Deciphering bidirectional causal links between oxidative stress and lung cancer risk through Mendelian randomization
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View abstract on PubMed
Summary
This summary is machine-generated.Oxidative stress injury biomarkers (OSIBs) show distinct roles in lung cancer development. This study used Mendelian randomization to find that higher albumin may reduce adenocarcinoma risk, while elevated monounsaturated fatty acids and lactate are linked to increased risk for other lung cancer types.
Area Of Science
- Oncology
- Genetics
- Biochemistry
Background
- Lung cancer is a leading global cause of cancer mortality.
- Suboptimal survival rates for advanced lung cancer necessitate novel prevention strategies.
- Oxidative stress (OS), an imbalance of reactive oxygen species (ROS) and antioxidants, is implicated in lung cancer pathogenesis.
Purpose Of The Study
- To investigate bidirectional causal relationships between genetically predicted oxidative stress injury biomarkers (OSIBs) and lung cancer risk.
- To utilize Mendelian randomization (MR) for assessing these causal links.
Main Methods
- A two-sample bidirectional MR approach was employed.
- Causal effects of 16 OSIBs on lung cancer subtypes (small cell lung cancer, squamous cell carcinoma, adenocarcinoma) and vice versa were assessed.
- Genetic data were sourced from large-scale genome-wide association studies in European populations.
Main Results
- Higher albumin levels were associated with a reduced risk of adenocarcinoma (OR=0.599, P=0.039).
- Elevated monounsaturated fatty acids were linked to an increased risk of squamous cell carcinoma (OR=1.742, P=0.019).
- Increased lactate levels were positively associated with small cell lung cancer risk (OR=4.565, P=0.049).
- Reverse MR analysis did not indicate causal effects of lung cancer on OSIBs.
Conclusions
- OSIBs play distinct roles in lung cancer risk.
- Oxidative stress is pivotal in cancer development.
- Further research is warranted to validate these biomarkers for early detection and prevention.
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