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Researchers have discovered a ‘genomic tug of war’ in animal studies that could influence how well certain patients — or certain cancers — respond to decitabine, a drug used to treat myelodysplastic syndromes that is plagued by drug resistance issues. For the first time, researchers show that decitabine causes coding and non-coding regions of DNA to engage in a tug of war for a gene activator, called H2A.Z. Typically, deticabine draws this gene activator away from coding DNA, causing gene expression to grind to a halt and cells to die. However, many types of cancer have very high levels of H2A.Z, which may help them overcome this decitabine-induced tug of war, allowing the cancer to grow.