HER2-driven Lung Cancer Sensitive to Chemotherapy
Human epidermal growth factor receptor 2 (HER2)-driven non-small cell lung cancers (NSCLC) are sensitive to chemotherapy.
Human epidermal growth factor receptor 2 (HER2)-driven non-small cell lung cancers (NSCLC) are sensitive to chemotherapy, with HER2-targeted agents being potential therapies of interest, a new study published online ahead of print in the journal Annals of Oncology has shown.1
Although HER2 mutations have been identified as oncogenic drivers in 1% to 2% of lung adenocarcinomas, there is currently no standard of care for these patients. Therefore, researchers sought to evaluate the therapeutic outcomes of patients with HER2 mutations and lung cancer and to determine the efficacy of various drug regimens.
For the retrospective cohort study, researchers analyzed data from 101 patients with advanced NSCLC and a known HER2 exon-20 insertion, who were treated with chemotherapy and/or HER2-targeted agents. Of those, 60.4% were never smokers and all were adenocarcinomas. Five patients had concomitant EGFR mutations, 1 had concomitant ALK translocations, and 1 had ROS translocations.
Results showed that median overall survival was 24 months. The overall response rate and median progression-free survival with conventional chemotherapy were 43.5% and 6 months in first-line therapies, and 10% and 4.3 months in second-line therapies.
A total of 65 patients received HER2-targeted therapies, of whom 57 received trastuzumab, 14 received neratinib, 9 received afatinib, and 5 received lapatinib. The overall response rate was 50.9% with trastuzumab and progression-free survival was 4.8 months.
“Our results should help to define the best therapeutic strategy for these patients and to orient future clinical trials,” the authors conclude.
1. Maziéres J, Barlesi F, Filleron T, et al. Lung cancer patients with HER2 mutations treated with chemotherapy and HER2-targets drugs: results from the European EUHER2 cohort [published online ahead of print November 23, 2015]. Ann Oncol. doi:10.1093/annonc/mdv573.