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. 2018 Feb 28;9:867. doi: 10.1038/s41467-018-03058-6

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — Analytical study approach. An overview of the analytical approach for each of the 1000 most-Mendelian probes in the multiple-case family-based analyses (a) and for the replication study of 24 probes in the population-based, case–control analyses (b). A measure of Mendelian heritability was calculated for all probes not on a sex chromosome or within 10 base pairs of a SNP (not depicted). For each of the 1000 most-Mendelian probes, a Mendelian model was fitted to the probe’s M-values and this was used to calculate carrier probabilities (e.g., for a hypothetical genetic variant that causes aberrant DNA methylation at the probe), then these carrier probabilities were tested for association with breast cancer (note that unbiased p-values could be calculated but unbiased risks could not because we could not adjust for ascertainment). This gave 24 highly heritable methylation marks that were associated with breast cancer, and a nested case–control study was used to test the M-values of each of these probes for association with breast cancer and to estimate the corresponding odds ratios (ORs)