Fig. 2: Occurrence of mutations in lung adenocarcinoma (LUAD) drivers in other lung cancer histologies and their association with a low/never-smoking profile.
From: Lineage plasticity and histological transformation: tumor histology as a spectrum
a, b Oncoprint showing LUAD driver mutations, as profiled by MSK-IMPACT next-generation sequencing, and smoking history of Memorial Sloan Kettering Cancer Center (MSK) lung adenosquamous (LUAS, n = 93) and lung squamous carcinoma (LUSC, n = 1379) cohorts (a), as well as MSK combined histology small cell lung cancer (cSCLC, n = 84), large cell neuroendocrine carcinoma (LCNEC, n = 223), and small cell lung cancer (SCLC, n = 772) cohorts (b). cSCLC tumors are defined as tumors containing both SCLC and non-small cell lung cancer (NSCLC Like SCLC tumors) histologic subtypes, where the NSCLC subtype can be LUAD, LUSC, large cell carcinoma (LCC), LCNEC or any other minor NSCLC histologic subtype. c, d Barplots showing the percentage of different patient smoking profiles for patients with LUAS or LUSC (c) or with cSCLC, LCNEC and SCLC (d). Altered groups represent patients with tumors harboring mutations in genes that are known LUAD drivers and are associated with a low smoking profile in the LUAD setting (EGFR, ALK, RET, ROS1). Unaltered groups represent patients with tumors that do not harbor mutations in the previously mentioned genes. Distribution of smoking history groups was compared using χ2 test. *P < 0.05, **P < 0.01, ***P < 0.001. Figures were generated in cBioPortal.org247,248,249 with data from the MSK-IMPACT clinical cohort.250 Histology annotations were obtained from clinical diagnosis, in the style of real word data (RWD). “n” represents the number of patients.
