Epigenetic alterations and smoking-associated lung cancer: An integrative review

Abstract

Introduction: Cancer has been one of the leading causes of mortality over the last decade, ranking as the first or second leading cause of premature death (i.e., before age 70) in most countries. Objective: To understand the mechanisms of DNA methylation and their influence on the development of lung cancer, as well as to analyze the potential of these epigenetic alterations as complementary diagnostic tools, particularly in smokers. Methods: This is a literature review conducted via active searches in the MEDLINE and LILACS databases. Descriptors related to lung neoplasms, smoking, DNA/RNA methylation, RNA damage, and epigenetics were used, combined with Boolean operators. Pre-defined inclusion and exclusion criteria were applied, resulting in the selection of seven articles for analysis. Results: The studies analyzed demonstrated that DNA methylation alterations—specifically hypomethylation—are associated with the onset of lung cancer oncogenesis, contributing to the inactivation of tumor suppressor genes. A strong relationship was also observed between tobacco smoke exposure and these epigenetic modifications. Evidence indicates that DNA methylation plays a central role in the molecular mechanisms underlying lung cancer development and could be explored as an epigenetic marker for disease screening in smokers. Conclusion: DNA methylation is a significant factor in pulmonary carcinogenesis and holds potential as an auxiliary tool for early diagnosis, thereby helping to improve patient survival.