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. 2021 Apr 13:11:644895.
doi: 10.3389/fonc.2021.644895. eCollection 2021.

Unique Profile of Driver Gene Mutations in Patients With Non-Small-Cell Lung Cancer in Qujing City, Yunnan Province, Southwest China

Yongchun Zhou  1 , Feng Ge  2 , Yaxi Du  1 , Quan Li  1 , Jingjing Cai  1 , Xin Liu  1 , Yinjin Guo  1 , Zhenghai Shen  3 , Lincan Duan  4 , Zhan Huang  5 , Fei Yao  5 , Changbin Zhu  5 , Hutao Shi  6 , Yunchao Huang  7
Affiliations

Unique Profile of Driver Gene Mutations in Patients With Non-Small-Cell Lung Cancer in Qujing City, Yunnan Province, Southwest China

Yongchun Zhou et al. Front Oncol. .

Abstract

Objective: Qujing City, Yunnan Province, China, has a high incidence of lung cancer and related mortality. The etiology of NSCLC in Qujing area and distribution of associated molecular aberrations has not been fully elucidated. This study aimed to reveal the profile of driver gene mutations in patients with non-small-cell lung cancer (NSCLC) in Qujing and explore their relationships with clinicopathological characteristics.

Methods: In this study, the mutation profiles of NSCLC driver genes, including EGFR, ALK, ROS1, KRAS, BRAF, RET, MET, HER2, NRAS, and PIK3CA, were investigated in patients with NSCLC from Qujing and compared with those from other regions in Yunnan Province. The associations between molecular mutations and clinicopathological characteristics were further analyzed.

Results: A distinct profile of driver gene mutations was discovered in patients with NSCLC from Qujing. Interestingly, a higher proportion of EGFR compound mutations, including G719X + S768I (19.65% vs 3.38%, P < 0.0001) and G719X + L861Q (21.10% vs 2.82%, P < 0.0001), was observed in patients with NSCLC in Qujing compared with patients in non-Qujing area, besides significantly different distributions of EGFR (46.01% vs. 51.07%, P = 0.0125), ALK (3.17% vs. 6.97%, P = 0.0012), ROS1 (0.5% vs. 2.02%, P = 0.0113), and KRAS (23.02% vs. 7.85%, P < 0.0001). Further, EGFR compound mutations were more likely associated with the occupation of patients (living/working in rural areas, e.g., farmers). Moreover, KRAS G12C was the dominant subtype (51.11% vs 25.00%, P = 0.0275) among patients with NSCLC having KRAS mutations in Qujing.

Conclusions: Patients with NSCLC in Qujing displayed a unique profile of driver gene mutations, especially a higher prevalence of EGFR compound mutations and dominant KRAS G12C subtype, in this study, indicating a peculiar etiology of NSCLC in Qujing. Therefore, a different paradigm of therapeutic strategy might need to be considered for patients with NSCLC in Qujing.

Keywords: ALK; EGFR; KRAS; Qujing; ROS1; mutation profile; non-small-cell lung cancer.

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Conflict of interest statement

ZH, FY, and CZ were employed by Amoy Diagnostics Co., Ltd. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Flowchart of participant selection in this study.
Figure 2
Figure 2
Mutation frequencies of 10 lung cancer driver genes in patients with NSCLC according to the regions in Yunnan Province.
Figure 3
Figure 3
Mutation frequencies of ALK and ROS1 in patients with NSCLC from Qujing and non-Qujing regions.
Figure 4
Figure 4
Frequencies of EGFR mutations, EGFR subtypes, and compound mutations in patients with NSCLC from Qujing and non-Qujing areas. (A) the prevalence of EGFR mutation in Qujing patients was compared with non-Qujing patients. (B) the point mutation frequencies of G719X, S768I, and L861Q were higher in Qujing patients, and the point mutation of 19Del and L858R were lower in Qujing patients. (C, D) the distribution of EGFR mutation subtypes in Qujing and non-Qujing patients. (E, F) the distribution of EGFR compound mutation subtypes in Qujing and non-Qujing patients.
Figure 5
Figure 5
Profile of KRAS mutation and subtypes in patients with NSCLC from Qujing and non-Qujing areas. (A) the prevalence of KRAS mutation in Qujing patients was compared with non-Qujing patients. (B, C) the distribution of KRAS mutation subtypes in Qujing and non-Qujing patients.
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