Buccal Epithelium, Cigarette Smoking, and Lung Cancer: Review of the Literature

Saba, Raya; Halytskyy, Oleksandr; Saleem, Nasir; Oliff, Ira

doi:10.1159/000479796

Cited by 10 publications

(9 citation statements)

References 41 publications

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“…Cigarette smoking traits also exhibited distinct associations not observed in alcohol use traits. For instance, we noted lung development to be associated with both ND and CPD which supports epidemiological findings of lung morbidities linked to cigarette smoking 48, 49 .…”

Section: Resultssupporting

confidence: 88%

Chromatin architecture in addiction circuitry elucidates biological mechanisms underlying cigarette smoking and alcohol use traits

Won

Akbarian

Hancock

et al. 2021

Preprint

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Cigarette smoking and alcohol use are among the most prevalent substances used worldwide and account for a substantial proportion of preventable morbidity and mortality, underscoring the public health significance of understanding their etiology. Genome-wide association studies (GWAS) have successfully identified genetic variants associated with cigarette smoking and alcohol use traits. However, the vast majority of risk variants reside in non-coding regions of the genome, and their target genes and neurobiological mechanisms are unknown. Chromosomal conformation mappings can address this knowledge gap by charting the interaction profiles of risk-associated regulatory variants with target genes. To investigate the functional impact of common variants associated with cigarette smoking and alcohol use traits, we applied Hi-C coupled MAGMA (H-MAGMA) built upon cortical and midbrain dopaminergic neuronal Hi-C datasets to GWAS summary statistics of nicotine dependence, cigarettes per day, problematic alcohol use, and drinks per week. The identified risk genes mapped to key pathways associated with cigarette smoking and alcohol use traits, including drug metabolic processes and neuronal apoptosis. Risk genes were highly expressed in cortical glutamatergic, midbrain dopaminergic, GABAergic, and serotonergic neurons, suggesting them as relevant cell types in understanding the mechanisms by which genetic risk factors influence cigarette smoking and alcohol use. Lastly, we identified pleiotropic genes between cigarette smoking and alcohol use traits under the assumption that they may reveal substance-agnostic, shared neurobiological mechanisms of addiction. The number of pleiotropic genes was ∼26-fold higher in dopaminergic neurons than in cortical neurons, emphasizing the critical role of ascending dopaminergic pathways in mediating general addiction phenotypes. Collectively, brain region- and neuronal subtype-specific 3D genome architecture refines neurobiological hypotheses for smoking, alcohol, and general addiction phenotypes by linking genetic risk factors to their target genes.

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Section: Resultssupporting

confidence: 88%

Chromatin architecture in addiction circuitry elucidates biological mechanisms underlying cigarette smoking and alcohol use traits

Won

Akbarian

Hancock

et al. 2021

Preprint

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“…AgNORs count method was widely used in oral exfoliative cytology particularly among cigarette smokers to predict early cellular proliferative activity indicating neoplastic change [19], but its use for lung cytology is scarce [20]. It was reported that cellular proliferative quantified by AgNORs might play a substantial role in the early detection and diagnosis of premalignant and malignant lesions in the absence of clinical manifestations [21].…”

Section: Discussionmentioning

confidence: 99%

The Utility of Nucleolar Organizer Regions Quantitation in Early Prediction of Lung Neoplastic Transformation

Ahmed

Hag

Binsaleh

et al. 2020

Cureus

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Background: Cancer burden can be reduced by early detection of early neoplastic changes applying suitable screening methods. This study aimed to assess the utility of nucleolar organizer regions (NORs) quantitation in early prediction of lung neoplastic transformation. Methodology: This study investigated 200 apparently healthy individuals categorized into two groups; smoking exposed individuals (N=100), and were categorized as cases, and smoking nonexposed (N=100), and were ascertained as controls. Sputum specimen was attained from each participant (paying all indispensable safety precautions and sample adequacy processes). Results: Out of the 200 volunteers assessed in the present study, mean NORs counts of >2.00 were identified in 16/200(8%) of the study subjects. All 16/16(100%) cases were found with lung epithelial metaplasia (squamous metaplasia). Out of the 100 cases, mean NORs counts of >2.00 were identified in 16/100(16%), hence, all the controls were identified with mean NORs counts of <2.00. The risk of lung cellular proliferative changes associated with smoking exposure are odds ratio (OR) (95% confidence interval, CI) = 39.2485 (2.3199-664.0052), p = 0.0110, z statistic = 2.543. Conclusion: NORs count is a simple, specific, cost-effective, and reliable method that can give a quantitative measurement for the risk of lung neoplastic transformation. For at risk-population (tobacco users), it is recommended to perform the argyrophilic NORs (AgNORs) method beside sputum cytology.

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“…In contrast, only a few studies report on the effects of cigarette smoke in oral mucosa 13 . Clinically, cigarette smoke results in oral mucosa dysplasia, leukoplakia, and finally carcinoma 14 .…”

Section: Introductionmentioning

confidence: 99%

Early effects of cigarette smoke extract on human oral keratinocytes and carcinogenesis in head and neck squamous cell carcinoma

et al. 2020

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Background Cigarette smoking is a major risk factor for head and neck squamous cell carcinoma. Still, the effect of cigarette smoke on the molecular level is unclear. The aim of the present study was to investigate the early effects of cigarette smoke on carcinogenesis of head and neck squamous cell carcinoma. Methods Human oral keratinocytes were exposed for 1 week to standardized cigarette smoke extract, and subsequently RT‐quantitative PCR array was performed. Protein expression of dysregulated genes was determined by immunohistochemistry in tissue samples of oral squamous cell carcinoma, oral leukoplakia, and tonsil mucosa. Results RT‐PCR revealed upregulation of ITGA‐2 and MMP‐1, whereas TEK receptor tyrosine kinase was downregulated in human oral keratinocytes. ITGA‐2 and MMP‐1 were significantly overexpressed in tissue samples of oral squamous cell carcinoma in comparison to normal mucosa (P <.01 in all experiments). Conclusion Upregulation of ITGA‐2 and MMP‐1 induced by cigarette smoke contributes significantly to oral carcinogenesis.

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Buccal Epithelium, Cigarette Smoking, and Lung Cancer: Review of the Literature

Cited by 10 publications

References 41 publications

Chromatin architecture in addiction circuitry elucidates biological mechanisms underlying cigarette smoking and alcohol use traits

Chromatin architecture in addiction circuitry elucidates biological mechanisms underlying cigarette smoking and alcohol use traits

The Utility of Nucleolar Organizer Regions Quantitation in Early Prediction of Lung Neoplastic Transformation

Early effects of cigarette smoke extract on human oral keratinocytes and carcinogenesis in head and neck squamous cell carcinoma

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