Optimal management of mantle cell lymphoma in the primary setting

ABSTRACT

Introduction: The management of mantle cell lymphoma (MCL) has significantly improved since the use of intensified induction and autologous stem cell transplant consolidation. Evolving developments in minimal residual disease detection and novel agent therapy are now challenging this frontline treatment paradigm.

Areas covered: This review discusses both the established role of induction and transplant consolidation in MCL, followed by evolving concepts in the use of novel agents in the frontline setting, and the use of minimal residual disease as a driver of MCL management.

Expert opinion: In an era of novel agents and improved biologic understanding of MCL, our goal for frontline management should evolve toward personalized therapy for individual patients to maximize efficacy and survival whilst minimizing treatment-related toxicities.

KEYWORDS:

• Mantle cell lymphoma
• autologous stem cell transplant
• minimal residual disease
• chemotherapy
• lymphoma

Article highlights

• A watch-and-wait approach is appropriate in a subset of patients with MCL but requires careful consideration of both clinical (nodal vs. non-nodal) and biologic factors (SOX-11, Ki67%, and TP53 status).

• The achievement of MRD-negative status is an important therapeutic goal associated with improved outcomes.

• The clinical utility of MRD monitoring and MRD-driven maintenance strategies are areas that require further prospective validation.

• Risk stratification of MCL patients at diagnosis remains difficult. The presence of TP53 mutation identifies a high-risk group for whom intensive induction and consolidation remain inadequate treatment.

• Novel targeted therapies are currently being moved forward into the frontline setting and may challenge the existing paradigm of autologous stem cell transplant consolidation in MCL.

Declaration of interest

J Kuruvilla has research support from the Canadian Cancer Society, the Leukemia and Lymphoma Society Canada, the Princess Margaret Cancer Foundation, Roche and Janssen, and previously received honoraria and/or served on the advisory boards for Abbvie, Astra Zeneca, BMS, Celgene, Gilead, Janssen, Karyopharm, Merck, Roche and Seattle Genetics. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or conflict with the subject matter or materials discussed in this manuscript apart from those disclosed.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was not funded.