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Cancer epigenetics is the study of somatically heritable changes to molecular processes that influence the flow of information between the DNA of cancer cells and their gene expression patterns. This includes comparative (tumour cell versus normal cell) investigation of nuclear organization, DNA methylation, histone modification and the consequences of genetic mutations in genes encoding epigenetic regulators.
Epigenetic aberrations can affect gene regulation and impact diseases, but understanding these regulatory connections remains challenging. Here, the authors present MethNet, a pipeline to integrate DNA methylation and gene expression profiles across multiple cancers to uncover distal cis-regulatory element hubs and their functional impact.
MYCN-amplified neuroblastoma remains an aggressive childhood cancer with its core regulatory circuits less understood. Here, the authors identify that the transcriptional corepressor Runx1t1 is indispensable for MYCN-driven neuroblastoma tumorigenesis.
SHP2 interacts with ACK1 kinase to erase pY54-H3 (Tyr54-phosphorylation of histones H3) epigenetic marks and triggers Androgen receptor transcriptional program. It explains genital abnormalities and infertility in LEOPARD syndrome patients, and AR upregulation in prostate cancer.
Parreno et al. provide evidence for epigenetically initiated cancers in Drosophila and show that cancer develops after transient loss of Polycomb group proteins in the absence of recurrent mutations.
In a recent Developmental Cell paper, Falvo et al. establish a role for epigenetic memory of inflammatory injury in promoting pancreatic tumorigenesis.
Rahme et al. establish an in vivo model for low-grade glioma, and use it to demonstrate that Pdgfra insulator loss and Cdkn2a promoter silencing are epigenetic drivers of gliomagenesis.