New research taking place at the University of Plymouth's Brain Tumour Research Centre of Excellence, and supported by the Children’s Tumor Foundation, will trial combinations of drugs to try and find the first effective non-surgical treatments for patients with neurofibromatosis type 2 (NF2)

Engineered oncolytic bacteria have emerged as a promising therapeutic platform for precision cancer treatment, offering tumor-specific colonization, immune activation, and controllable therapeutic delivery. This review summarizes recent advances in the design and application of synthetic biological strategies that enhance bacterial precision, safety, and efficacy in tumor therapy. These strategies are categorized into three major regulatory modes: exogenous input–responsive gene circuits, autonomous bacterial signal–responsive gene circuits, and tumor microenvironment-responsive gene circuits.

DNA–protein cross-links (DPCs) represent a severe form of DNA damage that can disrupt essential chromatin-based processes. Among them, DNA–histone cross-links (DHCs) occur frequently within nucleosomes, yet their structural and functional consequences remain poorly understood due to their instability and low natural abundance.

This study investigates the molecular mechanisms underlying ligand recognition, subtype selectivity, and activation of neuropeptide FF receptor 1 (NPFFR1)—a Gi/o-coupled receptor that responds to endogenous RF-amide peptides (RFRP-3 from pro-NPFFB, NPFF from pro-NPFFA) and regulates physiological processes like opioid function, pain, and energy homeostasis. To address gaps in understanding its role in opioid modulation (due to lack of selective ligands), the authors used cryo-electron microscopy (cryo-EM) to resolve atomic structures of two NPFFR1-Gi complexes: RFRP-3-bound and NPFF-bound. GloSensor cAMP assays confirmed ligand potency differences, and mutagenesis/MD simulations validated key interactions.

Fibrosis, resulting from excess extracellular matrix (ECM) deposition, is a feature of adipose tissue (AT) dysfunction and obesity-related insulin resistance.

Preclinical studies indicate that cavity-resident macrophages in the peritoneal and pleural spaces contribute to immunosuppression and cancer progression. While these macrophages typically accumulate on organ surfaces rather than deeply infiltrating into tissues, their behavior and function in tumors remains unclear.

Hypertrophic chondrocytes are deeply involved in the growth of mammalian bones. Researchers find that these cells transform into multiple functional cell types, including those responsible for lengthening bones, maintaining the periosteum, and promoting the invasion of blood vessels that supply newly formed bone. Thrombospondin-4, a key signaling molecule produced by these cells, drives blood vessel formation. These findings open new avenues for enhancing bone repair and healing injured bones.

Myelodysplastic syndrome (MDS) arises from defective blood stem cells that progressively lose their normal functions. Japanese researchers have revealed how changes in chromatin accessibility—how DNA is packaged—reprogram these stem cells toward faulty myeloid gene activity. This shift disrupts the balance of blood cell development and drives disease progression. The team also developed a chromatin-based “progenitor score” that accurately reflects disease severity and predicts patient prognosis in MDS.