Mogamulizumab for the treatment of T-cell lymphoma

ABSTRACT

Introduction: T-cell lymphoma is a relatively rare hematologic malignancy that accounts for 10–20% of non-Hodgkin lymphomas. Treatment strategies for T-cell lymphomas are different from that for B-cell lymphomas and have poor prognoses. Among various subtypes of T-cell lymphomas, adult T-cell leukemia-lymphoma (ATL) has the worst prognosis. To achieve further improvement in the treatment outcome of T-cell lymphomas, several novel agents such as brentuximab vedotin, lenalidomide, romidepsin, and pralatrexate are actively being studied. Mogamulizumab, an anti-CC chemokine receptor 4 (CCR4) monoclonal antibody, is one of the promising agents for CCR4-positive T-cell lymphomas, especially for ATL.

Areas covered: First, basic information about the current treatment strategy of T-cell lymphomas including ATL is described. Then, the authors discuss the current clinical development of mogamulizumab and its clinical implications for T-cell lymphomas.

Expert opinion: Mogamulizumab has potent clinical efficacy against CCR4-positive T-cell lymphomas, especially against ATL. Among various toxicities associated with mogamulizumab, skin eruptions are the most significant. Although there are several effective competitors, mogamulizumab has a unique mechanism and is expected to be a key agent for treating CCR4-positive T-cell lymphomas, especially ATL.

KEYWORDS:

• Adult T-cell leukemia-lymphoma
• ATL
• CCR4
• Mogamulizumab
• PTCL
• CTCL
• T-cell lymphoma

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Erratum

Acknowledgments

The authors appreciate Dr Akiko M. Maeshima (Department of Pathology, National Cancer Center Hospital, Tokyo, Japan) for providing the photomicrographs in Figures 2 and 3. The authors had this manuscript language edited by editage by CACTUS.

Declaration of interest

S Makita has received honoraria from Chugai Pharmaceutical Co. Ltd and Celgene. K Tobinai has received honoraria from Zenyaku Kogyo, Eisai, Takeda, Mundipharma, Janssen Pharmaceuticals, HUYA Bioscience, Kyowa Hakko Kirin, Celgene, Chugai Pharmaceutical. Co. Ltd, and Ono Pharmaceutical Co. Ltd; and has received research funding from Chugai Pharmaceutical Co. Ltd, Kyowa Hakko Kirin, Ono Pharmaceutical Co. Ltd, Celgene, Janssen Pharmaceuticals, GlaxoSmithKline, Eisai, Mundipharma, Takeda, Servier, and AbbVie. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

Additional information

Funding

This work was supported in part by the National Cancer Center​​ Research and Development Fund [26-A-4, 29-A-3].