New study reveals how controlling sunburn-triggered inflammation may prevent skin cancer
Peer-Reviewed Publication
Updates every hour. Last Updated: 31-Dec-2025 06:11 ET (31-Dec-2025 11:11 GMT/UTC)
A new University of Chicago study explores how prolonged exposure to ultraviolet (UV) radiation can trigger inflammation in skin cells through degradation of a key protein called YTHDF2. This protein acts as a gatekeeper in preventing normal skin cells from becoming cancerous. The finding opens the door to develop potential new approaches to skin cancer prevention and treatment.
Scientists at Gladstone Institutes and UC San Francisco (UCSF) have mapped the intricate network of genetic switches that immune cells use to fine-tune levels of FOXP3. Their findings, published in Immunity, have important implications for developing immune therapies and address a long-standing mystery about why this gene behaves differently in humans than in mice.
The aberrant overexpression of Lysine-specific demethylase 1 (LSD1/KDM1A) is a common feature across a wide spectrum of human cancers, and its elevated levels correlate with poor survival of cancer patients, making it an attractive target for pharmacological intervention. However, the clinical trials of LSD1 small-molecule inhibitors are facing few serious challenges, including toxicity at therapeutic doses. Here, the authors reported the discovery of LD-110 as a potent PROTAC degrader via the ubiquitin-proteasome system, leading to significantly growth suppression of cancer cells both in vitro and in vivo.