Please use this identifier to cite or link to this item: 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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