Correlation between cancer cachexia and immune-related adverse events in HCC
Peer-Reviewed Publication
Updates every hour. Last Updated: 1-Jan-2026 03:11 ET (1-Jan-2026 08:11 GMT/UTC)
Cancer cachexia is commonly present in various cancers, including live, pancreatic, gastroesophageal, and bile duct cancers, and is associated with chemotherapy toxicity. M-MDSC induces mTEC apoptosis and impairs T cell negative selection, which leads to autoimmune T-cell infiltration of normal organs and serves as a prerequisite for the occurrence of irAEs. In addition, irAEs patients have higher levels of circulating M-MDSCs. M-MDSCs associated with cancer cachexia can serve as potential predictive biomarkers for irAE in advanced cancer patients.
This review highlights how natural polysaccharide-based microneedles (PMNs) are emerging as a transformative platform for cancer immunotherapy. We report their unique dual role in drug delivery and immune regulation, the innovative use of 3D printing for precision fabrication, and their smart responsiveness to the tumor environment. By integrating biocompatibility, enhanced drug loading, and controlled release, polysaccharide-based microneedles (PMNs) offer a promising strategy to overcome challenges in traditional cancer immunotherapies, potentially supporting the development of more effective and personalized treatments.
Researchers uncover a cunning new trick by which breast cancer cells evade immune attack. While the cGAS-STING pathway normally detects cytosolic DNA and activates anti-tumor immunity via IRF3-interferon signaling, aggressive tumors overexpress a long noncoding RNA, FAM83H-AS1, redirecting cGAS-STING signaling toward NF-κB-driven chronic inflammation that supports tumor growth. Critically, this shift creates a therapeutic vulnerability: NF-κB upregulates PD-L1, rendering these tumors highly susceptible to existing immunotherapies. This discovery reveals both a key mechanism for how cancer evades immunity and a promising way to fight back.
Exosomes facilitate cell-to-cell communication and are involved in key biological processes. Understanding the mechanisms regulating exosome production could offer new therapeutic insights for various diseases. Here, Prof. Zhong’s team demonstrates that exosome secretion is significantly inhibited when glucose is replaced with galactose as the primary carbon source in the culture medium. This glycometabolic regulation of exosome secretion is dependent on the cellular hexosamine biosynthetic pathway (HBP). Inhibition of HBP via gene knockdown, pharmacological blockade, or metabolite deprivation markedly suppresses exosome secretion. Mechanistically, HBP regulates multivesicular body (MVB) outward trafficking and its fusion with the plasma membrane via synaptosomal-associated protein 25 (SNAP25). O-GlcNAcylation of SNAP25 promotes soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex assembly, thereby facilitating exosome release. In summary, these findings reveal a critical role of HBP and protein O-GlcNAcylation in exosome secretion, which may provide new therapeutic targets for exosome-associated diseases, including cancer and inflammatory disorders.
Immune cells called B cells make antibodies that fight off invading bacteria, viruses and other foreign substances. During their preparation for this battle, B cells transiently revert to a more flexible, or plastic, stem-cell-like state in the lymph nodes, according to a new preclinical study from Weill Cornell Medicine investigators. The results could help explain how many lymphomas develop from mature B cells rather than from stem cells, as many other cancers do, and guide researchers in developing better treatments.