Autologous stem-cell collection following VTD or VRD induction therapy in multiple myeloma: a single-center experience

Triplet-drug regimen bortezomib-thalidomide-dexamethasone (VTD) and bortezomib-lenalidomide-dexamethasone (VRD) are considered as standard of care induction prior autologous stem-cell transplantation (ASCT) in myeloma. In addition to improve response rate, induction therapy should preserve an adequate stem-cell collection. In the present retrospective study, we analyzed stem-cell collection in 325 newly diagnosed myeloma patients who received either VTD or VRD induction before ASCT. Stem-cell mobilization consisted of intravenous cyclophosphamide plus G-CSF. Plerixafor was administered preemptively to rescue mobilization. In comparison with VTD, VRD induction was associated with a more frequent use of plerixafor (19.3% versus 5.4%,p = 0.004) and with an increased number of apheresis to reach adequate collection (>2 apheresis required in 42.3% versus 30.2%,p = 0.05). Moreover, more patients experienced collection failure in the VRD group (6% versus 1.8%,p = 0.004). The median number of CD34-positive cells (x10(6)/kg) was lower in the VRD group: 8.5 versus 9.3 (p = 0.05) in the VTD group. The vast majority of patients underwent ASCT (93% versus 98%, in VRD and VTD group, respectively). These data highlight the need of optimal stem-cell collection strategy, especially in the context of tandem transplantation and incorporation of anti-CD38 monoclonal antibody into induction.

Automated summary

The triplet-drug regimens VTD and VRD are standard of care induction prior to ASCT in myeloma. VRD induction was associated with more frequent use of plerixafor, increased number of apheresis, and higher collection failure rate compared to VTD. The median number of CD34-positive cells was lower in the VRD group, although the majority of patients in both groups underwent ASCT. Optimizing stem-cell collection strategy is crucial, especially in the context of tandem transplantation and incorporating anti-CD38 monoclonal antibody into induction.