A review article by researchers at Boston University School of Medicine (BUSM) proposes a new epigenetic hypothesis linked to tumor production and novel ideas about what causes progenitor cells to develop into cancer cells. Published in the February 2013 issue of Epigenomics, the article provides examples of how epigenetic drug treatments could be beneficial in treating cancers while also decreasing the likelihood of cancer relapse.
The article was written by researchers at the Boston University Cancer Center. Sibaji Sarkar, PhD, adjunct instructor of medicine at BUSM, is the article's corresponding author.
Cancer is a complex disease characterized by uncontrolled cell growth, division and invasion into other tissues. A 2004 review article published in Nature Medicine suggests that epigenetics, which is the phenomena whereby genetically identical cells express their genes differently resulting in different phenotypes and other factors play an important role in the formation of cancer originating from cancer stem cells.
Sarkar and colleagues propose that epigenetic processes, specifically DNA methylation, may trigger cancer progenitor cell formation from somatic cells in coordination with other cellular and environmental events. DNA methylation is a process that changes the DNA and causes genes to be silenced. In the absence of definitive proof of the existence of cancer stem cells, this hypothesis discusses a possible explanation for the formation and existence of cells that may develop into cancer. The researchers also explore why only some individuals develop cancer, despite identical genetic predispositions.
In cancer cells, the enzyme that maintains high levels of methylation in tumor suppressor genes is highly expressed, allowing uncontrolled growth. At the same time, many oncogenes, or genes with the potential to cause cancer, are activated and have lower levels of methylation. The apparent anomaly of the existence of both low and high rates of methylation could be explained with either the compartmentalization of these two processes and/or by the existence of both a methylation and demethylation system operating simultaneously at specific locations with the help of various accessory proteins.