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SCIENTIFIC PROGRAMME
SESSION I
HOW I TREAT
SMOLDERING MYELOMA
(SMM)
SESSION II
HOW I TREAT NEWLY
DIAGNOSED MULTIPLE
MYELOMA
SESSION III
FROM RISK
STRATIFICATION TO
RISK-BASED THERAPY?
DEBATE 1
SHOULD WE USE MRD
TESTING TO DETERMINE
THERAPY IN MULTIPLE
MYELOMA?
DEBATE 2
IS THERE A FUTURE ROLE
OF AUTOLOGOUS STEM
CELL TRANSPLANTATION?
SESSION IV
HOW I TREAT RELAPSED
MULTIPLE MYELOMA
DEBATE 3
SHOULD EVERY PATIENT
RECEIVE DARATUMUMAB
IN FIRST LINE?
ROUNDTABLE
MULTIPLE MYELOMA
FROM THE PERSPECTIVE
OF FDA/EMEA AND
FOUNDATIONS
SESSION V
YOU CAN’T BE IMMUNE
FOR IMMUNE THERAPY
ANYMORE
SESSION VI
OTHER PLASMA CELL
DYSCRASIAS
KEYNOTE LECTURES
THE FUTURE OF
MULTIPLE MYELOMA
SELECTED ABSTRACTS
FOR AN ORAL
PRESENTATION
ABSTRACTS SELECTED
AS POSTERS
DISCLOSURES
C. OLA LANDGREN (MIAMI)
IS THERE A FUTURE ROLE OF AUTOLOGOUS STEM CELL TRANSPLANTATION?
NO!
M.D., Ph.D., Professor of Medicine; Chief, Myeloma Program, Division of Hematology
Leader, Experimental Therapeutics Program; Sylvester Comprehensive Cancer Center, University of Miami,
Miami, Florida
High-dose melphalan chemotherapy followed by autologous stem cell transplant (HDM-ASCT) was
developed almost 50 years ago. The concept was launched in an era when there were no other effective
treatment options available. At that time, the addition of HDM-ASCT – after delivery of existing
combination chemotherapy – offered a deepening of the treatment response, which typically (but not
always) translated into longer progression-free survival. In some, but not all, randomized clinical trials, an
overall survival benefit was noted. These facts have continued to support a role for HDM-ASCT in newly
diagnosed multiple myeloma patients for several decades. However, the past 5-10 years, driven by
increased access to better drugs and more sensitive assays to determine response to therapy (i.e., MRD
assays), the role of HDM-ASCT in newly diagnosed multiple myeloma patients has been increasingly
questioned. In 2020, at 8 years of follow-up, a large randomized study (IFM 2009 “Determination study”)
found no survival benefit of upfront (versus delayed) HDM-ASCT in newly diagnosed multiple myeloma
patients treated with VRd combination therapy. An increasing number of studies show high rates of deep
treatment responses. For example, modern 4-drug combination therapies show over 70% MRD negativity
rates in the absence of HDM-ASCT. On a drug safety note, genomic studies have recently shown that
exposure to high-dose melphalan chemotherapy translates into >20% increased mutational burden. Also,
long-term clinical studies show that multiple myeloma patients exposed to high-dose melphalan
chemotherapy (versus the general population) have a 50- to 100-fold higher relative risk of developing
MDS/AML. Given the rapidly evolving therapeutic field with a large number of promising bi-specific
monoclonal antibodies as well as cell-based treatment options in development, it seems logical to
conjecture that HDM-ASCT belongs to an older era which no longer will be part of the treatment of newly
diagnosed multiple myeloma patients. Instead, its future role will be in selected patients with
relapsed/refractory multiple myeloma. The speed of this change will be regulated by the access to newer
therapies. In countries where access to modern drugs is limited and change will be slow(er), HDM-ASCT
will likely remain as a main option for newly diagnosed multiple myeloma patients for several years. For
these reasons, there is no role for autologous stem cell transplantation in newly diagnosed multiple
myeloma patients in the future.