New research on older Floridians reveals a striking disparity in melanoma outcomes. Men experience roughly twice as many melanoma-related deaths as women. Non-Hispanic and white populations also face higher rates of melanoma diagnosis and death than Hispanic groups. Researchers suggest differences likely reflect a combination of higher UV exposure, lower sun-protective behaviors and screening in men, disparities in access to care, and possible biological sex differences in immune response. The findings underscore an uneven burden and urgent need for targeted prevention and early detection.

Bladder cancer remains one of the most prevalent urological malignancies worldwide and is frequently associated with high recurrence rates, metastatic progression, and unfavorable long-term clinical outcomes. Although immune checkpoint blockade targeting the PD-1/PD-L1 axis has substantially improved therapeutic management for subsets of patients with advanced bladder cancer, durable clinical responses remain limited because of intrinsic and acquired resistance mechanisms within the tumor microenvironment.

Lung cancer is the leading cause of cancer-related deaths globally, and for patients with advanced EGFR-mutated non-small cell lung cancer (NSCLC), targeted epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) like gefitinib and osimertinib are standard first-line therapies. However, the inevitable emergence of acquired drug resistance severely limits long-term patient survival. While metabolic reprogramming and aerobic glycolysis are known hallmarks of tumor progression, the specific epigenetic pathways fueling TKI resistance remain elusive.

The UCLA study, conducted in mouse models and human cells and published in iScience, shows dendritic cells — the immune cells that direct killer T cells to attack cancer — ramp up their intake of creatine inside tumors and depend on it to function effectively in this nutrient-poor environment.

Damage to DNA in cancer cells can lead to pieces breaking off chromosomes and floating away, like icebergs cracking off from a glacier. Scientists at Sanford Burnham Prebys Medical Discovery Institute and their colleagues published findings May 28, 2026, in Genome Medicine demonstrating significant similarities between samples of tumors featuring these stranded DNA fragments and research models developed using these tumor samples. This close match provides scientists with greater confidence in using these models to learn how to better diagnose and treat cancers with these splintered spots of DNA.

Many repetitive regions of the genome have been considered “junk DNA” because the technologies available did not allow them to be studied at sufficient resolution. This is the case with the SST1/NBL2 macrosatellites, considered irrelevant and, until now, virtually invisible, which could have a more complex and decisive biological role than previously thought in nuclear organization, genome regulation, chromosomal instability and even cancer.