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Avastin and chemotherapy followed by a KRAS stratified randomization to maintenance treatment for first line treatment of metastatic colorectal cancer

ABSTRACT: Primary objectives: To demonstrate that maintenance treatment with bevacizumab + erlotinib following first line chemo- and anti-angiogenetic therapy results in a significant increase in progression-free survival (PFS) rate at 3 months among patients without KRAS mutation as compared to maintenance treatment with bevacizumab alone. Primary endpoints: To evaluate maintenance treatment with bevacizumab+erlotinib versus bevacizumab alone in patients with KRAS WT tumors following first line chemo- and anti-angiogenetic therapy by comparing progression-free survival rate at 3 months.

DISEASE(S): Metastatic Colorectal Cancer,Patients With Previously Untreated Metastatic Colorectal Carcinoma.

PROVIDER: 2528060 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Project description: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. Here, 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. 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 KRAS locus was assessed using high resolution genome-wide array CGH and the expression levels of 17 miRNAs targeting KRAS were determined by real-time PCR. Good response was associated with 12p12.1 copy number loss, even in patients with a KRAS mutation, while copy number gain in wild-type KRAS patients was correlated with a poor response. In KRAS mutated tumours increased miR-200b and decreased miR-143 expression were associated with a good response. In wild-type KRAS patients, miRNA expression did not predict response in a multivariate model. Thus, assessment of KRAS CNA and miRNAs targeting KRAS might further optimize the selection of patients eligible for anti-EGFR therapy. Copy number detection was performed using NimbleScan and Nexus software Formalin-fixed paraffin-embedded primary tumour tissue was used from 34 metastisized colorectal cancer patients in a phase III trial (CKTO 2005-02; ClinTrials.gov NCT00208546) of the Dutch Colorectal Cancer Group (DCCG), 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.

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Avastin and chemotherapy followed by a KRAS stratified randomization to maintenance treatment for first line treatment of metastatic colorectal cancer

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