Reference : Breast and prostate cancer risk: the interplay of polygenic risk, high-impact monogen...
E-prints/Working papers : Already available on another site
Life sciences : Genetics & genetic processes
Systems Biomedicine
http://hdl.handle.net/10993/47445
Breast and prostate cancer risk: the interplay of polygenic risk, high-impact monogenic variants, and family history 2021.06.04.21258277
English
Hassanin, Emadeldin [> >]
May, Patrick mailto [University of Luxembourg > Luxembourg Centre for Systems Biomedicine (LCSB) > Bioinformatics Core]
Aldisi, Rana [> >]
Spier, Isabel [> >]
Forstner, Andreas J. [> >]
Nothen, Markus M. [> >]
Aretz, Stefan [> >]
Krawitz, Peter [> >]
Bobbili, Dheeraj Reddy mailto [University of Luxembourg > Luxembourg Centre for Systems Biomedicine (LCSB) > Bioinformatics Core]
Maj, Carlo [> >]
4-Jun-2021
Cold Spring Harbor Laboratory Press
No
[en] Purpose: Investigate to which extent polygenic risk scores (PRS), high-impact monogenic variants, and family history affect breast and prostate cancer risk by assessing cancer prevalence and cancer cumulative lifetime incidence. Methods 200,643 individuals from the UK Biobank were stratified as follows: 1. carriers or non-carriers of high impact constitutive, monogenic variants in cancer susceptibility genes, 2. high or non-high PRS (90th percentile threshold), 3. with or without a family history of cancer. Multivariable logistic regression was used to compare the odds ratio (OR) across the different groups while Cox proportional hazards models were used to compute the cumulative incidence through life. Results Breast and prostate cancer cumulative incidence by age 70 is 7 and 5 for non-carriers with non-high PRS and reaches 37 and 32 among carriers of high-impact variants in cancer susceptibility genes with high PRS. The additional presence of family history is associated with a further increase of the risk of developing cancer reaching an OR of 14 and 21 for breast and prostate cancer, respectively. Conclusion: High PRS confers a cancer risk comparable to high-impact monogenic variants. Family history, monogenic variants, and PRS contribute additively to breast and prostate cancer risk.
Luxembourg Centre for Systems Biomedicine (LCSB): Bioinformatics Core (R. Schneider Group)
The FNR supported P.M. as part of the National Centre of Excellence in Research on Parkinson's disease (NCER-PD, FNR11264123) and the DFG Research Units FOR2715 (INTER/DFG/17/11583046) and FOR2488 (INTER/DFG/19/14429377)
Researchers ; Professionals
http://hdl.handle.net/10993/47445
10.1101/2021.06.04.21258277
https://www.medrxiv.org/content/early/2021/06/09/2021.06.04.21258277
https://doi.org/10.1101/2021.06.06.21253270
FnR ; FNR14429377 > Anne Grünewald > ProtectMove II > Reduced Penetrance In Hereditary Movement Disorders: Elucidating Mechanisms Of Endogenous Disease Protection > 01/07/2020 > > 2020

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