CD38 antibody (Azide Free)
- Known as:
- CD38 (anti-) (Azide Free)
- Catalog number:
- 10r-cd38cmsp
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- CD38 antibody (Azide Free)
Related genes to: CD38 antibody (Azide Free)
- Gene:
- CD38 NIH gene
- Name:
- CD38 molecule
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 4p15.32
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2014-11-18
Related products to: CD38 antibody (Azide Free)
Related articles to: CD38 antibody (Azide Free)
- Extramedullary disease (EMD) in multiple myeloma (MM) is associated with poor outcomes due to aggressive disease kinetics and therapy resistance. The bone marrow (BM) tumour microenvironment (TME) promotes cell survival and drug resistance in marrow restricted MM, but little is known about the TME in EMD. To characterize the tissue architecture of these tumors, we performed spatial transcriptomics on tumour biopsies. Like BM-restricted MM, we identified significant inter-patient heterogeneity in plasma cell (PC) expression profiles, although still maintaining a characteristic plasma cell transcriptome. The TME was dominated by macrophages with a suppressive "M2" phenotype. CD8+ T-cells frequently expressed exhaustion markers LAG3 and TIGIT, consistent with a suppressive TME. We identified three recurrent TME niches based on immune-cell composition: immune excluded, immune suppressed and immune permissive. The immune excluded niche comprised the bulk of tumors, reflecting spatial exclusion of immune cells. The suppressive extracellular matrix from abundant tumour-associated fibroblasts in the immune suppressive niche may further contribute to T-cell exclusion. Cell-cell interaction modelling revealed a complex, bidirectional network: PC modulated the TME through PGE2 and VEGFB, while receiving canonical pro-survival signals through CD38, CXCR4 and BCMA. Notably, TME cells, particularly fibroblasts and macrophages, are predicted to collectively promote the suppressive macrophage phenotype and fibrotic extracellular matrix, reinforcing an immunosuppressive milieu that supports local disease progression. These findings reveal the spatial organization of EMD, highlighting niche substitution rather than niche independence, and identify clinically tractable microenvironmental niches and signaling networks in this high-risk myeloma subset. - Source: PubMed
Publication date: 2026/06/30
Bingham Nicholas EardleyBoiko Julie RJones Daniel CWong DanielKhong TiffanyMithraprabhu SridurgaEnsbey Kathleen SElz Anna ENewell Evan WSpencer AndrewHill Geoffrey R - Este estudio tiene como objetivo presentar un caso clínico de Mieloma Múltiple (MM) con una presentación oral inusual, subrayando la importancia de la vigilancia bucal en el diagnóstico integral de enfermedades hematológicas. Caso Clínico: Se presenta el caso de una paciente femenina de 70 años que acudió a la Cátedra de Estomatología "A" de la Facultad de Odontología de la Universidad Nacional de Córdoba con lesiones gingivales bimaxilares de 6 meses de evolución. La paciente, sin antecedentes patológicos conocidos, presentó pérdida de peso significativa y síntomas sistémicos graves. Al examen clínico, se observaron masas hiperplásicas gingivales dolorosas, con movilidad dental generalizada. La ortopantomografía y la tomografía revelaron reabsorción alveolar y áreas osteolíticas. Los análisis de laboratorio mostraron anemia, leucopenia, trombocitopenia, y marcadores inflamatorios elevados. La biopsia reveló una proliferación de células plasmáticas monoclonales positivas para CD38 y cadenas kappa, lo que llevó al diagnóstico de MM. La paciente fue remitida a oncohematología, pero falleció rápidamente. Conclusión: Este caso destaca la importancia del reconocimiento temprano de manifestaciones orales de MM, que pueden ser un desafío diagnóstico debido a su similitud con otras afecciones orales comunes. La identificación oportuna de estas lesiones por parte de los odontólogos puede ser crucial para reducir la morbilidad y mortalidad asociadas a esta enfermedad hematológica. - Source: PubMed
Publication date: 2026/06/22
Gilligan Gerardo MarceloRomero Panico Juan CruzPanico Rene - [This corrects the article DOI: 10.1093/ckj/sfaf283.]. - Source: PubMed
Publication date: 2026/06/26
- Vitamin D (VitD) is an important immunometabolic regulator of T cell function. Its active form, 1,25-dihydroxyvitamin D, signals through the VitD receptor (VDR), which is highly expressed in activated CD4 T cells. Although VDR signaling suppresses glycolysis by reducing glucose uptake and glycolytic enzyme expression, early T cell expansion is preserved, suggesting the involvement of alternative metabolic pathways. Since glutaminolysis is essential for T cell activation and proliferation, we investigated whether VitD modulates glutamine metabolism during early CD4 T cell activation. - Source: PubMed
Publication date: 2026/06/11
Vera Agustín AHernandez MauricioCartes Ricardo ALlerena FarydCisterna Solange EQuiroga Romina ASanhueza Sergio AMuñoz-Grez Camila PVergara FranciscoMoena DanielAlarcón Pablo ABurgos RafaelRivas Coralia IUribe ElenaArgüello Rafael JAlmarza CristopherUrra Felix ATapia-Belmonte FranciscoFerrada LucianoLamperti Liliana INova-Lamperti Estefanía - Immune thrombocytopenia (ITP) is the most common acquired bleeding disorder where considerable dysfunction of regulatory T cells (Tregs) contributes to loss of immune tolerance. CD38 is a transmembrane glycoprotein equipped with ectoenzymatic activities. It affects other nicotinamide adenine dinucleotide (NAD) consuming enzymes such as deacetylase Sirtuin-1 (Sirt-1), which is pivotal for Treg stability. Anti-CD38 monoclonal antibody exerts ectoenzyme modulating capacity and has been proved to rapidly boost and maintain platelet levels in patients with ITP. - Source: PubMed
Publication date: 2026/06/26
Zhu MingfangWang HaoyiXu YitongLi YubinWang WanruWang LingjunWang RuixueZhang PingWang RutingCao JunyingWang LinShi YanHou MingHou Yu