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https://hdl.handle.net/11499/10246
Title: | MYD88 Expression and L265P Mutation in Mature B-Cell Non-Hodgkin Lymphomas | Authors: | Caner, Vildan. Sen Turk, N. Baris, I.C. Cetin, G.O. Tepeli, E. Hacioglu, S. Sari, Hakan İsmail |
Keywords: | myeloid differentiation factor 88 MYD88 protein, human adult advanced cancer aged Article B cell lymphoma cancer genetics carcinogenesis controlled study female gain of function mutation gene expression gene overexpression gene sequence genetic association human human tissue immunohistochemistry large cell lymphoma major clinical study male mutation rate real time polymerase chain reaction scoring system biosynthesis genetic association study genetics metabolism mutation pathology single nucleotide polymorphism Adult Female Gene Expression Genetic Association Studies Humans Lymphoma, Large B-Cell, Diffuse Male Mutation Myeloid Differentiation Factor 88 Polymorphism, Single Nucleotide Real-Time Polymerase Chain Reaction |
Publisher: | Mary Ann Liebert Inc. | Abstract: | 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. © Copyright 2015, Mary Ann Liebert, Inc. | URI: | https://hdl.handle.net/11499/10246 https://doi.org/10.1089/gtmb.2015.0041 |
ISSN: | 1945-0265 |
Appears in Collections: | PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection Tıp Fakültesi Koleksiyonu WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection |
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