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Tumor genotyping to predict response

Nature Reviews Clinical Oncology volume 7, page 551 (2010)Cite this article

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Mutations in KRAS confer resistance to anti-EGFR therapy. Patients with metastatic colorectal cancer (mCRC) are, therefore, profiled for seven KRAS mutations before receiving cetuximab or panitumumab. In a study published in the Lancet Oncology, primary tumor samples (n = 773) were collected from patients with chemotherapy-refractory mCRC treated with cetuximab. The effects of KRAS, BRAF, NRAS, and PIK3CA mutations on the efficacy of cetuximab plus chemotherapy were evaluated. “We used a centralized and advanced mutation detection technology to ensure that all samples were analyzed by the same method, that the number of potentially occurring mutations assessed were maximized, and high sensitivity meant our analysis was not affected by the quality of the tumor samples,” says lead investigator Sabine Tejpar.

Objective response was the primary end point, and progression-free survival and overall survival were secondary end points. Multivariate analyses confirmed significant associations between outcome and KRAS, PIK3CA exon 20, NRAS and BRAF mutation status. “Our results provide a clear picture of the efficacy of cetuximab plus chemotherapy in chemotherapy-refractory mCRC according to the presence or absence of activating mutations in these genes,” says Tejpar.

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ORIGINAL RESEARCH PAPER

  1. De Roock, W. et al. Effects of KRAS, BRAF, NRAS, and PIK3CA mutations on the efficacy of cetuximab plus chemotherapy in chemotherapy-refractory metastatic colorectal cancer: a retrospective consortium analysis. Lancet Oncol. 11, 753–762 (2010)

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  1. Helene Myrvang
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Myrvang, H. Tumor genotyping to predict response. Nat Rev Clin Oncol 7, 551 (2010). https://doi.org/10.1038/nrclinonc.2010.144

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