Rapid profiling of point mutations in the KRAS, BRAF and PIK3CA genes
Colorectal cancer (CRC) is the third most common cancer worldwide and prognosis for patients with metastatic CRC (mCRC) remains poor. Monoclonal antibodies like cetuximab and panitumumab have proven to be effective in combination with chemotherapy or as single agents for the treatment of mCRC. They block the signal from EGFR inhibiting downstream signalling including KRAS, BRAF and PIK3CA mediated events.
However, when KRAS, BRAF and PIK3CA are mutated they are permanently turned on, permitting downstream events irrespective of anti-EGFR therapy. The Randox KRAS, BRAF, PIK3CA Array allows the clinician to detect important mutations in these genes, enabling the appropriate selection of patients for therapy.
Studies have shown that patients with mCRC carrying activating KRAS gene mutations do not benefit from anti-EGFR moAb therapy. KRAS mutations have emerged as the major negative predictor of efficacy in patients receiving cetuximab or panitumumab. The occurrence of KRAS mutations however only accounts for 35-45% of nonresponsive patients. Identification of additional genetic determinants of primary resistance to EGFR targeted therapies in CRC is therefore important. Recent studies have shown mutations in BRAF and PIK3CA genes to affect patient response to EGFR-targeted moAbs.
• Streamlined workflow – optimised for the molecular laboratory
• Compatible with FFPE tissue and fresh/frozen tissue
• Detection of 1% mutant in a background of wildtype genomic DNA
• Only a single DNA sample required
• Mutations are also implicated in other cancers such as KRAS in lung cancer and PIK3CA in breast cancer
*PIK3CA for research use only