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CD79B and MYD88 Mutations in Splenic Marginal Zone Lymphoma

The mutation status of genes involved in the NF-κB signaling pathway in splenic marginal zone lymphoma was examined. DNA sequence analysis of four genes was performed: CD79A, CD79B, CARD11, and MYD88 that are activated through BCR signaling or Toll-like and interleukin signaling. A single point muta...

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Detalles Bibliográficos
Autores principales: Trøen, Gunhild, Warsame, Abdirashid, Delabie, Jan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3556831/
https://www.ncbi.nlm.nih.gov/pubmed/23378931
http://dx.doi.org/10.1155/2013/252318
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author Trøen, Gunhild
Warsame, Abdirashid
Delabie, Jan
author_facet Trøen, Gunhild
Warsame, Abdirashid
Delabie, Jan
author_sort Trøen, Gunhild
collection PubMed
description The mutation status of genes involved in the NF-κB signaling pathway in splenic marginal zone lymphoma was examined. DNA sequence analysis of four genes was performed: CD79A, CD79B, CARD11, and MYD88 that are activated through BCR signaling or Toll-like and interleukin signaling. A single point mutation was detected in the CD79B gene (Y196H) in one of ten SMZL cases. Additionally, one point mutation was identified in the MYD88 gene (L265P) in another SMZL case. No mutations were revealed in CD79A or CARD11 genes in these SMZL cases. Neither were mutations detected in these four genes studied in 13 control MZL samples. Interestingly, the two cases with mutations of CD79B and MYD88 showed increased numbers of immunoblasts spread among the smaller and typical marginal zone lymphoma cells. Although SMZL shows few mutations of NF-κB signaling genes, our results indicate that the presence of these mutations is associated with a higher histological grade.
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spelling pubmed-35568312013-02-01 CD79B and MYD88 Mutations in Splenic Marginal Zone Lymphoma Trøen, Gunhild Warsame, Abdirashid Delabie, Jan ISRN Oncol Research Article The mutation status of genes involved in the NF-κB signaling pathway in splenic marginal zone lymphoma was examined. DNA sequence analysis of four genes was performed: CD79A, CD79B, CARD11, and MYD88 that are activated through BCR signaling or Toll-like and interleukin signaling. A single point mutation was detected in the CD79B gene (Y196H) in one of ten SMZL cases. Additionally, one point mutation was identified in the MYD88 gene (L265P) in another SMZL case. No mutations were revealed in CD79A or CARD11 genes in these SMZL cases. Neither were mutations detected in these four genes studied in 13 control MZL samples. Interestingly, the two cases with mutations of CD79B and MYD88 showed increased numbers of immunoblasts spread among the smaller and typical marginal zone lymphoma cells. Although SMZL shows few mutations of NF-κB signaling genes, our results indicate that the presence of these mutations is associated with a higher histological grade. Hindawi Publishing Corporation 2013-01-10 /pmc/articles/PMC3556831/ /pubmed/23378931 http://dx.doi.org/10.1155/2013/252318 Text en Copyright © 2013 Gunhild Trøen et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Trøen, Gunhild
Warsame, Abdirashid
Delabie, Jan
CD79B and MYD88 Mutations in Splenic Marginal Zone Lymphoma
title CD79B and MYD88 Mutations in Splenic Marginal Zone Lymphoma
title_full CD79B and MYD88 Mutations in Splenic Marginal Zone Lymphoma
title_fullStr CD79B and MYD88 Mutations in Splenic Marginal Zone Lymphoma
title_full_unstemmed CD79B and MYD88 Mutations in Splenic Marginal Zone Lymphoma
title_short CD79B and MYD88 Mutations in Splenic Marginal Zone Lymphoma
title_sort cd79b and myd88 mutations in splenic marginal zone lymphoma
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3556831/
https://www.ncbi.nlm.nih.gov/pubmed/23378931
http://dx.doi.org/10.1155/2013/252318
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