Genomic landscape of Epstein–Barr virus-positive extranodal marginal zone lymphomas of mucosa-associated lymphoid tissue

2021 ◽  
Author(s):  
Bryan Rea ◽  
Yen-Chun Liu ◽  
Alanna Maguire ◽  
Lorinda A. Soma ◽  
Chris M. Bacon ◽  
...  
Keyword(s):  
Lymphoid Tissue ◽  
Epstein Barr Virus ◽  
Marginal Zone ◽  
Barr Virus ◽  
Genomic Landscape ◽  
Epstein Barr

A Survey of Epstein-Barr Virus DNA in Lymphoid Tissue: Frequent Detection in Hodgkin’s Disease

1989 ◽  
Vol 91 (1) ◽  
pp. 1-5 ◽  
Author(s):  
Stephen P. Staal ◽  
Richard Ambinder ◽  
William E. Beschorner ◽  
Gary S. Hayward ◽  
Risa Mann
Keyword(s):  
Hodgkin's Disease ◽  
Lymphoid Tissue ◽  
Epstein Barr Virus ◽  
Hodgkin’S Disease ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals Case Report: EBV-Positive Extra-Nodal Marginal Zone Lymphoma Associated With XMEN Disease Caused by a Novel Hemizygous Mutation in MAGT1

2021 ◽  
Vol 11 ◽  
Author(s):  
Xin Huang ◽  
Dan Liu ◽  
Zifen Gao ◽  
Cuiling Liu
Keyword(s):  
Epstein Barr Virus ◽  
Marginal Zone ◽  
Pediatric Population ◽  
Genetic Disorder ◽  
Marginal Zone Lymphoma ◽  
Epstein Barr Virus Infection ◽  
Loss Of Function ◽  
Barr Virus ◽  
Epstein Barr ◽  
Nodal Marginal Zone Lymphoma

BackgroundX-linked immunodeficiency with magnesium defect and Epstein-Barr virus infection and neoplasia (XMEN) disease is an X-linked genetic disorder of immune system caused by loss-of-function mutation in gene encoding Magnesium transporter 1 (MAGT1). Individuals with XMEN disease are prone to developing Epstein Barr Virus (EBV)-associated lymphomas. Herein, we report the first known case of an EBV+ EMZL associated with XMEN disease.Case presentationThe patient was an 8-year-old Chinese boy who suffered from recurrent infections from birth. Six months before, the patient presented with a painless mass on his upper lip and excisional biopsy revealed an EBV-positive extra-nodal marginal zone lymphoma (EBV+ EMZL). Furthermore, molecular investigations with next-generation sequencing identified a novel germline mutation in MAGT1 (c.828_829insAT) in the patient. The c.828_829insAT variant was predicted to cause premature truncation of MAGT1 (p.A277M.fs*11) and consequently was defined as likely pathogenic. The mutation was inherited from his asymptomatic heterozygous carrier mother. Hence the patient was diagnosed with an XMEN disease both clinically and genetically.ConclusionOur results expand the genetic spectrum of XMEN disease and also the clinical spectrum of EBV+ EMZL. We highlight the importance of the genetic etiology underlying EBV+ lymphoma in the pediatric population.

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