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000157090 1001_ $$aWent, Molly$$b0
000157090 245__ $$aSearch for multiple myeloma risk factors using Mendelian randomization.
000157090 260__ $$aWashington, DC$$bAmerican Society of Hematology$$c2020
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000157090 520__ $$aThe etiology of multiple myeloma (MM) is poorly understood. Summary data from genome-wide association studies (GWASs) of multiple phenotypes can be exploited in a Mendelian randomization (MR) phenome-wide association study (PheWAS) to search for factors influencing MM risk. We performed an MR-PheWAS analyzing 249 phenotypes, proxied by 10 225 genetic variants, and summary genetic data from a GWAS of 7717 MM cases and 29 304 controls. Odds ratios (ORs) per 1 standard deviation increase in each phenotype were estimated under an inverse variance weighted random effects model. A Bonferroni-corrected threshold of P = 2 × 10-4 was considered significant, whereas P < .05 was considered suggestive of an association. Although no significant associations with MM risk were observed among the 249 phenotypes, 28 phenotypes showed evidence suggestive of association, including increased levels of serum vitamin B6 and blood carnitine (P = 1.1 × 10-3) with greater MM risk and ω-3 fatty acids (P = 5.4 × 10-4) with reduced MM risk. A suggestive association between increased telomere length and reduced MM risk was also noted; however, this association was primarily driven by the previously identified risk variant rs10936599 at 3q26 (TERC). Although not statistically significant, increased body mass index was associated with increased risk (OR, 1.10; 95% confidence interval, 0.99-1.22), supporting findings from a previous meta-analysis of prospective observational studies. Our study did not provide evidence supporting any modifiable factors examined as having a major influence on MM risk; however, it provides insight into factors for which the evidence has previously been mixed.
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000157090 7001_ $$aCornish, Alex J$$b1
000157090 7001_ $$aLaw, Philip J$$b2
000157090 7001_ $$aKinnersley, Ben$$b3
000157090 7001_ $$avan Duin, Mark$$b4
000157090 7001_ $$aWeinhold, Niels$$b5
000157090 7001_ $$0P:(DE-He78)f26164c08f2f14abcf31e52e13ee3696$$aFörsti, Asta$$b6$$udkfz
000157090 7001_ $$aHansson, Markus$$b7
000157090 7001_ $$aSonneveld, Pieter$$b8
000157090 7001_ $$aGoldschmidt, Hartmut$$b9
000157090 7001_ $$aMorgan, Gareth J$$b10
000157090 7001_ $$0P:(DE-He78)19b0ec1cea271419d9fa8680e6ed6865$$aHemminki, Kari$$b11$$udkfz
000157090 7001_ $$aNilsson, Björn$$b12
000157090 7001_ $$aKaiser, Martin$$b13
000157090 7001_ $$aHoulston, Richard S$$b14
000157090 773__ $$0PERI:(DE-600)2876449-3$$a10.1182/bloodadvances.2020001502$$gVol. 4, no. 10, p. 2172 - 2179$$n10$$p2172 - 2179$$tBlood advances$$v4$$x2473-9537$$y2020
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