Daratumumab, a monoclonal antibody targeting CD38, has been approved for use with standard myeloma regimens. An evaluation of subcutaneous daratumumab combined with bortezomib, lenalidomide, and dexamethasone (VRd) for the treatment of transplantation-eligible patients with newly diagnosed multiple myeloma is needed.
METHODS
In this phase 3 trial, we randomly assigned 709 transplantation-eligible patients with newly diagnosed multiple myeloma to receive either subcutaneous daratumumab combined with VRd induction and consolidation therapy and with lenalidomide maintenance therapy (D-VRd group) or VRd induction and consolidation therapy and lenalidomide maintenance therapy alone (VRd group). The primary end point was progression-free survival. Key secondary end points were a complete response or better and minimal residual disease (MRD)–negative status.
RESULTS
At a median follow-up of 47.5 months, the risk of disease progression or death in the D-VRd group was lower than the risk in the VRd group. The estimated percentage of patients with progression-free survival at 48 months was 84.3% in the D-VRd group and 67.7% in the VRd group (hazard ratio for disease progression or death, 0.42; 95% confidence interval, 0.30 to 0.59; P<0.001); the P value crossed the prespecified stopping boundary (P=0.0126). The percentage of patients with a complete response or better was higher in the D-VRd group than in the VRd group (87.9% vs. 70.1%, P<0.001), as was the percentage of patients with MRD-negative status (75.2% vs. 47.5%, P<0.001). Death occurred in 34 patients in the D-VRd group and 44 patients in the VRd group. Grade 3 or 4 adverse events occurred in most patients in both groups; the most common were neutropenia (62.1% with D-VRd and 51.0% with VRd) and thrombocytopenia (29.1% and 17.3%, respectively). Serious adverse events occurred in 57.0% of the patients in the D-VRd group and 49.3% of those in the VRd group.
CONCLUSIONS
The addition of subcutaneous daratumumab to VRd induction and consolidation therapy and to lenalidomide maintenance therapy conferred a significant benefit with respect to progression-free survival among transplantation-eligible patients with newly diagnosed multiple myeloma.
Daratumumab, a monoclonal antibody targeting CD38, has been approved for use with standard myeloma regimens. An evaluation of subcutaneous daratumumab combined with bortezomib, lenalidomide, and dexamethasone (VRd) for the treatment of transplantation-eligible patients with newly diagnosed multiple myeloma is needed.
Methods
In this phase 3 trial, we randomly assigned 709 transplantation-eligible patients with newly diagnosed multiple myeloma to receive either subcutaneous daratumumab combined with VRd induction and consolidation therapy and with lenalidomide maintenance therapy (D-VRd group) or VRd induction and consolidation therapy and lenalidomide maintenance therapy alone (VRd group). The primary end point was progression-free survival. Key secondary end points were a complete response or better and minimal residual disease (MRD)–negative status.
Results
At a median follow-up of 47.5 months, the risk of disease progression or death in the D-VRd group was lower than the risk in the VRd group. The estimated percentage of patients with progression-free survival at 48 months was 84.3% in the D-VRd group and 67.7% in the VRd group (hazard ratio for disease progression or death, 0.42; 95% confidence interval, 0.30 to 0.59; P<0.001); the P value crossed the prespecified stopping boundary (P=0.0126). The percentage of patients with a complete response or better was higher in the D-VRd group than in the VRd group (87.9% vs. 70.1%, P<0.001), as was the percentage of patients with MRD-negative status (75.2% vs. 47.5%, P<0.001). Death occurred in 34 patients in the D-VRd group and 44 patients in the VRd group. Grade 3 or 4 adverse events occurred in most patients in both groups; the most common were neutropenia (62.1% with D-VRd and 51.0% with VRd) and thrombocytopenia (29.1% and 17.3%, respectively). Serious adverse events occurred in 57.0% of the patients in the D-VRd group and 49.3% of those in the VRd group.
Conclusions
The addition of subcutaneous daratumumab to VRd induction and consolidation therapy and to lenalidomide maintenance therapy conferred a significant benefit with respect to progression-free survival among transplantation-eligible patients with newly diagnosed multiple myeloma.
Longer PFS with carfilzomib, lenalidomide, and dexamethasone, interim analysis shows
Use of a triple-drug maintenance combination appeared to improve progression-free survival (PFS) in patients with newly diagnosed multiple myeloma following induction therapy and autologous stem-cell transplantation, an interim analysis of the phase III ATLAS trialopens in a new tab or window suggested.
In an intention-to-treat analysis, the median PFS was 59.1 months for patients treated with carfilzomib (Kyprolis), lenalidomide (Revlimid), and dexamethasone (KRd) compared with 41.4 months for those treated with lenalidomide alone (HR 0.51, 95% CI 0.31-0.86, P=0.012) at a median follow-up of 33.8 months, reported Andrzej J. Jakubowiak, PhD, of the University of Chicago Medical Center, and colleagues.
In addition, the minimal residual disease (MRD) negativity rate, as evaluated after six treatment cycles, was 53% in the KRd group compared with 31% in the lenalidomide group (P=0.0035), they noted in Lancet Oncologyopens in a new tab or window.
“To our knowledge, this study is the first randomized phase III trial suggesting superiority of an alternative maintenance therapy to lenalidomide alone,” the authors wrote.
“Longer follow-up of ATLAS will allow confirmation of these results and assessment of sustained minimal residual disease negativity, efficacy in patients with high-risk disease, and overall survival,” they added.
At data cutoff, 76% of patients in the KRd group versus 71% in the lenalidomide group reached complete response or better, with no significant difference seen in terms of depth of response.
There were nine deaths in the KRd group and 11 in the lenalidomide group. Jakubowiak and team observed no statistically significant difference in overall survival between the groups.
In an accompanying commentaryopens in a new tab or window, Monika Engelhardt, MD, and Ralph Wäsch, MD, both of the University of Freiburg in Germany, noted that “ATLAS is a key trial suggesting that maintenance approaches with more than one drug, including lenalidomide, should be studied further.”
“These results also align with those of the FORTE trialopens in a new tab or window, in which carfilzomib plus lenalidomide maintenance improved progression-free survival compared with lenalidomide alone after carfilzomib-based induction with or without autologous stem-cell transplantation,” they continued.
Regarding safety, the most common grade 3 and 4 adverse events were neutropenia (48% in the KRd group vs 60% in the lenalidomide group), thrombocytopenia (13% vs 7%), and lower respiratory tract infections (8% vs 1%). Serious adverse events were reported in 30% of patients in the KRd group and 22% in the lenalidomide group.
One treatment-related adverse event led to death — respiratory failure due to severe pneumonia — in the KRd group.
Jakubowiak and colleagues acknowledged that, as expected, there were more toxic effects observed in the KRd group than the lenalidomide-alone group, but with “an acceptable level of safety and tolerability.”
Moreover, they pointed out that “using a minimal residual disease-directed and risk-adapted design, we show that to reduce the number of toxic effects with extended carfilzomib, lenalidomide, and dexamethasone treatment, patients with standard-risk disease who reach minimal residual disease negativity after six cycles of treatment can de-escalate to maintenance with lenalidomide alone while maintaining the benefit conferred by carfilzomib, lenalidomide, and dexamethasone.”
Engelhardt and Wäsch noted that carfilzomib combinations involve more intensive treatment and visits compared with lenalidomide alone, adding that clinicians will need to decide who will benefit from this combination in routine practice.
Additionally, they suggested that questions remain about the best regimen for high-risk patients, treatment length, and which combination doses and schedules should be used.
“Molecular analysis and minimal residual disease assessment to detect those who might benefit most from treatment are required,” they concluded. “Until the primary analysis of ATLAS is available, the interim data suggest that carfilzomib, lenalidomide, and dexamethasone in patients with newly diagnosed multiple myeloma after autologous stem-cell transplantation can be considered.”
ATLAS is an ongoing investigator-initiated, open-label, randomized trial, which is being conducted across 12 centers in the U.S. and Poland among 180 patients with newly diagnosed multiple myeloma. All patients had completed a type of induction and had stable disease or better, had undergone autologous stem-cell transplantation within 100 days, initiated induction 12 months before enrollment, and had an Eastern Cooperative Oncology Group performance status of 0 or 1.
Patients were assigned to KRd (n=93) or lenalidomide alone (n=87) from June 2016 to October 2020. Median age was 59, and 53% were men. Both groups received treatment for up to 3 years (36 cycles). Patients in the KRd group who had no detectable MRD, as well as standard-risk cytogenetics, received lenalidomide alone after completion of cycle eight.
PURPOSE: With the initial analysis of POLLUX at a median follow-up of 13.5 months, daratumumab in combination with lenalidomide and dexamethasone (D-Rd) significantly prolonged progression-free survival versus lenalidomide and dexamethasone (Rd) alone in patients with relapsed or refractory multiple myeloma (RRMM). We report updated efficacy and safety results at the time of final analysis for overall survival (OS).
METHODS: POLLUX was a multicenter, randomized, open-label, phase III study during which eligible patients with = 1 line of prior therapy were randomly assigned 1:1 to D-Rd or Rd until disease progression or unacceptable toxicity. After positive primary analysis and protocol amendment, patients receiving Rd were offered daratumumab monotherapy after disease progression.
RESULTS: Significant OS benefit was observed with D-Rd (hazard ratio, 0.73; 95% CI, 0.58 to 0.91; P = .0044) at a median (range) follow-up of 79.7 (0.0-86.5) months. The median OS was 67.6 months for D-Rd compared with 51.8 months for Rd. Prespecified analyses demonstrated an improved OS with D-Rd versus Rd in most subgroups, including patients age = 65 years and patients with one, two, or three prior lines of therapy, International Staging System stage III disease, high-risk cytogenetic abnormalities, and refractoriness to their last prior line of therapy or a proteasome inhibitor. The most common (= 10%) grade 3/4 treatment-emergent adverse events with D-Rd versus Rd were neutropenia (57.6% v 41.6%), anemia (19.8% v 22.4%), pneumonia (17.3% v 11.0%), thrombocytopenia (15.5% v 15.7%), and diarrhea (10.2% v 3.9%).
CONCLUSION: D-Rd significantly extended OS versus Rd alone in patients with RRMM. To our knowledge, for the first time, our findings, together with the OS benefit observed with daratumumab plus bortezomib and dexamethasone in the phase III CASTOR trial, demonstrate OS improvement with daratumumab-containing regimens in RRMM (ClinicalTrials.gov identifier: NCT02076009 [POLLUX]).
Introduction Lenalidomide maintenance after autologous stem cell transplant (ASCT) is standard of care for myeloma (MM) patients, based on trials in which lenalidomide was planned to continue until disease progression. As outcomes for myeloma patients continue to improve, understanding whether time limited maintenance is as effective as treatment to progression is a critical question. Optimal duration may differ in subgroups of patients e.g. those with standard vs high-risk genetics or those who have achieved minimal residual disease negativity (MRD-ve). Data from the UK NCRI Myeloma XI trial were analysed to explore these questions.
Methods Myeloma XI is a phase III randomised controlled trial which recruited newly diagnosed patients with pathways for both transplant eligible (TE) and ineligible patients. In the TE pathway there was a maintenance randomisation at 3 months after ASCT with patients allocated to either lenalidomide maintenance (10mg D1-21/28, planned to continue until disease progression) or observation.
Progression-free survival (PFS) data were analysed landmarked from multiple time points (2, 3, 4, and 5 years) after the time of maintenance randomisation, including all patients who had not had an event or were censored prior to that time point. Data were analysed for all patients, within genetic risk sub-groups and by MRD status. MRD was assessed at the time of maintenance randomisation using flow cytometry with a median sensitivity of 0.004%. Molecular high-risk (HiR) was defined as the presence of del(17p), gain(1q), t(4,14), t(14;16) or t(14;20). The percentage of patients experiencing key side effects over time was also explored including all patients taking lenalidomide in each 6-month time interval.
Results In the TE pathway 1248 patients entered the maintenance randomisation and were allocated to observation (n=518) or lenalidomide (n=730). Median follow up was 44.7 months (IQR 32.4-62.7). As previously reported, lenalidomide maintenance was associated with a significant PFS benefit, median PFS from randomisation was 64 months for those receiving lenalidomide vs 32 months for those observed (HR 0.52, [95%CI 0.45, 0.61], p<0.001). This was consistent for both SR (HR 0.40, [95%CI 0.28, 0.58], p<0.0001) and HiR (HR 0.50, [95%CI 0.35, 0.70], p<0.0001) patients and for those MRD-ve (HR 0.72, [95%CI 0.55, 0.95], p=0.022) and MRD+ve (HR 0.37, [95%CI 0.27, 0.50], p<0.0001) at the start of maintenance therapy.
The magnitude of the PFS benefit was consistent when landmarked from 2y after randomisation (HR 0.51 [95%CI 0.40, 0.66], p<0.001), 3y (HR 0.47, [95%CI 0.33, 0.67], p<0.0001) and 4y (HR 0.56 [95%CI 0.33, 0.95], p=0.031), but the benefit appeared to diminish at subsequent time points.
There was more evidence for the benefit of longer duration of lenalidomide maintenance in patients MRD+ve at the start of maintenance therapy than those MRD-ve. In MRD +ve patients landmarked from 2y the HR was 0.34 [95%CI 0.19, 0.59], p<0.0001, 3y HR 0.26 [95%CI 0.11, 0.58], p=0.001 and 4y HR 0.14 [95%CI 0.04, 0.48], p=0.002. In MRD -ve patients landmarked from 2y the HR was 0.63 [95%CI 0.43, 0.94], p=0.025 but from 3y was no longer statistically significant (3y HR 0.65 [95%CI 0.36, 1.15], 4y HR 0.68 [95%CI 0.27, 1.69]). In patients with both standard and high-risk disease there was evidence of ongoing benefit of lenalidomide maintenance beyond 2-3 years.
Patients continuing lenalidomide maintenance long term did not experience worsening bone marrow suppression. In the first 6 months neutropenia was seen in 57% of patients, grade 1 (G1) 21%, G2 19%, G3 15% and G4 2.5%. This gradually reduced the longer patients were on maintenance therapy, e.g. during months 54-60 neutropenia was seen in only 40% of patients G1 20%, G2 17%, G3 3%, G4 0%.
Discussion In this analysis there is clear evidence that continuing lenalidomide maintenance beyond 3 years is associated with improved PFS, supporting recent findings from the DETERMINATION and STAMINA studies. There does, however, appear to be a time after ASCT at which continuing maintenance may no longer have ongoing benefit over observation. The current analysis suggests that between 4 and 5 years the impact diminished in all patients, earlier in the subgroup of patients MRD-ve after ASCT. Ongoing long term follow up of this and other studies is needed to define the optimal time point at which a randomised trial of stopping or continuing maintenance should be implemented.
Purpose: PD-1/PD-L1 signaling promotes tumor growth while inhibiting effector cell–mediated antitumor immune responses. Here, we assessed the impact of single and dual blockade of PD-1/PD-L1, alone or in combination with lenalidomide, on accessory and immune cell function as well as multiple myeloma cell growth in the bone marrow (BM) milieu.
Experimental Design: Surface expression of PD-1 on immune effector cells, and PD-L1 expression on CD138+ multiple myeloma cells and myeloid-derived suppressor cells (MDSC) were determined in BM from newly diagnosed (ND) multiple myeloma and relapsed/refractory (RR) multiple myeloma versus healthy donor (HD). We defined the impact of single and dual blockade of PD-1/PD-L1, alone and with lenalidomide, on autologous anti–multiple myeloma immune response and tumor cell growth.
Results: Both ND and RR patient multiple myeloma cells have increased PD-L1 mRNA and surface expression compared with HD. There is also a significant increase in PD-1 expression on effector cells in multiple myeloma. Importantly, PD-1/PD-L1 blockade abrogates BM stromal cell (BMSC)-induced multiple myeloma growth, and combined blockade of PD-1/PD-L1 with lenalidomide further inhibits BMSC-induced tumor growth. These effects are associated with induction of intracellular expression of IFNγ and granzyme B in effector cells. Importantly, PD-L1 expression in multiple myeloma is higher on MDSC than on antigen-presenting cells, and PD-1/PD-L1 blockade inhibits MDSC-mediated multiple myeloma growth. Finally, lenalidomide with PD-1/PD-L1 blockade inhibits MDSC-mediated immune suppression.
Conclusions: Our data therefore demonstrate that checkpoint signaling plays an important role in providing the tumor-promoting, immune-suppressive microenvironment in multiple myeloma, and that PD-1/PD-L1 blockade induces anti–multiple myeloma immune response that can be enhanced by lenalidomide, providing the framework for clinical evaluation of combination therapy.
Background Lenalidomide plus dexamethasone is a reference treatment for relapsed multiple myeloma. The combination of the proteasome inhibitor carfilzomib with lenalidomide and dexamethasone has shown efficacy in a phase 1 and 2 study in relapsed multiple myeloma. Methods We randomly assigned 792 patients with relapsed multiple myeloma to carfilzomib with lenalidomide and dexamethasone (carfilzomib group) or lenalidomide and dexamethasone alone (control group). The primary end point was progression-free survival. Results Progression-free survival was significantly improved with carfilzomib (median, 26.3 months, vs. 17.6 months in the control group; hazard ratio for progression or death, 0.69; 95% confidence interval [CI], 0.57 to 0.83; P=0.0001). The median overall survival was not reached in either group at the interim analysis. The Kaplan-Meier 24-month overall survival rates were 73.3% and 65.0% in the carfilzomib and control groups, respectively (hazard ratio for death, 0.79; 95% CI, 0.63 to 0.99; P=0.04). The rates of overall response (partial response or better) were 87.1% and 66.7% in the carfilzomib and control groups, respectively (P<0.001; 31.8% and 9.3% of patients in the respective groups had a complete response or better; 14.1% and 4.3% had a stringent complete response). Adverse events of grade 3 or higher were reported in 83.7% and 80.7% of patients in the carfilzomib and control groups, respectively; 15.3% and 17.7% of patients discontinued treatment owing to adverse events. Patients in the carfilzomib group reported superior health-related quality of life. Conclusions In patients with relapsed multiple myeloma, the addition of carfilzomib to lenalidomide and dexamethasone resulted in significantly improved progression-free survival at the interim analysis and had a favorable risk-benefit profile.
For patients with smoldering multiple myeloma, the standard of care is observation until symptoms develop. However, this approach does not identify high-risk patients who may benefit from early intervention.
METHODS
In this randomized, open-label, phase 3 trial, we randomly assigned 119 patients with high-risk smoldering myeloma to treatment or observation. Patients in the treatment group received an induction regimen (lenalidomide at a dose of 25 mg per day on days 1 to 21, plus dexamethasone at a dose of 20 mg per day on days 1 to 4 and days 12 to 15, at 4-week intervals for nine cycles), followed by a maintenance regimen (lenalidomide at a dose of 10 mg per day on days 1 to 21 of each 28-day cycle for 2 years). The primary end point was time to progression to symptomatic disease. Secondary end points were response rate, overall survival, and safety.
RESULTS
After a median follow-up of 40 months, the median time to progression was significantly longer in the treatment group than in the observation group (median not reached vs. 21 months; hazard ratio for progression, 0.18; 95% confidence interval [CI], 0.09 to 0.32; P<0.001). The 3-year survival rate was also higher in the treatment group (94% vs. 80%; hazard ratio for death, 0.31; 95% CI, 0.10 to 0.91; P=0.03). A partial response or better was achieved in 79% of patients in the treatment group after the induction phase and in 90% during the maintenance phase. Toxic effects were mainly grade 2 or lower.
CONCLUSIONS
Early treatment for patients with high-risk smoldering myeloma delays progression to active disease and increases overall survival.
The 21st century has seen great strides in treatment for multiple myeloma, a cancer of the bone marrow once considered a death sentence. In fact, thanks to research by Dana-Farber scientists, this blood cancer that took the lives ofGeraldine Ferraro and Leonard P. Zakim has become a chronic disease for many patients.
Ken Anderson, MD, and his colleagues have helped transform multiple myeloma into a more manageable illness by shepherding many novel drugs from the laboratory to the patient bedside.
Over a decade ago, median survival in multiple myeloma was just 2 to 3 years. Today, James (Jim) Bond of Cleveland, Ohio, who bicycles across his home state every year to raise money for cancer research, has been living with multiple myeloma for 20 years. Bond credits Dana-Farber’s clinical trials for his longevity.
Multiple myeloma is estimated to strike 22,350 people in the U.S. in 2013. Although there is still no cure, Dana-Farber researchers have contributed to the following advances.
Velcade. In 2003, the FDA approved a drug called bortezomib (Velcade), which today is standard treatment for newly diagnosed myeloma, thanks to research conducted by Anderson,Paul Richardson, MD, and their colleagues at Harvard Medical School and elsewhere.
Studying the tumor’s “neighborhood.”Around the time that Velcade was approved, Anderson and his team were also investigating the drug thalidomide (Thalomid) as a treatment for myeloma. They explored the effect of medications not just on the tumor cells but also on those surrounding the tumor, including non-cancerous immune and other cells.
Thalidomide, Revlimid and Pomalidomide. Anderson and his team discovered that thalidomide and its close cousin lenalidomide (Revlimid) actively recruit immune cells to fight cancer. Clinical trials led by Richardson and colleagues set the stage for the approval of lenalidomide to treat advanced myeloma in 2006. The most potent immunomodulator studied by both the laboratory and clinical team to date, called pomalidomide (Pomalyst), was approved in February 2013.
Combination drugs. Because many genetic mutations drive a single tumor, cancer is often best treated with combinations of therapies. Dana-Farber researchers hope to personalize multiple myeloma treatment by categorizing patients based on the molecular pathways that drive their cancer, and prescribe the appropriate combinations of drugs.
Stem cell transplant. This procedure is still a key component of treatment for multiple myeloma. DF/BWCC is a leading provider of stem cell transplantation, which involves giving the patient healthy bone marrow harvested from his or her own stem cells, or sometimes those of a donor.
Lenalidomide improved progression-free survival after first-line induction therapy but increased risk for second cancers.
Response rates and remission durations have improved for patients with multiple myeloma since the advent of more effective induction regimens and autologous stem-cell transplant (ASCT) consolidation. Nonetheless, most patients experience disease progression within 3 to 4 years. To assess the role of maintenance lenalidomide after initial therapy to improve progression-free survival (PFS), investigators conducted three phase III, multicenter, randomized, double-blind, placebo-controlled trials involving previously untreated multiple myeloma patients.
In an industry-supported study by Palumbo and colleagues, 459 patients (aged 65) with newly diagnosed, symptomatic disease who were ineligible for ASCT were randomized to one of three regimens: melphalan plus prednisone followed by placebo (MP), MP plus lenalidomide (Revlimid; 10 mg of on days 1–21 of 28-day cycle) for 9 cycles followed by placebo (MPR), or MPR induction followed by the same dosage of lenalidomide until relapse or unacceptable toxicity (MPR-R). At median follow-up of 30 months, median PFS was longer with MPR-R (31 months) than with MPR (14 months; P<0.001) or MP (13 months; P<0.001); PFS benefit was achieved by patients aged 65 to 75 but not by those older than 75. Overall survival (OS) was not improved with lenalidomide. The rate of grade 4 neutropenia was higher with lenalidomide versus without (32%–35% vs. 8%), as was the 3-year rate of second primary cancers (7% vs. 3%).
In an industry-supported study by Attal and colleagues, 614 patients (aged <65) without disease progression after induction therapy and ASCT were randomized to placebo or lenalidomide (10 mg daily for 3 months, increased to 15 mg if tolerated) until relapse or unacceptable toxicity. At median follow-up of 30 months, the median PFS was longer with lenalidomide than with placebo (41 vs. 23 months; P<0.001). OS was not improved with lenalidomide. At median follow-up of 45 months, the rate of second primary cancers was higher with lenalidomide than with placebo (3.1 vs. 1.2 per 100 person-years; P=0.002).
In a study by McCarthy and colleagues, 460 patients (aged <71) who achieved stable disease or partial or complete remission at 100 days after ASCT were randomized to placebo or lenalidomide (10 mg daily, dose-adjusted to 5–15 mg as tolerated) until relapse. After a planned interim analysis at median follow-up of 18 months showed a benefit for lenalidomide, 86 of the 128 patients remaining on placebo crossed over to lenalidomide. At a median follow-up of 34 months, the median time to disease progression (the primary outcome) was longer with lenalidomide than with placebo (46 vs. 27 months; P<0.001). The rate of OS at 3 years was higher with lenalidomide than with placebo (88% vs. 80%; 2-sided P=0.03). The rate of grade 3 or 4 neutropenia was higher with lenalidomide than with placebo (P<0.001), as was the cumulative incidence of a second primary cancer (P=0.008).
Comment: Each of these trials showed that lenalidomide improved PFS, and one showed that it improved OS. Further analysis and longer follow-up will be important to better assess toxicities (especially the increased risk for second malignancies) and the response to further therapy in patients with disease progression after lenalidomide maintenance. The benefit of lenalidomide maintenance versus lenalidomide therapy at the time of progression is also of interest, especially for patients in complete remission after initial induction. As an editorialist noted, it is necessary to consider the high cost of lenalidomide. In aggregate, these important phase III trials establish maintenance lenalidomide as an option for myeloma patients who respond to first-line induction therapy.
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