Chemotherapy drugs that target a common mutation in colorectal cancer rapidly lose efficacy in patients, leading to relapse. According to a new preclinical study by Weill Cornell Medicine and MD Anderson Cancer Center investigators, colorectal tumors often find multiple ways to survive treatment, including additional genetic mutations and activation of cellular pathways typically associated with inflammation and regeneration. Targeting this tumor-specific inflammatory process could enhance the efficacy of some anticancer therapies and prevent drug resistance.

IBD, which comprises the inflammatory conditions Crohn’s disease and ulcerative colitis, affects about 1.6 million Americans, many of whom cannot be effectively treated. This mostly is due to a lack in understanding of what exactly causes the increased inflammation, fibrosis, and compromised intestinal barrier that underlie this disease and its manifold symptoms. 

A new study, published in Nature Biomedical Engineering and led by Wyss Founding Director Donald Ingber, developed donor-specific microfluidic Organ Chip models of colon that replicate major hallmarks of IBD in vitroin an unprecedented way. Their approach pinpointed new drivers of IBD progression and, for the first time, demonstrated a direct impact of pregnancy hormones on IBD severity in female IBD patient chips and recapitulated the enhanced initiation of cancer formation in IBD tissues.

High-altitude exposure, characterized by hypobaric hypoxia, cold, and intense radiation, profoundly remodels the gut microbiota, triggering a cascade of physiological and pathological changes that extend far beyond the gastrointestinal tract. As millions travel to or reside in regions above 2500 meters, understanding this gut-centric axis has become critical for managing health risks. Hypoxia disrupts the delicate balance of the gut ecosystem, leading to dysbiosis, impaired barrier function, and increased intestinal permeability. This allows bacterial translocation and systemic inflammation, which underpin conditions like acute and chronic mountain sickness. Crucially, the gut microbiome acts as a dynamic environmental sensor; its altered production of metabolites—particularly short-chain fatty acids (SCFAs) and bile acids—directly influences host energy metabolism, immune responses, and acclimatization capacity. These changes are increasingly implicated in a spectrum of diseases, from metabolic disorders to colorectal cancer, positioning the gut as a central mediator of high-altitude health. This review synthesizes evidence from human and animal studies to elucidate how high-altitude stress reshapes the microbial landscape, explores the mechanisms linking microbiota to disease, and evaluates emerging microbiome-based interventions for promoting resilience.