Fig. 4: Genomic alterations in STK11 and genes within the Notch signaling family in different lung cancer histologies.
From: Lineage plasticity and histological transformation: tumor histology as a spectrum
a Frequency of driver mutations in STK11 in the different lung cancer histologic subtypes, large cell neuroendocrine carcinoma (LCNEC), lung adenocarcinoma (LUAD), lung adenosquamous (LUAS), combined small cell lung cancer (cSCLC), squamous cell lung carcinoma (LUSC) and SCLC. b Oncoprint showing mutations in genes of interest in the LCNEC Memorial Sloan Kettering Cancer Center (MSK) cohort. c Co-occurrence or mutual exclusion of mutations in the LCNEC MSK cohort, quantifying how strongly the presence or absence of alterations in A are associated with the presence or absence of alterations in B in the selected samples. d Oncoprint showing mutations in genes related to the Notch signaling pathway in the lung cancer MSK cohort, divided by histological subtypes. e Frequency of genomic alterations in genes related to the Notch pathway (see d) in the different lung cancer histological subtypes from the MSK cohort. Odds Ratio = (Neither × Both)/(A Not B × B Not A). p-values are derived from two-sided Fisher Exact Test and q-values were derived from a Benjamini-Hochberg false discovery rate correction procedure. Log2ratio > 0: tendency towards co-occurrence; log2ratio ≤ 0: tendency towards mutual exclusivity. q-value < 0.05: significant association. 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 RWD. MSK LUAD (n = 9789), LUAS (n = 93), LUSC (n = 1379), cSCLC (n = 84), LCNEC (n = 223), and SCLC (n = 772) cohorts are depicted. “n” represents the number of patients.
