Chromatin structure defines the state in which genetic information, in the form of DNA, is organized within a cell. This organization of the genome dictates the abilities of genes to be activated or silenced. Though each cell of a multicellular organism harbours the same genome (barring some of the adaptive immune cells and germline cells due to chromosomal recombination), epigenetic mechanisms are primarily responsible for the development and maintenance of tissue specific expression patterns. Recent reports and studies on cancer epigenetics have shown extensive reprogramming of every component of the epigenetic machinery in cancer, including DNA methylation, histone modification, and nucleosome positioning. These genetic and epigenetic alterations interact at all stages of cancer development, working together to promote cancer progression.

Rapidly growing tumour cells provide a microenvironment rich in reactive oxygen and nitrogen species (ROS and RNS). ROS and RNS are capable of bringing modification at a nucleotide level by conversion of 5-methylcytosine (5-mC) to 5-hydroxymethylcytosine (5-hmC). This oxidative environment also promotes DNA strand breaks, as DNA modification is further amplified under oxidative stress as DNA repair machinery is compromised due to inhibition of DNA repair enzymes. Mitochondrial manganese superoxide dismutase (MnSOD or SOD2) is reported to be repressed in certain types of tumours, such as breast cancer. SOD2 deficiency results in a significant decrease in global histone epigenetic marks such as 2meH3K4, 3meH3K9, 2meH3K27, 3meH3K27 and AcH3K9. Certain classes of histone deacetylases (HDACs) like sirtuins are also redox regulated.

The aim of this Special Issue, in light of these findings, is to invite authors to contribute original research articles, as well as review articles, exploring the role of redox regulated epigenetics landscape in cancer.

Potential topics include but are not limited to the following:

• Reactive oxygen species (ROS) mediated genomic and epigenomic instability
• Redox signalling as a driving force for epigenetic modifications
• Redox responsive RNAi for cancer therapy
• Modulation of mitochondrial bioenergetics post epigenetic changes in cancer
• The Warburg effect as a source to generate redox equivalents in tumour micro-environment
• Metabolic signalling of epigenetic changes in cancer
• Redox mediated metal sensitivity in cancer
• Redox modulation of TET enzymes in cancer
• Modulation of oncogenic microRNAs (onco-miRs) by redox signalling in cancer