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.

Scientists at Peking University have identified a mitochondrial protein that is essential for protecting motor neurons, offering new insight into how amyotrophic lateral sclerosis (ALS) may develop. The study, led by Dr. Xianhua Wang and Dr. Heping Cheng at the College of Future Technology, Peking University, shows that loss of the mitochondrial protein ROMO1 causes progressive damage to motor neurons and muscles in mice, closely resembling key features of human ALS. The findings were published online in Science Bulletin.

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.