000167736 001__ 167736 000167736 005__ 20240229133546.0 000167736 0247_ $$2doi$$a10.14309/ctg.0000000000000317 000167736 0247_ $$2pmid$$apmid:33646204 000167736 0247_ $$2altmetric$$aaltmetric:101082423 000167736 037__ $$aDKFZ-2021-00502 000167736 041__ $$aEnglish 000167736 082__ $$a610 000167736 1001_ $$0P:(DE-He78)c392ec8a090dcfbe801f135a6212caf9$$aChen, Xuechen$$b0$$eFirst author 000167736 245__ $$aSmoking, Genetic Predisposition, and Colorectal Cancer Risk. 000167736 260__ $$aLondon$$bNature Publ. Group$$c2021 000167736 3367_ $$2DRIVER$$aarticle 000167736 3367_ $$2DataCite$$aOutput Types/Journal article 000167736 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1637159765_23141 000167736 3367_ $$2BibTeX$$aARTICLE 000167736 3367_ $$2ORCID$$aJOURNAL_ARTICLE 000167736 3367_ $$00$$2EndNote$$aJournal Article 000167736 500__ $$a#EA:C070#LA:C070#2021 Mar 1;12(3):e00317 000167736 520__ $$aSmoking and genetic predisposition are established risk factors for colorectal cancer (CRC). We aimed to assess and compare their individual and joint impact on CRC risk using the novel approach of genetic risk equivalent (GRE).Data were extracted from the Darmkrebs: Chancen der Verhütung durch Screening study, a large population-based case-control study in Germany. A polygenic risk score (PRS) based on 140 CRC-related single nucleotide polymorphisms was derived to quantify genetic risk. Multiple logistic regression was used to estimate the individual and joint impact of smoking and PRS on CRC risk, and to quantify the smoking effect in terms of GRE, the corresponding effect conveyed by a defined difference in PRS percentiles.There were 5,086 patients with CRC and 4,120 controls included. Current smokers had a 48% higher risk of CRC than never smokers (adjusted odds ratio 1.48, 95% confidence interval 1.27-1.72). A PRS above the 90th percentile was significantly associated with a 3.6-, 4.3-, and 6.4-fold increased risk of CRC in never, former, and current smokers, respectively, when compared with a PRS below the 10th percentile in never smokers. The interaction between smoking and PRS on CRC risk did not reach statistical significance (P = 0.53). The effect of smoking was equivalent to the effect of having a 30 percentile higher level of PRS (GRE 30, 95% confidence interval 18-42).Both smoking and the PRS carry essentially independent CRC risk information, and their joint consideration provides powerful risk stratification. 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