TY - JOUR
T1 - Decoding the pathophysiology and the genetics of multiple myeloma to identify new therapeutic targets
AU - Lawasut, Panisinee
AU - Groen, Richard W.J.
AU - Dhimolea, Eugen
AU - Richardson, Paul G.
AU - Anderson, Kenneth C.
AU - Mitsiades, Constantine S.
N1 - Funding Information:
C.S.M. is supported by the Shawna Ashlee Corman Investigatorship in Multiple Myeloma Research; the Multiple Myeloma Research Foundation, and the Leukemia and Lymphoma Society. C.S.M. and P.G.R. are supported by the de Gunzburg Myeloma Research Fund. C.S.M. and K.C.A. are supported by NIH grants R01CA050947 and P01CA155258. R.W.J.G. is supported by the People Programme (Marie Curie Actions) of the European Union's Seventh Framework Programme FP7/2007-2013/ under REA grant agreement N° [302428]. The authors would like to acknowledge the assistance of Jeffrey D. Sorrell in the preparation of the manuscript.
PY - 2013/10
Y1 - 2013/10
N2 - In recent years, significant progress has been achieved in the characterization of the transcriptional profiles, gene mutations and structural chromosomal lesions in myeloma cells. These studies have identified many candidate therapeutic targets, which are recurrently deregulated in myeloma cells. However, these targets do not appear, at least individually, to represent universal driver(s) of this disease. Furthermore, evaluation of these recurrent lesions does not suggest that they converge to a single molecular pathway. Detailed integration of molecular and functional data for these candidate targets and pathways will hopefully dissect which of them play more critical roles for each of the different individual molecular defined subtypes of this disease. This review focuses on how recent updates in our understanding of myeloma pathogenesis and molecular characterization may impact ongoing and future efforts to develop new therapeutics for this disease.
AB - In recent years, significant progress has been achieved in the characterization of the transcriptional profiles, gene mutations and structural chromosomal lesions in myeloma cells. These studies have identified many candidate therapeutic targets, which are recurrently deregulated in myeloma cells. However, these targets do not appear, at least individually, to represent universal driver(s) of this disease. Furthermore, evaluation of these recurrent lesions does not suggest that they converge to a single molecular pathway. Detailed integration of molecular and functional data for these candidate targets and pathways will hopefully dissect which of them play more critical roles for each of the different individual molecular defined subtypes of this disease. This review focuses on how recent updates in our understanding of myeloma pathogenesis and molecular characterization may impact ongoing and future efforts to develop new therapeutics for this disease.
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U2 - 10.1053/j.seminoncol.2013.07.010
DO - 10.1053/j.seminoncol.2013.07.010
M3 - Article
C2 - 24135398
AN - SCOPUS:84886931146
SN - 0093-7754
VL - 40
SP - 537
EP - 548
JO - Seminars in oncology
JF - Seminars in oncology
IS - 5
ER -