Impact of Smoking on Lung Cancer Treatment Effectiveness: A Review

Abstract

Tobacco smoke contains more than 4000 detectable substances, such as polycyclic aromatic hydrocarbons, nicotine, carbon monoxide and heavy metals, which are considered powerful enzymatic inducers that have notable influence on the efficacy and tolerability of many medications through complex pharmacokinetic and pharmacodynamic interactions. As a result, adjustments of drug dosages are required in smokers, both if they continue to smoke or if they quit after smoking cessation treatment. The purpose of this review is to examine the main drug interactions with tobacco smoke clinically relevant, with a closer look on patients developing oncologic diseases.

Lipid‐soluble Cigarette Smoke Particles Induced Vascular Endothelin Type A Receptor Up‐Regulation through Activation of ERK1/2 Signal Pathways

“…In addition to this, the endothelium was removed, so the interaction between endothelial cells and smooth muscle cells could not be involved. More than 4000 substances were identified in cigarette smoke . Unfortunately, we were unable to clarify which substance(s) are directly involved in the present study.…”

Nicotinic-nAChR signaling mediates drug resistance in lung cancer

“…Both epithelial growth factor receptor (EGFR) mutation and gene amplification status may be notable in determining chemoresistance in NSCLC [6]. Several studies have revealed that never-smokers with lung cancer are more responsive to EGFR-tyrosine kinase inhibitor (EGFR-TKI) therapy than smokers [7,8]. Tumor progression and chemoresistance mediated by nicotine and its metabolites have been partly attributed to phosphoinositide 3-kinase (PI3K)/AKT, nuclear factor-κB (NF-κB), and mitochondrial signaling pathways [7,9,10].…”

“…Several studies have revealed that never-smokers with lung cancer are more responsive to EGFR-tyrosine kinase inhibitor (EGFR-TKI) therapy than smokers [7,8]. Tumor progression and chemoresistance mediated by nicotine and its metabolites have been partly attributed to phosphoinositide 3-kinase (PI3K)/AKT, nuclear factor-κB (NF-κB), and mitochondrial signaling pathways [7,9,10]. Therefore, resistance is an inevitable barrier limiting lung cancer therapy effectiveness and reducing enthusiasm, making it today's pervasive challenge for long-term disease control.…”

Tobacco influence in heavy metals levels in head and neck cancer cases

“…To the present time, more than 7000 chemical substances have been identified in cigarette smoke, including aromatic hydrocarbons, aldehydes, ketones, and heavy metals (Condoluci et al 2016;Stewart and Wild 2014). Although some metals are considered essential for biological functions, balance, high exposure to lead (Pb), cadmium (Cd), arsenic (As), nickel (Ni), and chromium (Cr), which are present in soil, contaminating food, and tobacco smoke, are also considered risk factors for cancer (Condoluci et al 2016;Galazyn-Sidorczuk et al 2008;Koedrith et al 2013;Maret 2016;Tsai et al 2017;Viana et al 2011). From the contamination of soil, tobacco leaves can be exposed to the metals: lead (Pb), cadmium (Cd), arsenic (As), nickel (Ni), and chromium (Cr), copper (Cu), and zinc (Zn), but its concentrations are dependent on plant growth and soil pH (the lower soil pH, the higher the metal contamination capacity) (Golia et al 2009).…”

“…Some carcinogens as physical, chemical, or viral agents are well known, but heavy metal's relation to malignant neoplasms and the mechanism by which it induces carcinogenesis remain unclear (Condoluci et al 2016;Galazyn-Sidorczuk et al 2008;Koedrith et al 2013;Maret 2016;Tsai et al 2017;Viana et al 2011;Wise et al 2017). Metals such as cadmium, arsenic, nickel, and chromium are already classified as carcinogenic to humans (Groups 1 and 2) by the International Agency for Research on Cancer (WHO-IARC.…”