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

Guest editorial: Genetic and epigenetic alterations in hematopoietic malignancies

This is an excerpt from the content

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 ...