DNA repair eukaryotic cells have additional protective mechanisms that avoid uncontrolled interaction of different parts of the chromatin and damaged regions. Key factors here are the regulation of chromatin density and mobility. The 4D (temporal and spatial) organization of chromatin is controlling this security barrier by regulating the accessibility of genes, flexibility of DNA, and its ability to move inside the nucleus. How this regulation mechanisms are involved in DNA repair upon radiation damage is until now rarely known but an important part to understand the enhanced effectiveness of high linear energy transfer (LET) particles. The damage recognition via PARP1 and the subsequent chromatin decondensation via PARylation is a crucial step in the DNA damage response (DDR). Upon We used the SNAKE microbeam with a beam spot size of <1 µm to induce highly localized DNA damage in living cells using 55 MeV Carbon ions to investigate the chromatin rearrangements in the early stage of DDR.

The promising results of immune checkpoint inhibitors (ICIs) in tumors have changed the current treatment modality for cancer. ICIs response prediction is urgently needed for the personalized therapy approach. In the recent issue of the Journal of Oncology, Zixin Hu et al. proposed that DNA methylation alternations contribute to tumor microenvironment (TME) reshapement to predict the ICIs response. Notwithstanding the global DNA methylation loss, the repression of T cell receptor signaling and the fellow costimulators by DNA hypermethylation contributed to the cold TME and ICIs resistance.

H3K9 demethylases can remove the repressive H3K9 methylation marks on histones to alter chromatin structure, gene transcription and epigenetic state of cells. By counteracting the function of H3K9 methyltransferases, H3K9 demethylases have been shown to play an important role in numerous biological processes, including diseases such as cancer. 

The chromosomal passenger complex (CPC), comprising Survivin, Aurora B kinase, INCENP, and Borealin, is classically known for its essential functions during mitosis. However, recent findings expand the CPC's role beyond cell division, uncovering novel functions in replication stress response and genome stability maintenance.

DNA polymerase epsilon subunit 2 (POLE2) is a vital component of the DNA polymerase epsilon complex, essential for leading-strand DNA synthesis and maintaining genomic stability. Recent cancer studies have highlighted POLE2's oncogenic importance, as it is overexpressed in breast, lung, liver, and kidney cancers. Elevated POLE2 levels often correlate with poor overall and relapse-free survival, though some cancer types show contradictory associations, suggesting context-dependent roles.