P4, N=36, Not yet recruiting, Affiliated Hospital of Guizhou Medical University; Affiliated Hospital of Guizhou Medical University

In contrast, IL18 promoter variation showed various associations: rs1946518 G allele correlated with peroneal nerve shorter compound motor action potential (CMAP) distal latency and lower ulnar nerve sensory nerve action potential (SNAP) amplitude...We confirmed the presence of acetate, propionate, and butyrate in human CSF and demonstrated serum-CSF equivalence for these SCFAs, while stool concentrations were higher, as expected. Collectively, IL18 polymorphisms and SCFAs readouts emerge as biologically grounded candidates for patient stratification in CIDP; these findings warrant validation in larger, multicenter cohorts integrating electrophysiology with CSF/serum biomarkers and microbiome profiling.

We conclude that the optimal use of PARP inhibitors, PSMA-targeted RLT, and ARPIs requires a personalized strategy guided by molecular profiling, functional imaging, prior treatment exposure, and safety considerations. This clinically focused overview aims to support evidence-based decision-making in an increasingly complex treatment landscape.

P2, N=64, Completed, Memorial Sloan Kettering Cancer Center | Active, not recruiting --> Completed | Trial completion date: May 2026 --> Jan 2026 | Trial primary completion date: May 2026 --> Jan 2026

Cyclocircadins A, C, D, and F-H delayed the phase of the circadian rhythm, and reduced the amplitude of bioluminescence oscillations. In addition, cyclocircadins A, C, F, and G tended to lengthen the circadian period, whereas cyclocircadin E tended to shorten it. Cyclocircadins A and F-H were more active at lower concentrations than cyclocircadins C-E, indicating that structural variations in the seven-membered ring are critical for their activity.

P2, N=31, Completed, Montefiore Medical Center | Active, not recruiting --> Completed

AR alterations in ctDNA accumulate at progression in mCRPC patients treated with ARPIs, especially in those with initially durable responses. These findings support the use of liquid biopsy to serially track resistance mechanisms and inform precision therapy in advanced prostate cancer.

Their structures were elucidated by 1D and 2D NMR spectroscopy, high-resolution mass spectrometry (HR-ESIMS), interproton distance analysis using NOE peak amplitude normalization for improved cross-relaxation (PANIC), Snatzke's method, and computational ECD and DP4⁺ probability calculations...Overall, compound 3 exhibited the most consistent and potent cell-line specific anticancer effects across both models, highlighting its potential as a promising lead candidate for further anticancer drug development. Collectively, these results suggest concentration-dependent anticancer activity of T. crispa diterpenoids in liver and lung cancer models and further support compound 3 as promising leading candidate targeting key survival signaling pathways in cancer.

Advanced multimetabolic APTw-CEST and 2-deoxy-D-glucose-CEST postprocessing metrics allowed adequate preclinical murine BC subtyping. AREX showed potential for 2-deoxy-D-glucose-CEST in tumor characterization; however, APTw-CEST remains superior. MTRasym failed to distinguish between tumor subtypes in CEST-MRI.

Of all trials, only MAGNITUDE, evaluating niraparib and abiraterone, led to aligned conclusions from both the EMA and FDA, as its design effectively identified the subgroup most likely to benefit. Currently, there is a need for harmonisation in biomarker-driven trial designs and the definition of homologous recombination repair deficiency (HRD). Access to biomarker and clinical data from all PARP-inhibitor trials would allow researchers to clarify the impact of different HRR mutations on outcomes.

However, for BRCA-mutated mCRPC, olaparib combined with abiraterone improved PFS (HR = 0.61, 95% CrI = 0.41-0.91) and OS (HR = 0.41, 95% CrI = 0.21-0.80) significantly. For patients with changes in other related DNA repair genes (but not BRCA), olaparib alone was an effective treatment. This information may assist doctors and patients in choosing the most suitable treatment based on the cancer's genetic characteristics.

Our findings unveil a brain-cartilage circuit that regulates cartilage regeneration, providing valuable insights into the inherent limitations of tissue regeneration and suggesting a promising treatment strategy for enhancing cartilage regeneration.