserin aut Beyond <it<KRAS</it< mutation status: influence of <it<KRAS</it< copy number status and microRNAs on clinical outcome to cetuximab in metastatic colorectal cancer patients 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<<it<KRAS</it< mutation is a negative predictive factor for treatment with anti-epidermal growth factor receptor (EGFR) antibodies in metastatic colorectal cancer (mCRC). Novel predictive markers are required to further improve the selection of patients for this treatment. We assessed the influence of modification of <it<KRAS</it< by gene copy number aberration (CNA) and microRNAs (miRNAs) in correlation to clinical outcome in mCRC patients treated with cetuximab in combination with chemotherapy and bevacizumab.</p< <p<Methods</p< <p<Formalin-fixed paraffin-embedded primary tumour tissue was used from 34 mCRC patients in a phase III trial, who were selected based upon their good (n = 17) or poor (n = 17) progression-free survival (PFS) upon treatment with cetuximab in combination with capecitabine, oxaliplatin, and bevacizumab. Gene copy number at the <it<KRAS</it< locus was assessed using high resolution genome-wide array CGH and the expression levels of 17 miRNAs targeting <it<KRAS</it< were determined by real-time PCR.</p< <p<Results</p< <p<Copy number loss of the <it<KRAS</it< locus was observed in the tumour of 5 patients who were all good responders including patients with a <it<KRAS</it< mutation. Copy number gains in two wild-type <it<KRAS</it< tumours were associated with a poor PFS. In <it<KRAS</it< mutated tumours increased miR-200b and decreased miR-143 expression were associated with a good PFS. In wild-type <it<KRAS</it< patients, miRNA expression did not correlate with PFS in a multivariate model.</p< <p<Conclusions</p< <p<Our results indicate that the assessment of <it<KRAS</it< CNA and miRNAs targeting <it<KRAS</it< might further optimize the selection of mCRC eligible for anti-EGFR therapy.</p< Neoplasms. Tumors. Oncology. Including cancer and carcinogens Tol Jolien verfasserin aut Dijkstra Jeroen R verfasserin aut de Krijger Inge verfasserin aut Vink-Börger M verfasserin aut van Vliet Shannon verfasserin aut Teerenstra Steven verfasserin aut Kamping Eveline verfasserin aut Verwiel Eugène verfasserin aut Koopman Miriam verfasserin aut Meijer Gerrit A verfasserin aut van Krieken J Han JM verfasserin aut Kuiper Roland verfasserin aut Punt Cornelis JA verfasserin aut Nagtegaal Iris D verfasserin aut In BMC Cancer BMC, 2003 12(2012), 1, p 292 (DE-627)326643710 (DE-600)2041352-X 14712407 nnns volume:12 year:2012 number:1, p 292 https://doi.org/10.1186/1471-2407-12-292 kostenfrei https://doaj.org/article/0bf1a254f99f41f19d8735d421926b94 kostenfrei http://www.biomedcentral.com/1471-2407/12/292 kostenfrei https://doaj.org/toc/1471-2407 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2012 1, p 292
spelling	10.1186/1471-2407-12-292 doi (DE-627)DOAJ050090364 (DE-599)DOAJ0bf1a254f99f41f19d8735d421926b94 DE-627 ger DE-627 rakwb eng RC254-282 Mekenkamp Leonie JM verfasserin aut Beyond <it<KRAS</it< mutation status: influence of <it<KRAS</it< copy number status and microRNAs on clinical outcome to cetuximab in metastatic colorectal cancer patients 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<<it<KRAS</it< mutation is a negative predictive factor for treatment with anti-epidermal growth factor receptor (EGFR) antibodies in metastatic colorectal cancer (mCRC). Novel predictive markers are required to further improve the selection of patients for this treatment. We assessed the influence of modification of <it<KRAS</it< by gene copy number aberration (CNA) and microRNAs (miRNAs) in correlation to clinical outcome in mCRC patients treated with cetuximab in combination with chemotherapy and bevacizumab.</p< <p<Methods</p< <p<Formalin-fixed paraffin-embedded primary tumour tissue was used from 34 mCRC patients in a phase III trial, who were selected based upon their good (n = 17) or poor (n = 17) progression-free survival (PFS) upon treatment with cetuximab in combination with capecitabine, oxaliplatin, and bevacizumab. Gene copy number at the <it<KRAS</it< locus was assessed using high resolution genome-wide array CGH and the expression levels of 17 miRNAs targeting <it<KRAS</it< were determined by real-time PCR.</p< <p<Results</p< <p<Copy number loss of the <it<KRAS</it< locus was observed in the tumour of 5 patients who were all good responders including patients with a <it<KRAS</it< mutation. Copy number gains in two wild-type <it<KRAS</it< tumours were associated with a poor PFS. In <it<KRAS</it< mutated tumours increased miR-200b and decreased miR-143 expression were associated with a good PFS. In wild-type <it<KRAS</it< patients, miRNA expression did not correlate with PFS in a multivariate model.</p< <p<Conclusions</p< <p<Our results indicate that the assessment of <it<KRAS</it< CNA and miRNAs targeting <it<KRAS</it< might further optimize the selection of mCRC eligible for anti-EGFR therapy.</p< Neoplasms. Tumors. Oncology. Including cancer and carcinogens Tol Jolien verfasserin aut Dijkstra Jeroen R verfasserin aut de Krijger Inge verfasserin aut Vink-Börger M verfasserin aut van Vliet Shannon verfasserin aut Teerenstra Steven verfasserin aut Kamping Eveline verfasserin aut Verwiel Eugène verfasserin aut Koopman Miriam verfasserin aut Meijer Gerrit A verfasserin aut van Krieken J Han JM verfasserin aut Kuiper Roland verfasserin aut Punt Cornelis JA verfasserin aut Nagtegaal Iris D verfasserin aut In BMC Cancer BMC, 2003 12(2012), 1, p 292 (DE-627)326643710 (DE-600)2041352-X 14712407 nnns volume:12 year:2012 number:1, p 292 https://doi.org/10.1186/1471-2407-12-292 kostenfrei https://doaj.org/article/0bf1a254f99f41f19d8735d421926b94 kostenfrei http://www.biomedcentral.com/1471-2407/12/292 kostenfrei https://doaj.org/toc/1471-2407 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2012 1, p 292
allfields_unstemmed	10.1186/1471-2407-12-292 doi (DE-627)DOAJ050090364 (DE-599)DOAJ0bf1a254f99f41f19d8735d421926b94 DE-627 ger DE-627 rakwb eng RC254-282 Mekenkamp Leonie JM verfasserin aut Beyond <it<KRAS</it< mutation status: influence of <it<KRAS</it< copy number status and microRNAs on clinical outcome to cetuximab in metastatic colorectal cancer patients 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<<it<KRAS</it< mutation is a negative predictive factor for treatment with anti-epidermal growth factor receptor (EGFR) antibodies in metastatic colorectal cancer (mCRC). Novel predictive markers are required to further improve the selection of patients for this treatment. We assessed the influence of modification of <it<KRAS</it< by gene copy number aberration (CNA) and microRNAs (miRNAs) in correlation to clinical outcome in mCRC patients treated with cetuximab in combination with chemotherapy and bevacizumab.</p< <p<Methods</p< <p<Formalin-fixed paraffin-embedded primary tumour tissue was used from 34 mCRC patients in a phase III trial, who were selected based upon their good (n = 17) or poor (n = 17) progression-free survival (PFS) upon treatment with cetuximab in combination with capecitabine, oxaliplatin, and bevacizumab. Gene copy number at the <it<KRAS</it< locus was assessed using high resolution genome-wide array CGH and the expression levels of 17 miRNAs targeting <it<KRAS</it< were determined by real-time PCR.</p< <p<Results</p< <p<Copy number loss of the <it<KRAS</it< locus was observed in the tumour of 5 patients who were all good responders including patients with a <it<KRAS</it< mutation. Copy number gains in two wild-type <it<KRAS</it< tumours were associated with a poor PFS. In <it<KRAS</it< mutated tumours increased miR-200b and decreased miR-143 expression were associated with a good PFS. In wild-type <it<KRAS</it< patients, miRNA expression did not correlate with PFS in a multivariate model.</p< <p<Conclusions</p< <p<Our results indicate that the assessment of <it<KRAS</it< CNA and miRNAs targeting <it<KRAS</it< might further optimize the selection of mCRC eligible for anti-EGFR therapy.</p< Neoplasms. Tumors. Oncology. Including cancer and carcinogens Tol Jolien verfasserin aut Dijkstra Jeroen R verfasserin aut de Krijger Inge verfasserin aut Vink-Börger M verfasserin aut van Vliet Shannon verfasserin aut Teerenstra Steven verfasserin aut Kamping Eveline verfasserin aut Verwiel Eugène verfasserin aut Koopman Miriam verfasserin aut Meijer Gerrit A verfasserin aut van Krieken J Han JM verfasserin aut Kuiper Roland verfasserin aut Punt Cornelis JA verfasserin aut Nagtegaal Iris D verfasserin aut In BMC Cancer BMC, 2003 12(2012), 1, p 292 (DE-627)326643710 (DE-600)2041352-X 14712407 nnns volume:12 year:2012 number:1, p 292 https://doi.org/10.1186/1471-2407-12-292 kostenfrei https://doaj.org/article/0bf1a254f99f41f19d8735d421926b94 kostenfrei http://www.biomedcentral.com/1471-2407/12/292 kostenfrei https://doaj.org/toc/1471-2407 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2012 1, p 292
allfieldsGer	10.1186/1471-2407-12-292 doi (DE-627)DOAJ050090364 (DE-599)DOAJ0bf1a254f99f41f19d8735d421926b94 DE-627 ger DE-627 rakwb eng RC254-282 Mekenkamp Leonie JM verfasserin aut Beyond <it<KRAS</it< mutation status: influence of <it<KRAS</it< copy number status and microRNAs on clinical outcome to cetuximab in metastatic colorectal cancer patients 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<<it<KRAS</it< mutation is a negative predictive factor for treatment with anti-epidermal growth factor receptor (EGFR) antibodies in metastatic colorectal cancer (mCRC). Novel predictive markers are required to further improve the selection of patients for this treatment. We assessed the influence of modification of <it<KRAS</it< by gene copy number aberration (CNA) and microRNAs (miRNAs) in correlation to clinical outcome in mCRC patients treated with cetuximab in combination with chemotherapy and bevacizumab.</p< <p<Methods</p< <p<Formalin-fixed paraffin-embedded primary tumour tissue was used from 34 mCRC patients in a phase III trial, who were selected based upon their good (n = 17) or poor (n = 17) progression-free survival (PFS) upon treatment with cetuximab in combination with capecitabine, oxaliplatin, and bevacizumab. Gene copy number at the <it<KRAS</it< locus was assessed using high resolution genome-wide array CGH and the expression levels of 17 miRNAs targeting <it<KRAS</it< were determined by real-time PCR.</p< <p<Results</p< <p<Copy number loss of the <it<KRAS</it< locus was observed in the tumour of 5 patients who were all good responders including patients with a <it<KRAS</it< mutation. Copy number gains in two wild-type <it<KRAS</it< tumours were associated with a poor PFS. In <it<KRAS</it< mutated tumours increased miR-200b and decreased miR-143 expression were associated with a good PFS. In wild-type <it<KRAS</it< patients, miRNA expression did not correlate with PFS in a multivariate model.</p< <p<Conclusions</p< <p<Our results indicate that the assessment of <it<KRAS</it< CNA and miRNAs targeting <it<KRAS</it< might further optimize the selection of mCRC eligible for anti-EGFR therapy.</p< Neoplasms. Tumors. Oncology. Including cancer and carcinogens Tol Jolien verfasserin aut Dijkstra Jeroen R verfasserin aut de Krijger Inge verfasserin aut Vink-Börger M verfasserin aut van Vliet Shannon verfasserin aut Teerenstra Steven verfasserin aut Kamping Eveline verfasserin aut Verwiel Eugène verfasserin aut Koopman Miriam verfasserin aut Meijer Gerrit A verfasserin aut van Krieken J Han JM verfasserin aut Kuiper Roland verfasserin aut Punt Cornelis JA verfasserin aut Nagtegaal Iris D verfasserin aut In BMC Cancer BMC, 2003 12(2012), 1, p 292 (DE-627)326643710 (DE-600)2041352-X 14712407 nnns volume:12 year:2012 number:1, p 292 https://doi.org/10.1186/1471-2407-12-292 kostenfrei https://doaj.org/article/0bf1a254f99f41f19d8735d421926b94 kostenfrei http://www.biomedcentral.com/1471-2407/12/292 kostenfrei https://doaj.org/toc/1471-2407 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2012 1, p 292
allfieldsSound	10.1186/1471-2407-12-292 doi (DE-627)DOAJ050090364 (DE-599)DOAJ0bf1a254f99f41f19d8735d421926b94 DE-627 ger DE-627 rakwb eng RC254-282 Mekenkamp Leonie JM verfasserin aut Beyond <it<KRAS</it< mutation status: influence of <it<KRAS</it< copy number status and microRNAs on clinical outcome to cetuximab in metastatic colorectal cancer patients 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<<it<KRAS</it< mutation is a negative predictive factor for treatment with anti-epidermal growth factor receptor (EGFR) antibodies in metastatic colorectal cancer (mCRC). Novel predictive markers are required to further improve the selection of patients for this treatment. We assessed the influence of modification of <it<KRAS</it< by gene copy number aberration (CNA) and microRNAs (miRNAs) in correlation to clinical outcome in mCRC patients treated with cetuximab in combination with chemotherapy and bevacizumab.</p< <p<Methods</p< <p<Formalin-fixed paraffin-embedded primary tumour tissue was used from 34 mCRC patients in a phase III trial, who were selected based upon their good (n = 17) or poor (n = 17) progression-free survival (PFS) upon treatment with cetuximab in combination with capecitabine, oxaliplatin, and bevacizumab. Gene copy number at the <it<KRAS</it< locus was assessed using high resolution genome-wide array CGH and the expression levels of 17 miRNAs targeting <it<KRAS</it< were determined by real-time PCR.</p< <p<Results</p< <p<Copy number loss of the <it<KRAS</it< locus was observed in the tumour of 5 patients who were all good responders including patients with a <it<KRAS</it< mutation. Copy number gains in two wild-type <it<KRAS</it< tumours were associated with a poor PFS. In <it<KRAS</it< mutated tumours increased miR-200b and decreased miR-143 expression were associated with a good PFS. In wild-type <it<KRAS</it< patients, miRNA expression did not correlate with PFS in a multivariate model.</p< <p<Conclusions</p< <p<Our results indicate that the assessment of <it<KRAS</it< CNA and miRNAs targeting <it<KRAS</it< might further optimize the selection of mCRC eligible for anti-EGFR therapy.</p< Neoplasms. Tumors. Oncology. Including cancer and carcinogens Tol Jolien verfasserin aut Dijkstra Jeroen R verfasserin aut de Krijger Inge verfasserin aut Vink-Börger M verfasserin aut van Vliet Shannon verfasserin aut Teerenstra Steven verfasserin aut Kamping Eveline verfasserin aut Verwiel Eugène verfasserin aut Koopman Miriam verfasserin aut Meijer Gerrit A verfasserin aut van Krieken J Han JM verfasserin aut Kuiper Roland verfasserin aut Punt Cornelis JA verfasserin aut Nagtegaal Iris D verfasserin aut In BMC Cancer BMC, 2003 12(2012), 1, p 292 (DE-627)326643710 (DE-600)2041352-X 14712407 nnns volume:12 year:2012 number:1, p 292 https://doi.org/10.1186/1471-2407-12-292 kostenfrei https://doaj.org/article/0bf1a254f99f41f19d8735d421926b94 kostenfrei http://www.biomedcentral.com/1471-2407/12/292 kostenfrei https://doaj.org/toc/1471-2407 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2012 1, p 292
language	English
source	In BMC Cancer 12(2012), 1, p 292 volume:12 year:2012 number:1, p 292
sourceStr	In BMC Cancer 12(2012), 1, p 292 volume:12 year:2012 number:1, p 292
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Neoplasms. Tumors. Oncology. Including cancer and carcinogens
isfreeaccess_bool	true
container_title	BMC Cancer
authorswithroles_txt_mv	Mekenkamp Leonie JM @@aut@@ Tol Jolien @@aut@@ Dijkstra Jeroen R @@aut@@ de Krijger Inge @@aut@@ Vink-Börger M @@aut@@ van Vliet Shannon @@aut@@ Teerenstra Steven @@aut@@ Kamping Eveline @@aut@@ Verwiel Eugène @@aut@@ Koopman Miriam @@aut@@ Meijer Gerrit A @@aut@@ van Krieken J Han JM @@aut@@ Kuiper Roland @@aut@@ Punt Cornelis JA @@aut@@ Nagtegaal Iris D @@aut@@
publishDateDaySort_date	2012-01-01T00:00:00Z
hierarchy_top_id	326643710
id	DOAJ050090364
language_de	englisch
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callnumber-first	R - Medicine
author	Mekenkamp Leonie JM
spellingShingle	Mekenkamp Leonie JM misc RC254-282 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens Beyond <it<KRAS</it< mutation status: influence of <it<KRAS</it< copy number status and microRNAs on clinical outcome to cetuximab in metastatic colorectal cancer patients
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topic_title	RC254-282 Beyond <it<KRAS</it< mutation status: influence of <it<KRAS</it< copy number status and microRNAs on clinical outcome to cetuximab in metastatic colorectal cancer patients
topic	misc RC254-282 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
topic_unstemmed	misc RC254-282 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
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title	Beyond <it<KRAS</it< mutation status: influence of <it<KRAS</it< copy number status and microRNAs on clinical outcome to cetuximab in metastatic colorectal cancer patients
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title_full	Beyond <it<KRAS</it< mutation status: influence of <it<KRAS</it< copy number status and microRNAs on clinical outcome to cetuximab in metastatic colorectal cancer patients
author_sort	Mekenkamp Leonie JM
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author_browse	Mekenkamp Leonie JM Tol Jolien Dijkstra Jeroen R de Krijger Inge Vink-Börger M van Vliet Shannon Teerenstra Steven Kamping Eveline Verwiel Eugène Koopman Miriam Meijer Gerrit A van Krieken J Han JM Kuiper Roland Punt Cornelis JA Nagtegaal Iris D
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author-letter	Mekenkamp Leonie JM
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title_sort	beyond <it<kras</it< mutation status: influence of <it<kras</it< copy number status and micrornas on clinical outcome to cetuximab in metastatic colorectal cancer patients
callnumber	RC254-282
title_auth	Beyond <it<KRAS</it< mutation status: influence of <it<KRAS</it< copy number status and microRNAs on clinical outcome to cetuximab in metastatic colorectal cancer patients
abstract	<p<Abstract</p< <p<Background</p< <p<<it<KRAS</it< mutation is a negative predictive factor for treatment with anti-epidermal growth factor receptor (EGFR) antibodies in metastatic colorectal cancer (mCRC). Novel predictive markers are required to further improve the selection of patients for this treatment. We assessed the influence of modification of <it<KRAS</it< by gene copy number aberration (CNA) and microRNAs (miRNAs) in correlation to clinical outcome in mCRC patients treated with cetuximab in combination with chemotherapy and bevacizumab.</p< <p<Methods</p< <p<Formalin-fixed paraffin-embedded primary tumour tissue was used from 34 mCRC patients in a phase III trial, who were selected based upon their good (n = 17) or poor (n = 17) progression-free survival (PFS) upon treatment with cetuximab in combination with capecitabine, oxaliplatin, and bevacizumab. Gene copy number at the <it<KRAS</it< locus was assessed using high resolution genome-wide array CGH and the expression levels of 17 miRNAs targeting <it<KRAS</it< were determined by real-time PCR.</p< <p<Results</p< <p<Copy number loss of the <it<KRAS</it< locus was observed in the tumour of 5 patients who were all good responders including patients with a <it<KRAS</it< mutation. Copy number gains in two wild-type <it<KRAS</it< tumours were associated with a poor PFS. In <it<KRAS</it< mutated tumours increased miR-200b and decreased miR-143 expression were associated with a good PFS. In wild-type <it<KRAS</it< patients, miRNA expression did not correlate with PFS in a multivariate model.</p< <p<Conclusions</p< <p<Our results indicate that the assessment of <it<KRAS</it< CNA and miRNAs targeting <it<KRAS</it< might further optimize the selection of mCRC eligible for anti-EGFR therapy.</p<
abstractGer	<p<Abstract</p< <p<Background</p< <p<<it<KRAS</it< mutation is a negative predictive factor for treatment with anti-epidermal growth factor receptor (EGFR) antibodies in metastatic colorectal cancer (mCRC). Novel predictive markers are required to further improve the selection of patients for this treatment. We assessed the influence of modification of <it<KRAS</it< by gene copy number aberration (CNA) and microRNAs (miRNAs) in correlation to clinical outcome in mCRC patients treated with cetuximab in combination with chemotherapy and bevacizumab.</p< <p<Methods</p< <p<Formalin-fixed paraffin-embedded primary tumour tissue was used from 34 mCRC patients in a phase III trial, who were selected based upon their good (n = 17) or poor (n = 17) progression-free survival (PFS) upon treatment with cetuximab in combination with capecitabine, oxaliplatin, and bevacizumab. Gene copy number at the <it<KRAS</it< locus was assessed using high resolution genome-wide array CGH and the expression levels of 17 miRNAs targeting <it<KRAS</it< were determined by real-time PCR.</p< <p<Results</p< <p<Copy number loss of the <it<KRAS</it< locus was observed in the tumour of 5 patients who were all good responders including patients with a <it<KRAS</it< mutation. Copy number gains in two wild-type <it<KRAS</it< tumours were associated with a poor PFS. In <it<KRAS</it< mutated tumours increased miR-200b and decreased miR-143 expression were associated with a good PFS. In wild-type <it<KRAS</it< patients, miRNA expression did not correlate with PFS in a multivariate model.</p< <p<Conclusions</p< <p<Our results indicate that the assessment of <it<KRAS</it< CNA and miRNAs targeting <it<KRAS</it< might further optimize the selection of mCRC eligible for anti-EGFR therapy.</p<
abstract_unstemmed	<p<Abstract</p< <p<Background</p< <p<<it<KRAS</it< mutation is a negative predictive factor for treatment with anti-epidermal growth factor receptor (EGFR) antibodies in metastatic colorectal cancer (mCRC). Novel predictive markers are required to further improve the selection of patients for this treatment. We assessed the influence of modification of <it<KRAS</it< by gene copy number aberration (CNA) and microRNAs (miRNAs) in correlation to clinical outcome in mCRC patients treated with cetuximab in combination with chemotherapy and bevacizumab.</p< <p<Methods</p< <p<Formalin-fixed paraffin-embedded primary tumour tissue was used from 34 mCRC patients in a phase III trial, who were selected based upon their good (n = 17) or poor (n = 17) progression-free survival (PFS) upon treatment with cetuximab in combination with capecitabine, oxaliplatin, and bevacizumab. Gene copy number at the <it<KRAS</it< locus was assessed using high resolution genome-wide array CGH and the expression levels of 17 miRNAs targeting <it<KRAS</it< were determined by real-time PCR.</p< <p<Results</p< <p<Copy number loss of the <it<KRAS</it< locus was observed in the tumour of 5 patients who were all good responders including patients with a <it<KRAS</it< mutation. Copy number gains in two wild-type <it<KRAS</it< tumours were associated with a poor PFS. In <it<KRAS</it< mutated tumours increased miR-200b and decreased miR-143 expression were associated with a good PFS. In wild-type <it<KRAS</it< patients, miRNA expression did not correlate with PFS in a multivariate model.</p< <p<Conclusions</p< <p<Our results indicate that the assessment of <it<KRAS</it< CNA and miRNAs targeting <it<KRAS</it< might further optimize the selection of mCRC eligible for anti-EGFR therapy.</p<
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title_short	Beyond <it<KRAS</it< mutation status: influence of <it<KRAS</it< copy number status and microRNAs on clinical outcome to cetuximab in metastatic colorectal cancer patients
url	https://doi.org/10.1186/1471-2407-12-292 https://doaj.org/article/0bf1a254f99f41f19d8735d421926b94 http://www.biomedcentral.com/1471-2407/12/292 https://doaj.org/toc/1471-2407
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Novel predictive markers are required to further improve the selection of patients for this treatment. We assessed the influence of modification of <it<KRAS</it< by gene copy number aberration (CNA) and microRNAs (miRNAs) in correlation to clinical outcome in mCRC patients treated with cetuximab in combination with chemotherapy and bevacizumab.</p< <p<Methods</p< <p<Formalin-fixed paraffin-embedded primary tumour tissue was used from 34 mCRC patients in a phase III trial, who were selected based upon their good (n = 17) or poor (n = 17) progression-free survival (PFS) upon treatment with cetuximab in combination with capecitabine, oxaliplatin, and bevacizumab. Gene copy number at the <it<KRAS</it< locus was assessed using high resolution genome-wide array CGH and the expression levels of 17 miRNAs targeting <it<KRAS</it< were determined by real-time PCR.</p< <p<Results</p< <p<Copy number loss of the <it<KRAS</it< locus was observed in the tumour of 5 patients who were all good responders including patients with a <it<KRAS</it< mutation. Copy number gains in two wild-type <it<KRAS</it< tumours were associated with a poor PFS. In <it<KRAS</it< mutated tumours increased miR-200b and decreased miR-143 expression were associated with a good PFS. In wild-type <it<KRAS</it< patients, miRNA expression did not correlate with PFS in a multivariate model.</p< <p<Conclusions</p< <p<Our results indicate that the assessment of <it<KRAS</it< CNA and miRNAs targeting <it<KRAS</it< might further optimize the selection of mCRC eligible for anti-EGFR therapy.</p<</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Neoplasms. 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Beyond <it<KRAS</it< mutation status: influence of <it<KRAS</it< copy number status and microRNAs on clinical outcome to cetuximab in metastatic colorectal cancer patients

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