Mekenkamp, Leonie J.M;
Tol, Jolien;
Dijkstra, Jeroen;
De Krijger, Inge;
Vink-Borger, M Elisa;
Teerenstra, Steven;
Verwiel, Eugene;
Koopman, Miriam;
Meijer, Gerrit A.;
van Krieken, J. Han J.M.;
Kuiper, Roland;
Punt, Cornelis J.A.;
Nagtegaal, Iris D.
Abstract 235: Beyond KRAS mutation status: Influence of KRAS copy number alteration and microRNAs in response to cetuximab in metastatic colorectal cancer patients
Sie können Bookmarks mittels Listen verwalten, loggen Sie sich dafür bitte in Ihr SLUB Benutzerkonto ein.
Medientyp:
E-Artikel
Titel:
Abstract 235: Beyond KRAS mutation status: Influence of KRAS copy number alteration and microRNAs in response to cetuximab in metastatic colorectal cancer patients
Beteiligte:
Mekenkamp, Leonie J.M;
Tol, Jolien;
Dijkstra, Jeroen;
De Krijger, Inge;
Vink-Borger, M Elisa;
Teerenstra, Steven;
Verwiel, Eugene;
Koopman, Miriam;
Meijer, Gerrit A.;
van Krieken, J. Han J.M.;
Kuiper, Roland;
Punt, Cornelis J.A.;
Nagtegaal, Iris D.
Erschienen:
American Association for Cancer Research (AACR), 2011
Beschreibung:
<jats:title>Abstract</jats:title>
<jats:p>Introduction: KRAS 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 KRAS 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.</jats:p>
<jats:p>Patients and methods: Formalin-fixed paraffin-embedded primary tumor tissue was used of 34 mCRC patients from a phase III trial (CAIRO2), who were selected based upon their good (n=17) and poor (n=17) progression-free survival (PFS) upon treatment with cetuximab in combination with capecitabine, oxaliplatin, and bevacizumab. Gene CNA at the KRAS locus was assessed using a high resolution genome-wide array CGH and the expression levels of 17 miRNAs targeting KRAS were determined by real-time PCR.</jats:p>
<jats:p>Results: Copy number loss of the KRAS locus was observed in the tumor of 5 patients who were all good responders including patients with a KRAS mutation. Copy number gains in two wild type-KRAS tumors were associated with a poor PFS. Increased expression of several miRNAs (presented at the meeting) targeting KRAS correlated with PFS of patients treated with cetuximab, bevacizumab and chemotherapy.</jats:p>
<jats:p>Conclusion: Our results indicate that the assessment of KRAS CNA and miRNAs targeting KRAS further optimize the selection of mCRC eligible for anti-EGFR therapy, in addition to KRAS mutation status.</jats:p>
<jats:p>Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 235. doi:10.1158/1538-7445.AM2011-235</jats:p>