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van Duin, M.

Publications and source records attributed to van Duin, M..

3 recordsLinked to original sources

Expression profile of CASSIOPEIA patients refines prognostic value of MRD negativity in multiple myeloma

Long-term follow-up of the CASSIOPEIA trial (NCT02541383) demonstrated superior progression-free survival (PFS) with daratumumab, both in combination with bortezomib, thalidomide, and dexamethasone during induction and consolidation, and during maintenance therapy, in transplant- eligible patients newly diagnosed with multiple myeloma (MM). However, outcomes among CASSIOPEIA patients remain heterogeneous across treatment groups. Measurable residual disease (MRD) is a strong indicator of the depth and duration of therapeutic response and is independently associated with both PFS and overall survival (OS), but it does not fully capture the biological diversity of MM. We performed a risk prediction analysis based on transcriptomic subgroups in CASSIOPEIA patients. A subset of 628 patients was characterized using RNA sequencing and consensus clustering identified five transcriptomic subtypes of MM. Long-term follow-up allowed the definition of three transcriptomic risk categories, with estimated 72-month PFS rates of 70%, 51%, and 27% for low, intermediate, and high-risk groups, respectively, among patients who received daratumumab in at least one treatment phase. In these patients, MRD negativity rates after consolidation and six months later were significantly higher in the low and high-risk groups compared with the intermediate-risk group. In the high-risk group, MRD status was not associated with PFS or OS. This suggests that, although daratumumab administered during both the induction/consolidation and maintenance phases improves the clinical outcomes of patients with activation of NSD2 or overexpressing members of the MAF family, highly aggressive minor clones may rapidly expand. These findings emphasize the need for novel therapeutic strategies in this high-risk population.

cancer biology↗

Multi-omics data integration reveals molecular mechanisms of carfilzomib resistance in multiple myeloma

Multiple myeloma represents a complex hematological malignancy, characterized by its wide array of genetic and clinical events. The introduction of proteasome inhibitors, such as carfilzomib or bortezomib, into the therapeutic landscape has notably enhanced the quality of life and survival rates for patients suffering from this disease. Nonetheless, a significant obstacle in the long-term efficacy of this treatment is the inevitable development of resistance to PIs, posing a substantial challenge in managing the disease effectively. Our study investigates the molecular mechanisms behind carfilzomib resistance by analyzing multi-omics profiles from four multiple myeloma cell lines: AMO-1, KMS-12-PE, RPMI-8226 and OPM-2, together with their carfilzomib-resistant variants. We uncovered a significant downregulation of metabolic pathways linked to strong mitochondrial dysfunction in resistant cells. Further examination of patient samples identified key genes - ABCB1, RICTOR, PACSIN1, KMT2D, WEE1 and GATM - potentially crucial for resistance, guiding us towards promising carfilzomib combination therapies to circumvent resistance mechanisms. The response profiles of tested compounds have led to the identification of a network of gene interactions in resistant cells. We identified two already approved drugs, benidipine and tacrolimus, as potential partners for combination therapy with carfilzomib to counteract resistance. This discovery enhances the clinical significance of our findings.

cancer biology↗

An IL-1β driven neutrophil-stromal cell axis fosters a BAFF-rich microenvironment in multiple myeloma

The bone marrow permanently harbors high numbers of neutrophils, and a tumor-supportive bias of these cells could significantly impact bone marrow-confined malignancies. In multiple myeloma, the bone marrow is characterized by inflammatory stromal cells with the potential to influence neutrophils. We investigated myeloma-associated alterations in marrow neutrophils and the impact of stromal inflammation on neutrophil function. Mature neutrophils in myeloma marrow are activated and tumor-supportive, transcribing increased levels of IL-1{beta}, and myeloma cell survival factor BAFF. Interactions with inflammatory stromal cells can induce neutrophil activation, including BAFF secretion, in a STAT3-dependent manner and once activated, neutrophils gain the ability to reciprocally induce stromal activation. After first-line myeloid-depleting treatment, patient bone marrow retains residual stromal inflammation and newly-formed neutrophils are reactivated. Combined, we identify a neutrophil-stromal cell feed-forward loop driving tumor-supportive inflammation that persists after treatment and warrants novel strategies to target both stromal and immune microenvironments in multiple myeloma.

immunology↗