Genetic differences between smokers and never-smokers with lung cancer

Kuśnierczyk, Piotr

doi:10.3389/fimmu.2023.1063716

Cited by 12 publications

(6 citation statements)

References 137 publications

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“…Smoking likely worsens outcomes in ARDS and COPD exacerbations by heightening inflammation. For cardiovascular disease, smoking impairs endothelial function, reduces nitric oxide, and promotes atherosclerosis through oxidized LDL and effects on adhesion molecules (Kuśnierczyk 2023). As illustrated in Fig.…”

Section: Mechanisms Of Smoking-induced Diseasementioning

confidence: 99%

Oxidative stress and inflammation: elucidating mechanisms of smoking-attributable pathology for therapeutic targeting

Addissouky,

El Sayed,

Ali

et al. 2024

Bull Natl Res Cent

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Background Tobacco smoking remains a major preventable cause of disease and death worldwide. Combustible cigarettes release thousands of chemicals that can initiate inflammatory pathways leading to smoking-related illness. This review aims to synthesize current scientific knowledge on mechanisms of smoking-induced disease, epidemiological trends, and clinical strategies from recent literature. Main body of the abstract At the cellular level, cigarette smoke triggers oxidative stress through reactive oxygen species (ROS), causing DNA damage. This provokes inflammatory signaling cascades mediated by damage-associated molecular patterns (DAMPs), receptors like RAGE and TLRs, and downstream cytokines. Smoking also disrupts apoptosis and autophagy. In the lungs, oxidative stress and inflammation from smoking play central roles in COPD pathogenesis. Smoking-induced oxidative DNA damage, chronic inflammation, and impaired immunity combine to promote lung carcinogenesis. For cardiovascular disease, smoking triggers endothelial dysfunction, platelet activation, and atherogenesis through oxidized LDL and effects on nitric oxide and adhesion molecules. Short conclusion Given the unequivocal evidence of health risks, smoking cessation is critical to reducing preventable death and disability. Both counseling and pharmacotherapy have proven efficacy for quitting, but efficacy remains limited long-term. Emerging nicotine products like e-cigarettes have unknown impacts on cessation and population health. Comprehensive efforts encompassing prevention, screening, treatment innovation, harm reduction, and policy reform focused on curbing smoking-attributable morbidity and mortality are warranted.

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Section: Mechanisms Of Smoking-induced Diseasementioning

confidence: 99%

Oxidative stress and inflammation: elucidating mechanisms of smoking-attributable pathology for therapeutic targeting

Addissouky,

El Sayed,

Ali

et al. 2024

Bull Natl Res Cent

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“…They recruited 232 NSLSC NS patients and established three genetic subtypes unique to NS. TMB was almost sevenfold lower in NS than in smokers [1,21] and significantly associated with tumour stage, histology, and age, but not tumour purity. A higher frequency of EGFR mutations was found in females than in males.…”

Section: Setd2mentioning

confidence: 78%

“…Therefore, analysis of the genomic differences between NS and CS will aid in uncovering the cellular and molecular pathways of malignant transformation. Indeed, although NS patients have a lower number of mutations compared to CS, they seem to be conducive for the malignant transformation, whereas, in CS, the numerous mutations seem to be mostly passenger mutations [21]. Even so, there are specific changes that occur in the TME and distinct driver genes, as well as genetic pathway alterations, in NS.…”

Section: Setd2mentioning

confidence: 99%

A Functional Genomics Review of Non-Small-Cell Lung Cancer in Never Smokers

Hamouz,

Hammouz,

Bajwa

et al. 2023

IJMS

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There is currently a dearth of information regarding lung cancer in never smokers (LCINS). Additionally, there is a difference in somatic mutations, tumour mutational burden, and chromosomal aberrations between smokers and never smokers (NS), insinuating a different disease entity in LCINS. A better understanding of actionable driver alterations prevalent in LCINS and the genomic landscape will contribute to identifying new molecular targets of relevance for NS that will drastically improve outcomes. Differences in treatment outcomes between NS and smokers, as well as sexes, with NSCLC suggest unique tumour characteristics. Epidermal growth factor receptor (EGFR) tyrosine kinase mutations and echinoderm microtubule-associated protein-like 4 anaplastic lymphoma kinase (EML4-ALK) gene rearrangements are more common in NS and have been associated with chemotherapy resistance. Moreover, NS are less likely to benefit from immune mediators including PD-L1. Unravelling the genomic and epigenomic underpinnings of LCINS will aid in the development of not only novel targeted therapies but also more refined approaches. This review encompasses driver genes and pathways involved in the pathogenesis of LCINS and a deeper exploration of the genomic landscape and tumour microenvironment. We highlight the dire need to define the genetic and environmental aspects entailing the development of lung cancer in NS.

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“…Furthermore, it should be considered that there are many differences between lung cancer in smokers versus non-smokers. These multiple differences relate to histology, genetics, lifetime risk, and the role played by environmental risk factors [57]. It is possible that the lower lifetime risk of lung cancer, in addition to the greater role played by environmental factors in the etiology of lung cancer in never-smokers, may confound the results in this subgroup.…”

Section: Discussionmentioning

confidence: 99%

Adherence to Data-Driven Dietary Patterns and Lung Cancer Risk: A Systematic Review and Dose–Response Meta-Analysis

Fabiani,

La Porta,

Li Cavoli

et al. 2023

Nutrients

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The effect of dietary patterns on lung cancer risk is currently debated. In this study, we evaluated the association between different “a posteriori” dietary patterns and lung cancer risk. The search was carried out (February 2023) through Scopus, Web of Science, and PubMed databases. Meta-analysis was performed by a random-effects model using risk values (RR and OR) extracted from the 12 selected studies. Two main dietary patterns were identified and named “Western/meat” and “Healthy/prudent”. The highest adherence to the “Western/meat” dietary pattern significantly increased the lung cancer risk (OR = 1.39; 95% CI: 1.17–1.65; p = 0.0002) while the highest adherence to the “Healthy/prudent” pattern reduced it (OR = 0.65; 95% CI: 0.51–0.83; p = 0.001). A linear trend between both dietary patterns and lung cancer risk was observed. However, a statistically significant inverse dose–response trend was found only for the “Healthy/prudent” dietary pattern (regression coefficient = −0.0031, p = 0.003). Subgroup analyses showed that the “Western/meat” pattern significantly increased the lung cancer risk in former (n = 4) (OR = 1.93, 95% CI: 1.11–3.36) and current smokers (n = 7) (OR = 1.35, 95% CI: 1.06–1.71). Similarly, the “Healthy/prudent” pattern exerts a protective effect on former (n = 4) (OR = 0.61, 95% CI: 0.44–0.85) and current smokers (n = 8) (OR = 0.64, 95% CI: 0.46–0.88). For both dietary patterns, no significant effect was observed on never-smokers.

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Genetic differences between smokers and never-smokers with lung cancer

Cited by 12 publications

References 137 publications

Oxidative stress and inflammation: elucidating mechanisms of smoking-attributable pathology for therapeutic targeting

Oxidative stress and inflammation: elucidating mechanisms of smoking-attributable pathology for therapeutic targeting

A Functional Genomics Review of Non-Small-Cell Lung Cancer in Never Smokers

Adherence to Data-Driven Dietary Patterns and Lung Cancer Risk: A Systematic Review and Dose–Response Meta-Analysis

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