CD44 (CD44 Molecule)

CD44 expression can aid in staging carcinoma. These results add to growing literature suggesting that HPV interaction changes biology of EGFR by preventing degradation.

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Inactivation of Cdh1 alone in Cd44-expressing cells is sufficient to induce DGC in mice. Tumour growth is significantly accelerated by concurrent Trp53 inactivation.

Assays using a rhodamine-labelled polymer reveal a positive relationship between cellular internalization and CD44 expression levels in breast cancer cells. Conjugation of paclitaxel to the polymer enhances paclitaxel potency in CD44-expressing cancer cells compared to free paclitaxel.

This study highlights subtype-specific epithelial signatures, identifies key signaling pathways (e.g., MIF), and pinpoints candidate therapeutic targets (CD44, CD74). These discoveries shed new light on the distinct pathogenic mechanisms of LUSC and LUAD and provide actionable insights to facilitate the clinical translation of subtype-specific personalized immunotherapies.

These findings are highly relevant for clinicians and researchers aiming to enhance ICI effectiveness in solid tumors. Given the ongoing clinical evaluation of iRGD, this simple, non-conjugated strategy offers a feasible and rapidly translatable approach to overcome a key limitation of current ICI therapy and improve outcomes for patients with HCC.

This self-reinforcing mechanism enables a highly efficient synergistic combination of microwave thermal and dynamic therapies, achieving potent tumor ablation through localized hyperthermia, cytotoxic reactive oxygen species generation, as validated both in vitro and in vivo. This work establishes a paradigm of using endogenous metabolites for autonomous motion, advancing nanomaterials for precise cancer therapy.

The cell type-dependence of the effect of hPSC-derived EV treatment was postulated to be due to occurrence of an EMT for cells located at different locations along the epithelial-mesenchymal spectrum, leading to either an increase or decrease in tumorigenicity. Therefore, exposure to EVs does not always reduce the tumorigenicity of cancer cells but is cell type-dependent.

In contrast, the efficacy was significantly lower in CD44-negative SNU-216 cells (IC50 = 5.22 μg•mL-1). This work highlights the strategic use of His as a bridge to create a synergistic HA-ZIF-8 platform, offering a powerful and promising approach to the targeted therapy of CD44-overexpressing cancers.

Our data demonstrated that CD80 modulated tumor-cell stemness and malignant phenotype while restraining antitumor T cell immunity. Targeting CD80 augments antitumor immunity and provides a compelling strategy to enhance treatment responses to neoadjuvant chemoimmunotherapy in HNSCC.

Patients with high expression of HSPA5, YAP, and TAZ exhibited significantly poorer overall survival. Collectively, our findings suggested that HSPA5 promotes PMT through the stabilization of YAP/TAZ and identified HSPA5 as a promising therapeutic target for GBM patients.

TCE significantly altered the expression of approximately 25% of miRNAs related to cancer pathway in the miRNA array panel, as it upregulated 19 miRNAs and downregulated 4 miRNAs of the tested 84 miRNAs. Considering the effects on chromatin modification, proliferation rate, and miRNAs, it can be concluded that these mechanisms may be involved in TCE-induced nephrotoxicity.