These conjugates exhibited high antiproliferative potency against a number of cancer cell lines, including the epidermal growth factor receptor (EGFR) L858R/T790M mutant cell.
The purpose of this study was to clarify the relationship between the EGFR-L858R mutation and cancer cell invasion ability and to investigate the molecular mechanisms involved in the formation of MPE.
The results of cancer tissue specimens were identical to those with existing systems (nucleic acid-locked nucleic acid PCR clamp or cycleave PCR), except for two samples that showed both exon 19 deletions and L858R.
Importantly, we observed that the combination of PI3K-mTOR and MEK inhibitors effectively shrunk tumors in a transgenic and xenograft model of EGFR T790M-L858Rcancers.