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Background  Several genetic driver alterations have been identified in micropapillary lung adenocarcinoma (MPA). However, the frequency of co-alteration of  ROS1 ,  EGFR , and  EML4-ALK  is yet unclear. Herein, we investigated the relationship between clinicopathologic characteristics and well-identified driver mutations of MPA compared with non-micropapillary lung adenocarcinoma (LA).    Methods  Formalin-fixed paraffin-embedded (FFPE) sections derived from lung adenocarcinoma patients who never received adjuvant chemotherapy or radiation therapy prior to surgical resection were collected from October 2016 to June 2019.  EGFR  mutations,  ROS1  rearrangements, and  EML4-ALK  fusion were identified in a set of 131 MPA and LA cases by using the amplification refractory mutation system (ARMS). The response rate and duration of response were assessed using Response Evaluation Criteria in Solid Tumors version 1.1 (RECIST 1.1).    Results   EGFR  mutations had occurred in 42 (76.4%) MPA patients and 42 (55.3%) LA patients. Interestingly,  ROS1  rearrangements were highly enriched only in the MPA cases (6/55, 10.9%) but rarely in the LA cases (1/76, 1.3%). Furthermore, 7.3% (4/55) MPA samples had double gene mutations, while only 1.3% (1/76) LA cases had double gene alterations. Of 5 patients with harboring two driver oncogene mutations, four patients (80%) obtained partial response, and one patient (20%) suffered recurrence.    Conclusions  A higher prevalence of  ROS1  rearrangement or combined mutations of  ROS1 ,  EGFR , and  EML4-ALK  may play a critical role in the tumorigenesis of MPA. These findings provide a novel therapeutic strategy for patients with malignant MPA through combining TKIs than one TKI.

A comprehensive study on the oncogenic mutation and molecular pathology in Chinese lung adenocarcinoma patients