Combined siRNA-mediated silencing of MSH3 and HTT has synergistic therapeutic effects in a mouse model of Huntington’s disease.

Angiopoietin-1 RNA therapy slows the progression of WT1 glomerular disease in a preclinical mouse model.

Mutant p53 reactivation combined with DNA demethylation kills AML/MDS cells, showing efficacy in a pilot clinical trial.

Zika virus particles can assemble in the absence of the full-length premembrane structural protein.

In Fig. 3A of the Research Article “Follistatin gene delivery enhances muscle growth and strength in nonhuman primates” by Kota et al., the ELISpot data for the MCK promoter were erroneously duplicated as the data for the CMV promoter. The figure has been revised to illustrate the correct ELISpot data for the CMV promoter. This discrepancy did not affect the conclusions of the paper.

A genetic mouse model of IDH-mutant glioma responds to mutant IDH inhibitor (mIDHi) and shows that prior mIDHi treatment improves response to chemoradiation.

Fecal microbiome transplant up-regulates immune tolerance pathways in food allergy.

Dynamic immune and JAK-STAT–IFN signaling across time points after liver transplant parallels rejection outcomes.

A 2D NIR-II nanozyme achieves surgical navigation at single-cell–level resolution and enables catalytic phototherapy as a precise glioma theranostic.

In human rotator cuff surgical samples, a DLK1+ subset of fibroadipogenic progenitor cells is identified that can limit fatty infiltration in mice.

Engineered human spinal interneurons rebuild damaged motor circuits after injury, enabling functional recovery through synaptic integration.

Targeting the immune microenvironment suppresses pathological retinal angiogenesis.

Somatosensory nerves drive pathologic bony bar formation via pleiotrophin signaling, and TrkA inhibition or bupivacaine attenuates it in mice.

Cancers hijack the nervous system to fuel growth and evade targeting; decoding this interface opens avenues for patient care.

Neural signals link physiological history to tumor biology, shaping metastasis risk and therapeutic response across time.

Preexisting nerve architecture protects early tumors, suggesting that therapies should disrupt neural organization rather than target individual signaling molecules.

Bidirectional cross-talk between neural circuits and tumors drives cancer progression and can be therapeutically targeted through drug repurposing.

Pathogenic interactions between neurons and malignant cells drive childhood brain cancers.

Overcoming glioblastoma therapy resistance will require integration of precision oncology, immunotherapy, and advanced delivery technologies.

Ciltacabtagene autoleucel–associated non-ICANS neurotoxicities are driven by high CD4+ CAR T cell expansion.