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Review

The role of SLAMF7 in multiple myeloma: impact on therapy

, &
Pages 67-75 | Received 01 May 2016, Accepted 30 Jun 2016, Published online: 18 Jul 2016
 

ABSTRACT

Introduction: Multiple myeloma (MM), a mature B-cell neoplasm, is the second most common hematologic malignancy worldwide. Despite significant improvements in outcome with new therapies, the majority of responding patients will eventually develop resistance to treatment. Furthermore, patients swith disease refractory to both proteasome inhibitors and immunomodulatory drugs (IMiDs) have a poor prognosis.

Areas covered: Several new therapeutic approaches are emerging and immunotherapeutic strategies present an important advance for the treatment of patients with relapsed or refractory MM. Among the monoclonal antibodies under development in MM, those targeting SLAMF7 and CD38 have shown the most consistent benefit in trials to date. In this review, we will specifically focus on elotuzumab (anti-SLAMF7 antibody), and provide a summary of the mechanism of action, the clinical results and the safety profile of this new drug.

Expert commentary: Although elotuzumab has no single agent activity in MM, randomized trials in relapsed/refractory MM have demonstrated significantly improved progression-free survival when the agent is added to bortezomib-dexamethasone or lenalidomide-dexamethasone. Furthermore, this agent with its novel mechanism of action can be combined with standard therapies without a significant increase in toxicity. Elotuzumab is a highly effective therapy and future data are necessary to identify the best place for this therapy in the setting of MM.

Declaration of Interest

P Moreau has received honoraria and acted on advisory boards for BMS, Takeda, Janssen, Novartis, Celgene and Amgen. 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 paper was not funded.

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