ADAM10 (ADAM Metallopeptidase Domain 10)

TIMPs display contrasting expression profiles and distinct pathway associations in breast cancer. TIMP1 emerges as the only consistently overexpressed inhibitor, while TIMP4 appears as a promising prognostic marker with unique MMP correlations that may influence tumor behaviors.

When combined with lipidomics as a third modality, the platform correctly determines 97.4% cancer stage accuracy, with only one misclassification. This study establishes a multimodal EV-based activity/affinity assay as a robust framework for liquid biopsy, providing accurate cancer staging, improved prognostics, and offering a potential platform for pan-disease diagnostics.

Mechanistically, CI upregulated the expression of ADAM10, which plays a key role in converting membrane-bound CX3CL1 to its soluble form. This study provided evidence that chronic inflammation could promote tumor progression through the activation of ADAM10/CX3CL1 axis in gastric cancer.

Current first- and second-line therapies rely on oxaliplatin- or irinotecan-based combination chemotherapies combined with antibody-mediated inhibition of EGFR- or VEGF-dependent signaling, but these regimens are associated with significant side effects that limit long-term use and effectiveness. Finally, treatment studies in CRC cell line-derived xenograft models revealed marked antitumorigenic properties of 1H5. Together, these findings demonstrate that selective targeting of the active conformation of ADAM10 enables simultaneous inhibition of multiple oncogenic pathways involved in CRC growth and progression and represents a promising therapeutic strategy warranting further clinical evaluation.

Androgen signaling modulates APP processing in cancer, particularly through the non-amyloidogenic pathway; however, significant knowledge gaps remain. Further studies are needed to explore the interaction between androgens and APP processing in other cancer types, as well as to elucidate downstream signaling pathways regulated at the gene expression level.

We propose that interventions targeting this axis must move beyond traditional agonist/antagonist approaches toward spatiotemporally specific precision control strategies, including intelligent delivery systems, CRISPR-based cell engineering, and AI-driven personalized treatments. Rationally reprogramming the functional orientation of this axis holds promise in overcoming immune checkpoint inhibitor resistance and provides a theoretical foundation for the development of a new generation of cancer immunotherapies.

These results reveal to what extent EV purification methods impact both, EV composition and function. This methodological awareness is critical for advancing EV-based biomarker discovery, diagnostics, and therapeutic platforms.

Multiple therapeutic modalities have been validated, including small-molecule inhibitors (INCB7839, INCB3619, GI254023X) that suppress ligand shedding and enhance trastuzumab efficacy, RNA interference (siRNA/miRNA) for targeted gene silencing, and engineered nanocarrier drug delivery platforms that overcome therapeutic resistance. The epigenetic regulation, post-translational modifications, and diagnostic advancements, such as SERS-based serum profiling, further underscore their value as biomarkers and druggable targets. Collectively, ADAM/ADAMTS-centered interventions represent a promising direction for precision oncology and therapeutic targets for improving clinical outcomes in breast cancer.

The analysis highlights the presence of variants with high pathogenicity scores, suggesting their significant role in disease mechanisms. This study identifies potentially pathogenic nsSNPs in ADAM10 and ADAM17 that may affect their alpha-secretase activity and contribute to AD pathogenesis. Further experimental validation is essential to confirm these results and clarify their roles in disease mechanisms.

CD24 therefore emerged as an effective target in BCP-ALL, and the combination of CD24 and CD123 as a potential effective double-targeting strategy. The combination of different recognition modalities (eg, a CAR and CD16) should be tested to determine whether it provides synergistic cytotoxic activity in triple targeting.

When combined with lipidomics as a third modality, the platform correctly determined 97.4% cancer stage accuracy, with only one misclassification. This study establishes a multimodal EV-based activity/affinity assay as a robust framework for liquid biopsy, providing accurate cancer staging, improved prognostics, and offering a potential platform for pan-disease diagnostics.

The present study demonstrated that lower pleural sRAGE is a potential predictive biomarker for talc pleurodesis failure despite inferiority to pleural acidity. Imbalance between sRAGE and HMGB1 in MPE may be associated with the underlying mechanism for talc pleurodesis failure.