The detectability of the pretreatment EGFR T790M mutations in lung adenocarcinoma using CAST-PCR and digital PCR

Adenocarcinoma is the most common histological class of lung carcinoma, and its relative incidence is increasing (1). A great deal of progress has been made in targeted therapy for non-small cell lung cancer (NSCLC), largely as a result of the development of small-molecular inhibitors, such as epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) (2-4) and anaplastic lymphoma kinase (ALK) inhibitors (5). However, molecular targeted therapy is associated with some problems. A gatekeeper T790M mutation is known to cause resistance to EGFR-TKIs (6-10). This mutation is reported in 50–60% of cases with acquired resistance to EGFR-TKIs (7,9). The mutation detected rates are different from the mutation detection methods (11). T790M substitution has been shown to alter the proper binding of the drug to the ATP pocket of EGFR and/or return the affinity of the ATP to the drug to the wild-type level (8,9)