• Colorectal Dis · Nov 2014

    Review Meta Analysis

    KRAS status and resistance to epidermal growth factor receptor tyrosine-kinase inhibitor treatment in patients with metastatic colorectal cancer: a meta-analysis.

    • W Li, Q Shi, W Wang, J Liu, J Ren, Q Li, and F Hou.
    • Oncology Department, Shanghai Municipal Hospital of Traditional Chinese Medicine affiliated to Shanghai TCM University, Shanghai, China.
    • Colorectal Dis. 2014 Nov 1;16(11):O370-8.

    AimThis study reviewed the association between KRAS mutation and resistance to treatment with epidermal growth factor receptor (EGFR) tyrosine-kinase inhibitors (TKIs) in patients with metastatic colorectal cancer (mCRC).MethodA search was carried out of PubMed, MEDLINE, EMBASE and the Cochrane Library databases (to November 2013) without language restrictions.ResultsTen studies were included in the final meta-analysis, consisting of 1339 patients with mCRC, of whom 427 (32%) had a KRAS mutation. The objective response rate (ORR) of mCRC patients with KRAS mutation was 8% (33/427), whereas the ORR of mCRC patients with wild-type KRAS was 34% (306/912). The overall pooled response rate (RR) for the ORR was 1.297 (95% CI 1.244-1.353, P < 0.01). Subgroup analysis comparing cetuximab monotherapy treatment with cetuximab plus chemotherapy, showed a pooled RR of 1.26 (95% CI 1.12-0.63, P < 0.01) and 1.30 (95% CI 1.25-1.36, P < 0.01), respectively. For patients receiving anti-EGFR with monoclonal antibodies (mAb) given as first-line treatment or not, the pooled RRs were 1.34 (95% CI 1.23-1.46, P < 0.01) and 1.29 (95% CI 1.23-1.35, P < 0.01). The data on progression-free survival from five studies in the meta-analysis gave a hazard ratio (HR) of 1.99 with a 95% CI of 1.69-2.29. Finally, the data for overall survival in mCRC patients were pooled from the only three studies reporting the HR (1.80; 95% CI 1.50-2.10). None of the results had any evidence of heterogeneity.ConclusionAll the results favoured a stronger link between mutant KRAS and anti-EGFR mAb, but due to a mutually exclusive relationship between KRAS and other gene mutations the clinical usefulness of KRAS mutation as a selection marker for sensitivity to EGFR TKIs in mCRC is limited.Colorectal Disease © 2014 The Association of Coloproctology of Great Britain and Ireland.

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