The Open Leukemia Journal

2010, 3 : 1-8
Published online 2010 January 7. DOI: 10.2174/1876816401003010001
Publisher ID: TOLEUKEMIAJ-3-1

RESEARCH ARTICLE
 The Common Leukemic Fusions in Pathogenesis and in Treatment Response in Acute Myeloid Leukemia

Temesgen Fufan , Shafqat Ahmed and Jenny L Persson*
Division of Experimental Cancer Research, Department of Laboratory Medicine, Clinical Research Center in Malmö, Lund University, 205 02, Malmö, Sweden

* Address correspondence to this author at the Clinical Research Cancer, Division of Experimental Cancer Research, Lund University, Malmö University Hospital, 205 02, Malmö, Sweden; Tel: +46-40-391106; Fax: +46-40-391222; E-mail: jenny_l.persson@med.lu.se

ABSTRACT

Chromosomal abnormalities are the most common alterations in acute myeloid leukemia (AML). Among those abnormalities, chromosomal translocations that produce the oncogenic fusion proteins have been frequently observed in different subtypes of AML. Although molecular mechanisms underlying the consequences of the oncogenic transformation resulted from the fusion proteins have been extensively studied, little is known about the molecular events cooperative with the oncogenic fusion proteins in the pathogenesis of leukemia and the cellular mechanisms with regard to the predictive roles of the fusions in treatment response. In this article, we will present an overview of the important aspects of AML-associated fusion proteins and their regulated transcriptional networks in pathogenesis and prognosis of AML. We will also discuss the recent findings pertaining to the functional link between the oncogenic fusions and response of leukemic cells to the treatment. Understanding the regulation of AML-associated fusions and their association with disease characteristics, patient outcome and treatment response will be of fundamental importance for predicting the effectiveness of the treatment and design the specific therapeutic strategies.

Keywords:

Acute myeloid leukemia, chromosome translocations, leukemic fusion proteins, transcriptional factors, treatment response.