Smoking, Genetic Predisposition, and Colorectal Cancer Risk.
Aged
Biomarkers, Tumor
/ genetics
Case-Control Studies
Colorectal Neoplasms
/ epidemiology
Ex-Smokers
/ statistics & numerical data
Female
Genetic Predisposition to Disease
Germany
/ epidemiology
Humans
Male
Middle Aged
Non-Smokers
/ statistics & numerical data
Polymorphism, Single Nucleotide
Risk Assessment
/ statistics & numerical data
Risk Factors
Smokers
/ statistics & numerical data
Smoking
/ adverse effects
Smoking Cessation
Journal
Clinical and translational gastroenterology
ISSN: 2155-384X
Titre abrégé: Clin Transl Gastroenterol
Pays: United States
ID NLM: 101532142
Informations de publication
Date de publication:
01 03 2021
01 03 2021
Historique:
received:
23
10
2020
accepted:
27
01
2021
entrez:
1
3
2021
pubmed:
2
3
2021
medline:
14
9
2021
Statut:
epublish
Résumé
Smoking 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. Abstinence from smoking can compensate for a substantial proportion of genetically determined CRC risk.
Identifiants
pubmed: 33646204
doi: 10.14309/ctg.0000000000000317
pii: 01720094-202103000-00002
pmc: PMC7925134
doi:
Substances chimiques
Biomarkers, Tumor
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e00317Informations de copyright
Copyright © 2021 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of The American College of Gastroenterology.
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