Bortezomib (PS‐341) in patients with human herpesvirus 8‐associated primary effusion lymphoma

Boulanger, Emmanuelle; Meignin, Véronique; Oksenhendler, Éric

doi:10.1111/j.1365-2141.2008.07057.x

Cited by 29 publications

(18 citation statements)

References 8 publications

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“…9 The presence of EBV-induced cellular proliferation through the NF-B pathway also suggests the potential for treatment with agents that down-regulate this pathway, such as bortezomib. 10 Lenalidomide, an immunomodulatory agent, has also been used successfully. 11 …”

Section: Therapymentioning

confidence: 99%

HIV-associated non-Hodgkin lymphoma: viral origins and therapeutic options

Krishnan¹,

Zaia

2014

Hematology

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HIV infection is associated with an increased risk of malignancy, especially B-cell lymphoid malignancies. Many of these lymphomas are further driven by concomitant infection with viruses such as Epstein-Barr virus or Human Herpesvirus 8, the latter being implicated in uncommon types of lymphomas seen in the setting of HIV-1 infection. Treatment outcomes have improved due to infusional chemotherapy, high-dose chemotherapy, and effective antiretroviral therapy. Successful functional cure of HIV-1 infection has been demonstrated with the use of allogeneic hematopoietic stem cell transplantation. This result spurred a change in the field of HIV-1 management so that, ultimately, the goals of therapy would shift from not only curing the underlying lymphoma, but also curing the HIV-1 infection. Treatment options will be discussed with an emphasis on hematopoietic cell-based therapy for the underlying HIV infection.

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Section: Therapymentioning

confidence: 99%

HIV-associated non-Hodgkin lymphoma: viral origins and therapeutic options

Krishnan¹,

Zaia

2014

Hematology

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“…Thus, the Nf-κB pathway represents an appropriate target for the molecular therapy of PEL, and several Nf-κB inhibitors are already potential candidates (24)(25)(26). One of these candidates, the proteasome inhibitor bortezomib, has been shown to inhibit Nf-κB activity and induce the apoptosis of PEL cell lines in vitro (27,28); however, bortezomib failed to control the progression of PEL in a clinical trial (29), indicating that …”

Section: Discussionmentioning

confidence: 99%

“…preclinical anti-tumor activity does not necessarily translate directly into activity in patients, and that preclinical studies using animal models are required to determine the actual advantage of NF-κB inhibitors in PEL (29). Malignant lymphomas are characterized by a high degree of radioresponsiveness.…”

Section: A B Cmentioning

confidence: 99%

Therapeutic effects of γ-irradiation in a primary effusion lymphoma mouse model

Shiraishi

Gotoh²,

Towata

et al. 2009

Exp Med

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Abstract. Primary effusion lymphoma (PEL) is a unique and recently identified non-Hodgkin's lymphoma in immunocompromised individuals. PEL is caused by the Kaposi sarcoma-associated herpes virus/human herpes virus 8 (KSHV/ HHV-8) and has a peculiar presentation involving liquid growth in the serous body cavity, chemotherapy resistance and poor prognosis. In search of a new therapeutic modality for PEL, we examined the effect of γ-irradiation on PEL-derived cell lines (BCBL-1, BC-1, and BC-3) in vitro and in vivo. An MTT assay and trypan blue exclusion assay revealed that irradiation significantly suppressed cell proliferation in the PEL cell lines in a dose-dependent manner, and induced apoptosis. The PEL cell lines were relatively radiosensitive compared with other hematological tumor cell lines (Raji, Jurkat, and K562 cells). Inoculation of the BC-3 cell line into the peritoneal cavity of Rag2/Jak3 double-deficient mice led to massive ascites formation, and subcutaneous injection of BCBL-1 led to solid lymphoma formation. Total body irradiation (4 Gy x 2) with bone marrow transplantation resulted in the complete recovery of both types of PEL-inoculated mice. These results suggest that total body irradiation with bone marrow transplantation can be successfully applied for the treatment of chemotherapyresistant PEL.

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“…PEL cells typically express a hematolymphoid marker, CD45, but they usually lack expressions of B-cell markers (CD19, CD20, CD79a, surface and cytoplasmic immunoglobulin) (20). PEL cells express plasma cell markers, including CD138, VS38c and MUM-1/IRF4.…”

Section: Laboratory Featuresmentioning

confidence: 99%