DR LOVE: I was wondering where things stand from your point of view, with the use of checkpoint inhibitors in people with targetable mutations. There’s been discussion that maybe these people don’t respond as well, less PD-1. They’re nonsmokers. Does that change your algorithm? You were talking about kind of a standard second-line approach. What about in patients with targetable mutations?

DR BLUMENSCHEIN: So we’re actually doing a study right now where we’re looking at the combination of an EGFR inhibitor plus a PD-1 inhibitor. But to get to your point, the data sets that have come out from a number of trials demonstrate that patients who have higher mutational burden, generally smokers, have a higher response rate, I think it’s about 25% if there’s a higher mutational burden. And then those that don’t, the response rates are lower and they’re lower than the usual 18%. So there is a correlation with higher genetic mutational load, et cetera, and benefit when you’re treated with a PD-1 or PD-L1 inhibitor.

In routine practice, no. If someone has an EGFR mutation or an ALK translocation, I’ll treat them with the appropriate compound or compounds, depending on how their tumor progresses and their treatment progresses. I’m not using those combinations off study. I do think that immunotherapies are a reasonable option for those patients at progression if there’s not a third-generation EGFR TKI that’s available for them or if they’ve run through the gamut of ALK inhibitors.

First- and second-generation EGFR tyrosine kinase inhibitors (TKIs) for EGFR mutation-positive non-small cell lung cancer (NSCLC)

Osimertinib and treatment options for patients with disease progression on an EGFR TKI

Other targetable mutations in NSCLC: ALK rearrangement; MET exon 14 splice mutation

Application of immune checkpoint inhibitors in NSCLC

Systemic and localized treatment approaches for NSCLC

Small cell lung cancer, mesothelioma and squamous NSCLC