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@ARTICLE{Kar:142999,
author = {S. P. Kar and I. L. Andrulis and H. Brenner$^*$ and S.
Burgess and J. Chang-Claude$^*$ and D. Considine and T.
Dörk and D. G. R. Evans and M. Gago-Domínguez and G. G.
Giles and M. Hartman and D. Huo and R. Kaaks$^*$ and J. Li
and A. Lophatananon and S. Margolin and R. L. Milne and K.
R. Muir and H. Olsson and K. Punie and P. Radice and J.
Simard and R. M. Tamimi and E. Van Nieuwenhuysen and C.
Wendt and W. Zheng and P. D. P. Pharoah},
title = {{T}he association between weight at birth and breast cancer
risk revisited using {M}endelian randomisation.},
journal = {European journal of epidemiology},
volume = {34},
number = {6},
issn = {1573-7284},
address = {Dordrecht [u.a.]},
publisher = {Springer Science + Business Media B.V.},
reportid = {DKFZ-2019-00624},
pages = {591-600},
year = {2019},
abstract = {Observational studies suggest that higher birth weight (BW)
is associated with increased risk of breast cancer in adult
life. We conducted a two-sample Mendelian randomisation (MR)
study to assess whether this association is causal. Sixty
independent single nucleotide polymorphisms (SNPs) known to
be associated at P < 5 × 10-8 with BW were used to
construct (1) a 41-SNP instrumental variable (IV) for
univariable MR after removing SNPs with pleiotropic
associations with other breast cancer risk factors and (2) a
49-SNP IV for multivariable MR after filtering SNPs for data
availability. BW predicted by the 41-SNP IV was not
associated with overall breast cancer risk in
inverse-variance weighted (IVW) univariable MR analysis of
genetic association data from 122,977 breast cancer cases
and 105,974 controls (odds ratio = 0.86 per 500 g
higher BW; $95\%$ confidence interval 0.73-1.01).
Sensitivity analyses using four alternative methods and
three alternative IVs, including an IV with 59 of the 60
BW-associated SNPs, yielded similar results. Multivariable
MR adjusting for the effects of the 49-SNP IV on birth
length, adult height, adult body mass index, age at
menarche, and age at menopause using IVW and MR-Egger
methods provided estimates consistent with univariable
analyses. Results were also similar when all analyses were
repeated after restricting to estrogen receptor-positive or
-negative breast cancer cases. Point estimates of the odds
ratios from most analyses performed indicated an inverse
relationship between genetically-predicted BW and breast
cancer, but we are unable to rule out an association between
the non-genetically-determined component of BW and breast
cancer. Thus, genetically-predicted higher BW was not
associated with an increased risk of breast cancer in adult
life in our MR study.},
cin = {C070 / C120 / C020 / L101},
ddc = {610},
cid = {I:(DE-He78)C070-20160331 / I:(DE-He78)C120-20160331 /
I:(DE-He78)C020-20160331 / I:(DE-He78)L101-20160331},
pnm = {311 - Signalling pathways, cell and tumor biology
(POF3-311)},
pid = {G:(DE-HGF)POF3-311},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:30737679},
doi = {10.1007/s10654-019-00485-7},
url = {https://inrepo02.dkfz.de/record/142999},
}