Anti-Human CD38 FITC 100 tests
- Known as:
- Antibody toHuman CD38 fluorecein 100 tests
- Catalog number:
- 11-0389-42
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Human CD38 FITC 100 tests
Related genes to: Anti-Human CD38 FITC 100 tests
- 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: Anti-Human CD38 FITC 100 tests
Related articles to: Anti-Human CD38 FITC 100 tests
- Cribriform tumor of the skin (formerly primary cutaneous cribriform carcinoma/primary cutaneous cribriform apocrine carcinoma) is a rare adnexal neoplasm of uncertain malignant potential. Recent studies have identified recurrent co-deletion of the long arm of chromosomes 6 and 9 and CD38 overexpression as potential diagnostic features, but their sensitivity and specificity remain incompletely defined. We identified 11 cribriform tumors with classic morphologic features, including several previously reported molecular characterized cases and additional unpublished cases, from multiple institutions. CD38 immunohistochemistry was performed on all tumors and compared with a panel of morphologic mimics, including adenoid cystic carcinoma (n = 8), digital papillary adenocarcinoma (n = 8), eccrine/apocrine adenomas (n = 7), hidradenoma (n = 2), and endocrine mucin-producing sweat gland carcinoma (n = 3). SNP array analysis was available in nine cases. Patients had a median age of 47 years with a slight female predominance (64%). Tumors commonly involved the extremities and ranged from 0.3 to 2.0 cm. Histologically, all cases demonstrated a well-circumscribed dermal neoplasm of bland epithelial cells arranged in cribriform architecture with characteristic thread-like intraluminal bridging, without high-grade features. CD38 expression was identified in 9/11 cases (82%), typically with moderate-to-strong diffuse cytoplasmic staining. All morphologic mimics (n = 28) were CD38 negative. Recurrent chromosomal deletions involving 6q and/or 9q were identified in 7/8 (88%) successfully tested cases. Two morphologically classic cribriform tumors lacked CD38 expression, including one with confirmed 6q/9q codeletion, while one CD38-positive case lacked detectable genomic copy number alterations. These findings further support cribriform tumors as a molecularly distinct, low-grade adnexal neoplasm characterized by recurrent 6q/9q deletions and frequent CD38 expression. CD38 appears to be a useful adjunctive diagnostic marker with high specificity among the selected mimics tested, although its sensitivity is incomplete, and absence of staining does not exclude the diagnosis. - Source: PubMed
Publication date: 2026/09/07
Kalomeris TaylorCloutier Jeffrey MRonen ShiraLezcano CeciliaPulitzer Melissa PMoy Andrea PChen Joyce MZhang YanmingDehner Carina AHonaker Eric CBridges AlinaMagro Cynthia MBusam Klaus JLinos Konstantinos - This single-institution retrospective study evaluated a measurable residual disease (MRD)-guided induction intensification strategy in transplant-eligible patients with newly diagnosed multiple myeloma treated in the anti-CD38 antibody era. Sixty patients undergoing autologous stem cell transplantation (ASCT) between 2020 and 2025 were included. Most received bortezomib, lenalidomide, and dexamethasone as initial therapy. Patients with persistent MRD by multiparameter flow cytometry underwent treatment intensification, commonly with daratumumab, carfilzomib, and dexamethasone before ASCT. Among 52 evaluable patients, 35 (67.3%) achieved MRD negativity before ASCT, and 30 of 32 (93.8%) were MRD-negative after ASCT. Stem cell mobilization and engraftment were successful. After median follow-up of 28.5 months, 2-year progression-free and overall survival were 87.3% and 98.0%. R-ISS stage III and extramedullary disease were associated with inferior progression-free survival. High-risk cytogenetics showed poorer outcomes. This MRD-adapted strategy was feasible, achieved deep responses, and preserved mobilization, but high-risk disease remained prone to relapse, supporting post-transplant intensification. - Source: PubMed
Publication date: 2026/09/06
Yokoyama DaizoMinakata DaisukeFujiwara Shin-IchiroHonda SeinaTominaga RyutaroNoguchi AtsutoFuruki ShukaKoyama ShunsukeMurahashi RuiNakashima HirotomoHyodo KazukiKawaguchi Shin-IchiroToda YumikoUmino KentoUeda MasuzuAshizawa MasahiroYamamoto ChihiroHatano KaoruSato KazuyaOhmine KenKanda Yoshinobu - CD38 is a highly conserved multifunctional enzyme that regulates intracellular calcium signaling and NAD⁺ metabolism. Although extensively studied in cancer and autoimmune diseases, growing evidence points to a critical role for CD38 in both normal and diseased liver physiology. In hepatic tissue, CD38 is expressed on multiple cell types. Aberrant CD38 activity contributes to increased oxidative stress, inflammation, and diminished tissue repair. Recent studies suggest that CD38 may also promote cellular senescence partly through its regulation of intracellular NAD⁺ and calcium. This review examines the role of CD38 in maintaining hepatic homeostasis and explores its involvement in liver injury, chronic liver diseases, and carcinogenesis. We also highlight the contribution of CD38-mediated signaling to hepatic fibrogenesis and end-stage liver failure as well as its potential role in liver transplantation, particularly post-transplant related conditions including ischemic injury and acute cellular rejection. Given its impact on multiple intracellular processes, CD38 has emerged as a promising therapeutic target. New findings describe how CD38 inhibition preserves NAD⁺ levels, supports tissue recovery, and mitigates disease progression in the liver. Finally, we outline new frontiers for CD38 in liver biology and the advancement of CD38-targeted therapeutic strategies. - Source: PubMed
Publication date: 2026/09/05
Eng Jason WPeterson Blake RBlack Sylvester - Daratumumab, an Anti-CD38 monoclonal antibody, is now widely used in frontline induction for transplant-eligible multiple myeloma. Although highly effective, concerns remain regarding its potential impact on CD34⁺ stem cell mobilization and early outcomes after autologous hematopoietic stem cell transplantation, particularly when combined with lenalidomide. This study aims to evaluate whether prior daratumumab exposure affects CD34⁺ mobilization, stem cell collection, engraftment, or early post-autologous hematopoietic stem cell transplantation complications. - Source: PubMed
Publication date: 2026/09/05
Dos Anjos Arthur SousaMendonça Claudio VertiMaradei Simone Cunhade Azevedo Juliana Pessoa RivelloKaufman JacquesMoreira Maria ClaudiaMorgado MoniqueGarnica MarciaMaiolino Angelo - Central nervous system (CNS) involvement in multiple myeloma (MM) is a rare but devastating complication associated with poor prognosis and limited therapeutic options. We report a 73-year-old woman with high-risk IgG kappa MM harboring TP53 [del(17p)] and 13q deletion who developed extramedullary and CNS disease after six prior lines of therapy, including two autologous stem cell transplants, and was triple-class refractory to proteasome inhibitors, immunomodulatory agents, and anti-CD38 monoclonal antibodies. At CNS relapse, cerebrospinal fluid (CSF) cytology demonstrated abundant atypical and binucleated plasma cells, and MRI showed diffuse leptomeningeal enhancement. Elranatamab was initiated using a standard step-up dosing schedule, combined with intrathecal methotrexate and dexamethasone. Within two months, MRI showed complete resolution of leptomeningeal disease and CSF became acellular. Systemic evaluation confirmed a complete response by IMWG criteria, with normalization of serum immunofixation, protein electrophoresis, and free light chains. No cytokine release syndrome or neurotoxicity was observed. The remission has been sustained and remains ongoing at 18 months. This case suggests that BCMA-targeted bispecific antibodies, combined with CNS-directed therapy, may induce deep and durable CNS remission in heavily pretreated MM, and supports further investigation of bispecific antibodies in CNS-involved myeloma. - Source: PubMed
Publication date: 2026/08/07
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