Premium
Advances in the treatment of acute myeloid leukemia: From chromosomal aberrations to biologically targeted therapy
Author(s) -
Lübbert Michael,
MüllerTidow Carsten,
Hofmann WolfKarsten,
Koeffler H. Phillip
Publication year - 2008
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.21770
Subject(s) - acute promyelocytic leukemia , myeloid leukemia , cancer research , imatinib , myelodysplastic syndromes , targeted therapy , thalidomide , lenalidomide , biology , leukemia , myeloid , medicine , immunology , bioinformatics , retinoic acid , bone marrow , genetics , multiple myeloma , cancer , gene
We describe several recent advances in our understanding and treatment of acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) including the use of cytogenetics to classify these diseases and to identify therapies that are specific for the abnormalities. Cell lines have provided readily available and very relevant models to understand these diseases. The two clear successes include the use of retinoic acid for acute promyelocytic leukemia and tyrosine kinase inhibitors (e.g., imatinib) for chronic myelogenous leukemia. Very recent results suggest a particular activity of lenalidomide, an analogue of thalidomide, in MDS patients with deletions of the long arm of chromosome 5 (so‐called 5q minus syndrome), and notable activity of azanucleoside DNA demethylating agents in MDS with loss of chromosome 7. However, for the vast majority of cytogenetic abnormalities found in AML/MDS, no specific therapies have been identified. The use of a variety of molecular biology techniques have identified a large number of genomic abnormalities; the challenge of the next several decades is to identify specific therapies for these molecular defects. J. Cell. Biochem. 104: 2059–2070, 2008. © 2008 Wiley‐Liss, Inc.