This study reveals how lipid metabolism dysregulation promotes colorectal cancer liver metastasis (CRLM) through a novel YTHDF3-mediated mechanism involving m⁶A RNA modification and liquid-liquid phase separation.

Though it has long been recognized that the liver exhibits remarkable immune tolerance, the underlying mechanisms driving this phenomenon remain poorly understood. Here, we explore the liver’s unique immune tolerance—a critical feature that enables it to process gut- and diet-derived inflammogens without eliciting excessive inflammation. We propose that entero-pancreatic peptide hormones (e.g., GLP-1, GIP, CCK, glucagon, VIP, amylin) and postprandially reabsorbed bile acids (BAs), delivered at high concentrations via the portal vein, activate G protein-coupled receptors and trigger cAMP signalling pathways that ultimately promote anti-inflammatory responses through mechanisms such as PKA–CREB and Epac activation. These pathways have been implicated in suppressing inflammation, and fostering a tolerogenic phenotype in resident immune cells.

Lymphatic malformations (LMs) are congenital vascular anomalies characterized by abnormal lymphatic development, leading to disfigurement and severe clinical complications. However, the immunopathological mechanisms underlying LMs remain poorly defined. Here, we provide a comprehensive single-cell immune landscape of LMs by integrating single-cell RNA, T-cell receptor, and B-cell receptor sequencing (scRNA-seq, scTCR-seq, and scBCR-seq) on peripheral blood and pleural effusion samples, uncovering profound immune dysregulation and chronic inflammation.

The intestinal epithelium undergoes rapid renewal every 3–5 days, a process driven by intestinal stem cells (ISCs) located at the base of crypts. While ISCs play an essential role in epithelial regeneration following injury, such as that induced by chemotherapy or radiation, the underlying regulatory mechanisms remain incompletely understood.

In recent decades, scientists have debated whether a seven-million-year-old fossil was bipedal—a trait that would make it the oldest human ancestor. A new analysis by a team of anthropologists offers powerful evidence that Sahelanthropus tchadensis—a species discovered in the early 2000s—was indeed bipedal by uncovering a feature found only in bipedal hominins.

For the first time, scientists have reconstructed ancient genomes of Human betaherpesvirus 6A and 6B (HHV-6A/B) from archaeological human remains more than two millennia old. The study, led by the University of Vienna and University of Tartu (Estonia) and published in Science Advances, confirms that these viruses have been evolving with and within humans since at least the Iron Age. The findings trace the long history of HHV-6 integration into human chromosomes and suggest that HHV-6A lost this ability early on.

New study reveals that bacteria can survive antibiotic treatment through two fundamentally different “shutdown modes,” not just the classic idea of dormancy. The researchers show that some cells enter a regulated, protective growth arrest, a controlled dormant state that shields them from antibiotics, while others survive in a disrupted, dysregulated growth arrest, a malfunctioning state marked by vulnerabilities, especially impaired cell membrane stability. This distinction is important because antibiotic persistence is a major cause of treatment failure and relapsing infections even when bacteria are not genetically resistant, and it has remained scientifically confusing for years, with studies reporting conflicting results. By demonstrating that persistence can come from two distinct biological states, the work helps explain those contradictions and provides a practical path forward: different persister types may require different treatment strategies, making it possible to design more effective therapies that prevent infections from coming back.

Why does cancer sometimes recur after chemotherapy? Why do some bacteria survive antibiotic treatment? In many cases, the answer appears to lie not in genetic differences, but in biological noise — random fluctuations in molecular activity that occur even among genetically identical cells.

Biological systems are inherently noisy, as molecules inside living cells are produced, degraded, and interact through fundamentally random processes. Understanding how biological systems cope with such fluctuations — and how they might be controlled — has been a long-standing challenge in systems and synthetic biology.

Although modern biology can regulate the average behavior of a cell population, controlling the unpredictable fluctuations of individual cells has remained a major challenge. These rare “outlier” cells, driven by stochastic variation, can behave differently from the majority and influence system-level outcomes.

This longstanding problem has been answered by a joint research team led by Professor KIM Jae Kyoung (KAIST, IBS Biomedical Mathematics Group), KIM Jinsu (POSTECH), and Professor CHO Byung-Kwan (KAIST), which has developed a novel mathematical framework called the “Noise Controller” (NC). This achievement establishes a level of single-cell precision control previously thought impossible, and it is expected to provide a key breakthrough for longstanding challenges in cancer therapy and synthetic biology.