Vicky-2 BCMA (mouse)
- Known as:
- Vicky-2 BCMA (mouse)
- Catalog number:
- mc-113
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Vicky-2 BCMA (mouse)
Related genes to: Vicky-2 BCMA (mouse)
- Gene:
- TNFRSF17 NIH gene
- Name:
- TNF receptor superfamily member 17
- Previous symbol:
- BCMA
- Synonyms:
- BCM, CD269, TNFRSF13A
- Chromosome:
- 16p13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-20
- Date modifiied:
- 2016-10-05
Related products to: Vicky-2 BCMA (mouse)
Related articles to: Vicky-2 BCMA (mouse)
- This meta-analysis systematically evaluated the efficacy and safety of B-cell maturation antigen (BCMA)-directed chimeric antigen receptor (CAR) T-cell therapy in patients with relapsed or refractory multiple myeloma (RRMM) with extramedullary disease (EMD). - Source: PubMed
Publication date: 2026/04/22
Li Yan-LingLi Meng-JiaoLi Jia-JiaChen DanLi Cai-YangQiu LingHe YingFan Jian-ChunRen Shi-HuiYao HaoFan Fang-Yi - Chimeric antigen receptor (CAR) T-cell therapy has transformed the management of hematologic malignancies, achieving high remission rates in relapsed or refractory B-cell acute lymphoblastic leukemia, large B-cell lymphoma, and multiple myeloma. By redirecting autologous or allogeneic T lymphocytes against tumor-associated antigens such as and , CAR T-cells overcome resistance to conventional therapies. Progressive optimization of CAR design-from early constructs to armored and logic-gated platforms-has enhanced persistence, specificity, and safety. Pivotal trials and real-world evidence confirm durable responses, although challenges remain, including cytokine release syndrome, neurotoxicity, manufacturing complexity, high cost, and limited global access. Emerging strategies, such as multi-antigen targeting, gene editing technologies, and CAR delivery, aim to improve efficacy and scalability. Integration of artificial intelligence and point-of-care manufacturing may further streamline production and patient selection. Continued innovation will determine the long-term impact of CAR T-cell therapy as a scalable pillar of precision hematologic oncology. - Source: PubMed
Publication date: 2026/03/04
Hernández-Idarraga Karol JArias-Rozo Andrea JArango-Rodríguez Martha LSossa Claudia LBecerra-Bayona Silvia M - There is limited systemic data on the dynamics of BCMA-target antigen expression with BCMA CAR-T at relapse. We analyzed 76 patients receiving standard-of-care BCMA-directed CAR-T who underwent real-time BCMA expression evaluation at baseline (n = 50), relapse (6), or both (20) using flow cytometry (FC) and/or immunohistochemistry (IHC). BCMA was universally expressed at baseline with significant heterogeneity in expression level. No concordance was seen between FC and IHC in categorizing high vs. low expression (Spearman: 0.07, Cohen kappa: 0). Plasma cell BCMA expression by FC correlated with clinical outcomes, whereas IHC did not. High BCMA expression by FC was associated with increased likelihood for VGPR/CR (p = 0.007) and longer time to progression (p = 0.005), including the ciltacabtagene autoleucel cohort (median: 23.0 vs. 7.7 months, p = 0.02). Relapsed patients retained BCMA expression by FC, though 29% (5/16) had BCMA loss by IHC, with 4/5 showing concurrent positive BCMA expression by FC. BCMA expression at relapse by FC was significantly lower than baseline (p = 0.04); downregulation (≥25% decrease) occurred in 50% (8/16) with paired samples. Higher BCMA expression by FC correlated with higher likelihood of deep, durable responses following BCMA-directed CAR-T. While BCMA loss is rare, decreased expression is common at relapse, with implications for sequencing BCMA-directed therapies. - Source: PubMed
Publication date: 2026/04/04
Rana Masooma ShifaFernandez-Pol SebastianJensen AlexandriaHovanky VannaVelayati ArashOak Jean SSilva OscarAmes ErikMuffly Lori SSahaf BitaArai SallyKennedy Vanessa EBharadwaj SushmaIberri David JLiedtke MichaelaNatkunam YasodhaShiraz ParveenWeng Wen-KaiSmith MelodyFrank Matthew JMackall Crystal LDahiya SaurabhMikkilineni LekhaMiklos David BHosoya HitomiSidana Surbhi - Programmed death-ligand 1 (PD-L1) positivity is associated with a favorable response to immune checkpoint blockade (ICB) in urothelial bladder cancer (BLCA). However, the efficacy of ICB in BLCA exhibits considerable heterogeneity, leading to the need for complementary predictive biomarkers. Recent studies suggest that a high degree of plasma cell infiltration is correlated with improved benefit from ICB, but a specific plasma cell marker in BLCA has not been identified. The aim of this study was to evaluate tumor necrosis factor receptor superfamily member 17 (TNFRSF17) as a plasma cell-specific marker in BLCA and test its utility, combined with PD-L1, for patient stratification receiving ICB therapy. - Source: PubMed
Publication date: 2026/04/03
Chen JiawenLi BingshengGan YuLi Pan - Patients with relapsed/refractory multiple myeloma (RRMM) who are penta-drug refractory, defined as resistant to two proteasome inhibitors, two immunomodulatory agents, and an anti-CD38 monoclonal antibody, face a dismal prognosis, particularly after exposure to T-cell-redirecting therapies. Selinexor, an oral exportin-1 inhibitor, offers a distinct mechanism of action and may retain efficacy in this difficult setting. We conducted a retrospective analysis at six German tertiary centers (2023-2025) to evaluate the efficacy and safety of selinexor plus bortezomib and dexamethasone (SVd) in penta-refractory MM after both BCMA- and GPRC5D-targeted therapies. Eighteen patients were identified, with a median of seven prior lines of therapy. High-risk cytogenetic abnormalities were present in seven cases, including del17p in six. The overall response rate (ORR) was 61%, including one complete, five very good partial, and five partial responses, and median progression-free survival (PFS) was 4.3 months. Among nine patients (50%) with extramedullary disease (EMD), three achieved complete and one near-complete EMD resolution. Two patients who had relapsed after CAR T-cell treatment with idecabtagene vicleucel achieved partial and very good partial responses and were successfully transitioned to a second CAR T-cell therapy with ciltacabtagene autoleucel. Hematologic toxicities under SVd were manageable, and no treatment-related deaths occurred. SVd demonstrates meaningful activity in patients with penta-refractory MM and prior failure of BCMA/GPRC5D-targeted immunotherapies. The ORR of 61%, disease control in 78% of patients, and median PFS of 4.3 months support further evaluation of SVd in this highly refractory setting after failure of BCMA- and GPRC5D-directed approaches. - Source: PubMed
Publication date: 2026/03/31
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