ADAM17 (ADAM Metallopeptidase Domain 17)

Our data identify ADAM17 as an easily quantifiable, longitudinal biomarker that concurrently reflects tumor development stage and renal function damage in MM patients. Incorporation of ADAM17 into existing risk algorithms may enhance prognostic precision and enable earlier, patient-tailored intervention.

TAB16 is a modifiable backbone to which additional functional components can be added, such as IL-15 (TAB16/15) for consolidated and multifaceted activity. Our ADAM17-engaging platform offers a unique approach for targeted ADAM17 inhibition to augment the anti-tumor function of endogenous and therapeutic NK cells.

Deletion of iRhom2 provided protection against neuropathic changes, without altering glucose levels, revealing a glucose-independent mechanism. These findings establish iRhom2 as a promising therapeutic target, offering new translational opportunities to prevent or treat diabetic neuropathy.

Clinically, elevated serum levels of soluble MerTK (s-Mer) correlated with hepatic injury severity and Caspase-1 activation in patients after partial hepatectomy or liver transplantation. Our findings suggest a potential therapeutic strategy for LIRI prevention and treatment.

Tracheal epithelial cells were stimulated with GM-CSF and then treated after 24 h by lentivirus-mediated ADAM17 RNAi and mitomycin C. A model of severe traumatic tracheal stenosis was established in Beagle dogs...In conclusion, it was showed that TAPI-1 combined with silicone stents can significantly alleviate severe traumatic tracheal stenosis in Beagle dogs by inhibiting the ADAM17/TGF-β1 signaling pathway and expanding the narrowed trachea. TAPI-1 combined with silicone stents can be considered as a novel therapeutic approach for treating severe tracheal stenosis after trauma.

In conclusion, bevacizumab remains an integral component of OC treatment. Future progress will depend on biomarker-driven, prospectively designed clinical trials and the integration of multi-omic data and machine learning approaches to enable precision application of anti-angiogenic strategies, maximising clinical benefit while minimising toxicity.

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.

KRASG12D-driven tumorigenesis requires both autocrine and paracrine signaling regulated by ADAM17. Beyond activating EGFR to drive acinar cell transdifferentiation, ADAM17 also promotes neoplastic progression by modulating additional protumor signaling that shape the fibroinflammatory microenvironment. These findings highlight a pivotal role for ADAM17 in orchestrating epithelial plasticity, cellular signaling, and stromal remodeling during pancreatic tumorigenesis.

This study emphasized the importance of UBL3 in VEGFRi resistance in RCC and proposed that UBL3 activated NOTCH signaling through two distinct pathways, thereby suppressing cancer apoptosis and promoting resistance to VEGFRis. These findings provided a solid scientific foundation and paved the way for the development of novel therapeutic strategies for patients with advanced RCC.

gasseri significantly decreased the levels of the pro-inflammatory cytokine TNF and reduced immune cell infiltration in stained gastric tissues. Together, these findings suggest that certain lactobacilli can counteract the H. pylori-mediated induction of HBEGF and TGF-α expression, and indicate that ADAM17 could be targeted to inhibit the cancer-related effects of H. pylori.

Finally, by employing multiplex immunofluorescence imaging to visualize the spatial proximity between epithelial and immune cells, we elucidate their functional cross-talk within the tissue microenvironment. The findings demonstrate that our computer-optimized peptide carrier achieves transdermal siRNA delivery and reprograms the psoriasis-associated inflammatory microenvironment.