The cGAS‑STING pathway detects cellular DNA to trigger type I interferons and cytokines. This review integrates mechanistic immunology with clinical oncology perspectives, dissecting pathway components, regulatory factors, and therapeutic potential for cancer and diverse diseases, bridging fundamental discoveries to clinical applications.

 Researchers have developed a novel molecular classification system for endometrial cancer using network perturbation analysis. By analyzing 783 patient samples across four cohorts, the team identified three distinct subtypes with significantly different survival outcomes. The most aggressive subtype (C1) exhibits hormone signaling loss, immune exclusion, and specific sensitivity to paclitaxel and proteasome inhibitors, enabling precision treatment selection for high-risk patients.

We proposed a multidimensional, real-world framework to benchmark LLM versus physician decision-making in challenging lung cancer cases, using a curated set of 50 cases (complex/rare/refractory) and blinded three-dimensional Likert scoring (comprehensiveness, specificity, readability) to compare four LLMs, physicians across seniority levels, and AI-assisted juniors. DeepSeek R1 showed the most balanced overall performance, scoring between intermediate and senior physicians across dimensions. Performance was strongly case-type dependent: LLMs exceeded intermediate physicians in rare cases but underperformed—particularly in specificity—in refractory cases that require longitudinal reasoning. Notably, AI assistance substantially improved junior physicians in rare cases, while providing limited benefit and slightly reducing specificity in refractory cases; overall error profiling highlighted complementary strengths between clinicians and LLMs.

This review systematically analyzes the molecular mechanisms of five core DDR pathways (Homologous Recombination Repair, Non-Homologous End Joining, Base Excision Repair, Nucleotide Excision Repair, and Mismatch Repair) in mediating chemotherapy resistance in tumors, and thoroughly elucidates the correlation between key molecular events. The research presents an innovative molecular synergy model between DDR regulation and Immune Checkpoint Blockade. This article also provides perspectives on multidimensional intervention strategies based on the DDR network, including the development of inhibitors targeting novel DDR targets, the establishment of DDR pathway functional assessment systems based on multidimensional biomarkers, and the investigation of synergistic paradigms between DDR and novel therapeutic modalities.

 

A comprehensive review led by researchers from Southern Medical University and Fudan University uncovers how the body’s circadian clock regulates tumor biology, immune function, and the effectiveness of immune checkpoint inhibitors. The study integrates molecular, cellular, and clinical findings to propose “chronotherapy” as a new strategy to optimize cancer immunotherapy outcomes through time-of-day–based dosing and tumor microenvironment modulation.

Researchers have systematically mapped approximately 260,000 cancer-specific small RNAs, called oncRNAs, across 32 cancer types, revealing distinctive molecular "barcodes" that can identify cancer type with over 90% accuracy and predict patient outcomes through simple blood tests. In a study published January 23 in Cell Reports Medicine, Arc Institute Core Investigator Hani Goodarzi and colleagues found that each cancer produces unique patterns of these orphan non-coding RNAs, with about 30% actively secreted into the bloodstream. In 192 breast cancer patients from the I-SPY 2 trial, those with high residual oncRNA levels after chemotherapy had nearly 4-fold worse overall survival. This finding required only 1 milliliter of serum and remained significant even when controlling for standard clinical measures. Because cancer cells actively secrete these RNAs rather than passively shedding DNA, oncRNA-based liquid biopsies could enable earlier detection of recurrence and real-time treatment monitoring, addressing a key challenge in cancers that don't shed much DNA into the bloodstream.

Hepatocellular carcinoma (HCC) is the most common subtype of primary liver cancer and continues to be a major cause of cancer-related mortality, particularly in regions of China with a high hepatitis B virus prevalence. Early-stage diagnosis remains challenging due to its asymptomatic onset and the limited sensitivity of conventional biomarkers, which together contribute to delayed detection, suboptimal therapeutic outcomes, and poor prognosis. These limitations underscore the urgent need for reliable, sensitive, and specific biomarkers to enable timely detection and targeted intervention. Protein induced by vitamin K absence or antagonist-II, an abnormal prothrombin variant generated under vitamin K deficiency or antagonism, has emerged as a promising candidate with diagnostic and therapeutic relevance in HCC. This review critically examines the molecular and biological characteristics of protein induced by vitamin K absence or antagonist-II, evaluates its clinical utility in HCC diagnosis and management, and delineates the current limitations hindering its broader application. Furthermore, future perspectives are proposed to guide translational research and clinical implementation. Collectively, this review aims to provide a comprehensive theoretical framework to advance precision diagnosis and individualized treatment strategies for HCC.