MyD88 L265P mutation and B cell tumor.
10.7534/j.issn.1009-2137.2014.01.048
- Author:
Hai-Min CHEN
1
;
Jian HOU
2
;
Author Information
1. Department of Hematology, Zhabei Branch of Changzheng Hospital, The Second Military Medical University, Shanghai 200070, China.
2. Department of Hematology, Zhabei Branch of Changzheng Hospital, The Second Military Medical University, Shanghai 200070, China
- Publication Type:Journal Article
- MeSH:
Carcinogenesis;
Humans;
Lymphoma, Large B-Cell, Diffuse;
Mutation;
Myeloid Differentiation Factor 88;
genetics;
Signal Transduction
- From:
Journal of Experimental Hematology
2014;22(1):241-244
- CountryChina
- Language:Chinese
-
Abstract:
Myeloid differentiation factor (MyD88) is an important adaptor protein mediating the signal transduction of most Toll-like receptors (TLR), interleukin-1 receptor (IL-1R) and interleukin-18 receptor (IL-18R) that play a key role to mediate innate immune response. Recently, activating of MYD88 L265 mutation has been reported in about of 90% lymphoplasmacytoid lymphoma/Waldenström's Macroglobulinemia, about of 29% activated type diffuse large B-cell lymphoma and other subtypes of B cell tumors demonstrating the MyD88 signaling plays an important role in B cell tumorigenesis, and inhibitors targeting MyD88 might become a new remedy for B cell tumors. In this review, the latest advances in the roles of MyD88 L265P mutation in B cell tumorigenesis were summarized.
