In conclusion, USP7 was a key regulator of DNA repair in pNENs. The combination of cisplatin and P005091 therefore holds promise as a therapeutic strategy for pNENs.
Combining cytokine mRNA immunotherapy with cytotoxic killing and immune checkpoint blockade can reactivate antitumour immunity, offering a promising strategy for treating advanced PDAC.
Our studies reveal that CMV-specific viral memory T cells can be re-directed to control a solid tumor normally refractory to immunotherapy via a simple, intravenous injection of T-cell peptide epitopes. This mutation-agnostic approach has significant potential for the development of "off-the-shelf" therapeutics by stimulating pre-existing antiviral memory, and it is widely applicable due to the high prevalence of CMV.
Time-dependent ROC analyses demonstrated that MCM4 positivity achieved AUCs of 0.817 (95% CI: 0.763-0.864) at 3 years and 0.777 (95% CI: 0.720-0.828) at 5 years for postoperative metastasis assessment. Taken together, these findings identify MCM4 positivity as an independent prognostic biomarker for postoperative metastasis risk assessment in SPN.
Single cell RNA sequencing data confirmed the elevated TIGIT expression on CD4+ T cells and increased exhausted CD4+ T cells in CLCG-low PDACs. These findings uncovered the unique underlying mechanisms of immune suppression in CLCG-deficient PDACs and identified CLCG as potential biomarkers to identify those who may benefit from TIGIT-targeting immunotherapies.
1 day ago
Journal • PD(L)-1 Biomarker • IO biomarker
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PD-L1 (Programmed death ligand 1) • HAVCR2 (Hepatitis A Virus Cellular Receptor 2) • TIGIT (T Cell Immunoreceptor With Ig And ITIM Domains 2) • CD4 (CD4 Molecule)
Our study demonstrates that KRT17 marks a distinct transcriptional signature in a subpopulation of epithelial cells within histologically low-grade IPMN. This population of cells likely represents a transitional state of histologically low-grade epithelial cells undergoing progression to a higher grade of dysplasia and thus may represent a higher risk of progression to carcinoma.
Furthermore, Meflin deficiency reduced the area of tumor vessels in a TNBC mouse model, highlighting its role in CAF-mediated inhibition of TNBC progression and improvement of drug delivery. Accordingly, Meflin plays a role as a potential functional marker of rCAFs in TNBC.
In vivo studies demonstrated that CFMCP NPs exhibit excellent biocompatibility, significantly inhibit tumor growth, and exert direct cytotoxic effects. In summary, the development of this novel composite nanomaterial, which induces ferroptosis through mitochondrial Ca2+ overload, provides a valuable reference for synergistic and highly effective tumor therapy.