Bortezomib plus CHOP for the treatment of HIV-associated plasmablastic lymphoma: clinical experience in three patients

Fernández-Álvarez, Rubén; González-Rodríguez, Ana Pilar; Rubio-Castro, Arturo; González, María E.; Payer, Ángel Ramírez; Alonso-Garcia, Ana; Rodriguez-Villar, Diana; Domínguez-Iglesias, Francisco; Sancho, Juan‐Manuel

doi:10.3109/10428194.2015.1050666

Cited by 28 publications

(16 citation statements)

References 13 publications

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“…Reanalysis of our gene expression data (3 EBV + PT-PBL vs 20 EBV + PT-DLBCL, fold change 2, FDR < 0.05[ 95 ]) confirmed enhanced MYC signaling and demonstrated unfolded protein response endoplasmic reticulum stress signaling in PBL (unreported data). These findings provide an explanation for the success of bortezomib treatment in PBL case reports[ 96 , 97 ] and suggest that BET bromodomain inhibitors may represent a potential new therapeutic strategy, as has been successfully demonstrated in experimental models of multiple myeloma[ 98 ].…”

Section: Discussionmentioning

confidence: 94%

Recent insights in the pathogenesis of post-transplantation lymphoproliferative disorders

Morscio¹,

Tousseyn²

2016

WJT

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Post-transplant lymphoproliferative disorder (PTLD) is an aggressive complication of solid organ and hematopoietic stem cell transplantation that arises in up to 20% of transplant recipients. Infection or reactivation of the Epstein-Barr virus (EBV), a ubiquitous human herpesvirus, in combination with chronic immunosuppression are considered as the main predisposing factors, however insight in PTLD biology is fragmentary. The study of PTLD is complicated by its morphological heterogeneity and the lack of prospective trials, which also impede treatment optimization. Furthermore, the broad spectrum of underlying disorders and the graft type represent important confounding factors. PTLD encompasses different malignant subtypes that resemble histologically similar lymphomas in the general population. Post-transplant diffuse large B-cell lymphoma (PT-DLBCL), Burkitt lymphoma (PT-BL) and plasmablastic lymphoma (PT-PBL) occur most frequently. However, in many studies various EBV+ and EBV- PTLD subtypes are pooled, complicating the interpretation of the results. In this review, studies of the gene expression pattern, the microenvironment and the genetic profile of PT-DLBCL, PT-BL and PT-PBL are summarized to better understand the mechanisms underlying post-transplantation lymphomagenesis. Based on the available findings we propose stratification of PTLD according to the histological subtype and the EBV status to facilitate the interpretation of future studies and the establishment of clinical trials.

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Section: Discussionmentioning

confidence: 94%

Recent insights in the pathogenesis of post-transplantation lymphoproliferative disorders

Morscio¹,

Tousseyn²

2016

WJT

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“…The use of antimyeloma agents has been based on the fact of the plasmacytic differentiation of PBL cells and on the detection of common genetic abnormalities between ΜΜ undergoing blastic transformation and PBL [ 19 ] although the experience is limited to case reports. The proteasome inhibitor bortezomib constitutes the cornerstone of frontline treatment in MM achieving rapid responses, protecting kidney function, and overcoming the adverse prognosis of poor cytogenetics.…”

Section: Discussionmentioning

confidence: 99%

“…The proteasome inhibitor bortezomib constitutes the cornerstone of frontline treatment in MM achieving rapid responses, protecting kidney function, and overcoming the adverse prognosis of poor cytogenetics. In addition, bortezomib has been shown to be effective in patients with post-germinal center (GC) diffuse large B-cell lymphoma (DLBCL), inducing higher response and survival rates when used in combination with anthracycline-containing regimens [ 19 ] and has been shown promising in PBL patients in combination with CHOP or CHOP-like regimens both in HIV-positive [ 9 ] and in HIV-negative patients [ 20 ]. As a result, the combination of CHOP plus bortezomib appeared a suitable choice for our patient.…”

Section: Discussionmentioning

confidence: 99%

Plasmablastic Lymphoma in an Immunocompetent Patient with MDS/MPN with Ring Sideroblasts and Thrombocytosis—A Case Report

Bouchla

Tsakiraki

Glezou

et al. 2018

Case Reports in Hematology

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Plasmablastic lymphoma (PBL) is a rare, aggressive type of B-cell non-Hodgkin lymphoma with the vast majority of patients responding poorly to treatment or progressing shortly thereafter. Cyclophosphamide-doxorubicin-vincristine-prednisolone (CHOP) or CHOP-like regimens have disappointing results in this setting. We report a case of PBL arising in a previously diagnosed myelodysplastic/myeloproliferative (MDS/MPN) with ring sideroblasts and thrombocytopenia (RS-T), HIV-negative patient treated with the combination of CHOP and bortezomib. The patient achieved complete metabolic response, which has lasted one year, longer by far than would have been expected with the sole use of CHOP.

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“…In a short series, out of six patients treated with bortezomib alone, five achieved a PR – two as frontline therapy and three as a salvage treatment 45. Bortezomib has been used in combination with CHOP as frontline therapy in three HIV-associated PbL patients, all of them achieved a CR, and two of them were alive 14 and 22 months after V-CHOP 46. However, the most frequently used chemotherapy regimen in combination with bortezomib has been infusional EPOCH.…”

Section: Treatmentmentioning

confidence: 99%

Plasmablastic lymphoma: current perspectives

López¹,

Abrisqueta²

2018

BLCTT

111

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Plasmablastic lymphoma (PbL) is a rare and aggressive B-cell malignancy with large neoplastic cells, most of them resembling plasmablasts that have a CD20-negative phenotype. Although initially described as being associated with HIV, over the years it has also been identified in patients with solid organ transplant and immunocompetent patients. Little is known about molecular basis that drives PbL, and still its diagnosis remains challenging given its rarity. However, proper recognition of its clinical characteristics, localization, and morphological features can establish a correct diagnosis of PbL within the spectrum of CD20-negative large B-cell lymphomas (LBCLs). PbL is characterized by CD20 and PAX5 negativity together with the expression of CD38, CD138, MUM1/IRF4, Blimp1, and XBP1 plasmacytic differentiation markers. It is usually associated with Epstein–Barr virus infections, and MYC gene rearrangements. PbL should be carefully differentiated from other CD20-negative B-cell neoplasms, ie, primary effusion lymphoma, anaplastic lymphoma kinase-positive (ALK) large B-cell lymphoma, and LBCL in human herpesvirus 8-associated multicentric Castleman disease. Despite our improved understanding of this disease, its prognosis remains dismal with short overall survival. There is no standard of care for this entity. Several chemotherapy combinations have been used with hardly any differences on its outcome. Thus, new approaches with the addition of novel molecules are needed to overcome its poor prognosis. Our current understanding and knowledge of PbL relies primarily on case reports and small case series. In this review, we revise through an extensive literature search, the clinical and biological characteristics of this entity, and the potential therapeutic options.

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Bortezomib plus CHOP for the treatment of HIV-associated plasmablastic lymphoma: clinical experience in three patients

Cited by 28 publications

References 13 publications

Recent insights in the pathogenesis of post-transplantation lymphoproliferative disorders

Recent insights in the pathogenesis of post-transplantation lymphoproliferative disorders

Plasmablastic Lymphoma in an Immunocompetent Patient with MDS/MPN with Ring Sideroblasts and Thrombocytosis—A Case Report

Plasmablastic lymphoma: current perspectives

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