2008
DOI: 10.1016/j.mrrev.2008.04.002
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Multiple roles of nicotine on cell proliferation and inhibition of apoptosis: Implications on lung carcinogenesis

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Cited by 126 publications
(101 citation statements)
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“…[15][16][17][18][19] Nicotine is non-carcinogenic, but in vitro and animal studies have proved that nicotine plays a role in tumor promotion through angiogenesis and inhibition of apoptosis. [20,21] In the present study, nicotine levels were detected only in less number of samples by TLC method. Analysis by GC method showed that there is more percentage of blood nicotine levels (>1.425 ug/ml) in 55% cases of cancer group, alarming a possibility to acquire laryngopharyngeal cancer if there is prolonged consumption of tobacco.…”
Section: Discussioncontrasting
confidence: 47%
“…[15][16][17][18][19] Nicotine is non-carcinogenic, but in vitro and animal studies have proved that nicotine plays a role in tumor promotion through angiogenesis and inhibition of apoptosis. [20,21] In the present study, nicotine levels were detected only in less number of samples by TLC method. Analysis by GC method showed that there is more percentage of blood nicotine levels (>1.425 ug/ml) in 55% cases of cancer group, alarming a possibility to acquire laryngopharyngeal cancer if there is prolonged consumption of tobacco.…”
Section: Discussioncontrasting
confidence: 47%
“…Nicotine and its derivatives play important roles in the stimulation of NSCLC growth (Catassi et al, 2008;. In this regard, nicotinic acetylcholine receptors (nAChRs), beta-ARs (Schuller et al, 1999) and the activation of the betaadrenergic signaling cascade (Schuller et al, 1999;Laag et al, 2006) and the Akt pathway (Carlisle et al, 2007) are important, as shown in many animal studies (Schuller and Orloff, 1998;Schuller et al, 2000;West et al, 2004;Arredonda et al, 2006;Schuller, 2008;2009).…”
Section: Discussionmentioning
confidence: 99%
“…Nicotine causes a deficiency in GABA, an antagonist of betaadrenergic signalling . nAChRs are important for the autocrine-proliferative network that facilitates the growth of neoplastic cells (Catassi et al, 2008;. Regarding the intensity of the adrenergic and muscarinic cholinergic receptors in lung cancer tissue versus normal lung parenchyma, a study showed that beta-ARs were decreased, whereas muscarine receptors were increased in pulmonary adenocarcinoma (Kondratenko et al, 1991).…”
Section: Discussionmentioning
confidence: 99%
“…It comes as no surprise that the development of pathogenic oxidative processes in human organism is lifestyle dependent. [2] Thus, cigarette smoking, which is considered in the literature as a risk factor for various pathological developments and diseases (such as chronic bronchitis, emphysema, cardiovascular disease, carcinogenic developments, and tumour growth [7][8][9][10][11][12][13][14] ) causes, in particular, the oxidative damage of cell membranes and biological macromolecules. [6,[15][16][17][18][19][20][21][22][23] Cigarette smoke is a complex chemical conglomerate that contains high concentrations of two distinctly different fractions of free radicals, one in its gas phase (GP) and another one in the particulate matter (tar).…”
Section: Introductionmentioning
confidence: 99%