In the last decade, chemotherapies were the SoC in advanced NSCLC treatment with limited benefit to long-term survival. Discovery of EGFR/ALK and PD1/PDL1 followed by of approval targeted therapies (TTs) and immunotherapies (IOs), respectively, marked two major treatments shifts. In addition, science advancement on drug resistance issued from TTs and new drug gable mutations continue to transform the treatment landscape and options for patients with advanced NSCLC.
This study used IMS Oncology Analyzer™ a syndicated, retrospective, longitudinal cancer treatment database collecting anonymized patient-level oncology data in EU5, projected to national level. Data collected between 2005 and 2016 was used to identify changes in the treatment paradigm in advanced NSCLC. Three time period groups have been compared: period 1: from 2005 to 2008; period 2: from 2009 to 2014 and period 3: 2015 and 2016.
Of the currently 1,602,026 (projected number) treated populations, there is an increase in protein kinase Inhibitors (TKIs) usage, mainly represented by anti EGFR and anti ALK, from 8% to 23% to 30% in period 1, 2 and period 3 respectively. Monoclonal antibodies (MAb) follows a similar trend increasing from 1% to 15% in the last years, respectively, while the platinum agents slightly decreases. IOs captures 52% in the last couple of years from the overall MAb group. Till recently, bevacizumab (BEVA) was leading this therapeutic class. Increased granularity in patient stratification, will allow identification of more spectacular treatment changes or identification of those who would have passed unnoticed. In 1L, mutant segment, paradigm switch occurred end 2008 when TKIs reached directly 84%. In 2L, IOs jump is much less noticeable, entering directly in the last analyzed period with 25% from MAb group. In WT segment, we can notice 2 switches: one in 1L, end 2014 when BEVA reached directly 13% and a second one in 2L, end 2016, when MAbs captured 28%, with IOs representing 90% from this therapeutic group.
Currently, the advent of IOs has completely overshadowed existing TTs. Emerging genetic markers (ROS-1, KRAS, RET), specific EGFR/ALK mutations due to resistance along with combinations of IOs and TTs will continue to add new treatment options.
Clinical trial identification
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All authors have declared no conflicts of interest.