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

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 apop...

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Published inRecent patents on anti-cancer drug discovery Vol. 14; no. 1; p. 39
Main Authors Santoro, Alessia, Tomino, Carlo, Prinzi, Giulia, Lamonaca, Palma, Cardaci, Vittorio, Fini, Massimo, Russo, Patrizia
Format Journal Article
LanguageEnglish
Published United Arab Emirates 01.01.2019
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Abstract 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. To understand the genetic, molecular and cellular biology of addiction, chronic obstructive pulmonary disease and lung cancer. 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. 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. 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.
AbstractList 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. To understand the genetic, molecular and cellular biology of addiction, chronic obstructive pulmonary disease and lung cancer. 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. 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. 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.
Author Russo, Patrizia
Tomino, Carlo
Lamonaca, Palma
Cardaci, Vittorio
Prinzi, Giulia
Santoro, Alessia
Fini, Massimo
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Issue 1
Keywords lung cancer
nicotine
patent
Addiction
cancer hallmarks
nicotinic receptor
genetic variant
COPD
Language English
License Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
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Snippet The morbidity and mortality associated with tobacco smoking is well established. Nicotine is the addictive component of tobacco. Nicotine, through the...
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StartPage 39
SubjectTerms Animals
Humans
Lung Neoplasms - chemically induced
Lung Neoplasms - drug therapy
Lung Neoplasms - metabolism
Nicotinic Antagonists - metabolism
Nicotinic Antagonists - pharmacology
Nicotinic Antagonists - therapeutic use
Patents as Topic
Pulmonary Disease, Chronic Obstructive - chemically induced
Pulmonary Disease, Chronic Obstructive - drug therapy
Pulmonary Disease, Chronic Obstructive - metabolism
Receptors, Nicotinic - metabolism
Risk Factors
Smoking Cessation - methods
Smoking Cessation Agents - metabolism
Smoking Cessation Agents - pharmacology
Smoking Cessation Agents - therapeutic use
Tobacco Smoking - drug therapy
Tobacco Smoking - metabolism
Tobacco Use Disorder - drug therapy
Tobacco Use Disorder - metabolism
Title Tobacco Smoking: Risk to Develop Addiction, Chronic Obstructive Pulmonary Disease, and Lung Cancer
URI https://www.ncbi.nlm.nih.gov/pubmed/30605063
Volume 14
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