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Review
. 2020 May 17;12(5):1265.
doi: 10.3390/cancers12051265.

Assessing the Current State of Lung Cancer Chemoprevention: A Comprehensive Overview

Md Ashraf-Uz-Zaman  1 , Aditya Bhalerao  1 , Constantinos M Mikelis  1   2 , Luca Cucullo  1   2 , Nadezhda A German  1   2   3
Affiliations
Review

Assessing the Current State of Lung Cancer Chemoprevention: A Comprehensive Overview

Md Ashraf-Uz-Zaman et al. Cancers (Basel). .

Abstract

Chemoprevention of lung cancer is thought to significantly reduce the risk of acquiring these conditions in the subpopulation of patients with underlying health issues, such as chronic obstructive pulmonary disorder and smoking-associated lung problems. Many strategies have been tested in the previous decades, with very few translating to successful clinical trials in specific subpopulations of patients. In this review, we analyze these strategies, as well as new approaches that have emerged throughout the last few years, including synthetic lethality concept and microbiome-induced regulation of lung carcinogenesis. Overall, the continuous effort in the area of lung chemoprevention is required to develop practical therapeutical approaches. Given the inconsistency of results obtained in clinical trials targeting lung cancer chemoprevention in various subgroups of patients that differ in the underlying health condition, race, and gender, we believe that individualized approaches will have more promise than generalized treatments.

Keywords: cigarette smoke; inflammation; nicotine; oxidative stress; repurposing; tumorigenesis.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Stages of morphological cellular adaptations and molecular changes leading to lung cancer. Representative illustration highlighting morphological alterations of the epithelial cells during the gradual transition towards lung cancer and key molecular alterations contributing to this process.
Figure 2
Figure 2
Formation of the DNA adducts by benzo[a]pyrene (B[a]P) and 4-aminobiphenyl (4-ABP).
Figure 3
Figure 3
Role of nicotine-derived metabolites in the formation of DNA adducts.
Figure 4
Figure 4
Reactive oxygen species (ROS) promote cellular inflammatory response and oxidative damage, which may impact cell and tissue viability in the lungs. The figure is a schematic illustration depicting the primary point of mutual interference between Nrf2 and NF-κB. Note the cellular regulation of Nrf2 and NF-κB under normal and stressed conditions. Both Nrf2 and NF-κB are nuclear transcription factors that balance and counteract each other’s activity. Note also that the predominant activation of the NF-κB pathway through ROS exposure (generated either endogenously and/or exogenously) promotes genotoxicity, lipid peroxidation, and protein degradation leading to cellular and tissue damage.
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