Ask about this productRelated genes to: CD44 antibody
- Gene:
- CD44 NIH gene
- Name:
- CD44 molecule (Indian blood group)
- Previous symbol:
- MIC4, MDU2, MDU3
- Synonyms:
- IN, MC56, Pgp1, CD44R, HCELL, CSPG8
- Chromosome:
- 11p13
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2019-04-23
Related products to: CD44 antibody
Related articles to: CD44 antibody
- The clinical application of cancer stem cell marker CD44 in breast cancer prognosis has been widely explored. However, data on the association between CD44 expression and prognostication across molecular subtypes of breast cancer remain limited. In this study we evaluated CD44 expression in various breast carcinoma subtypes and its association with clinicopathological prognostic parameters. Further, molecular docking studies were performed to investigate molecular interactions involving CD44. A cross-sectional study was conducted on breast tissue specimens collected from 60 patients over a period of two years. Immunohistochemistry analyses were performed to assess CD44 expression in paraffin-embedded breast tissue samples. Clinicopathological prognostic parameters were analysed in relation to CD44 expression. Of the 60 cases, CD44 staining was positive in 34 cases (57%) and negative in 26 (43%). Increased CD44 expression was correlated with histological grade (p=0.022), lymphovascular invasion (p=0.039), and lymph node status (p=0.033) in invasive breast carcinoma. Notably, high CD44 expression was also observed in patients with triple-negative breast cancer. Further, protein docking analysis revealed significant interactions between CD44 and molecular markers such as ER, PR, HER2/neu, and Ki-67, with HER2/neu showing the strongest correlation. Several new targeted treatments for breast cancer were also identified through docking studies. These findings highlight that induced CD44 expression could be a potential marker of aggressive tumour behaviour in invasive breast carcinoma and across multiple molecular subtypes, including triple-negative breast cancer. - Source: PubMed
Publication date: 2026/05/25
Krishnappa AmitaKanakapura Paramesh HrushikeshSuresh RamyaPrashantha KalappaVivek Hamse KameshwarNarasaraju Telugu Akula - This work aimed to establish a translationally viable, xeno-free, serum-free platform and protocol for the isolation and expansion of human salivary stem/progenitor cells (hS/PCs) suitable for regulatory qualification and future FDA-approved first-in-human autologous regenerative therapy trials for the treatment of hyposalivation disorders. Parotid gland specimens from non-cancerous regions/tissues were collected from consented surgical patients. Primary hS/PCs were isolated from tissue specimens, cultured in animal-component-free conditions, expanded to produce millions of cells, then enriched for CD44+ stem/progenitor cells by magnetic cell sorting. Normal epithelial purity was assessed using cytokeratins 5/14. Anti-CD133/PROM1 (cancer marker) and anti- fibroblast (clone TE-7) antibodies were used to demonstrate a lack of contaminating cells. Phenotype validation was performed by flow cytometry and immunocytochemistry on both CD44+ sorted and unsorted populations. Senescence-associated beta-galactosidase (SA-β-gal) assays were performed across serial passages (P1-P6). Pluripotency was demonstrated by culture under conditions supporting lineage-specific differentiation. Primary hS/PCs demonstrated consistent expansion and epithelial morphology under serum-free conditions. CD44 expression remained high (>95%) throughout expansion, with negligible detection of CD133 or fibroblast markers, confirming epithelial purity and absence of tumorigenic or stromal contamination. Immunocytochemistry corroborated these expression profiles. SA-β-gal staining revealed only a minor, passage-dependent increase (5-16%) in senescent cells from multiple donors, indicating retention of proliferative potential. Our defined, animal-free culture system supports stable expansion of pure low passage hS/PCs under conditions compatible with good manufacturing practice (GMP). - Source: PubMed
Publication date: 2026/05/13
Geremias Thaise Cda Costa Fabio H BMohyuddin Nadia GLombaert Isabelle MFarach-Carson Mary CWu Danielle - The efficient targeted delivery and on-demand release of nanomedicines still present significant challenges in tumor therapy. In the present study, we developed a novel strategy of tumor ferroptosis therapy through the synergistic effect of nanomedicines (biomimetic liposomes) and a medical device (high-intensity focused ultrasound, HIFU). It was found that HIFU irradiation induced heightened expressions of CD44 and reactive oxygen species (ROS) in tumor cells by 1.43-fold and 2.64-fold, respectively. This allowed the gambogic acid-loaded, platelet-mimicking liposomes (PLip) to more precisely target the tumor cells through the interaction of CD44 and P-selectin on the PLip and subsequently ROS-responsively release the drug from PLip, thus effectively killing tumor cells. Crucially, gambogic acid also significantly enhanced ROS production, leading to lipid peroxidation and augmented ferroptosis induced by HIFU. In summary, HIFU demonstrates immense potential in synergizing with nanomedicines to combat tumors. - Source: PubMed
Publication date: 2026/03/03
Xu RuizheLi XuejingSu XiaominQin XifengHe YingWang SiyuLiu YueWu JiayiWang TingLiu MingyangOuyang BoshuLi JiaYang WuliZhang BoPang Zhiqing - The glycocalyx is a carbohydrate-rich layer formed by glycoproteins, glycolipids, proteoglycans, and glycosaminoglycans at the outer cell surface. In cancer, this layer is not a passive coating. Its thickness, composition, charge, and nanoscale organization are altered by oncogenic signaling, dysregulated glycosyltransferases, protease-mediated shedding, and reciprocal interactions with stromal and immune cells. These changes affect how tumor cells sense force, bind the extracellular matrix, cluster receptors, evade immune surveillance, survive in circulation, and arrest at distant vascular beds. Studies in the past decade have linked a bulky glycocalyx to integrin activation and growth factor signaling, identified hyaluronan-CD44 and selectin-dependent steps in metastatic dissemination, and placed the sialoglycan-Siglec axis among the immune suppressive circuits operating in the tumor microenvironment. Meanwhile, pathology, imaging, glycoproteomics, and liquid-biopsy studies have started to define glycocalyx-derived biomarkers with diagnostic and prognostic value, especially in hepatocellular carcinoma, pancreatic cancer, breast cancer, and hematologic malignancies. This review summarizes the structure of the cancer glycocalyx, the molecular programs that remodel it, and the consequences of these changes for tumor progression. It also discusses analytical approaches, biomarker development, and therapeutic strategies aimed at mucins, proteoglycans, glycosyltransferases, hyaluronan signaling, heparanase, and tumor-associated sialoglycans. A central theme is that the glycocalyx should be viewed as an integrated biophysical and signaling interface, and its clinical value will depend on spatially resolved, context-specific analysis rather than single-marker measurements alone. - Source: PubMed
Publication date: 2026/05/25
Tomita Hiroyuki - Cancer stem cells (CSCs) drive colorectal cancer (CRC) therapeutic resistance through metabolic reprogramming, particularly aerobic glycolysis. Strategies simultaneously targeting CSC metabolism and stemness remain limited. - Source: PubMed
Publication date: 2026/05/17
Xue YulingZheng YifengZhong YonghongLi JinYang TingtingHong ShicuiWang ShengqiXie JianhuiXiong WenjunYang XiaoboWang ZhiyuWang Wei