- To provide an update on the setting of patients with EGFR-mutated advanced non-small cell lung cancer (NSCLC) and implications for targeted treatments
- To provide a summary of data from clinical studies with EGFR tyrosine kinase inhibitors (TKIs) in patients with advanced NSCLC
- To provide an update on the mechanisms of resistance to EGFR TKIs and how to overcome it
|Title||Duration||Content||CME Points||CME Test|
|Important Pathways to Target in (Advanced) NSCLC: A Focus on EGFR-Inhibition and Implications for Clinical Practice||50 min.||82 slides||1||Take test|
This E-Learning module elaborates the role of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) in patients with EGFR-mutated non-small cell lung cancer (NSCLC) and provides the timeline of the development of different generations of EGFR TKIs with illustration of results from relevant clinical trials, putting the achievements, in terms of improved outcomes, into a clinically relevant context.
The authors contextualize clinical practice messages in terms of selection of treatment options for patients with EGFR mutation-positive NSCLC. They discuss the data from relevant clinical trials in terms of first and second generation of EGFR TKIs, elaborate acquired resistance to EGFR-TKIs and discuss the data on third-generation EGFR TKIs.
The module details treatment strategies for patients who develop resistance mutation and analyses the type of progression that drives therapy, as well as the role of re-biopsy and liquid biopsy.
In particular, the authors underline that in NSCLC patients with activating EGFR mutations, EGFR TKIs therapy statistically significantly delays disease progression and should be considered as front-line therapy. In EGFR wild-type patients, EGFR TKIs are not recommended in first-line, being inferior to chemotherapy and no better than placebo.
At the time of progression, patients on EGFR TKIs should undergo additional molecular testing to select the optimal therapy. Blood based testing may be considered in patients where a biopsy is not always possible, if blood is negative a biospy should be performed. The authors advise to consider both plasma and tumour analysis to confirm presence or absence of T790M mutation. Osimertinib is preferred to chemotherapy in patients with T790M positive tumours at the time of progression. They state that the switch to chemotherapy is standard of care for T790M negative patients. Furthermore, the authors advise to consider clinical trials for T790M negative population to assess new agents e.g. Axl, MET, HER2 and other inhibitors.
This module has been developed from a previous E-Learning module that elaborated different pathways relevant for targeted treatments in patients with advanced NSCLC. The authors have presented here the new data since then.
The authors have reported no conflicts of interest