The KRAS, BRAF, PIK3CA Array is designed for the rapid qualitative simultaneous detection of point mutations within the KRAS, BRAF and PIK3CA genes from fresh/frozen and formalin fixed paraffin embedded (FFPE) tissue DNA for predictive and prognostic mutation profiling. PIK3CA for research use only.
Colorectal cancer (CRC) is the third most common cancer worldwide and prognosis for patients with metastatic CRC (mCRC) remains poor, with a median overall survival (OS) of 18 to 21 months. Monoclonal antibodies (moAbs) 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.
Studies have shown that patients with mCRC carrying activating KRAS gene mutations do not benefit from anti-EGFR moAb therapy and 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.
However, when KRAS, BRAF and PIK3CA are mutated they are permanently ‘turned on’, permitting downstream signalling, 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.
In addition to colorectal cancer, KRAS, BRAF and PIK3CA mutations have been implicated in lung cancer, head and neck cancer, thyroid cancer and malignant melanoma and breast cancer.