New research from The University of Texas at Arlington helps explain a longstanding puzzle in melanoma treatment: why continuous targeted therapy performed better than planned on-and-off treatment schedules in clinical trials, despite promising laboratory studies of intermittent dosing.

Researchers from Insilico Medicine, the University of Copenhagen, and international academic partners have identified NDRG1 as a previously unrecognized regulator of DNA damage repair and a potential therapeutic vulnerability in genetically defined cancers. Published in Science Signaling, the study combined AI-assisted transcriptomic analysis, high-content genetic screening, molecular biology, patient survival data, and profiling across more than 130 cancer cell lines. The researchers found that the antimalarial drug quinacrine disrupts the interaction between NDRG1 and VCP, impairing the recruitment of proteins required for effective DNA repair. Colorectal cancer cells carrying mutations in the DNA repair–associated genes MLH1 or PARP3 were particularly sensitive to quinacrine treatment or NDRG1 knockdown, indicating a potential synthetic lethal relationship. Although quinacrine was used as an experimental tool compound, the findings provide a foundation for developing more selective therapies targeting the NDRG1 pathway in cancers with specific DNA repair deficiencies.

A Rutgers medical oncologist explains how one of the nation’s largest real-world treatment comparisons could help physicians personalize therapy.

After treatment for metastatic prostate cancer, a drop in prostate-specific antigen (PSA) levels in the blood is an indicator that the treatment is working. A recent real-world study published by Wiley online in CANCER indicates that reaching a PSA level below 0.2 ng/mL is an indicator of improved patient survival.