EBV-Associated Malignancies

Ocheni, S; Olusina, DB; Oyekunle, Anthony; Ibegbulam, Obike; Kröger, N.; Bacher, Ulrike; Zander, Axel R.

doi:10.2174/1874279301004010101

Cited by 10 publications

(9 citation statements)

References 102 publications

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“…Latency II (also called the “default program,” characterized by LMP1+/EBNA2−) is expressed in cells entering the germinal center reaction that mediates antibody affinity maturation whereas memory cells express latency I (or the “latency program,” characterized by LMP1−/EBNA2−) [40]. Although PTLD has been associated with latency III expression, this profile is probably only required in the early phases of B-cell infection as viral gene expression may vary within and between tumors [41]. …”

Section: The Epstein-barr Virus (Ebv) Exploits B-cell Differentiatmentioning

confidence: 99%

Molecular Pathogenesis of B-Cell Posttransplant Lymphoproliferative Disorder: What Do We Know So Far?

Morscio

Dierickx

Tousseyn

2013

Clinical and Developmental Immunology

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Posttransplant lymphoproliferative disorder (PTLD) is a potentially fatal disease that arises in 2%–10% of solid organ and hematopoietic stem cell transplants and is most frequently of B-cell origin. This very heterogeneous disorder ranges from benign lymphoproliferations to malignant lymphomas, and despite the clear association with Epstein-Barr Virus (EBV) infection, its etiology is still obscure. Although a number of risk factors have been identified (EBV serostatus, graft type, and immunosuppressive regimen), it is currently not possible to predict which transplant patient will eventually develop PTLD. Genetic studies have linked translocations (involving C-MYC, IGH, BCL-2), various copy number variations, DNA mutations (PIM1, PAX5, C-MYC, RhoH/TTF), and polymorphisms in both the host (IFN-gamma, IL-10, TGF-beta, HLA) and the EBV genome to B-cell PTLD development. Furthermore, the tumor microenvironment seems to play an important role in the course of disease representing a local niche that can allow antitumor immune responses even in an immunocompromised host. Taken together, B-cell PTLD pathogenesis is very complex due to the interplay of many different (patient-dependent) factors and requires thorough molecular analysis for the development of novel tailored therapies. This review aims at giving a global overview of the currently known parameters that contribute to the development of B-cell PTLD.

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Section: The Epstein-barr Virus (Ebv) Exploits B-cell Differentiatmentioning

confidence: 99%

Molecular Pathogenesis of B-Cell Posttransplant Lymphoproliferative Disorder: What Do We Know So Far?

Morscio

Dierickx

Tousseyn

2013

Clinical and Developmental Immunology

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“…On the other hand, in immunodepressed patients as well as in transplant recipients undergoing immunosuppression, CTLs are immobilized, allowing for the proliferation and immortalization of infected B cells [ 1 ]. EBV has been demonstrated to be involved in the development of numerous malignancies, both in immunocompetent hosts and in immunocompromised individuals [ 2 ]. The first association was with the endemic Burkitt’s lymphoma.…”

Section: Review Of Literaturementioning

confidence: 99%

The role of EBV in the pathogenesis of Burkitt’s Lymphoma: an Italian hospital based survey

Pannone

Zamparese²,

Pace

et al. 2014

Infect Agents Cancer

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The exact worldwide incidence of Burkitt’s lymphoma is not known. There are three distinct clinical variants of Burkitt’s lymphoma, each manifesting differences in epidemiology, clinical presentation, morphology, biology and genetic features: the endemic (African), the sporadic (non-endemic), and the immunodeficiency-associated form. In particular, we reported data regarding Burkitt’s lymphoma incidence in the world and across different European countries. Finally, we described clinic-pathological data of 48 Burkitt’s lymphomas occurred in Italy from 2003 to 2013, in 4 different hospitals, two of which located in east side, and the other ones located in the west-coast. Forty Burkitt’s lymphomas occurs in children (age range 3–12), and 8 were adulthood Burkitt’s lymphomas (age range 18–87). In the pediatric group the Male:Female ratio (M:F) was of 4:1, whereas the group of the adult patients has a M:F of 1:1.67. Immunohistochemical detection of Latent Membrane Protein 1 (LMP1) expression and Epstein-Barr virus Encoded RNA (EBER) In Situ Hybridization (ISH) procedures have been performed. Lymphocyte B monoclonal spread has been demonstrated using a Polymerase Chain Reaction (PCR) based method to amplify Fragment Restriction FR1, FR2 and FR3 immunoglobulin heavy chains DNA fragments. Only 38 cases out of 48 were analyzed for LMP-1 showing various percentage of stained cells in 47.4% of the patients.Considering ISH for EBER detection results: 1 out 2 (50%) adult analyzed cases was positive, with 50% of stained tumor cells (this patient was a 22 years old female, coming from Napoli);15 out 24 (62.5%) children analyzed Burkitt’s lymphomas resulted as positive for EBER;the overall positivity has been observed in 16/26 Burkitt’s lymphomas (61.53%).Finally, EBV has been detected in children and adult patients, one of them with deregulation of the oncogene c-MYC by chromosomal translocation.

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“…Studies have shown a strong association between EBV and the development of both nasopharyngeal carcinoma and hematologic malignancies, such as extranodal NK/T-cell lymphoma, nasal type, Burkitt's and Hodgkin's lymphoma. 5 Crucial in elucidating this case were the positive laboratory results, improvement with antibiotics, and corroborating immunohistochemical stain highlighting T pallidum. While a synchronous malignancy still cannot be excluded, close clinical follow-up has shown no further suspicious findings.…”

Section: Discussionmentioning

confidence: 67%

Section: Discussionmentioning

confidence: 99%