A new study from the University of Michigan Rogel Health Cancer Center, published in Science, sheds light on how two distinct classes of mutations in the FOXA1 gene—commonly altered in prostate cancer—drive tumor initiation formation and therapeutic resistance.

FOXA1, a key transcription factor that facilitates androgen receptor binding to DNA, is mutated in 10–40% of hormone-dependent prostate cancers. While common, the exact ways these mutations alter cancer cells have remained elusive—until now.

Rogel researchers, including Arul Chinnaiyan, M.D., Ph.D., S.P. Hicks Endowed Professor of Pathology and Urology, and Abhijit Parolia, Ph.D., Rogel Fellow and Assistant Professor of Pathology, used mouse models to understand the mechanisms underlying two major classes of FOXA1 mutations.

The discovery of an unknown organelle inside our cells could open the door to new treatments for devastating inherited diseases.

The organelle, a type of specialized structure, has been dubbed a “hemifusome” by its discoverers at the University of Virginia School of Medicine and the National Institutes of Health. This little organelle has a big job helping our cells sort, recycle and discard important cargo within themselves, the scientists say. The new discovery could help scientists better understand what goes wrong in genetic conditions that disrupt these essential housekeeping functions.

“This is like discovering a new recycling center inside the cell,” said researcher Seham Ebrahim, Ph.D., of UVA’s Department of Molecular Physiology and Biological Physics. “We think the hemifusome helps manage how cells package and process material, and when this goes wrong, it may contribute to diseases that affect many systems in the body.”