MYD88 Expression and L265P Mutation in Mature B-Cell Non-Hodgkin Lymphomas

被引:8
作者
Caner, Vildan [1 ]
Sen Turk, Nilay [2 ]
Baris, Ikbal Cansu [3 ]
Cetin, Gokhan Ozan [1 ]
Tepeli, Emre [1 ]
Hacioglu, Sibel [4 ]
Sari, Ismail [4 ]
Zencir, Sevil [3 ]
Dogu, Mehmet Hilmi [4 ]
Bagci, Gulseren [1 ]
Keskin, Ali [4 ]
机构
[1] Pamukkale Univ Hastanesi, Tibbi Genet AD, Denizli, Turkey
[2] Pamukkale Univ Hastanesi, Tibbi Patol AD, Denizli, Turkey
[3] Pamukkale Univ, Tibbi Biyol AD, TR-20070 Denizli, Turkey
[4] Pamukkale Univ Hastanesi, Hematol BD, Denizli, Turkey
关键词
CHRONIC LYMPHOCYTIC-LEUKEMIA; TOLL-LIKE RECEPTORS; WALDENSTROMS MACROGLOBULINEMIA; SOMATIC MUTATION; PREVALENCE; DISEASE;
D O I
10.1089/gtmb.2015.0041
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Background: Myeloid differentiation primary response 88 (MYD88) is a common adaptor protein that is responsible for signaling from several receptors; mutations in this gene may play a role in the pathogenesis of lymphoma. Aim: We aimed to determine the MYD88 L265P mutation frequency, the level of MYD88 expression, and their associations with clinicopathological parameters in mature B-cell non-Hodgkin lymphomas (NHLs). Methods: A total of 68 patients were included in the study. The presence of the MYD88 L265P mutation was analyzed by real-time polymerase chain reaction and direct sequencing. MYD88 protein expression was evaluated by immunohistochemistry (IHC) using two different scoring systems. Results:MYD88 L265P mutation was present in eight (18.6%) diffuse large B-cell lymphoma (DLBCL) patients. We also observed a significant association between the loss of MYD88 expression and advanced stage in both mature B-cell NHL and DLBCL according to the first IHC scoring systems (p=0.015 and p=0.024, respectively). An association was also seen between MYD88 overexpression and low clinical risk in both mature B-cell NHL and DLBCL according to the second IHC scoring system (p=0.027 and p=0.024, respectively). Conclusions: The L265P mutation may be helpful for understanding the pathogenesis of immune-privileged site-associated DLBCLs. The presence of the mutation, together with its protein overexpression, could also be used as a prognostic marker in advanced stage DLBCLs.
引用
收藏
页码:372 / 378
页数:7
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