TNFRSF11A (TNF Receptor Superfamily Member 11a)

This study provides and defines the first systematic snRNA-seq profiles under OXJF-treated HACE mice. The potential mechanisms of OXJF in treating HACE were related to maintaining energy metabolism, inflammation and BBB homeostasis.

Notably, kombucha did not induce renal or hepatic toxicity regardless of fermentation time. These findings suggest that kombucha, particularly after 4 days of fermentation, reduces inflammation and alveolar bone loss without systemic toxicity, supporting its potential as an adjunctive therapy for periodontitis.

miR-218-5p agomir treatment reduced cell pyroptosis in aorta of AS model mice and improved AS. Briefly, miR-218-5p repressed TNFRSF11A, repressed the NF-κB signaling, and disrupted NLRP3/caspase-1 activation, thereby alleviating pyroptosis and contributing to the improvement of AS.

We observed a reduced burden of MICs in the bone marrow (BM) of patients with stage I-III HER2+BC treated with IT DC1, compared with untreated patients and those treated with standard neoadjuvant HER2 therapies paclitaxel, with or without carboplatin, trastuzumab and pertuzumab (Taxol, Carboplatin, Herceptin and Perjeta or THP). We also treated a single patient with de novo stage IV HER2+ MBC with trastuzumab, pertuzumab and tamoxifen in combination with IT DC1. Remarkably, this treatment resulted in near-complete regression of primary tumor and metastatic disease, along with inhibition of MIC seeding in the BM. These findings suggest an intriguing strategy to inhibit the dissemination of MICs and prevent further overt metastasis in all patients with BC.

Denosumab facilitates the infiltration of CD8+ T cells into the interior of LC-BoM tissues. Based on this mechanism, we observed in both clinical cohorts and preclinical models that RANKL inhibitor can enhance the efficacy of immunotherapy in treating LC-BoM.

Downregulation of the RANK signalling predicts survival benefits in patients with primary breast cancer. Further investigation is warranted to explore the therapeutic potential of inhibiting RANK signalling in breast cancer.

Nevertheless, the patient's immunological status is not constant, and the relationship between aging and immune dysfunction is not fully understood. This review article offers an update on the current understanding of immunotherapeutic approaches in managing OsP and next-generation strategies that aim to develop tailored therapies for bone disorders.

Despite the effectiveness of treatments such as trastuzumab and lapatinib, many patients experience either primary or acquired resistance, leading to treatment failure. By identifying potential biomarkers and therapeutic targets, the review suggests that combining HER2 inhibitors with agents that target resistance pathways may enhance treatment efficacy and improve patient outcomes. Overall, this review underscores the complexity of HER2+ breast cancer treatment and the need for continued research to overcome resistance challenges.

This review emphasizes the critical need for incorporating immune-centric strategies into the management of CKD-MBD. It advocates for the development of biomarker-driven, personalized therapies and highlights the importance of conducting longitudinal studies to bridge the existing gaps in knowledge and improve patient outcomes.

The RANK-RANKL-OPG axis holds promise as a diagnostic and therapeutic target in dermatologic malignancies, warranting further clinical research.

AL is associated with increased KC incidence and mortality, mediated through inflammatory and metabolic proteins. These findings underscore chronic physiological stress as a significant factor in KC pathogenesis, providing potential biomarkers for early risk assessment and targeted prevention.

Notably, CYP2B6 emerged as a promising predictor of PARP inhibitor (PARPi) sensitivity, offering potential therapeutic implications. In conclusion, our study, harnessing machine learning and experimental validation, has uncovered novel biomarkers of HRD and PARPi sensitivity, shedding light on potential avenues for tailored clinical treatment strategies in COAD, thereby advancing personalized medicine.