Therapeutic Targeting of Tumorigenesis and Tumor Disease - For Clinical Analysis of Epigenetics and Epigenome

Tumorigenesis, in general, is originated from two types of gene alterations, a tumor suppressor gene and a proto-oncogene/oncogene. A tumor suppressor gene, or anti-oncogene, is a gene that protects a cell from tumorigenesis. When this gene mutates, it causes a loss or reduction in its protection[1]. A proto-oncogene is a normal gene coding proteins which regulate cell growth and differentiation in normal circumstance. Once the proto-oncogene has an activating mutation, it will cause aberrance of cell differentiation, finally resulting in tumorigenesis. Additionally, higher expression and chromosomal translocations of proto-oncogenes also could lead to tumorigenesis[2]. Although these DNA sequences of tumor suppressor gene and oncogene with their aberrant changes are extensively studied in tumor disease, some genetic changes are not involved in encoded DNA sequence rather than a gene switch on and off from external or environmental factors. Scientists concluded the aberrant changes as epigenetics (prefix epiGreek means over, outside of, around). The term ‘epigenetics’ regarding aberrant changes of tumor suppressor gene and oncogene emerged in the 1990s. The concept of epigenetics was described as “stably heritable phenotype resulting from changes in a chromosome without alterations in the DNA sequence” at a Cold Spring Harbor meeting in 2008. Currently, epigenetics is focusing on DNA methylation and histone modification for clinical analysis of therapeutic targeting of tumor prevention and treatment[3]. Department of Pediatrics, Section of Hematology/Oncology, Augusta, USA