Multi-Organoid PK/PD Platform Enables Personalized Therapy for NF1-Mutant Breast Cancer
Journal: Signal Transduction and Targeted Therapy
Author: Lim, J.H., Mun, S.J., Kang, H.M. et al., Republic of Korea
Researchers developed a patient-specific multi-organoid platform derived from induced pluripotent stem cells to model pharmacokinetics and pharmacodynamics across intestinal, liver, and kidney tissues in NF1-mutant breast cancer. Using this system, they identified Paxalisib combined with NF1 exon-skipping therapy as a synergistic treatment strategy, demonstrating the potential of integrating multi-organ PK/PD modeling with genotype-guided precision oncology.
Precancerous Microenvironment Remodeling Drives Early Tumor Survival
Journal: Nature
Author: Skrupskelyte, G., Rojo Arias, J.E., Ajith, H. et al., Switzerland / UK
Early-stage tumor cells can actively reshape their surrounding microenvironment, inducing fibroblasts to create a supportive precancerous niche through wound-healing responses and extracellular matrix remodeling. This fibronectin-rich stromal scaffold can promote tumor persistence and even confer tumor-like properties to normal epithelial cells, highlighting the critical role of stromal interactions in early tumor development.
Pyroptosome-Based In Situ Vaccine Strategy for Personalized Cancer Immunotherapy
Journal: Nature Materials
Author: Chen, B., Wan, F., Xia, H. et al. , China
Researchers developed a systemic injectable nanoadjuvant that induces tumor-cell pyroptosis, leading to the release of antigen-rich pyroptosomes and inflammatory signals that function as an in situ cancer vaccine. By combining pyroptosis with photoactivated TLR7/8 stimulation, the platform activates both innate and adaptive immunity to eliminate primary and metastatic tumors while minimizing systemic toxicity.
Early ECM Signaling Controls Metabolic Remodeling in Kidney Fibrosis
Journal: Nature Metabolism
Author: Gui, Y., Li, W., Liu, JJ. et al., USA
The extracellular matrix protein ECM1 acts as an early regulator of kidney fibrosis by controlling mechano-metabolic signaling within the fibrotic microenvironment. Suppressing ECM1 disrupts integrin–RhoC–YAP signaling, restores mitochondrial oxidative phosphorylation in kidney tubules, and promotes tissue repair, thereby limiting fibrotic progression.
