In the literature: December 2019

摘要

The introduction of new high-throughput technologies in oncology and the need to apply precision medicine for cancer patients has led to the detection of several molecular alterations. Among them, activating mutations of ERBB2 have been reported in many solid tumours. In the last years, several clinical trials with covalent tyrosine kinase inhibitors (TKIs) for ERBB2 mutant cancers have been conducted, with different results among several cancer types. In the SUMMIT trial, neratinib was most effective in breast cancer patients, with the majority of responders having tumours with L755S, V777L, or L869R ERBB2 mutations. In an elegant article published in by Robichaux , different TKI sensitivities between malignancies might be explained by cancer-specific mutational hotspots. In this experiment, specific exon 20 insertions were associated with neratinib sensitivity in breast cancer patients, nevertheless, these were associated with resistance in other cancer types, demonstrating that there may be other mechanisms underlying these tumour-type-specific differences.