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Randomised Phase II study of cetuximab alone or in combination with irinotecan in patients with metastatic colorectal cancer (CRC) with either KRAS WT or G13D mutation.

ABSTRACT: Interventions: Cetuximab & irinotecan combination therapy: Cetuximab 400mg/m2 Intravenous infusion (IVI) on Day 1, followed by 250mg/m2 Intravenous infusion (IVI) every week; Irinotecan 180mg/m2 Intravenous infusion (IVI) every 14 days; Treatment will continue until disease progression, unless there is unacceptable toxicity or either the patient or physician requests cessation of treatment. Primary outcome(s): To determine the 6 month PFS benefit of cetuximab alone or in combination with irinotecan in patients with KRAS WT or KRAS G13D mutated mCRC (PFS defined from time of randomisation to disease progression as defined by RECIST criteria version 1.1).[Patients will have a CT scan at baseline and every 6 weeks while on treatment. Patients will be followed up for 12 months after they progress on treatment.] Study Design: Purpose: Treatment; Allocation: Randomised controlled trial; Masking: Open (masking not used);Assignment: Parallel;Type of endpoint: Safety

DISEASE(S): Metastatic Colorectal Cancer,Cancer-bowel-back Passage (rectum) Or Large Bowel (colon)

PROVIDER: 2458601 | 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.

Dataset Information

Randomised Phase II study of cetuximab alone or in combination with irinotecan in patients with metastatic colorectal cancer (CRC) with either KRAS WT or G13D mutation.

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