We analyzed data from open-access research: MSK-IMPACT (molecular profiling data from patients receiving systemic antitumor
therapy) and MSK-TMB (molecular profiling data from patients receiving
immune checkpoint inhibitors). In both studies, high throughput sequencing was used for molecular profiling.
RESULTS: A total of 10,336 patients receiving antitumor
therapy (MSK-IMPACT study) and 1661 patients receiving
immune checkpoint inhibitors (MSK-TMB study) were included in the analysis. Co-mutation STK11/KRAS was found in 156 (1.5%) and 46 (2.8%) patients in the two studies, respectively. Most patients with the STK11/KRAS co-mutation had
non-small cell lung cancer (83% and 85% in the two studies, respectively). Among
non-small cell lung cancer patients, the STK11 mutation was associated with a worse outcome for patients receiving systemic antitumor
therapy, but not
immune checkpoint inhibition therapy (HR for OS 1.90 [95% CI 1.36-2.65] and 1.44 [95% CI 0.88-2.37]). Co-mutation STK11/KRAS was also not associated with patient outcome in any of the studies (HR for OS 0.93 [95% CI 0.56-1.52] and 1.09 [95% CI 0.54-2.19]). High
tumor mutational burden was associated with better outcome in the cohort of patients receiving
immune checkpoint inhibitors. An analogous analysis among patients in the pan-
cancer cohort (excluding patients with
non-small cell lung cancer) showed STK11 mutations and high
tumor mutational burden have a predictive role for the efficacy of
immune checkpoint inhibitors, but not STK11/KRAS co-mutation.
CONCLUSIONS: