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Tobacco Smoking: Risk to Develop Addiction, Chronic Obstructive Pulmonary Disease, and Lung Cancer

[ Vol. 14 , Issue. 1 ]

Author(s):

Alessia Santoro, Carlo Tomino, Giulia Prinzi, Palma Lamonaca, Vittorio Cardaci, Massimo Fini and Patrizia Russo*   Pages 39 - 52 ( 14 )

Abstract:


Background: The morbidity and mortality associated with tobacco smoking is well established. Nicotine is the addictive component of tobacco. Nicotine, through the non-neuronal α7nicotinic receptor, induces cell proliferation, neo-angiogenesis, epithelial to mesenchymal transition, and inhibits drug-induced apoptosis.

Objective: To understand the genetic, molecular and cellular biology of addiction, chronic obstructive pulmonary disease and lung cancer.

Methods: The search for papers to be included in the review was performed during the months of July- September 2018 in the following databases: PubMed (http://www.ncbi.nlm.nih.gov), Scopus (http://www.scopus.com), EMBASE (http://www.elsevier.com/online-tools/embase), and ISI Web of Knowledge (http://apps.webofknowledge.com/). The following searching terms: “nicotine”, “nicotinic receptor”, and “addiction” or “COPD” or “lung cancer” were used.

Patents were retrieved in clinicaltrials.gov (https://clinicaltrials.gov/). All papers written in English were evaluated. The reference list of retrieved articles was also reviewed to identify other eligible studies that were not indexed by the above-mentioned databases.

New experimental data on the ability of nicotine to promote transformation of human bronchial epithelial cells, exposed for one hour to Benzo[a]pyrene-7,8-diol-9-10-epoxide, are reported.

Results: Nicotinic receptors variants and nicotinic receptors upregulation are involved in addiction, chronic obstructive pulmonary disease and/or lung cancer. Nicotine through α7nicotinic receptor upregulation induces complete bronchial epithelial cells transformation.

Conclusion: Genetic studies highlight the involvement of nicotinic receptors variants in addiction, chronic obstructive pulmonary disease and/or lung cancer. A future important step will be to translate these genetic findings to clinical practice. Interventions able to help smoking cessation in nicotine dependence subjects, under patent, are reported.

Keywords:

Addiction, cancer hallmarks, COPD, genetic variant, lung cancer, nicotine, nicotinic receptor, patent.

Affiliation:

Clinical and Molecular Epidemiology, IRCSS San Raffaele Pisana, Via di Valcannuta 247, I-00166 Rome, Scientific Direction, IRCSS San Raffaele Pisana, Via di Valcannuta 247, I-00166 Rome, Clinical and Molecular Epidemiology, IRCSS San Raffaele Pisana, Via di Valcannuta 247, I-00166 Rome, Clinical and Molecular Epidemiology, IRCSS San Raffaele Pisana, Via di Valcannuta 247, I-00166 Rome, Pulmonary Rehabilitation, IRCCS San Raffaele Pisana, Via della Pisana, 235, I-00163 Rome, Scientific Direction, IRCSS San Raffaele Pisana, Via di Valcannuta 247, I-00166 Rome, Clinical and Molecular Epidemiology, IRCSS San Raffaele Pisana, Via di Valcannuta 247, I-00166 Rome



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