{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["14"],"submitter":["Springer C"],"pubmed_abstract":["In myeloma patients, high levels of soluble BCMA (sBCMA) can limit the efficacy of BCMA-directed therapies. Belantamab-mafodotin is a BCMA antibody-drug conjugate and shows good overall response rates in heavily pretreated patients but progression-free survival data are poor. As the drug induces apoptosis, we hypothesized that sBCMA includes extracellular vesicles (EV) and thus evaluated numbers of BCMA-EV before and during belantamab therapy in 10 myeloma patients. BCMA-EV were significantly higher in patients prior to Belantamab (median: 3227/μl; <i>p</i> = .013) than in other myeloma patients before therapy (<i>n</i> = 10; 1082/μl) or healthy volunteers (<i>n</i> = 10; 980/μl). During therapy, BCMA-EV showed a significant increase to a maximum of 8292/μl (<i>p</i> = .028). Maximal changes in BCMA-EV (Δmax = BCMA-EV at C1/maximal BCMA-EV) showed a strong inverse, logarithmic correlation (r = -.950; <i>p</i> < .001) with FLC ratio changes (Δmax = FLC ratio at C1/minimal FLC ratio) and BCMA-EV peaks often preceded FLC progression. Correlating increase of LDH and BCMA-EV levels, together with clinical symptoms, point to a mafodotin-induced eryptosis. In summary, BCMA-EV are a part of sBCMA, peak levels precede progression, and their measurement might be helpful in identifying resistance mechanisms and side effects of BCMA targeted therapies."],"journal":["Oncotarget"],"pagination":["949-956"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10691812"],"repository":["biostudies-literature"],"pubmed_title":["Plasma levels of BCMA-positive extracellular vesicles correlate to response and side effects in myeloma patients treated with belantamab-mafodotin."],"pmcid":["PMC10691812"],"pubmed_authors":["Trummer A","Krauter J","Springer C"],"additional_accession":[]},"is_claimable":false,"name":"Plasma levels of BCMA-positive extracellular vesicles correlate to response and side effects in myeloma patients treated with belantamab-mafodotin.","description":"In myeloma patients, high levels of soluble BCMA (sBCMA) can limit the efficacy of BCMA-directed therapies. Belantamab-mafodotin is a BCMA antibody-drug conjugate and shows good overall response rates in heavily pretreated patients but progression-free survival data are poor. As the drug induces apoptosis, we hypothesized that sBCMA includes extracellular vesicles (EV) and thus evaluated numbers of BCMA-EV before and during belantamab therapy in 10 myeloma patients. BCMA-EV were significantly higher in patients prior to Belantamab (median: 3227/μl; <i>p</i> = .013) than in other myeloma patients before therapy (<i>n</i> = 10; 1082/μl) or healthy volunteers (<i>n</i> = 10; 980/μl). During therapy, BCMA-EV showed a significant increase to a maximum of 8292/μl (<i>p</i> = .028). Maximal changes in BCMA-EV (Δmax = BCMA-EV at C1/maximal BCMA-EV) showed a strong inverse, logarithmic correlation (r = -.950; <i>p</i> < .001) with FLC ratio changes (Δmax = FLC ratio at C1/minimal FLC ratio) and BCMA-EV peaks often preceded FLC progression. Correlating increase of LDH and BCMA-EV levels, together with clinical symptoms, point to a mafodotin-induced eryptosis. In summary, BCMA-EV are a part of sBCMA, peak levels precede progression, and their measurement might be helpful in identifying resistance mechanisms and side effects of BCMA targeted therapies.","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Dec","modification":"2025-04-25T17:24:10.706Z","creation":"2025-04-06T04:05:30.451Z"},"accession":"S-EPMC10691812","cross_references":{"pubmed":["38039414"],"doi":["10.18632/oncotarget.28538"]}}