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Clin Translation Gastroenterology: The relationship between smoking, genetic susceptibility and risk of colorectal cancer

E. colorectal cancer (CRC) is the third largest and most common cancer in the world, and it is also the second largest cause of death -related deaths. There are about 1.8 million new cases each year and about 850,000 death cases. Like other diseases, the occurrence of CRC is the result of complex interaction between lifestyle and genetic factors. Among them, smoking is one of the most important risk factors for CRC. However, it is unclear to what extent it interacts with genetic susceptibility to it, which affects CRC risks. Although previous research has explored the interaction between smoking and a specific single CRC susceptible gene seat, it still lacks data on the correlation between smoking and overall genetic risks. Therefore, the purpose of this study is to evaluate CRC risks through the category of smoking and various genetic risk levels, and (ii) estimated to how much the genetically determined CRC risk can be reduced through smoking quitting.



This study is a large -scale case -based comparison study in Germany. Through the Gwas Research (GWAS), it was obtained by the 140 CRC -based single -nucleotide polypentine risk scores (PRS) to quantitatively genet risk. The multiple logic regression is used to estimate the individual and joint influence of smoking and PRS on CRC risks, and quantitative smoking effects with genetic risk equivalent (GRE). GRE is expressed by defined PRS percentage differences.

A total of 5086 CRC patients and 4,120 patients were included in this study. The current smokers are 48 % higher than those who have never smoked CRC (the adjustment of 1.48, 95 % of the confidence range of 1.27–1.72 after adjustment is 1.27–1.72). Compared with the PRS of less than 10 %, PRS, which is higher than 90 % percentage, enables those who never smoke. In the past, the risk of smokers and current smokers suffered 3.6 times, 4.3 times and 6.4 times, respectively. The interaction between smoking and PRS in CRC risks has not achieved statistical significance (P = 0.53). The effect of smoking is equivalent to 30 % increase in the level of PRS (GRE 30, 95 % confident interval 18-42).

This study has confirmed that smoking and PRS basically have the risk of increasing CRC. Quit smoking can make up a large part of the CRC risk caused by genetics.

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