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By Jack A. Roth, James D. Cox, Waun Ki Hong

Lung melanoma is a tremendous explanation for cancer-related deaths in women and men. even if, because the first variation of Lung melanoma used to be released 14 years in the past, speedy growth within the biology, prevention, analysis, and remedy of the disorder has been made.

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Genetic influences on smoking—a study of male twins. N Engl J Med 1992; 327:829–33. 95 Heath A, Kirk K, Meyer J, Martin N. Genetic and social determinants of initiation and age at onset of smoking in Australian twins. Behav Genet 1999; 29:395–407. 96 Koudsi N, Tyndale R. Genetic influences on smoking. Drug Monit 2005; 27(6):704–9. 97 Lerman C, Tyndale R, Patterson F et al. Nicotine metabolite ratio predicts efficacy of transdermal nicotine for smoking cessation. Clin Pharmacol Ther 2006; 79:600–8.

Segregation analyses of lung- and smoking-associated cancers Given the evidence for familial aggregation of lung and other smoking-associated cancers, after accounting for personal tobacco use and occupational/industrial risk factors, segregation analyses have been performed to determine whether patterns of transmission consistent with at least one major, high-penetrance genetic locus may be involved in lung cancer risk. Sellers et al. [80] performed genetic segregation analyses on the lung cancer proband families of Ooi et al.

Host susceptibility may also be involved in LC risk, since only a fraction of smokers develops LC [2–5]. Because carcinogenesis is a multistep process, multiple molecular events during this process account for the malignant transformation upon initial carcinogenic exposure. Understanding that multiple components contributing to LC can lead to the identification of high-risk subgroups, who may benefit from targeted screening or other interventions. Here, we provide a summary of recent advances in the molecular epidemiology of LC.

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