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Abstract
TP53 is a tumor-suppressor gene coding for p53, a protein responsible for cell-cycle arrest and DNA repair. Smoking has been demonstrated to lead to the methylation of tumor-suppressor genes in noncancerous lung biopsy tissues of smokers, and in bodily fluids, promoter hypermethylation occurs very early in the progression of cancer. Thus, DNA methylation changes may be initiated long before cells become cancerous. As this association has never been explored in young, healthy individuals, we decided to look at DNA isolated from urine and saliva samples taken from young male and female smoking and nonsmoking participants. While p53 methylation was not found in any of the samples tested, differences in DNA concentration between the two groups may shed light on the timing of epigenetic alterations, as well as better explain why the negative impact of smoking is not often found in young, healthy adults.
Acknowledgements
The authors of this report would like to thank the staff at Norgen Biotek Corporation (ON, Canada) for all of their help during the course of this study.
Financial & competing interests disclosure
Y Haj-Ahmad discloses conflicts of interest with products used in this study from Norgen Biotek Corporation (ON, Canada), as he is President and Chief Executive Officer of Norgen Biotek Corporation M Simkin, M Abdalla and M El-Mogy are also Norgen Biotek Corporation employees. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.