IGKC Antibody (OASA09221)
- Known as:
- IGKC Antibody (OASA09221)
- Catalog number:
- oasa09221
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- IGKC Antibody (OASA09221)
Related genes to: IGKC Antibody (OASA09221)
- Gene:
- IGKC NIH gene
- Name:
- immunoglobulin kappa constant
- Previous symbol:
- -
- Synonyms:
- HCAK1
- Chromosome:
- 2p11.2
- Locus Type:
- immunoglobulin gene
- Date approved:
- 2001-06-22
- Date modifiied:
- 2014-11-19
Related products to: IGKC Antibody (OASA09221)
Related articles to: IGKC Antibody (OASA09221)
- Lung squamous cell carcinoma (LUSC) is a heterogeneous cancer characterized by complex cellular interactions. Plasma cells, a critical immune population, exhibit functional diversity in LUSC. The aim of this study was to characterize plasma cell heterogeneity and their interactions with tumor cells using an integrative single-cell framework. - Source: PubMed
Publication date: 2026/05/30
Ma WenKuang JunjieHu XiaoyeHuang ShaohuiZhou JieLiao ZhiweiYuan Yan - The emergence of immune checkpoint inhibitors (ICIs) has transformed the treatment landscape of metastatic melanoma. However, despite its success, reliable biomarkers for predicting primary resistance are not available in clinical practice. This study seeks to identify predictors of primary resistance based on novel gene expression signatures. The transcriptomic profile of the tumor microenvironment was analyzed using tissue samples from 46 metastatic cutaneous melanoma patients collected prior to the initiation of ICIs therapy. A primary resistance predictive model was trained with the Discovery FFPE RNA-seq subcohort and validated using an independent external cohort of 54 samples. Additionally, liquid biopsy samples from peripheral blood mononuclear cells were analyzed in 8 patients using single-cell RNA sequencing (scRNA-seq) and in 46 patients using flow cytometry. We identified an 82-gene transcriptomic signature composed of tumor- and immune-related genes that stratifies metastatic cutaneous melanoma patients based on primary resistance to ICIs, with key markers including and . This signature achieved an AUC of 0.814. Immune deconvolution guided by scRNA-seq revealed four immune cell subsets (Plasma cells, Pre-B cells, memory CD4⁺ T cells, and naive CD4⁺ T cells) as prognostic indicators of resistance. We propose a transcriptomic biomarker signature that accurately predicts primary resistance to ICIs in metastatic cutaneous melanoma. Through the integration of immune deconvolution with circulating immune cell profiles, we derived an ImmuneSignature linked to patient survival. By combining these approaches, we provide a framework for enhancing the prediction of immunotherapy outcomes and offer a novel strategy for identifying therapeutic targets to overcome resistance. - Source: PubMed
Publication date: 2026/03/30
Onieva Juan LuisPérez-Ruiz ElisabethVilkki VilleBerciano-Guerrero MiguelFigueroa-Ortiz LauraZalabardo ManuelMartínez-Gálvez BeatrizBarragán IsabelRueda-Domínguez Antonio - Our previous preclinical studies demonstrated that non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin and naproxen significantly inhibited prostate tumorigenesis in a TMPRSS2-ERG fusion-driven model compared to non-fusion models. Since TMPRSS2-ERG fusion-positive tumors display heightened inflammatory signaling and substantial immune infiltration, we hypothesized that the differential efficacy of NSAIDs may arise from their ability to remodel the tumor immune microenvironment. Accordingly, in the present study, we systematically profiled innate and adaptive immune-cell populations: F4/80⁺ macrophages, mast cells, neutrophils, CD3⁺ T cells, CD8⁺ cytotoxic T cells, FoxP3⁺ regulatory T cells, CD20⁺ B cells, IgKC⁺ plasma cells, and Granzyme B⁺ effector cells in highly infiltrated dorso-lateral prostate regions of TMPRSS2-ERG fusion-driven and non-fusion PCa models, with and without NSAID intervention. Our analyses revealed pronounced macrophage infiltration in TMPRSS2-ERG. Pten and Hi-Myc model, which was further augmented by NSAIDs. Importantly, NSAID intervention shifted macrophage polarization toward an M1-like, pro-inflammatory state, contrasting with the M2-dominant phenotype characteristic of untreated tumors. NSAID treatment reduced mast cell density within the stromal compartment, suggesting suppression of mast cell-mediated tumor-promoting signals. In the fusion model, infiltration of total T cells and CD8⁺ cytotoxic T cells decreased following NSAID exposure, whereas FoxP3⁺ Tregs remained largely unaffected. Both models showed increased B-cell infiltration independent of NSAID efficacy, and no clear correlation was observed between plasma-cell presence and treatment response. Collectively, our findings offer new insight into NSAID-mediated immunomodulation in TMPRSS2-ERG fusion-driven PCa; however, further in-depth immune subtyping and spatial mapping could fully delineate the immunological mechanisms driving NSAID responsiveness. - Source: PubMed
Publication date: 2026/02/23
Tomar Munendra SinghRaina KomalMishra NehaKant RamaFox Jennifer TAgarwal ChaplaAgarwal Rajesh - Pancreatic ductal adenocarcinoma (PAAD) metastasis is driven by complex tumor-microenvironment interactions. Here, we integrated single-cell and bulk transcriptomic analyses of 104,855 cells from 10 patients to delineate the cellular and molecular landscape of primary versus metastatic PAAD. We identified metastasis-associated epithelial (LMO7⁺, TOP2A⁺, PIGR⁺), fibroblast (IGKC⁺, RGS5⁺), and M2-like macrophage (APOE⁺, CD14⁺, FOLR2⁺, SPP1⁺) subpopulations, validated via bulk deconvolution. Functional analyses revealed upregulated Wnt signaling, epithelial-mesenchymal transition, and angiogenesis in metastatic epithelial and fibroblast compartments. Intercellular communication analysis highlighted SPP1-mediated macrophage-epithelial/fibroblast crosstalk involving key receptor-ligand pairs, contributing to immune suppression and metastatic niche formation. Integrating gene expression and cell proportions, we developed a prognostic model with high predictive accuracy (C-index > 0.85), stratifying patients into risk groups with distinct immune landscapes. Furthermore, PTK6 was identified as a driver of PAAD proliferation, migration, and invasion. Collectively, our study elucidates TME-driven mechanisms of PAAD metastasis, identifies prognostic and therapeutic targets, and provides a framework for precision intervention. - Source: PubMed
Publication date: 2025/11/29
Shen ShijunLi ZhiqiangYang HongZhang XinweiChen GangPa Chengzhou - Pancreatic ductal adenocarcinoma (PDAC) genetic susceptibility is partially identified. The complement system (CS) influences carcinogenesis and participates in immunological defense and homeostasis; however, its role in PDAC genetic susceptibility and prognosis is underexplored. The association of SNPs within 111 CS-related genes with PDAC risk is assessed in the PanGenEU study and validated in the UKBiobank. We investigate the association between the CS-related gene variation and PDAC risk, followed by an in-depth functional in silico study using TCGA and ICGC data. We assess whether CS-related genes are associated with prognosis at the germline and somatic levels. We investigate the immune infiltration of PDAC tumors according to their transcriptomic profile. Genetic variation in FCN1 and PLAT is significantly associated with PDAC risk. PDAC patients with elevated expression of IGHG3, IGKC, IGHM, F2R, F2RL2, CFI, A2M, or C4A display improved survival and higher infiltration of CD8, B cells, and Th1 cells. Individuals with high expression levels of either FGA, SERPINE1, FGG, or F3 exhibit poorer survival, higher infiltration of Tregs, and lower infiltration of CD8 cells. Results from this study suggest that CS-related genes play a role in PDAC genetic susceptibility and survival through specific immune cell infiltration. - Source: PubMed
Publication date: 2025/11/28
Langtry AlbertoRabadan RaulAlonso LolaFilip IoanSabroso-Lasa SergioMoreno-Oya AneLawlor RitaCarrato AlfredoAlvarez-Gallego RafaelIglesias MarMolero XavierLöhr Matthias JMichalski Christoph WPerea JoséO'Rorke MichaelBarberà Victor MTardón AdoninaFarré AntoniMuñoz-Bellvís LuísCrnogorac-Jurcevic TatjanaDomínguez-Muñoz EnriqueGress Thomas MGreenhalf WilliamSharp LindaBalsells JoaquimCostello EithneKleeff JörgKong BoMora JosefinaO'Driscoll DamianScarpa AldoYe WeiminReal Francisco XLópez de Maturana EvangelinaMalats Núria