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Understanding Multiple Myeloma Symptoms
Reflecting on the pain I experienced before my diagnosis of multiple myeloma, I realized how important it was to pay attention to the related symptoms.
Ronald Chin received a diagnosis of multiple myeloma in January 2017 and has been in remission since October 2023. Catch up on all of Ronald's blogs here!
Many symptoms could be early warning signs of multiple myeloma. One of the most common is persistent bone pain, usually felt in the back, ribs or hips. Along with bone pain, individuals may experience fatigue, weakness and difficulty breathing.
I first noticed rib pain and sciatica in September 2016. Later that year, as I stepped onto the stage at a conference in Brazil, my body felt fragile, reminding me of the long-distance travel we had endured to get here. Even getting in and out of the car was challenging; my muscles strained from carrying heavy luggage and navigating crowded airports. The physical discomfort reminded me of the toll overseas traveling can take on a person's body.
However, it wasn't until January 2017, when I experienced shooting pain down my left leg, that I realized something was seriously wrong. I had lytic lesions throughout my body, and it was painful even to sneeze. Lytic lesions refer to areas of bone destruction that result in holes.
Multiple myeloma can also lead to a collapsed backbone in the spine, which can put pressure on the spinal cord and cause further complications. Unfortunately for me, five vertebrae quickly collapsed within weeks.
The elusive origin of myeloma remains a mystery, leaving those affected searching for answers. Deep within the bones lies the bone marrow, a vital source for creating blood cells. But something insidious occurs, transforming healthy plasma cells into malignant myeloma cells. As an architect frequently working on construction sites, it is possible that this environment may have played a role in developing myeloma. Yet, another factor cannot be disregarded — the overwhelming grief and stress from losing my mother in 2015 may have weakened my immune system, leaving me vulnerable to this disease.
The diagnosis is typically confirmed through a biopsy, an invasive procedure in which a specialized needle is used to extract a small sample of the bone marrow. This vital tissue, which produces all of the body's blood cells, is usually obtained from the pelvis. I underwent this procedure while confined to my hospital bed. My most recent bone marrow biopsy was performed in June 2023, revealing no trace of cancer in my body and bringing a wave of relief and hope for the future.
There are many notable figures who were diagnosed with multiple myeloma.
According to a new biography titled "Elizabeth: An Intimate Portrait"by Gyles Brandreth, it was revealed that Queen Elizabeth II may have had multiple myeloma before her death. A Newsweek article confirmed that she had this type of cancer before her passing. In October 2021, the queen experienced health issues that caused her to miss public appearances. In the next year, she faced mobility challenges and eventually passed away in September 2022. Her official cause of death is listed as "old age" on her death certificate. She died at the age of 96.
Tom Brokaw, aged 84, is a retired journalist and author known for his work on network news. In August of 2013, he was diagnosed with multiple myeloma. Over a year later, Brokaw announced that his cancer was in remission. It is uncertain whether he is currently undergoing any maintenance treatment. In his book, "A Lucky Life Interrupted: A Memoir of Hope," Brokaw recounts his experience with cancer.
Geraldine Ferraro was a notable figure in American politics, known for her roles as a politician, diplomat and lawyer. She gained even more attention when she became the Democratic Party's nominee for vice president during the 1984 presidential election alongside Walter Mondale. Sadly, in 1998, Ferraro was diagnosed with myeloma and died from the disease in 2011. She had gone to Mass General in Boston for treatment to manage her pain caused by a fracture, a common complication of multiple myeloma. Unfortunately, she contracted pneumonia and was unable to recover. She passed away at the age of 75.
Other notable people include:
American Secretary of State, Colin Powell.
Sam Walton, the American businessman who founded Walmart.
Eppie Friedman better known by the pen name Ann Landers and
Mickey Hargitay, 1955 Mr. Universe who married actress Jayne Mansfield.
According to medical professionals, multiple myeloma is a daunting and incurable disease. However, proper treatment and care can be effectively managed for years. After receiving three different lines of chemotherapy (what I call healing elixirs), I am now undergoing maintenance treatment with Darzalex (daratumumab). At my most recent appointment with my oncologist, she described my condition as "boring," a welcome label in the world of cancer. My blood results show no changes, and there are no signs of cancer, not even at the cellular level (also known as minimal residual disease or MRD). This means that I am in complete remission.
Through my involvement in various support groups with fellow warriors, I have learned that individuals with myeloma can live for years while undergoing treatment. The advancement of treatments is ongoing and constantly improving, providing hope for many. In some cases, those with multiple myeloma experience remissions lasting for years. Some choose not to continue with treatment, instead finding solace in their path toward healing. The resilience and courage displayed by these individuals are a testament to the strength of the human spirit in the face of adversity.
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Smoldering Multiple Myeloma: Risk Factors, Who To Treat, How To Treat
Speakers on precursor disease addressed distinctions between MGUS and smoldering multiple myeloma, risk stratification, and new thinking on the role of immunological aging, especially how it affects Black patients.
It's been almost 50 years since "monoclonal gammopathy of undetermined significance," or MGUS, was identified as a precursor to multiple myeloma. Yet the debate over when and how to treat patients who have not developed the organ damage associated with the blood cancer is as lively as ever, according to speakers at a session on precursor disease on the opening day of the International Myeloma Society 21st Annual Meeting & Exposition, taking place in Rio de Janiero, Brazil.
S. Vincent Rajkumar, MDImage credit: Mayo Clinic
High-risk smoldering multiple myeloma (SMM) has emerged as the condition where treatment yields the greatest benefit, said S. Vincent Rajkumar, MD, professor of medicine at Mayo Clinic. These patients are biologically distinct from those with MGUS, and those with high-risk features should be treated, he explained.
"Initially it was thought that smoldering myeloma is some in-between stage, between MGUS and smoldering multiple myeloma. But that's not what it is," he said. "We now know that smoldering multiple myeloma is a heterogeneous clinical condition, clinically defined where one-third of the patients have high-risk smoldering myeloma. They actually have myeloma, but they don't have the end organ damage, and two-thirds have MGUS."
Citing recommendations published in 2022, he said that patients with SMM should undergo risk stratification; those with high-risk SMM should receive either lenalidomide or lenalidomide with dexamethasone for 2 years, or they should enroll in a clinical trial. High-risk patients are those that have a time to progression of 2 years or less, as defined by an algorithm he outlined. Others should be observed every 3 to 4 months.1
For those who say it's better to wait for more trial data that compares early data to observation, Rajkumar said there's not much more data on the way. He is an investigator in the AQUILA trial (NCT03301220), which is studying the use of subcutaneous daratumumab in patients high-risk smoldering multiple myeloma. "We will know the results soon. But after that, there are no more randomized trials with observation along ongoing," he said.
For those who believe it's possible to observe patients and catch progression before it happens, Rajkumar said, "At Mayo, we have found out this is easier said than done." He reviewed results that showed the even at a top institution, "we miss the end organ damage 50% of the time….We want to prevent organ damage."
Approaches to Risk Stratification. Irene Ghobrial, MD, who is senior vice president for Experimental Medicine, director of the Center for Early Detection and Interception of Blood Cancers, and co-leader of the Lymphoma/Myeloma Cancer Center Program at Dana-Farber Cancer Institute, discussed risk stratification in high-risk patients; in SMM, she said, progression of SMM is about 10% a year.
Irene Ghobrial, MDImage credit: Dana-Farber Cancer Institute
The question, she said, is how to differentiate between those who will progress—and need early treatment—from those who are "more MGUS-like." She offered highlights from different models that have been developed to evaluate patient characteristics, and then discussed the elements to be evaluated, which include:
Genomic aberrations can help define precursor conditions, and Ghobrial detailed studies that have used whole genome sequencing, circulating tumor cells, and other strategies to create models that can predict progression. One of the discoveries, she explained, is that the genome for multiple myeloma is present long before a patient presents with full-blown disease.
"By the time we have overt myeloma, it's been there for 30 years," she said. For smoldering myeloma, "by the time it's progressing, it's already very mature and has a lot of genomic aberrations. For MGUS [it's] about 15 years."
Ghobrial then discussed the immune microenvironment. "You cannot look only at the cancer cells without looking at the immune cells. "A few years ago, we asked the question whether, by single cell sequencing, [if] the immune system is altered. And we indeed found that even as early as MGUS, you find that those patients have compositional changes."
On this topic, she noted that Friday's plenary session will feature a presentation by her Dana-Farber colleague, Romanos Sklavenitis-Pistofidis, MD, PhD, titled, "Single-Cell RNA Sequencing of 6 Million Tumor and Immune Cells in Patients With Plasma Cell Premalignancy Unveils Coregulation of Disease Progression by Tumor Biology and Immune Dysregulation."
Key findings will show that as we age, so does our immune system; in patients with MGUS and smoldering myeloma, Ghobrial said, "there is an accelerated immune aging that occurs despite the regular chronological age. And this is critical, because now you can identify specific signatures and specific cells that are changing even as early as MGUS in those patients, independent of age."
T-cell receptors shrink as disease progresses, and B cells age as well, she said.
How Common Is SMM? Sigurdur Kristinsson, MD, PhD, of the University of Iceland, offered an update and lessons learned from one of the most ambitious projects ever in research: what if you made screening for MGUS available to a population?
After its debut in 2021, the Iceland Screens, Treats, or Prevents Multiple Myeloma (iStopMM) study, has some important lessons about MGUS and SMM. First, both are more prevalent than they believed, at least among the people of Iceland—MGUS was found among .5% of the population over age 40. And second, SMM is also more common than was known before iStopMM.
"In particular, high risk smoldering myeloma that a lot of the individuals have it, so we really need to figure out who to treat and who definitely not to treat," Kristinsson said. On the positive side, those whose MGUS or SMM was caught early were managed differently than those who did not screen positive, but who later developed multiple myeloma and presented with acute symptoms in the emergency department. On average, he said, myeloma was detected a year earlier, with fewer acute features.
Finally, Kristinsson said, a population wide screening approach had to take into account the mental health effects of learning one had MGUS. Patients filled out a questionnaire after agreeing to take part in the study. How patients might deal with living with a finding of MGUS is a consideration for health systems.
Different Immune Responses by Population. Madhav Dhodapkar, MBBS, director, Center for Cancer Immunology at Winship Cancer Institute, Emory University, examined some key issues in the myeloma field: what drives the disease, and why does myeloma affect the Black population differently?
Madhav Dhodapkar, MBBSImage credit: Winship Cancer Institute
Dhodapkar said he would share stories "that relate to understanding mechanisms by which immune function is altered In early days of myelomogenesis," and offer an explanation of how "spatial aspects of [the] immune system actually evolve in the context of antigen specific immunity."
Understanding an immune-based theory of myeloma is not only critical for disease prevention, but preclinical models now show that immune-based therapies are "the mainstay of treating myeloma," he said.
First, Dhodapkar outlined the work his team is doing. The literature is full of interpretations based assumptions that T cells were exhausted; however, his work has shown that, in fact, in response to T-cell receptor engagement, T cells have "a fair bit of capacity for proliferation."2
"Interestingly, what these T cells are also able to do is actually produce cytokines. And in fact, patients with myeloma, T cells with myeloma make more cytokines, particularly those when you look at inflammatory cytokines and compared to the MGUS counterparts," he said.
He described 2 broad phenotypes of T cells that were delineated in studies; he said 1 type has been "implicated in the context of tissue inflammation," while the other expresses "known markers of T cell exhaustion in the context of inhibitory checkpoints."
What this means, he explained, is that in myeloma causes alterations that affect multiple inflammatory pathways, including for CD4 and CD8 T cells, "the 2 cell types that we are most interested in…as the immune system evolves over time."
This raised other questions, including whether there was increased DNA damage in myeloma and earlier on in MGUS, and whether this damage affected all populations equally.
"So that led us to hypothesize that perhaps what we were seeing was altered dysfunction in the context of what has been called immunologic aging," Dhodapkar said. The term has been used to refer to at age-related changes in immune cells, he said but many studies have had very few patients with African American ancestry, "as well as people in the first decade of life, where the great majority of ages will see that changes actually occur."
Of note, in the United States, 20% of all multiple myeloma diagnoses occur among Black patients, although they account for 14% of the overall population.3
Dhodapkar continued: "So we first went back and analyzed a cohort, a cohort of individuals, healthy individuals, between the first to seventh decade of life, including about 30% to 40% of Black patients in that cohort to create what we call an immuno-age calculator, then reapply that data into the data from similar assays into MGUS and myeloma patients."
"That led to the finding that patients with myeloma are approximately a couple of decades older immunologically compared to their MGUS counterparts," he said. "Interestingly, the biggest difference in the context of determinants of immunologic aging appears to be race-related, so the group that's at the highest risk for immunologic aging appears to be [those] with Black ancestry, wherein we see a greater aging, again, as early as MGUS, compared to their White counterparts. And it does correlate with immunologic function."
Dhodapkar even said this could explain why Black patients with myeloma as group have less robust responses to vaccines, including the COVID-19 vaccine. In taking another look at older data sets for the SARS-COV-2 vaccine, immunologic aging, not chronologic aging, was the better predictor of response the vaccine.
"What I think this data is beginning to point out is that there is, in fact, a significant amount of what we call maladaptive immune aging in myeloma that appears to be greater in myeloma compared to MGUS, that appears to be greater in Black patients," he said. "And [it] correlates with outcomes in these individuals."
References
1. Rakjumar SV, Kumar S, Lonial S, Mateos MV. Smoldering multiple myeloma current treatment algorithms. Blood Cancer J. 2022;12(9):129. Doi:10.1038/s41408-022-00719-0.
2. Dhodapkar MV, Immune-pathogenesis of myeloma. Hematol Oncol Clin North Am. 2024;38(2):281-291. Doi: 10.1016/j.Hoc.2023.12.011.
3. Disparities in African Americans. International Myeloma Foundation. Accessed September 25, 2024. Https://www.Myeloma.Org/IMF-Diversity-Equity-Inclusion-Policy/disparities-african-americans
Belantamab Mafodotin Quadruplet Shows Promise In Myeloma
A new combination therapy involving belantamab mafodotin, carfilzomib, lenalidomide, and dexamethasone showed promising results in patients with multiple myeloma who had received 1 prior line of therapy.
Shebli Atrash, MD, MS, FACP
Belantamab mafodotin-blmf (Blenrep) in combination with carfilzomib (Kyprolis), lenalidomide (Revlimid), and dexamethasone (KRd) was linked with a manageable safety profile, including manageable keratopathy, and early evidence of deep responses in patients with multiple myeloma who had received 1 prior line of therapy, according to findings from a phase 1 trial (NCT04822337) presented at the 21st International Myeloma Society Annual Meeting.1
Investigators determined the maximum tolerated dose (MTD) and recommended phase 2 dose (RP2D) of belantamab mafodotin in this regimen to be 1.9 mg/kg every 8 weeks.
The most common gastrointestinal (GI) adverse effects (AEs) seen with the combination across all treated patients (n = 19) included diarrhea (grade 1, 31.6%; grade 2, 15.8%), constipation (21.1%; 5.3%), vomiting (10.5%; 15.8%), nausea (10.5%; 21.1%), dysgeusia (5.3%; 5.3%), oral mucositis (5.3%; 5.3%), and anorexia (0%; 15.8%). No grade 3 or higher GI AEs were reported. Grade 3 and 4 hematological and infectious AEs included decreased platelet counts (grade 3, 5.3%; grade 4, 21.2%), decreased neutrophil counts (21.1%; not available [NA]), and all infections (15.8%; NA). Grade 1, 2, and 3 keratopathy was observed in 21.1%, 42.1%, and 31.6% of patients, respectively.
"Eye toxicity was reversible in all cases," Shebli Atrash, MD, MS, FACP, said in the presentation. "It seems that the duration [of eye toxicities] was less than the previously seen eye toxicity in [the phase 2] DREAMM-2 [trial (NCT03525678)] …It's important to note that [the rate of infections] sets this regimen apart from other BCMA-targeted approaches, including CAR T[-cell therapy] and bispecific [antibodies], given lower infection risks [with those agents]."
Atrash is a hematologist at the Atrium Health Levine Cancer Institute in Charlotte, North Caroline, as well as a clinical associate professor of hematology and oncology at the Wake Forest University School of Medicine in Winston-Salem.
Rationale for Investigating Belantamab Mafodotin-Based Quadruplets in MyelomaPrior research has shown the feasibility of quadruplet regimens containing KRd plus transplant in patients with transplant-eligible, newly diagnosed multiple myeloma. For instance, in the phase 2 FORTE trial (NCT02203643), KRd in combination with autologous stem cell transplant (ASCT; n = 315) elicited at least a very good partial response (VGPR) after induction in 70% of patients vs 53% of patients who received carfilzomib plus cyclophosphamide and dexamethsone plus ASCT (odds ratio [OR], 2.14; 95% CI, 1.44-3.19; P = .0002).2
Furthermore, in the phase 3 IsKia trial (NCT04483739), rates of minimal residual disease (MRD) negativity at a sensitivity of 10–6 improved over time throughout all trial phases in patients who received Isa-KRd (n = 151) vs those who received KRd alone (n = 151).3 The post-induction, post-ASCT, and post-consolidation MRD-negativity rates in the Isa-KRd arm were 27%, 52%, and 67%, respectively. These respective rates were 14% (OR, 2.36; P = .004), 27% (OR, 3.01; P < .001), and 48% (OR, 2.29; P < .001) in the KRd alone arm.
"All those results make us ask the question: Can we improve on the triplet regimen further?" Atrash asked.
Studies have also shown the efficacy of belantamab mafodotin in patients with relapsed/refractory multiple myeloma. In DREAMM-2, efficacy-evaluable patients who received the agent at 2.5 mg/kg (n = 97) achieved a median duration of response (DOR) of 11 months and an overall response rate (ORR) of 31% (97.5% CI, 20.8%-42.6%).4 Moreover, in the phase 3 DREAMM-7 trial (NCT04246047), belantamab mafodotin plus bortezomib (Velcade) and dexamethasone improved progression-free survival (PFS; HR, 0.41; 95% CI, 0.31-0.53; P < .001) and OS vs daratumumab (Darzalex) plus bortezomib and dexamethasone in patients with multiple myeloma who had progressed on at least 1 prior line of therapy.5
"Those results support the use of a quadruplet regimen with KRd with the addition of belantamab mafodotin," Atrash noted.1
Although DREAMM-2 showed that belantamab mafodotin is effective when administered every 3 weeks, the trial also demonstrated that the agent is associated with keratopathy, with similar rates of this AE observed regardless of the dose level.4 Among safety-evaluable patients who received the agent at 2.5 mg/kg (n = 95), grade 3 keratopathy or changes to the corneal epithelium was observed was observed in 27% of patients. Among safety-evaluable patients who received the agent at 3.4 mg/kg (n = 99), grade 3 keratopathy or changes to the corneal epithelium was observed was reported in 21% of patients.
"The rates of blurred vision and dry eye improved with lower doses of belantamab mafodotin, suggesting better tolerability with lower doses," Atrash said.1
Design of the Phase 1 TrialMultiple myeloma cells: © David A Litman - stock.Adobe.ComMultiple myeloma cells: © David A Litman - stock.Adobe.Com
This phase 1 study of belantamab mafodotin plus KRd enrolled patients with relapsed/refractory multiple myeloma who had received at least 1 prior line of therapy and had measurable disease. Patients needed to have an ECOG performance status of 0 to 2; an ANC of at least 1.5 x 103/mm3 if their marrow burden was less than 50% or an absolute neutrophil count (ANC) of at least 1.0 x 103/mm3 if their marrow burden was higher than 50%; a platelet count of at least 100,000 cells/mm3; total bilirubin levels at or below 1.5 times the upper limit of normal (ULN); aspartate aminotransferase and alanine aminotransferase levels at or below 2.5 times the ULN; creatinine clearance levels of at least 30 mL/min; and a left ventricular ejection fraction higher than 40%.
This phase 1 study included a 3+3 dose-escalation portion followed by a dose-expansion cohort to identify the RP2D. The primary objective was to establish the MTD of belantamab mafodotin. Key secondary objectives included ORR, depth of response, DOR, PFS, OS, and safety.
Patients received belantamab mafodotin plus KRd for a maximum of 18 cycles, followed by lenalidomide maintenance. Patients remained on treatment until disease progression or toxicity. Intravenous (IV) belantamab mafodotin was tested at 2 doses: 1.4 mg/kg or 1.9 mg/kg each over 30 to 60 minutes every 8 weeks. A backbone regimen of KRd was administered in 28-day cycles and consisted of IV carfilzomib at 20 or 56 mg/m2 on days 1, 8, and 15; oral lenalidomide at 25 mg on days 1 through 21; and oral dexamethasone at 20 or 40 mg weekly.
During the dose-escalation portion, 3 patients received belantamab mafodotin at 1.4 mg/kg. One DLT of grade 4 thrombocytopenia was observed at this dose level.
"It's important to note that the patient remained on the study and achieved MRD negativity later on," Atrash added.
Three more patients were enrolled at the dose level of 1.4 mg/kg. No additional DLTs were observed at this dose level, and the dose was escalated in 3 additional patients to 1.9 mg/kg. No DLTs were observed at this dose level, and 3 more patients were enrolled at the 1.9-mg/kg dose level to identify the MTD. Investigators did not observe any DLTs at the 1.9-mg/kg dose level, and this was identified as the MTD.
Notably, patients had received a median of 1 prior line of therapy (range, 1-3), and 42.1% of patients were Black. International Staging System information was available for 15 patients, 40%, 26.7%, and 33.3% of whom had stage I, II, and III disease, respectively. High-risk cytogenetics were observed in 47.3% of patients, and included 1q gain and 1p deletion (5.3%), 17 deletion (10.5%), and 1q gain (36%). Among all patients, 42.1% were refractory to lenalidomide, 10.5% were refractory to bortezomib, 26.3% were double refractory to a proteasome inhibitor and an immunomodulatory agent, and 26.3% were refractory to daratumumab.
Additional Safety DataBeyond keratopathy, the most common ophthalmological AEs seen at any point during treatment included blurred vision (5.2%; 42.1%; 42.1%), dry eye (36.8%; 5.3%; NA), cataract (0%; 10.5%; NA), photophobia (10.5%; 0%; NA), and conjunctivitis (0%; 5.3%; NA). No grade 4 ophthalmological AEs were observed.
Regarding the number of patients dosed in each treatment cycle, during cycle 1 (n = 19), 100% of patients were given treatment. During cycles 3 (n = 18), 5 (n = 15), 7 (n = 13), 9 (n = 11), 11 (n = 11), 13 (n = 9), 15 (n = 8), and 17 (n = 7), 61%, 47%, 58%, 36%, 64%, 44%, 25%, and 57% of patients enrolled in each cycle received treatment. Reasons for non-treatment in each cycle included dose toxicity, defined as grade 2 or higher keratopathy prior to dosing, as well as patient choice, Atrash explained.
"Keratopathy was manageable mainly with dose delays and to a lesser degree, with dose reductions," Atrash noted.
Efficacy DataBest responses included stringent complete response (CR; 37%), CR (16%), VGPR (5%), and PR (42%).
"Regarding MRD negativity, 10 out of 19 patients so far have MRD negativity at 10–5, whereas 40% of the patients had MRD negativity at 10–6," Atrash emphasized.
At a median follow-up of 16.8 months, 3 patients had progressed. The 24-month PFS, DOR, and OS rates were 80%, 81%, and 95%, respectively.
Based on these phase 1 findings, the phase 2 portion of the trial is planned, in which patients with high-risk, newly diagnosed multiple myeloma will undergo autologous stem cell transplant following induction with 8 cycles of belantamab mafodotin plus KRd.
Disclosures: Dr Atrash reports receiving research funding from Amgen, GSK, and Karyopharm; receiving honoraria from Janssen; and receiving consulting fees from Pfizer.
REFERENCES: 1. Atrash S. Results of a phase 1 clinical trial of belantamab mafodotin combined with carfilzomib, lenalidomide, and dexamethasone for multiple myeloma after one prior line of therapy. Presented at: 2024 International Myeloma Society Annual Meeting; September 25-28, 2024; Rio De Janeiro, Brazil. Abstract OA-57. 2. Gay F, Musto P, Rota-Scalabrini D, et al. Carfilzomib with cyclophosphamide and dexamethasone or lenalidomide and dexamethasone plus autologous transplantation or carfilzomib plus lenalidomide and dexamethasone, followed by maintenance with carfilzomib plus lenalidomide or lenalidomide alone for patients with newly diagnosed multiple myeloma (FORTE): a randomised, open-label, phase 2 trial. Lancet Oncol. 2021;22(12):1705-1720. Doi:10.1016/S1470-2045(21)00535-0 3. Gay F, Roeloffzen W, Dimopoulos MA, et al. Results of the phase III randomized Iskia trial: isatuximab-carfilzomib-lenalidomide-dexamethasone vs carfilzomib-lenalidomide-dexamethasone as pre-transplant induction and post-transplant consolidation in newly diagnosed multiple myeloma patients. Blood. 2023;142(suppl 1):4. Doi:10.1182/blood-2023-177546 4. Lonial S, Lee HC, Badros A, et al. Belantamab mafodotin for relapsed or refractory multiple myeloma (DREAMM-2): a two-arm, randomised, open-label, phase 2 study. Lancet Oncol. 2020;21(2):207-221. Doi:10.1016/S1470-2045(19)30788-0 5. Hungria V, Robak P, Hus M, et al. Belantamab mafodotin, bortezomib, and dexamethasone for multiple myeloma. N Engl J Med. 2024;391(5):393-407. Doi:10.1056/NEJMoa2405090
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