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.

A new review in the Journal of Pancreatology explores TIGIT as a pivotal immune checkpoint for cancer immunotherapy. It details TIGIT’s immunosuppressive mechanisms, its correlation with poor prognosis, and the superior efficacy of anti-TIGIT/PD-1 combination therapy in overcoming resistance to conventional immune checkpoint inhibitors.

The study, led by IRB Barcelona, shows that tumours with chromosomal instability can promote their own growth by damaging the surrounding healthy tissues.

Senescent tumour cells release signals that block the proliferation of neighbouring cells, ultimately inducing their death.

Published in EMBO Reports, the study identifies a new interaction mechanism between the tumour and its environment, which could open new avenues for researching targeted therapies against senescent cells.