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The KRAS / BRAF / PIK3CA Array* provides rapid detection of mutations within KRAS, BRAF and PIK3CA genes, enabling appropriate selection of patients for anti-EGFR therapy.

Colorectal cancer (CRC) is the third most common cancer worldwide 1. Metastatic disease accounts for 40-50% of newly diagnosed patients and is associated with high morbidity 1, 2. Despite recent therapeutic advances, the prognosis for patients with metastatic CRC (mCRC) remains poor 3. Early treatment is therefore critical. This array allows the clinician to correctly select appropriate patients for anti-EGFR therapy, thereby maximising drug efficacy and minimising adverse side effects to the patient.

Monoclonal antibodies (MoAbs) targeting the epidermal growth factor receptor (EGFR) have proven effective in combination with chemotherapy or as single agents for treatment of mCRC 4, 5. These molecules bind to the extracellular domain of EGFR with high affinity and competitively inhibit ligand binding, which leads to inhibition of phosphorylation and subsequent activation of downstream signalling pathways. However, only a subset of patients with mCRC clinically benefit from EGFR-targeted MoAbs.

Mutations in the KRAS gene are known to disrupt the EGFR pathway, rendering anti-EGFR therapy ineffective. Presence of KRAS mutations accounts for approximately 35-45% of non-responsive patients3. Oncogenic mutations in genes encoding key downstream effectors within the EGFR-signalling pathways may also be responsible for resistance to EGFR-targeted MoAbs6. Mutations within the BRAF 7 and PIK3CA 8 genes have now been reported to affect patient response to EGFR-targeted MoAbs.

Key Benefits


*PIK3CA for research use only.


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