"It's been known for decades that cancer can flatten healthy day-night stress hormone rhythms,” says CSHL’s Jeremy Borniger. “What causes that?” In mice, Borniger’s lab found that breast cancer disrupts the brain-body feedback loop that regulates these rhythms. Stimulating key neurons in the hypothalamus at certain times restored healthy function, pushing anti-cancer immune cells into tumors and shrinking them significantly.

A University of Maryland, Baltimore County (UMBC) study, published in Nature Communications, uncovers how enteroviruses—including those causing polio, myocarditis, encephalitis, and the common cold—hijack host cell machinery to replicate. Researchers determined the structure of a cloverleaf-shaped RNA element in the viral genome bound to the viral protein 3CD, which recruits host factors to form the viral replication complex. 3CD also acts as a switch between genome copying and protein synthesis. This highly conserved mechanism across all seven enteroviruses in the study presents a stable target for developing broad-spectrum antiviral drugs that could disrupt this essential interaction and prevent replication.

Researchers at the Icahn School of Medicine at Mount Sinai have developed a first-of-its-kind mRNA system that switches on therapeutic genes preferentially inside targeted cells—an advance demonstrated in studies in mice that could lay the groundwork for safer, more precise treatments for cancer and other diseases. The system, called the cell-selective modRNA translation system (cSMRTS), is an engineered form of mRNA designed to activate in specific cell populations. The findings were reported in the November 15 online issue of Molecular Therapy, a Cell Press journal.