Men diagnosed with nonmetastatic prostate cancer can generally expect to live for many years after their diagnosis. However, cardiovascular disease and other cancers remain important threats to their long-term health. For many survivors, this raises an important question: What can I do to live a longer, healthier life? A new study published in JAMA Network Open suggests that the type and source of dietary fat they consume may make a difference.

The study, co-led by researchers from the Research Institute of the McGill University Health Centre (The Institute) and Harvard T.H. Chan School of Public Health, included nearly 5,000 men with nonmetastatic prostate cancer and followed them for a median of 12.8 years, drawing on data collected over more than three decades. The researchers found that the type and source of fat consumed after diagnosis were associated with long-term survival. Higher saturated fat intake, as well as higher animal fat consumption (a major dietary source of saturated fat), were associated with greater all-cause mortality. These associations were driven primarily by deaths from cardiovascular disease and, to a lesser extent, other cancers—not by prostate cancer itself.

A real-world study of 145 resectable NSCLC patients who achieved pathological complete response after neoadjuvant chemoimmunotherapy found no significant disease-free or overall survival benefit from adding adjuvant immunotherapy. The findings suggest that patients with a pCR may not need further postoperative treatment, though larger prospective studies are required for confirmation.

A research team led by Prof. Yi Sun at Zhejiang University, reported a unexpected finding that the combination of Kras^G12D activation and genetic inactivation of UBE2M in the lung triggers the cGAS-STING-NF-κB signal to form a inflammatory tumor microenvironment (TME). Mechnistically, Kras^G12D promotes the mitochondrial biogenesis, whereas UBE2M depletion inhibits Parkin neddylation and mitophagy, together causing the cytoplasmic release of damaged mitochondrial DNA. The STING antagonist H-151 rescues TME, indicating a causal role of the cGAS-STING signal. The study therefore demonstrates a unexpected role of UBE2M in prevention TME induced by Kras mutant.