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Despite the astonishing outcomes after chimeric antigen receptor (CAR) T-cell therapy for relapsed refractory multiple myeloma (RRMM), most patients eventually relapse. There are only limited data available on salvage therapies following relapse after BCMA-directed CAR T-cell therapy. Here, we analyzed outcomes of post-CAR T-cell therapy relapse and impact of different salvage strategies in an international cohort of 139 patients (n = 130 ide-cel, n = 9 cilta-cel), receiving talquetamab (n = 28), teclistamab (n = 37), combinations of immunomodulating drugs (IMiDs), proteasome inhibitors (PIs) or CD38 monoclonal antibodies (n = 43), and others (n = 31). The median time to relapse after CAR T-cell therapy was 5 months, 53% had the extramedullary disease (EMD) at relapse, associated with dismal post-relapse outcome (P = 0.005). Overall response and complete response upon salvage therapies were 79% and 39% for talquetamab, 64% and 32% for teclistamab, 30% and 0% for IMiDs/PIs/CD38, and 26% and 3% for others (P < 0.001). Duration of response, as well as median survival, was significantly improved with bispecific antibodies (P < 0.001, respectively). Bispecific antibodies seemed to overcome the poor prognosis associated with early relapse and EMD, and were independent predictors for improved survival in multivariable analysis. In summary, these results suggest bispecific antibodies as the standard of care for relapse after CAR T-cell therapy for RRMM.
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http://dx.doi.org/10.1038/s41408-024-01197-2 | DOI Listing |
Zhong Nan Da Xue Xue Bao Yi Xue Ban
May 2025
Department of Pathology, First Clinical College, Changzhi Medical College, Changzhi 046000.
Objectives: Acute lung injury (ALI) is an acute respiratory failure syndrome characterized by impaired gas exchange. Due to the lack of effective targeted drugs, it is associated with high mortality and poor prognosis. (TW) has demonstrated anti-inflammatory activity in the treatment of various diseases.
View Article and Find Full Text PDFNan Fang Yi Ke Da Xue Xue Bao
August 2025
Clinical Laboratory, First Affiliated Hospital of Bengbu Medical University, Bengbu 233004, China.
Objectives: To investigate the therapeutic mechanism of 2,6-dimethoxy-1,4-benzoquinone (DMQ) for alleviating dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice.
Methods: Eighteen male C57BL/6J mice were equally randomized into control group, DSS group and DMQ treatment group. In DSS and DMQ groups, the mice were treated with DSS in drinking water to induce UC, and received intraperitoneal injections of sterile PBS or DMQ (20 mg/kg) during modeling.
Parasite Immunol
September 2025
Department of Zoology, Panjab University, Chandigarh, India.
Leishmania parasite adeptly evades the host's immune defences by infiltrating macrophages, exploiting apoptotic processes for further dissemination. Among the host's strategies to counter parasitic propagation, the pivotal role of B-cells, specifically B regulatory (Breg) cells, emerges. Recent evidence from in vitro and in vivo studies has thrust Breg cells into the spotlight, attributed to their IL-10 secretion and antigen presentation.
View Article and Find Full Text PDFCurr HIV Res
September 2025
Department of Hematology-Oncology, Chongqing University Cancer Hospital, Chongqing 400030, China.
HIV-associated lymphoma (HAL) is an aggressive malignancy directly linked to HIV infection and accounts for more than 30% of cancer-related deaths in people living with HIV (PLWH). HAL subtypes, including diffuse large B-cell lymphoma (DLBCL), Burkitt lymphoma (BL), primary effusion lymphoma (PEL), and plasmablastic lymphoma (PBL), exhibit five to ten times higher incidence rates and distinct molecular profiles compared to HIV-negative lympho-mas. Pathogenesis involves HIV-driven CD4+ T-cell depletion, chronic B-cell activation, and on-cogenic viral coinfection.
View Article and Find Full Text PDFFuture Oncol
September 2025
Division of Leukemia, Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL) is characterized by the fusion gene which produces a constitutively active tyrosine kinase which drives disease pathogenesis and is associated with resistance to conventional chemotherapy. Intensive cytotoxic chemotherapy followed by allogeneic hematopoietic stem cell transplantation (HSCT), the historical treatment paradigm for Ph+ ALL, was associated with poor outcomes. The introduction of inhibitors of ABL1 revolutionized the treatment of Ph+ ALL.
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