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Cigarette smoking is the leading cause of lung cancer (all histological types), accounting for about 89% and 70% of lung cancer deaths in men and women, respectively, in Europe and other regions where cigarette smoking is common.1 Oxidative damage to DNA by free radicals and oxidants in cigarette smoke (figure 1) is one of the major pathways that can lead to lung cancer development.2
As the heme pathway plays an important role against oxidative stress, uridine diphosphate-glucuronosyl-transferase 1-1 (UGT1A1) gene polymorphisms might be expected to protect against oxidative stress-induced cancer initiation.3 Congenital underexpression of hepatic UGT1A1 causes mild chronic unconjugated hyperbilirubinaemia, known as ‘Gilbert’s syndrome, GS’. Individuals with GS have mildly raised total bilirubin concentrations in the blood (>17 µmol/L) with normal serum activities of liver transaminases, biliary damage markers and red blood cell counts.4 The frequency of the Gilbert’s polymorphism is 30%–45%, however, phenotypic hyperbilirubinaemia is estimated to be 5%–10% in Caucasians.5 6 A remarkable body of evidence from experimental and clinical studies has demonstrated that bilirubin has substantial anti-inflammatory and antioxidative properties.4 The hypothesis that genetically raised bilirubin plays a role in lung …
Contributors HF conceived and wrote the manuscript. NSK, VV and KHW contributed to the final draft with intellectual importance.
Funding The authors declare receiving funding from the French National Cancer Institute (INCa, grant nr. 2016–043), the Austrian Science Fund (FWF, grant nr. P 29608) and the European Commission, BBMRI-LPC (FP7, grant nr. 313010).
Disclaimer Where authors are identified as personnel of the International Agency for Research on Cancer/WHO, the authors alone are responsible for the views expressed in this article and they do not necessarily represent the decisions, policy or views of the International Agency for Research on Cancer/WHO.
Competing interests None declared.
Patient consent for publication Not required.
Provenance and peer review Commissioned; externally peer reviewed.