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@ARTICLE{Wang:170190,
author = {X. Wang and E. Amitay$^*$ and T. A. Harrison and B. L.
Banbury and S. I. Berndt and H. Brenner$^*$ and D. D.
Buchanan and P. T. Campbell and Y. Cao and A. T. Chan and J.
Chang-Claude$^*$ and S. J. Gallinger and M. Giannakis and G.
G. Giles and M. J. Gunter and J. L. Hopper and M. A. Jenkins
and Y. Lin and V. Moreno and R. Nishihara and P. A. Newcomb
and S. Ogino and A. I. Phipps and L. C. Sakoda and R. E.
Schoen and M. L. Slattery and M. Song and W. Sun and S. N.
Thibodeau and A. E. Toland and B. Van Guelpen and M. O.
Woods and L. Hsu and M. Hoffmeister$^*$ and U. Peters},
title = {{A}ssociation {B}etween {S}moking and {M}olecular
{S}ubtypes of {C}olorectal {C}ancer.},
journal = {JNCI cancer spectrum},
volume = {5},
number = {4},
issn = {2515-5091},
address = {Oxford},
publisher = {Oxford University Press},
reportid = {DKFZ-2021-01813},
pages = {pkab056},
year = {2021},
abstract = {Smoking is associated with colorectal cancer (CRC) risk.
Previous studies suggested this association may be
restricted to certain molecular subtypes of CRC, but
large-scale comprehensive analysis is lacking.A total of
9789 CRC cases and 11 231 controls of European ancestry from
11 observational studies were included. We harmonized
smoking variables across studies and derived sex
study-specific quartiles of pack-years of smoking for
analysis. Four somatic colorectal tumor markers were
assessed individually and in combination, including BRAF
mutation, KRAS mutation, CpG island methylator phenotype
(CIMP), and microsatellite instability (MSI) status. A
multinomial logistic regression analysis was used to assess
the association between smoking and risk of CRC subtypes by
molecular characteristics, adjusting for age, sex, and
study. All statistical tests were 2-sided and adjusted for
Bonferroni correction.Heavier smoking was associated with
higher risk of CRC overall and stratified by individual
markers (P trend < .001). The associations differed
statistically significantly between all molecular subtypes,
which was the most statistically significant for CIMP and
BRAF. Compared with never-smokers, smokers in the fourth
quartile of pack-years had a $90\%$ higher risk of
CIMP-positive CRC (odds ratio = 1.90, $95\%$ confidence
interval = 1.60 to 2.26) but only $35\%$ higher risk for
CIMP-negative CRC (odds ratio = 1.35, $95\%$ confidence
interval = 1.22 to 1.49; P difference = 2.1 x 10-6). The
association was also stronger in tumors that were CIMP
positive, MSI high, or KRAS wild type when combined (P
difference < .001).Smoking was associated with differential
risk of CRC subtypes defined by molecular characteristics.
Heavier smokers had particularly higher risk of CRC subtypes
that were CIMP positive and MSI high in combination,
suggesting that smoking may be involved in the development
of colorectal tumors via the serrated pathway.},
cin = {C070 / C120 / HD01 / C020},
ddc = {610},
cid = {I:(DE-He78)C070-20160331 / I:(DE-He78)C120-20160331 /
I:(DE-He78)HD01-20160331 / I:(DE-He78)C020-20160331},
pnm = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
pid = {G:(DE-HGF)POF4-313},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:34377935},
pmc = {pmc:PMC8346704},
doi = {10.1093/jncics/pkab056},
url = {https://inrepo02.dkfz.de/record/170190},
}