Decoding the Pathophysiology and the Genetics of Multiple Myeloma to Identify New Therapeutic Targets

被引:8
|
作者
Lawasut, Panisinee [1 ,2 ,3 ,4 ]
Groen, Richard W. J. [1 ,2 ,5 ]
Dhimolea, Eugen [1 ,2 ]
Richardson, Paul G. [1 ,2 ]
Anderson, Kenneth C. [1 ,2 ]
Mitsiades, Constantine S. [1 ,2 ]
机构
[1] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA
[2] Harvard Univ, Sch Med, Dept Med, Boston, MA USA
[3] King Chulalongkorn Mem Hosp, Fac Med, Dept Med, Div Hematol, Bangkok, Thailand
[4] Chulalongkorn Univ, Thai Red Cross Soc, Bangkok, Thailand
[5] Univ Med Ctr Utrecht, Dept Cell Biol, Utrecht, Netherlands
关键词
BONE-MARROW; MOLECULAR PATHOGENESIS; SUPPRESSOR-CELLS; IN-VIVO; ANTIMYELOMA ACTIVITY; ANTITUMOR-ACTIVITY; DENDRITIC CELLS; STROMAL CELLS; T-CELLS; PHASE-I;
D O I
10.1053/j.seminoncol.2013.07.010
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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. (C) 2013 Published by Elsevier Inc.
引用
收藏
页码:537 / 548
页数:12
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