Mogamulizumab for the treatment of relapsed or refractory adult T-cell leukemia-lymphoma.
Frank T WinsettDaniel J LewisMadeleine DuvicPublished in: Expert review of hematology (2017)
Adult T-cell leukemia-lymphoma (ATL) is an aggressive variant of peripheral T-cell lymphoma of CD4+ T-malignant cells caused by human T-lymphotropic virus type-1. Despite aggressive treatment with multidrug combination chemotherapies, ATL confers a poor prognosis and commonly develops resistance to conventional treatments. Areas covered: Mogamulizumab is a humanized, defucosylated monoclonal antibody that acts by targeting the CC chemokine receptor 4 (CCR4) on malignant cells of ATL. In phase I and II clinical trials, it has achieved overall response rates of 31-50% in CCR4+ malignancies. The most commonly observed hematologic and non-hematologic adverse events included lymphocytopenia, neutropenia, leukocytopenia, infusion reaction, rash, and pyrexia. Expert commentary: Mogamulizumab has shown significant efficacy in treating ATL with moderately high response rates and has been approved in Japan for use in ATL. It may serve as a bridge therapy to achieve disease control prior to allogeneic hematopoietic stem cell transplantation. It also offers potential for use in combination with conventional chemotherapy. Determining the optimal combination of mogamulizumab with conventional and novel therapies remains an important strategy to improve the prognosis of patients with ATL.
Keyphrases
- poor prognosis
- acute myeloid leukemia
- monoclonal antibody
- allogeneic hematopoietic stem cell transplantation
- induced apoptosis
- acute lymphoblastic leukemia
- clinical trial
- diffuse large b cell lymphoma
- long non coding rna
- cell cycle arrest
- endothelial cells
- dendritic cells
- regulatory t cells
- low dose
- stem cells
- squamous cell carcinoma
- chemotherapy induced
- climate change
- locally advanced
- multiple myeloma
- radiation therapy
- replacement therapy
- cell death
- immune response
- open label
- multidrug resistant
- binding protein