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@ARTICLE{Pham:278646,
author = {T. T. Pham and K. Nimptsch and N. Papadimitriou and K.
Aleksandrova and M. Jenab and M. J. Gunter and L. Le
Marchand and L. Li and B. M. Lynch and S. Castellví-Bel and
A. I. Phipps and S. L. Schmit and H. Brenner$^*$ and S.
Ogino and E. Giovannucci and T. Pischon},
title = {{G}enetically determined circulating resistin
concentrations and risk of colorectal cancer: a two-sample
{M}endelian randomization study.},
journal = {Journal of cancer research and clinical oncology},
volume = {149},
number = {16},
issn = {0301-1585},
address = {Heidelberg},
publisher = {Springer},
reportid = {DKFZ-2023-01690},
pages = {14889-14900},
year = {2023},
note = {2023 Nov;149(16):14889-14900},
abstract = {Resistin, a novel pro-inflammatory protein implicated in
inflammatory processes, has been suggested to play a role in
colorectal development. However, evidence from observational
studies has been inconsistent. Mendelian randomization may
be a complementary method to examine this association.We
conducted a two-sample Mendelian randomization to estimate
the association between genetically determined circulating
resistin concentrations and risk of colorectal cancer (CRC).
Protein quantitative trait loci (pQTLs) from the SCALLOP
consortium were used as instrumental variables (IVs) for
resistin. CRC genetic summary data was obtained from
GECCO/CORECT/CCFR (the Genetics and Epidemiology of
Colorectal Cancer Consortium, Colorectal Cancer
Transdisciplinary Study, and Colon Cancer Family Registry),
and FinnGen (Finland Biobank). The inverse variance weighted
method (IVW) was applied in the main analysis, and other
robust methods were used as sensitivity analyses. Estimates
for the association from the two data sources were then
pooled using a meta-analysis approach.Thirteen pQTLs were
identified as IVs explaining together $7.80\%$ of
interindividual variation in circulating resistin
concentrations. Based on MR analyses, genetically determined
circulating resistin concentrations were not associated with
incident CRC (pooled-IVW-OR per standard deviation of
resistin, 1.01; $95\%$ CI 0.96, 1.06; p = 0.67. Restricting
the analyses to using IVs within or proximal to the
resistin-encoding gene (cis-IVs), or to IVs located
elsewhere in the genome (trans-IVs) provided similar
results. The association was not altered when stratified by
sex or CRC subsites.We found no evidence of a relationship
between genetically determined circulating resistin
concentrations and risk of CRC.},
keywords = {Colorectal cancer (Other) / Genetic (Other) / Instrumental
(Other) / Mendelian randomization (Other) / Resistin
(Other)},
cin = {C070 / C120 / HD01},
ddc = {610},
cid = {I:(DE-He78)C070-20160331 / I:(DE-He78)C120-20160331 /
I:(DE-He78)HD01-20160331},
pnm = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
pid = {G:(DE-HGF)POF4-313},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:37599317},
doi = {10.1007/s00432-023-05193-0},
url = {https://inrepo02.dkfz.de/record/278646},
}