期刊
BLOOD
卷 122, 期 7, 页码 1233-1242出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2013-01-481713
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资金
- National Institutes of Health grants NIH National Cancer Institute [CA109335, NIH CA122105, U56 CA112973]
- Dwoskin Family and Recio Family Foundations
- NIH National Cancer Institute [CA136387]
- AIDS Malignancies consortium NIH National Cancer Institute [U01 CA 1Z1947]
- NATIONAL CANCER INSTITUTE [R01CA136387, R01CA109335, U56CA112973, R01CA122105] Funding Source: NIH RePORTER
Primary effusion lymphoma (PEL) is an aggressive subtype of non-Hodgkin lymphoma characterized by short survival with current therapies, emphasizing the urgent need to develop new therapeutic approaches. Brentuximab vedotin (SGN-35) is an anti-CD30 monoclonal antibody (cAC10) conjugated by a protease-cleavable linker to a microtubuledisrupting agent, monomethyl auristatin E. Brentuximab vedotin is an effective treatment of relapsed CD30-expressing Classical Hodgkin and systemic anaplastic large cell lymphomas. Herein, we demonstrated that PEL cell lines and primary tumors express CD30 and thus may serve as potential targets for brentuximab vedotin therapy. In vitro treatment with brentuximab vedotin decreased cell proliferation, induced cell cycle arrest, and triggered apoptosis of PEL cell lines. Furthermore, in vivo brentuximab vedotin promoted tumor regression and prolonged survival of mice bearing previously reported UM-PEL-1 tumors as well as UM-PEL-3 tumors derived from a newly established and characterized Kaposi's sarcoma-associated herpesvirus-and Epstein-Barr virus-positive PEL cell line. Overall, our results demonstrate for the first time that brentuximab vedotinmay serve as an effective therapy for PEL and provide strong preclinical indications for evaluation of brentuximab vedotin in clinical studies of PEL patients.
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