CDX2 Monoclonal Antibody
- Known as:
- CDX2 Monoclonal Antibody
- Catalog number:
- 27189
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- CDX2 Monoclonal Antibody
Related genes to: CDX2 Monoclonal Antibody
- Gene:
- CDX2 NIH gene
- Name:
- caudal type homeobox 2
- Previous symbol:
- CDX3
- Synonyms:
- -
- Chromosome:
- 13q12.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-09-07
- Date modifiied:
- 2015-08-24
Related products to: CDX2 Monoclonal Antibody
Related articles to: CDX2 Monoclonal Antibody
- Cd[N(SiMe)] and MeCd react with (2-pyridylthio)methane ([Bptm]H) to afford [Bptm]CdN(SiMe) and [Bptm]CdMe, in which the LX [Bptm] ligand coordinates in a k-mode with a direct Cd-C bond that is distinct from {k-[Bptm]H}CdX complexes, in which the ligand is bidentate and serves as an L donor. The Cd-N(SiMe) bond of [Bptm]CdN(SiMe) is reactive, and [Bptm]CdN(SiMe) undergoes metathesis with RSiOH (R = Me, Ph) to form dimeric cadmium siloxides, {[Bptm]Cd(μ-OSiMe)} and {[Bptm]Cd(μ-OSiPh)}. In addition to the formation of {[Bptm]Cd(μ-OSiMe)} via this approach, {[Bptm]Cd(μ-OSiMe)} is also obtained by the reaction of [Bptm]CdN(SiMe) with CO, presumably via a sequence in which CO inserts into the Cd-N(SiMe) bond followed by elimination of MeSiNCO. The dimeric nature of {[Bptm]Cd(μ-OSiMe)} and {[Bptm]Cd(μ-OSiPh)} contrasts with the monomeric nature of the zinc counterpart, [Bptm]ZnOSiPh, an observation that is in accord with DFT calculations on {[Bptm]M(μ-OSiPh)} and [Bptm]MOSiPh (M = Zn, Cd). In addition to [Bptm]CdX compounds, [Bptm]Cd, a rare example of a six-coordinate dialkyl cadmium compound, which also features two [Bptm] ligands, has been obtained. - Source: PubMed
Publication date: 2026/05/12
Shlian Daniel GDaniels Josef DHummingbird EsheParkin Gerard - Early prediction of Alzheimer's disease (AD) progression from mild cognitive impairment (MCI) remains a major challenge, particularly when relying on non-invasive biomarkers. Identifying individuals with progressive MCI (pMCI) before conversion to AD could improve intervention strategies and clinical management. In this study, we developed a machine learning (ML) framework integrating blood-based multi-omics and demographic data to distinguish pMCI from stable MCI (sMCI). - Source: PubMed
Publication date: 2026/03/28
Vashishath YashuPijani Bizhan AlipourGoud Baddam NehaSaeed FahadBozdag Serdar - Glioblastoma (GBM), the most aggressive primary brain tumor, develops within a tumor microenvironment (TME) dominated by tumor-associated macrophages (TAMs) that critically influence disease progression. Through single-cell RNA sequencing (scRNA-seq) and bioinformatic analysis, we delineated macrophage heterogeneity within the GBM TME and identified a distinct VCAN⁺ macrophage subpopulation. Pseudotime trajectory analysis revealed these cells at the terminal stage of macrophage differentiation, where they exhibit enhanced granulocyte migration and chemotaxis pathways and exhibit a pro-tumorigenic phenotype that diverges from classical M1/M2 polarization. These VCAN⁺ macrophages displayed a distinct polarization state driven by tumor necrosis factor-α (TNF-α), contributing to both a pro-inflammatory and an immunosuppressive TME. CellChat analysis demonstrated their pivotal role in intercellular communication-predominantly mediating crosstalk with GBM tumor cells, endothelial cells, and CD8⁺ T cells via SPP1 signaling: SPP1 binding to CD44 on tumor cells enhances their invasiveness, while its interaction with CD47 on CD8⁺ T cells inhibits anti-tumor immunity. Transcriptional regulatory network analysis identified that CDX2 and MXI1 serve as key transcription factors modulating VCAN⁺ macrophage function and maintaining their specific polarization and homeostasis. Through machine learning, we identified seven hub genes-C1QA, C1QC, C3, CCL4, CD44, SERPINE1, and TREM2 (all highly expressed in VCAN⁺ macrophages and involved in their polarization or intercellular communication)-and constructed an effective GBM prognostic model (AUC = 0.83 in validation cohort), underscoring their roles in immune regulation, extracellular matrix remodeling, and VCAN⁺ macrophage-mediated tumor progression. Further studies with larger cohorts and functional validation will clarify this subpopulation's therapeutic potential and spatial distribution patterns. - Source: PubMed
Publication date: 2026/05/09
Guo JiaxinZhu ZhanshengTong NanyangXu DingdingZhang HuanLin ChenshiWan GuipingWang YameiZhou QingqingXia Liang - Pulmonary hepatoid adenocarcinoma (HAL) is an extremely rare and highly aggressive extrahepatic adenocarcinoma that exhibits hepatocellular carcinoma-like morphology and hepatocytic immunophenotype, often leading to diagnostic delay due to nonspecific respiratory presentations. We report a male patient in his 50s with a long history of heavy tobacco use who presented with a persistent cough initially treated as pneumonia without clinical improvement. Over subsequent weeks, he developed progressive dyspnea, weight loss, fatigue and diffuse bone pain. Computed tomography demonstrated left upper-lobe consolidation with pleural effusion and underlying collapse, mediastinal lymphadenopathy, and multiple lytic skeletal lesions consistent with metastatic disease, while triphasic abdominal imaging showed no focal hepatic lesions. Laboratory testing revealed mild anaemia with leukocytosis and thrombocytosis, markedly elevated carcinoembryonic antigen and normal alpha-fetoprotein. Tru-cut biopsy showed poorly differentiated adenocarcinoma with prominent signet ring cell differentiation. Immunohistochemistry demonstrated diffuse CK7 and HepPar-1 positivity with focal CDX2 positivity and negativity for TTF-1, CK20, p63, and D2-40, supporting a diagnosis of primary pulmonary hepatoid adenocarcinoma. The patient received 3 cycles of gemcitabine plus carboplatin but experienced rapid clinical deterioration. This case underscores that HAL may mimic nonresolving pneumonia and that normal AFP does not exclude the diagnosis; early biopsy and a targeted immunohistochemical panel are essential for timely recognition of this lethal entity. - Source: PubMed
Publication date: 2026/05/06
Khader RamiElhakim EsraaBdair MohammadSultan Rajaa AbuKhader AmeedAlmasalma MousaFerwana SalehBaraka Mohammed Z A - Early gastric carcinogenesis progresses from gastritis through intestinal metaplasia to early gastric cancer, yet the spatial origin of malignant transformation and subtype divergence remains unclear. Here we show, using spatial transcriptomics across human gastric tissues spanning disease progression, that an OLFM4-positive transitional subset emerges at the interface between gastric isthmus/glands and proliferative intestinal metaplasia crypts, consistent with an early step in intestinalization. From these crypts, transcriptional trajectories diverge toward distinct intestinal differentiation programs. Notably, proliferative crypt regions display the closest transcriptional similarity to early gastric cancer and are enriched for proliferation and DNA-repair pathways, supporting their role as a premalignant niche. We further identify increased activity of USF2-associated regulatory networks shared between crypt and cancer regions. Further stratification by Lauren subtype reveals that intestinal-type gastric cancer is characterized by a CDX2-dominated program, whereas diffuse-type gastric cancer exhibits developmental and stemness-related networks with SPP1 and CD44 co-occurring. Together, these findings highlight the intestinal metaplasia crypt as a premalignant niche and provide spatially resolved candidate markers for early detection and mechanistic investigation. - Source: PubMed
Publication date: 2026/05/08
Wen JingGong YuehuaSun LipingLin ZiqiXu QianJing JingjingHu LinglingDuan HanminYin HonghaoZhang HuanyuShen ShixuanDong NannanLi YilingTu HuakangYuan Yuan