No abstract

Breast cancers exhibit genome-wide aberrant DNA methylation patterns. To investigate how these affect the transcriptome and which changes are linked to transformation or progression, we apply genome-wide expression–methylation quantitative trait loci (emQTL) analysis between DNA methylation and gene expression. On a whole genome scale, in cis and in trans, DNA methylation and gene expression have remarkably and reproducibly conserved patterns of association in three breast cancer cohorts (n = 104, n = 253 and n = 277). The expression–methylation quantitative trait loci associations form two main clusters; one relates to tumor infiltrating immune cell signatures and the other to estrogen receptor signaling. In the estrogen related cluster, using ChromHMM segmentation and transcription factor chromatin immunoprecipitation sequencing data, we identify transcriptional networks regulated in a cell lineage-specific manner by DNA methylation at enhancers. These networks are strongly dominated by ERα, FOXA1 or GATA3 and their targets were functionally validated using knockdown by small interfering RNA or GRO-seq analysis after transcriptional stimulation with estrogen.

We theoretically study the Ruderman-Kittel-Kasuya-Yosida (RKKY) interaction between magnetic impurities in both Dirac and Weyl semimetals (SMs). We find that the internode process, as well as the unique three-dimensional spin-momentum locking, has significant influences on the RKKY interaction, resulting in both a Heisenberg and an Ising term, and an additional Dzyaloshinsky-Moriya term if the inversion symmetry is absent. These interactions can lead to rich spin textures and possible ferromagnetism in Dirac and time-reversal symmetry-invariant Weyl SMs. The effect of anisotropic Dirac and Weyl nodes on the RKKY interaction is also discussed. Our results provide an alternative scheme to engineer topological SMs and shed new light on the application of Dirac and Weyl SMs in spintronics.