Targeted therapies in many cancers have allowed unprecedented progress in the treatment of disease. However, routine implementation of genomic testing is constrained due to: 1) limited amounts of sample (pg–ng range) per biological specimen, 2) diagnostic turnaround time and workflow, 3) cost, and 4) difficulties in detection of mutational loads below 5%. KRAS is mutated in approximately 40% of colorectal cancers (CRCs). The majority of mutations affect codons 12, 13, and 61 and indicate a negative response to anti–epidermal growth factor receptor (EGFR) therapy. To optimize therapy strategies for personalized care, it is critical to rapidly screen patient samples for the presence of multiple KRAS mutations.
