, Volume 97, Issue 2, pp 163-164
Date: 09 Feb 2013

Guest editorial: Genetic and epigenetic alterations in hematopoietic malignancies

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It is now recognized that multiple gene alterations are required for the development of leukemia, as is the case with solid tumors. About a decade ago, these gene alterations were classified into two groups, called class I and class II mutations [1]. Class I mutations include activating mutations of tyrosine kinase receptors such as FLT-3 and c-Kit, tyrosine kinases such as JAK2, oncogenes such as Ras as well as inactivating mutations of tumor suppressors such as p53 and NF-1. Class I mutations induce cell proliferation or block apoptosis. Class II mutations, which include inactivating mutations of transcription factors such as AML1/Runx1 and chromosome modifying enzymes such as MLL, block hemopoietic differentiation. Class II mutations are often caused by chromosomal translocations resulting in fusion proteins such as AML1-ETO, PML-RARa and a variety of MLL-fusions. Combinations of class I and II mutations but not either class I or class II mutations alone induced acute leukemia in mo