Dr Danilov on Treatment Considerations in High-Risk MCL

Alexey Danilov, MD, PhD, associate director, Tino Stephenson Lymphoma Center, professor, Division of Leukemia, Department of Hematology & Hematopoietic Cell Transplantation, City of Hope, discusses considerations for varying treatment approaches in patients with high-risk mantle cell lymphoma (MCL).

The treatment of patients with MCL continues to trend toward a precision medicine approach, Danilov begins. In a patient who presents with high-risk features, such as blastoid MCL with multiple genetic abnormalities, TP53 aberrations—specifically TP53mutations—a complex karyotype, are generally not considered good candidates for induction therapy with intensive chemotherapy or an autologous stem cell transplantation (ASCT), due to lower efficacy associated with these options in high-risk patients, he adds. Additionally, they regimens are also associated with toxicities, and the lack of a progression-free survival benefit derived for these patients make chemotherapy or ASCT suboptimal options, Danilov says.

When selecting treatment options for high-risk patients with MCL, clinical trials serve as strong options; however, if a clinical trial is not available, novel therapy–based approaches are the preferred treatment choice, Danilov expands. These novel therapies could include lenalidomide (Revlimid), rituximab (Rituxan), or a BTK inhibitor–based approach, he notes.

The role of ASCT in the treatment of patients with MCL has continued to evolve, Danilov continues. Notably, in the phase 3 TRIANGLE trial (NCT02858258), the addition of ibrutinib (Imbruvica) to standard chemoimmunotherapy induction followed by ASCT and 2 years of maintenance ibrutinib significantly improved failure-free survival vs standard chemoimmunotherapy induction and ASCT alone in younger patients with MCL. Additionally, patients who received ibrutinib and did not receive transplant as consolidation did just as well as those who received ASCT, still leaving some questions to be answered regarding the role of ASCT in the MCL space, Danilov concludes.