Perturbed cell metabolism and energy regulation is a well established hallmark of cancer and has been studied since the middle of the nineteenth century. Cancer cells have been shown to exhibit greater activity of metabolic pathways including the glycolytic and glutaminolysis pathways and a reduced dependence on oxidative phosphorylation. However the mechanism by which cancer cells switch from traditional metabolic programs to their characteristic alternate programs remains poorly understood.
Such reprogramming events involve dynamic regulation of many genes and gene networks. My hypothesis is that these regulatory events are mediated through epigenetic means including chromatin modifications and functional long-noncoding RNAs. I am testing this hypothesis in the context of T-cell acute leukemia.
“Satisfaction of one's curiosity is one of the greatest sources of happiness in life.Linus Pauling