The cutting-edge advances in multivalent mRNA–exosome vaccines provides a mechanistic blueprint showing how these customized mRNA payloads can systematically reprogram the immunosuppressive architecture of “cold” tumor microenvironments and mobilize potent, antigen-specific cytotoxic T-lymphocyte responses to overcome cancer immunotherapy resistance.A primary challenge in oncology vaccinology is delivering payloads to lymphoid-resident antigen-presenting cells (APCs) without triggering systemic toxicities or rapid hepatic clearance. While synthetic lipid nanoparticles (LNPs) are standard for systemic delivery, they face hepatocyte sequestration driven by blood-borne apolipoprotein E (ApoE) binding, which limits extrahepatic bioavailability. To bypass this constraint, engineered exosomes offer a biological alternative. These cell-derived vesicles feature a native lipid bilayer enriched with cholesterol and sphingomyelin that shields mRNA from ribonuclease degradation. By presenting surface markers like CD47—a “don’t eat me” signal blocking macrophage phagocytosis via SIRPα—exosomes achieve extended circulation half-lives (Figure 1).

Hepatocellular carcinoma (HCC) remains one of the most lethal malignancies worldwide, ranking as the third leading cause of cancer-related mortality, with limited therapeutic targets and dismal prognosis for advanced disease. This study identifies P53 and DNA damage-regulated gene 1 (PDRG1) as a novel oncogenic driver in HCC, revealing a previously unrecognized regulatory axis promoting tumor progression. The researchers demonstrate that PDRG1 expression is significantly upregulated in HCC tissues compared with normal liver, and that high PDRG1 expression correlates with advanced tumor stage, higher histological grade, and poor patient survival, establishing PDRG1 as a potential prognostic biomarker. Functional studies reveal that PDRG1 knockdown suppresses HCC cell proliferation, migration, and invasion in vitro, and inhibits tumor growth and lung metastasis in vivo, while PDRG1 overexpression exerts opposite effects. Mechanistically, PDRG1 activates Wnt/β-catenin signaling, elevating levels of β-catenin, c-Myc, and phosphorylated GSK-3β, and the oncogenic effects of PDRG1 are reversed by the Wnt pathway inhibitor XAV939, confirming functional dependence on this pathway. Furthermore, the study identifies transcription factor Specificity Protein 1 (SP1) as an upstream regulator that binds directly to the PDRG1 promoter and activates its transcription, with rescue experiments confirming that SP1 exerts its pro-tumor effects through PDRG1.

A new review in Medicine Plus traces the evolution of mRNA lipid nanoparticles (mRNA-LNPs) from prophylactic vaccine vehicles to programmable therapeutic platforms. The authors detail clinical and preclinical progress across infectious disease, cancer, autoimmunity, rare genetic disease and tissue repair, while identifying key translational hurdles including extrahepatic targeting, repeat-dose immunogenicity, off-target editing risks, and scalable manufacturing.

People with lung cancer are more likely to have microplastics in their lungs and to have larger quantities of microplastics in their lungs, according to research that will be presented at the European Respiratory Society Congress in Barcelona, Spain. Researchers say their study adds to evidence that microplastics are entering our bodies via the air we breathe and suggests that there may be a link between microplastics and lung disease.

In two new studies, UCLA researchers used lab-grown brain organoids, donated human tissue and fused "assembloids" to investigate how radial glia — the stem cells that build the human cerebral cortex — decide which types of brain cells to make.

One study showed that how neural glia process nutrients helps determine which neurons they make. The other showed that physical contact from a neighboring region — the thalamus — drives the same cells to produce more of the neurons most expanded in the human brain.

Together, the findings recast radial glia's surroundings — its nutrients and physical connections — as active drivers of human brain development, offering new insight into how the cortex is built and how that process can go awry in neurodevelopmental disorders and cancer.

In a breakthrough study, researchers at The University of Texas MD Anderson Cancer Center discovered that psilocybin given before chemotherapy prevented the onset of nerve injury in preclinical models, even after repeated treatment cycles, which could help prevent pain, numbness and other common chemotherapy side effects.

New research reveals a promising new target for treating cancer by harnessing a type of molecule previously thought to do more harm than good.  

For decades, reactive oxygen species, or ROS, often called free radicals, have been viewed primarily as harmful molecules linked to aging, DNA damage and cancer. A new study co-led by Oregon Health & Science University finds that cancer-fighting T cells need small amounts of ROS to attack tumors.  

The investigators discovered that cancers exploit the T cell need for ROS by releasing an antioxidant protein that removes ROS from the tumor environment, effectively shutting down the attack by the immune system upon the cancer. 

Published today in the journal Science, the findings identify a previously unknown way tumors escape immune attack and point to a promising new target for cancer immunotherapy.