EGFR expression

BA exerts its anti-NSCLC effects via multi-target regulation of oncogenic signaling and metabolic reprogramming. This offers preliminary insights that could inform future applications in metabolic-targeted therapies and combination treatments.

Importantly, EGFR sialylation affected Cetuximab binding and receptor activation in a cell line-dependent manner, with cells bearing α2,6-sialylation showing modified antibody responsiveness. Overall, these findings demonstrate that EGFR sialylation modulates receptor behaviour and Cetuximab response in CRC, highlighting the inhibition of sialylation as a potential strategy to overcome glycosylation-mediated therapeutic resistance.

This preclinical NIR-PIT model would provide valuable insights into improving treatment strategies. (250 words).

P2, N=104, Suspended, Fudan University | Recruiting --> Suspended

The expression of IL-7R-IM confers cytokine independence and robust anti-tumor activity to NK and CAR-NK cells. This strategy offers a practical solution to improve the persistence and efficacy of off-the-shelf NK cell therapeutics for clinical application.

P2, N=104, Recruiting, Fudan University | N=52 --> 104

P2, N=40, Not yet recruiting, Eye & ENT Hospital of Fudan University

Sorafenib is the first-line therapy for advanced hepatocellular carcinoma (HCC)...Silencing ST3GAL1 significantly reduced Siglec-7 ligand expression on liver cancer cells, enhancing their susceptibility to NK-mediated cytotoxicity and cetuximab-induced antibody-dependent cellular cytotoxicity (ADCC) in epidermal growth factor receptor (EGFR)-expressing tumor cells...Moreover, its elevated expression is associated with adverse clinical outcomes in HCC. Targeting ST3GAL1 may represent a promising strategy to enhance NK cell-mediated anti-tumor immunity in HCC.

Combined positivity offered superior correlation with lymph node metastasis (p<0.001) and advanced clinical stage versus individual markers. Integrated p53/Ki-67/EGFR assessment advances OSCC prognostication, warranting routine pathological use for enhanced clinical decision-making.

Overall, our results suggest that multiple pathways of EV biogenesis may operate in glioma cells resulting in formation of complex EV landscapes consisting of EGFR-positive and EGFR-negative EV subsets. This heterogeneity may have important implications for EV functions and EV-based diagnostics.

Clinically, multiplex immunofluorescence of patient tumors demonstrated strong co-expression of EGFR, LC3, and SLC16A3, which correlated with poor disease-free survival. Our study reveals a previously unrecognized EGF-secretory autophagy axis that orchestrates metabolic remodeling in TNBC and highlights the therapeutic potential of targeting the secretory autophagy- SLC16A3-lactate pathway to restrain metastasis.

Izalontamab brengitecan (Iza-bren; BL-B01D1) is a bispecific ADC targeting EGFR and HER3 that has demonstrated activity in other malignancies. Importantly, tumor tissue obtained at progression after BL-B01D1 treatment confirmed ABCG2 upregulation, validating a clinically relevant resistance mechanism. These findings support BL-B01D1 as a promising therapeutic strategy in mCRPC and nominate ABCG2 as a rational target for overcoming resistance.