Molecular Mechanism and Malignant Clonal Evolution of Multiple Myeloma.
10.7534/j.issn.1009-2137.2015.05.056
- Author:
Fei DING
1
;
Ping ZHU
2
;
Xue-Qiang WU
1
Author Information
1. Institute of Hematology & Oncology, Beijing Aerospace General Hospital, Beijing 100076, China.
2. Laboratory of Hematology, Peking University First Hospital, Beijing 100034, China. E-mail: zhuping@bjmu.edu.cn.
- Publication Type:Journal Article
- MeSH:
Clonal Evolution;
Cyclin D1;
Genes, Immunoglobulin Heavy Chain;
Humans;
Multiple Myeloma;
genetics;
Translocation, Genetic
- From:
Journal of Experimental Hematology
2015;23(5):1513-1516
- CountryChina
- Language:Chinese
-
Abstract:
Almost all patients with multiple myeloma (MM) have chromosomal translocation which can result in genetic variation. There are mainly five types of chromosomal translocations, involving the IGH gene translocation to 11q13 (CCND1), 4p16 (FGFR/MMSET), 16q23 (MAF), 6p21 (CCND3) and 20q11 (MAFB). It is possible that all IGH translocations converge on a common cell cycle signal pathway. Some MM develops through a multistep transformation from monoclonal gammopathy of undetermined significance (MGUS) to smoldering MM (SMM) and eventually to MM and plasma cell leukemia (PCL). Similarly to what Darwin proposed in the mid-19th century-random genetic variation and natural selection in the context of limited resources, MM clonal evolution follow branching and nonlinear mode. The failure of MM treatment is usually related with the minimal subclone which is hardly found at newlydiagnosed.
