Alterations in the bacterial composition in various anatomical sites of the human body have been associated with tumorigenesis and the progression of multiple cancers; however, divergent results regarding enriched bacteria have been reported across studies of the same disease, indicating cohort-dependent bacterial compositional variance. To move beyond this inconsistency, a research team led by Professor Na Liu from Sun Yat-sen University Cancer Center proposes a fundamental shift in perspective. The team argues that it is the functional repertoire of bacterial communities, rather than their taxonomic identity, that serves as the core driver of tumor progression. The team proposes the unified nomenclature of bacterial functional constituents as “tumor-associated bacterial effectors” (TABEs), categorizing them into six functional classes according to their chemical nature, conserved structural features, and analogous mechanisms of action in regulating host cells. The researchers believe that exploring the mechanisms of TABEs in cancer represents a critical step toward harnessing their biological potential in real-life clinical settings.

Confronting the central challenge of how necroptosis reconciles high sensitivity to stimuli with robustness against intrinsic noise in complex living systems, this study systematically dissect the underlying design principles that govern cell-fate decisions. By integrating biophysical modelling with large-scale topological screening, we resolve the intricate biochemical reaction network into a minimal set of organizing rules. Our analysis identifies the incoherent feedforward loop (IFFL) as the core functional motif driving the observed dynamics. This topology endows the system with a distinctive bell-shaped input–output response, scale invariance, and the capacity to switch precisely between apoptotic and necrotic fates. Beyond elucidating the dynamical logic of cell death signalling, this work reveals, from a physics-informed perspective, a unifying “complexity-to-simplicity” design principle that may underlie the evolutionary construction of sophisticated signalling networks. It further provides a conceptual framework for understanding how dysregulation of cell-fate decisions contributes to pathological processes such as inflammation and tumorigenesis.

Liver organoids, three-dimensional structures derived from stem cells or hepatic progenitors, have emerged as a transformative technology. Unlike traditional two-dimensional cultures or animal models, organoids faithfully recapitulate the complex architecture and functionality of native liver tissue. This review summarizes recent advancements in liver organoid technology, detailing their development, classification, and key applications.

UC Davis researchers have mapped the structure and mechanics of a critical cellular machine that malfunctions in people with currently untreatable diseases such as infantile encephalopathy. These genetic disorders are caused by defects in the assembly of tubulin proteins that form the skeleton inside cells.

A largely overlooked structure inside our cells may play a crucial role in how the brain forms, offering new insight into developmental disorders and potential therapies.