CD46 (CD46 Molecule)

Importantly, MV-Blina did not induce either short- or long-term toxicity in in vitro neuronal models encompassing PBMCs, nor in immunocompromised CD46 transgenic mice, even under additional immunosuppression. Collectively, these findings support further investigations of MV-Blina as a potential treatment for patients with relapsed or refractory BCP-ALL.

P=N/A, N=1070, Recruiting, Beijing Children's Hospital Affiliated to Capital Medical University Baoding Hospital; Beijing Children's Hospital Affiliated to Capital Medical Unive

P=N/A, N=367, Active, not recruiting, AstraZeneca | Recruiting --> Active, not recruiting | N=1070 --> 367

By integrating orthogonal microtubule inhibition and high-linear-energy-transfer alpha irradiation on a single CD46 scaffold, potent, well-tolerated tumor control was achieved across diverse models. The dual-payload construct's compatibility with CD46 immuno-PET for real-time dosimetry further supports progression to early-phase clinical trials in prostate cancer and multiple myeloma.

Flow cytometric analysis conducted for proteomic expression of CD46 and CD55 on cell surfaces of leukemia patients showed a reduction in expression by 1.2-fold and 2.8-fold in AML patients, respectively. Post transcriptional knockdown of both genes in leukemic cell model using customized shRNA, followed by cell viability assays showed a significant reduction in the viability of cells by 3-fold, suggesting that although the expression of both proteins could be compromised by cancerous cells to evade complement attack mechanisms, they could also be vital to the viability of cancerous cells suggesting a dual role of complement in the tumor microenvironment.

Additionally, inflammation-to-cancer transition is a core mechanism in the development of OSCC, with the tumor inflammatory microenvironment acting as a "promoter" in the progression from OLK to OSCC. This study provides novel insights into the molecular mechanisms and targeted therapies for OSCC, holding significant theoretical and clinical application value.

Further functional experiments indicate that resting neutrophils phagocytose complement-opsonized NTDVs, leading to cell activation, including the production of reactive oxygen species (ROS). In conclusion, our data suggest a significant role for neutrophil-derived NTs in a wide range of inflammatory diseases and reveal a previously unknown mode of cell-cell communication.

Pre-treatment with EGCG blocked EGF-induced changes in CC cells. Collectively, these findings indicate the inflammatory role for EGF and attest the anti-inflammatory potential of EGCG in CC cells.

We identify subtype-specific protein signatures, with CD46, HNF1A, and ATP1B1 exclusively expressed in the aggressive group B. Finally, computational drug sensitivity prediction, validated by molecular docking, nominates Sunitinib as a potential therapy for group B patients. Our work provides a proteomic framework for improved prognostication and targeted therapy in high-risk HBV-HCC.

P2, N=75, Recruiting, FibroGen | Not yet recruiting --> Recruiting

Our findings suggest that E-cadherin inhibition is associated with early changes in EP300 chromatin localization, particularly at loci linked to epithelial-mesenchymal transition (EMT) and pluripotency. These changes may reflect an early chromatin-level response to altered cell adhesion, warranting further functional investigation.

LARRGs are crucial in the context of radiation resistant NSCLC, as they significantly influence tumor growth, the immune microenvironment, and drug response. This signature of LARRGs has the potential to serve as a prognostic biomarker and may also represent a promising therapeutic target for patients facing radiation resistant NSCLC.