MUSC researchers are tackling MASH, or metabolic dysfunction-associated steatohepatitis, a liver disease affecting hundreds of millions worldwide. It is also a leading cause of liver transplantation, yet treatment options remain limited. A new paper published in Nature partner journal (npj) Metabolic Health and Disease suggests that a widely used asthma medication, formoterol, could potentially offer a different therapeutic pathway altogether. Formoterol is a beta-2 adrenergic receptor agonist that has been prescribed for decades to open airways in conditions like asthma and chronic obstructive pulmonary disease.

Cancer cells frequently develop the ability to expel anticancer drugs before they can work - a phenomenon called multidrug resistance (MDR) - which is one of the leading reasons why chemotherapy fails in patients. This research addresses that problem with a fundamentally new strategy: instead of simply increasing drug doses or switching drugs, researchers engineered nanoparticles that first disable the cancer cell's drug-expulsion mechanism, and only then release the anticancer drug.

Published in Science Advances, St. Jude Children’s Research Hospital scientists used a mix of genetic cancer dependency data, artificial intelligence (AI) and naturally occurring mutations to prioritize safer cancer drug targets. They focused their efforts on targets most likely to be effective while limiting unwanted toxicity, identifying IRS4 as a potential dependency across multiple tumor types. The work provides a proof of principle for evaluating potential toxicity early in the search for novel therapeutics.

Every year, antibiotic-resistant Staphylococcus aureus, commonly known as “staph,” causes serious infections and outbreaks in hospitals and community settings, disproportionately affecting vulnerable populations, including the elderly and those with weakened immune systems. Methicillin-resistant strains, known as MRSA, are a leading contributor to deaths associated with antimicrobial resistance globally.

Cancer cells survive by repairing damage to their DNA - even damage that would normally be fatal. One of their most important defense systems is homologous recombination, a high-precision repair pathway that fixes broken DNA using key proteins such as RAD51 and CHK1. While therapies such as PARP inhibitors have successfully targeted this vulnerability, many tumors eventually regain their DNA repair ability and become resistant to treatment.