📈New Dataset: NR2F1 underlies persistence of residual disease in BRAF-mutant melanoma

Targeted therapies for melanoma, like BRAF and MEK inhibitors, can shrink tumors but often fail to completely eliminate all cancer cells. A small group of “persister” cells survives treatment and can cause the cancer to return later. In this dataset, we used expression profiling by high-throughput sequencing to find that a gene called NR2F1 is highly active in these surviving melanoma cells. Tumors with higher NR2F1 levels grew faster, were more invasive, and led to poorer survival after treatment. It was also discovered that NR2F1 is more active in older environments, suggesting that age may make it easier for these cells to persist. Blocking NR2F1 or its growth signals, such as the mTORC1 pathway, could be a new way to stop melanoma from coming back after therapy.