Diffuse large B-cell lymphomas with plasmablastic/plasmacytoid features are associated with TP53 deletions and poor clinical outcome

Simonitsch‐Klupp, Ingrid; Hauser, I. Jerome; Ott, German; Drach, Johannes; Ackermann, Jutta; Kaufmann, Jan; Weltermann, Ansgar; Greinix, Hildegard; Skrabs, Cathrin; Dittrich, Christian; Lutz, D.; Pötter, Richard; Mannhalter, Christine; Lechner, Klaus; Chott, Andreas; Jaeger, Ulrich

doi:10.1038/sj.leu.2403206

Cited by 50 publications

(27 citation statements)

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“…Autologous stem cell transplantation (SCT) in the management of HIV-associated lymphomas has shown to be feasible and effective [45,46], but its role in HIV-associated PBL is unclear. In fact, DLBCL with plasmablastic differentiation have shown to be resistant to standard chemotherapy and even SCT [43]. As mentioned earlier, PBL can be observed as a complication of SCT.…”

Section: Discussionmentioning

confidence: 94%

“…In our analysis, the overall survival of these two stages did not statistically differ. Several reasons that may account for this unexpected finding include: (1) differences in treatment between these two stages (e.g., a more aggressive and effective treatment of stage IV disease may offset its inherently worse prognosis than stage I disease), (2) inaccuracy in diagnosing or staging of PBL, (3) biological aggressiveness of lymphomas with plasmablastic morphology [43], (4) similarities of PBL with plasma cell myeloma [44] (e.g., myeloma staging and therapy differ greatly from those of lymphoma), (5) the retrospective nature and limitations of our data, and (6) inadequate reporting of survival in the analyzed articles. Because of these shortcomings, HIV-associated PBL cases should be followed prospectively to observe the outcome of these patients in the HAART era.…”

Section: Discussionmentioning

confidence: 99%

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HIV‐associated plasmablastic lymphoma: Lessons learned from 112 published cases

2008

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Plasmablastic lymphoma (PBL) is a distinct subtype of non-Hodgkin B-cell lymphoma, originally described with a strong predilection to the oral cavity of human immunodeficiency virus (HIV)-infected individuals. Data regarding patient age and gender, HIV status, initiation of and response to highly active antiretroviral therapy (HAART), tumor extent, pathology, treatment, and outcome were extracted from 112 cases of PBL identified in the literature. The median age at presentation was 38 years with a male predominance of 7:1, and the median CD41 count was 178 cells/mm 3 . PBL presented on average 5 years after diagnosis of HIV. Common primary sites of presentation included the oral cavity, gastrointestinal tract, and lymph nodes. Most cases presented with either stage I or stage IV disease. There was a variable expression of B-cell markers in tumor cells, but plasma cell markers were expressed in all cases. EBV was detected in 74%. Chemotherapy was used to treat 55% patients and was combined with radiotherapy in 21% cases. Complete response was obtained in 66% of treated cases; the majority of these responses were seen after CHOP (cyclophosphamide, doxorubicin, vincristine, prednisone). The refractory/relapsed disease rate was 54%. Death occurred in 53% of patients, with a median overall survival of 15 months. Sex, CD41 count, viral load, clinical stage, EBV status, primary site of involvement, and use of CHOP failed to show an association with survival. PBL is an aggressive B-cell lymphoma that presents in both oral and extra-oral sites of chronically HIV-infected immunosuppressed young men. Am. J. Hematol. 83:804-809, 2008. V

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

HIV‐associated plasmablastic lymphoma: Lessons learned from 112 published cases

2008

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“…Following morphological and immunohistochemical review, it appeared that 2 of them may actually be PBLs (with immunoblastic/plasmablastic morphology, low levels of expression of the B-cell markers PAX5 and CD20 and short time to failure of R-CHOP therapy). The other 3 may belong to the category described as DLBCL with secretory differentiation 4 on account of their strong CD20 and PAX5 positivity.…”

Section: Discussionmentioning

confidence: 99%

“…It is thought to derive from terminally differentiated B cells, exhibiting an immunophenotype of plasma cells (PC). 2,3 Differential diagnosis with ABC-DLBCL or DLBCL with marked secretory differentiation 4 and plasma cell myeloma with plasmablastic morphology is still a common problem because of the lack of a distinctive phenotype.…”

Section: Introductionmentioning

confidence: 99%

Aggressive large B-cell lymphoma with plasma cell differentiation: immunohistochemical characterization of plasmablastic lymphoma and diffuse large B-cell lymphoma with partial plasmablastic phenotype

Montes‐Moreno¹,

Gonzalez-Medina²,

et al. 2010

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The online version of this article has a Supplementary Appendix. BackgroundPlasmablastic lymphoma has recently come to be considered a distinct entity among mature B cell neoplasms, although the limits with diffuse large B-cell lymphoma (DLBCL) need to be more accurately defined. Design and MethodsHere we show the results of an immunohistochemical study of 35 cases of plasmablastic lymphoma compared with a set of 111 conventional DLBCLs . ResultsOur results demonstrate that the use of a limited combination of immunohistochemical markers (PAX5&CD20, PRDM1/BLIMP1 and XBP1s) enables the identification of a plasmablastic immunophenotype highly characteristic of plasmablastic lymphoma cases and associated with an aggressive clinical behavior. Additionally, the study shows that the acquisition of a partial plasmablastic phenotype (PRDM1/BLIMP1 expression) in DLBCL is associated with shorter survival in R-CHOP-treated patients. ConclusionsThe use of a restricted combination of immunohistochemical markers (PAX5&CD20, PRDM1/BLIMP1 and XBP1s) enables a more accurate definition of terminal differentiation for large B-cell lymphoma.Key words: plasmablastic lymphoma, terminal B-cell differentiation. Citation: Montes-Moreno S, Gonzalez-Medina

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“…23 MYC translocations may allow PBL cells to escape apoptosis. Along with the cell cycle dysregulation induced by MYC translocations, the impairment of the DNA damage response, through loss of p53, 24 may also play a critical role in the pathogenesis of plasmablastic transformation of low-grade B-cell lymphoproliferative disorders. 25 …”

Section: Pathogenesis and Cell Of Originmentioning

confidence: 99%

The biology and treatment of plasmablastic lymphoma

Castillo

Bibas

Miranda

2015

Blood

379

543

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Plasmablastic lymphoma (PBL) is an aggressive lymphoma commonly associated with HIV infection. However, PBL can also be seen in patients with other immunodeficiencies as well as in immunocompetent individuals. Because of its distinct clinical and pathological features, such as lack of expression of CD20, plasmablastic morphology, and clinical course characterized by early relapses and subsequent chemotherapy resistance, PBL can represent a diagnostic and therapeutic challenge for pathologists and clinicians alike. Despite the recent advances in the therapy of HIV-associated and aggressive lymphomas, patients with PBL for the most part have poor outcomes. The objectives of this review are to summarize the current knowledge on the epidemiology, biology, clinical and pathological characteristics, differential diagnosis, therapy, prognostic factors, outcomes, and potential novel therapeutic approaches in patients with PBL and also to increase the awareness toward PBL in the medical community.

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Diffuse large B-cell lymphomas with plasmablastic/plasmacytoid features are associated with TP53 deletions and poor clinical outcome

Cited by 50 publications

References 37 publications

HIV‐associated plasmablastic lymphoma: Lessons learned from 112 published cases

HIV‐associated plasmablastic lymphoma: Lessons learned from 112 published cases

Aggressive large B-cell lymphoma with plasma cell differentiation: immunohistochemical characterization of plasmablastic lymphoma and diffuse large B-cell lymphoma with partial plasmablastic phenotype

The biology and treatment of plasmablastic lymphoma

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