Little is known about association of mucin abundancy with oncogenic-driver alterations, immunohistochemical and clinicopathologic features in lung adenocarcinomas among Chinese. We here retrospectively examined the clinicopathologic and molecular characteristics of pulmonary mucin-producing adenocarcinoma (PMPA) and previously-reported non-mucinous lung adenocarcinomas collected at our institution. Among the 897 non-mucinous adenocarcinomas, 61 PMPA with ≤90% mucin and 39 PMPA with >90% mucin, ALK rearrangements were found in 47 (5.2%) non-mucinous adenocarcinomas, 9 (14.8%) PMPA with ≤90% mucin and 12 (30.8%) PMPA with >90% mucin, respectively, with an ordinal association (coefficient, 95% CI=0.11, 0.06 to 0.17). Similarly, KRAS mutations was found in 53 (5.9%) non-mucinous adenocarcinomas, 7 (11.5%) PMPA with ≤90% mucin and 14 (35.9%) PMPA with >90% mucin (coefficient, 95% CI=0.11, 0.05 to 0.16). However, mucinous abundancy was inversely, ordinally linked to the EGFR mutations (coefficient, 95% CI=-0.28, -0.33 to -0.22). Mucin abundancy seemed not associated with the alterations of HER2, BRAF, ROS1, MET and RET. We divided PMPA with >90% mucin into three histologic types, namely columnar mucinous cell with basal nuclei (type I, n=11), cuboidal cell with goblet cell feature (type II, n=16) and mucinous cribriform pattern (type III, n=12). These histologic subtypes were associated with alterations of ALK, KRAS and MET, and the immunohistochemical reactivity of MUC1, MUC2, MUC5ac, MUC6, TTF-1 and CK20, including high positive rate of MUC6 (90.9%) and CK20 (36.4%) in type I, MUC2 (50%) in type II and MUC1 (100%) in type III. In summary, mucin abundancy is associated with immunohistochemical and oncogenic-driver profiles of lung adenocarcinomas among Chinese.
Keywords: Lung cancer; adenocarcinoma; oncogenic driver; pathology; survival.