Molecular Marker Discovery and Evaluation: EGF rs1897990 and rs1524106 Variants in a China Lung Adenocarcinoma Young Population

TL;DR

This study finds that specific EGF gene variants and smoking increase the risk of lung adenocarcinoma in young people under 45 in China.

Contribution

Identifies EGF rs1897990 and rs1524106 as risk markers for young-onset lung adenocarcinoma, with smoking enhancing their effects.

Findings

EGF rs1897990 CT heterozygous mutation differs between young lung adenocarcinoma patients and controls (p=0.021).

T alleles of EGF rs1897990 and rs1524106 are significantly associated with disease risk (p=0.034 and p=0.023).

Smoking increases susceptibility to EGF variant-related lung adenocarcinoma in young individuals.

Abstract

The objective of this study is to investigate the genetic susceptibility and risk factors of EGF gene rs1897990 and rs1524106 in lung adenocarcinoma young patients aged ≤ 45 years.

A case–control study was conducted. DNA was extracted and identified from 88 samples from case and control groups by single‐nucleotide polymorphism assay. PCR amplification was performed by TaqMan probe method, and the factors of smoking, drinking, sex, and age were also included. To investigate the clinical factors and genotyping differences between case and control groups.

Smoking was an influential factor in young lung adenocarcinoma patients. The mutation frequency of EGF gene rs1897990 CT heterozygous mutant was different between the two groups (p = 0.021). The T alleles of EGF rs1897990 and rs1524106 were significantly different between the two groups (p = 0.034 and p = 0.023).

The young lung adenocarcinoma population (≤ 45 years old) is susceptible to EGF rs1897990 and rs1524106 variants, with smoking being another risk factor. Additionally, smoking may enhance the risk of EGF rs1897990 and rs1524106 variants threatening the development of lung adenocarcinoma.

The core EGF gene variants in string interaction network rs1897990 and rs1524106 are significant risk factors for lung adenocarcinoma in young individuals, particularly when combined with smoking. Tobacco use appears to potentiate the oncogenic effects of these variants, further increasing susceptibility to early‐onset lung adenocarcinoma.

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