Brentuximab Vedotin and Relapsing/Refractory NHL with High Expression of CD30
A recently published study by authors from South Korea focused on examining the efficacy of brentuximab vedotin in patients with non-Hodgkin lymphomas (NHL) that highly express CD30 (i.e., > 30% CD30-positive tumor cells based on immunohistochemistry), where the disease had relapsed or was refractory to previous treatments.
CD30 and Anti-CD30 Targeted Antibody
Brentuximab vedotin is an anti-CD30 targeted monoclonal antibody conjugated with the microtubule inhibitor auristatin.
The surface marker CD30 is uniformly expressed in Hodgkin lymphoma (HL) or anaplastic large cell lymphomas (ALCL). The efficacy of brentuximab vedotin has been confirmed in these indications. Subsequently, its effect has also been studied in other non-Hodgkin lymphomas: diffuse large B cell lymphoma (DLBCL), primary mediastinal B-cell lymphoma (PMBCL), peripheral T-cell lymphoma (PTCL), mycosis fungoides (MF), and various cutaneous T-cell lymphomas. Studies have shown that the response to brentuximab vedotin treatment was not directly proportional to the expression of CD30 on tumor cells.
Study Design and Objectives
The cited work is a phase II study, where brentuximab vedotin was administered at a dose of 1.8 mg/kg every 3 weeks to 33 patients with various types of NHL (excluding ALCL). The primary goal was to achieve more than 40% disease control, defined as complete response (CR), partial response (PR), or stable disease.
Key Findings
The overall disease control rate achieved was 48.5% (16/33), with 6 cases of CR and 6 cases of PR. A total of 6 patients (4 with CR and 2 with PR) maintained this response for the duration of 16 completed cycles. The response to brentuximab vedotin and patient survival were not associated with the level of CD30 expression.
The median follow-up duration for patients was 29.2 months, the median progression-free survival (PFS) was 1.9 months, and the median overall survival (OS) was 6.1 months.
The most common adverse events were fever, neutropenia, fatigue, and peripheral sensory neuropathy.
In a subsequent analysis that associated the treatment response with the oncogene MUM1 (Multiple myeloma oncogene 1), it was shown that MUM1-negative patients had a higher response rate (55.6%) than MUM1-positive patients (13.3%).
Conclusion
The efficacy of brentuximab vedotin in monotherapy for patients with relapsing/refractory NHL with high CD30 expression was very good, and the toxicity of this treatment was acceptable. Additionally, it was shown that MUM1 could be a suitable biomarker, where negativity predicts the effect of brentuximab vedotin in patients with CD30-positive lymphoma.
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Source: Kim S. J., Yoon D. H., Kim J. S. et al. Efficacy of brentuximab vedotin in relapsed or refractory high-CD30-expressing non-Hodgkin lymphomas: results of a multicenter, open-labeled phase II trial. Cancer Res Treat 2020 Apr; 52 (2): 374–387, doi: 10.4143/crt.2019.198.
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