Chromatin switching and transcriptional regulation in disease

Many human diseases are the result of inappropriate changes in gene expression resulting in deleterious phenotypes of specific cells. For example, loss of expression of tumour suppressors and/or ectopic expression of oncogenes underlie many cancers, a switch from an adult to a fetal gene-expression profile in cardiac myocytes results in cardiac hypertrophy and changes in the expression of many ion channel genes leads to a phenotypic switch from contractile to proliferative smooth muscle cells in vascular diseases such as neointimal hyperplasia and atherosclerosis. Understanding the molecular mechanisms responsible for these changes in gene expression is a major goal, in order to identify novel therapeutic targets.