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.

Researchers with the James P. Allison Institute™ at The University of Texas MD Anderson Cancer Center have discovered a new gene expression signature within tumors that can help identify patients with metastatic castration-resistant prostate cancer (mCRPC) who are more likely to experience lasting benefits from combined immunotherapy treatment.