Targeting Epigenetic Readers in Cancer

The principal tenet in oncology is that cancer is a disease that is initiated and driven by somatic aberrations of our genome. The challenge is to decipher how these genomic alterations culminate in malignant transformation and how they can be targeted for therapeutic gain. Molecular insights provided by the study of hematopoietic cancers have elucidated many fundamental principles in cancer biology. Recurrent chromosomal translocations involving transcriptional regulators in several hematopoietic cancers illustrate the importance of transcriptional dysregulation in cancer.1 The earliest detected translocations provided examples of abnormalities in both transcriptional activation and transcriptional repression.1,2 The introduction of more refined . . .