Plasmablastic lymphoma of the elderly: a clinicopathological comparison with age‐related Epstein–Barr virus‐associated B cell lymphoproliferative disorder

Liu, Fang; Asano, Naoki; Tatematsu, Akiko; Oyama, Takashi; Kïtamura, Kazuo; Suzuki, Kensaku; Yamamoto, Kazuhito; Sakamoto, Natsumi; Taniwaki, Masafumi; Kinoshita, Tomohiro; Nakamura, Shigeo

doi:10.1111/j.1365-2559.2012.04339.x

Cited by 54 publications

(41 citation statements)

References 40 publications

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“…MYC rearrangement has been found in 40% to 50% of the cases with the IG as major translocation partner (83% of cases) and associated with strong protein expression. [62][63][64] These rearrangements seem to be more common in HIV-related PBL than in other subgroups of patients and are associated with a shorter overall survival. 65 Some cases of PBL with MYC rearrangements have some overlapping features with plasma cell myeloma, such as monoclonal serum immunoglobulins and lytic bone lesions.…”

Section: Myc Activation In Other Aggressive Large B-cell Lymphomamentioning

confidence: 99%

MYC Alterations in Diffuse Large B-Cell Lymphomas

Karube

Campo

2015

Seminars in Hematology

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Section: Myc Activation In Other Aggressive Large B-cell Lymphomamentioning

confidence: 99%

MYC Alterations in Diffuse Large B-Cell Lymphomas

Karube

Campo

2015

Seminars in Hematology

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“…24 Using a reverse transcriptionpolymerase chain reaction method, Nguyen-Van et al 19 showed that many EBV-positive DLBCL of the elderly and EBV-positive PTLD resembling DLBCL shared features of EBV latency type III. A relatively high frequency of EBNA2 expression (28%-32%) has been observed in several studies.…”

Section: Epidemiologymentioning

confidence: 99%

“…18,42 Plasmablastic lymphoma of the elderly is another newly recognized entity with a relatively indolent clinical course and better prognosis compared with other agerelated EBV-positive B-cell LPDs. 24 Plasmablastic lymphoma of the elderly shares features with age-related EBV-positive B-cell LPDs, including older age, immunosenescence, EBV infection, HIV negativity, and an ABC immunophenotype, although contrasting features include more frequent extranodal involvement and MYC translocations and EBV type I latency pattern. 24 …”

Section: Clinical Featuresmentioning

confidence: 99%

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EBV-positive diffuse large B-cell lymphoma of the elderly

Papathomas

Medeiros

et al. 2013

Blood

202

179

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Epstein-Barr virus (EBV) positive diffuse large B-cell lymphoma (DLBCL) of the elderly, initially described in 2003, is a provisional entity in the 2008 World Health Organization classification system and is defined as an EBV-positive monoclonal large B-cell proliferation that occurs in patients >50 years of age and in whom there is no known immunodeficiency or history of lymphoma. These tumors are more common in Asia but also occur in North America and Europe at a low frequency. These neoplasms exhibit a morphologic continuum, from polymorphous to monomorphous, but morphologic features do not correlate with prognosis as all patients have a clinically aggressive course. Most EBV-positive DLBCL of the elderly patients have an activated B-cell immunophenotype and are characterized by prominent nuclear factor-κB activation. Cytogenetic complexity is usually low. In this review, we comprehensively delineate the data emerging from analyses of EBV latency program, microRNA-mediated EBV viral oncogenesis, functional genomics of EBV and its biology, and differential diagnosis challenge for EBV-positive DLBCL of the elderly. It is hoped that the improved understanding of these tumors will lead to the development of novel therapeutic approaches, enhance the effectiveness of clinical trials, and improve prognosis.

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“…These tumors usually present in extranodal sites and frequently in the mucosae of the head and neck region in patients with different immunodeficiency states, mainly HIV infection. [72][73][74] MYC translocations are encountered in 41% to 49% of PBL cases, virtually all of them with an IG gene as a partner and usually in the context of multiple chromosomal aberrations, and seem to confer an inferior prognosis. [73][74][75][76] MYC activation also seems to play a role in the progression of plasma cell neoplasms, particularly from monoclonal gammopathy of undetermined significance to PCM.…”

Section: Dh/th Lymphomamentioning

confidence: 99%

Understanding MYC-driven aggressive B-cell lymphomas: pathogenesis and classification

Ott

Rosenwald

Campo

2013

Blood

219

214

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MYC is a potent oncogene initially identified as the target of the t(8;14)(q24;q32) chromosome translocation in Burkitt lymphoma. MYC gene alterations have been identified in other mature B-cell neoplasms that are usually associated with an aggressive clinical behavior. Most of these tumors originate in cells that do not normally express MYC protein. The oncogenic events leading to MYC up-regulation seem to overcome the inhibitory effect of physiological repressors such as BCL6 or BLIMP1.Aggressive lymphomas frequently carry additional oncogenic alterations that cooperate with MYC dysregulation, likely counteracting its proapoptotic function. The development of FISH probes and new reliable antibodies have facilitated the study of MYC gene alterations and protein expression in large series of patients, providing new clinical and biological perspectives regarding MYC dysregulation in aggressive lymphomas. MYC gene alterations in large B-cell lymphomas are frequently associated with BCL2 or BCL6 translocations conferring a very aggressive behavior. Conversely, MYC protein up-regulation may occur in tumors without apparent gene alterations, and its association with BCL2 overexpression also confers a poor prognosis. In this review, we integrate all of this new information and discuss perspectives, challenges, and open questions for the diagnosis and management of patients with MYC-driven aggressive B-cell lymphomas. (Blood. 2013;122(24):3884-3891) Introduction MYC was initially identified as the target oncogene dysregulated by the t(8;14)(q24;q32) translocation in Burkitt lymphoma (BL). MYC rearrangements involving the heavy-and light-chain immunoglobulin (IGL) loci and different non-IG genes were subsequently detected in other lymphoid neoplasms usually associated with very aggressive clinical behavior.1,2 The transforming oncogenic potential of MYC was initially demonstrated in cell lines and transgenic animal models. However, MYC dysregulation alone does not cause lymphoma, 4 and the t(8;14) has been found at very low levels in blood and BM of healthy individuals, 5 indicating that this genetic alteration per se is not sufficient to trigger lymphomagenesis. BL and most lymphomas carrying MYC translocations are among the most proliferative tumors. However, MYC expression has been difficult to identify in the germinal center (GC), the lymphoid cell compartment with the highest proliferative fraction, where most of these tumors originate. Understanding the possible role of MYC in normal lymphoid regulation and particularly the modulation of the GC reaction has been elusive.Recent studies, including basic immunology analyses, new animal models, next-generation sequencing, and clinicopathological observations, are converging to provide a new perspective of the role of MYC in the lymphoid system and the pathogenesis of aggressive lymphomas. In this review, we integrate all of this new information and discuss new perspectives, challenges, and open questions for the diagnosis and management of patients. MYC as a transc...

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Plasmablastic lymphoma of the elderly: a clinicopathological comparison with age‐related Epstein–Barr virus‐associated B cell lymphoproliferative disorder

Cited by 54 publications

References 40 publications

MYC Alterations in Diffuse Large B-Cell Lymphomas

MYC Alterations in Diffuse Large B-Cell Lymphomas

EBV-positive diffuse large B-cell lymphoma of the elderly

Understanding MYC-driven aggressive B-cell lymphomas: pathogenesis and classification

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