Dnmt1 links BCR-ABLp210 to epigenetic tumor stem cell priming in myeloid leukemia

Abstract

The clonal nature of cancer evolution dictates that all tumor cells carry the same cancer-initiating genetic lesions. However, the latest findings have shown that the mode of action of oncogenes is not homogeneous throughout the developmental history of the tumor. Studies on different types of hematopoietic and solid tumors have shown that the contribution of some oncogenes to cancer development is mediated through the epigenetic reprogramming of the cancer-initiating target cell [1,2,3,4]. Epigenetic reprogramming is therefore a new type of interaction between oncogenes and tumor cells, in which the oncogene primes for cancer development by establishing a new pathological tumor cell identity. The current challenge is to test whether epigenetic remodeling in the absence of the driver oncogene is sufficient for tumorigenesis.