by A recent large-scale study conducted by researchers at the Keck School of Medicine delved into the intricate relationship between smoking and changes in DNA methylation across six distinct racial and ethnic groups. This study, funded by the National Institutes of Health, aimed to uncover the epigenetic mechanisms underlying the impact of smoking on gene expression, specifically in relation to the development of smoking-related diseases such as lung cancer.
Lead author Brian Huang, Ph.D., emphasized the importance of identifying epigenetic signatures of smoking to enhance risk prediction for smoking-related illnesses. The study analyzed data from 2,728 individuals and identified 408 DNA methylation markers associated with smoking, including two markers that exhibited variations based on race or ethnicity. The findings, featured in the American Journal of Human Genetics, shed light on the differences in how smoking affects individuals based on their genetic backgrounds.
Unique to this study was its multiethnic approach, encompassing a diverse range of racial and ethnic groups, a departure from previous research focusing on single or limited racial demographics. By quantifying smoking levels through measuring participants’ total nicotine equivalents (TNEs), the researchers obtained a more precise assessment of smoking dosages compared to conventional self-reported methods. This thorough examination provided insights into how smoking impacts health across different populations.
The study unveiled crucial information on the mechanisms through which smoking influences health outcomes, offering potential avenues for improved prediction, early detection, and treatment of smoking-related conditions. By scrutinizing DNA methylation patterns in conjunction with smoking habits, the researchers pinpointed key sites associated with smoking-induced epigenetic modifications, providing a deeper understanding of the disparities in lung cancer risk among various racial and ethnic groups.
Two significant DNA methylation sites exhibited distinct risk disparities based on race or ethnicity, emphasizing the intricate interplay between genetic variations and smoking-related health outcomes. These findings elucidated why certain populations face heightened risks of lung cancer compared to others, with African Americans and Latinos showing differential susceptibility to smoking-induced epigenetic changes.
To validate their discoveries, Huang and his team corroborated the results with data from additional participant groups, reinforcing the consistency of the identified CpG sites across different racial and ethnic backgrounds. This robust evidence supports the notion that specific epigenetic markers of smoking remain consistent across diverse populations, paving the way for tailored risk assessment and preventative strategies for smoking-related diseases.
Continuing their research endeavors, the team plans to delve into the interplay between DNA methylation patterns and lung cancer risk, aiming to elucidate how epigenetic changes heighten an individual’s susceptibility to lung cancer. By unraveling the intricate mechanisms linking DNA methylation to smoking and lung cancer risk, the researchers aspire to enhance predictive capabilities and refine interventions for mitigating the adverse health impacts of smoking. Additionally, ongoing investigations are underway to explore the epigenetic alterations associated with other smoking-related biomarkers, such as cadmium levels, to further expand our understanding of the complex interplay between smoking, genetics, and disease susceptibility.
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1. Source: Coherent Market Insights, Public sources, Desk research
2. We have leveraged AI tools to mine information and compile it.
