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WhileChimeric Antigen Receptor (CAR) T-celltherapy has achieved remarkable success in hematologic malignancies, this "living drug" has repeatedly hit a brick wall when confronting solid tumors. Worldwide, tens of millions of people are diagnosed each year with solid malignancies such as lung, gastric, and pancreatic cancers. Pancreatic cancer, for instance, has long stagnated at a 5-year survival rate of around 10%, while mortality rates for ovarian cancer remain grimly high. Within the dense microenvironment of these solid tumors, CAR-T cells face a dual dilemma: they fail to infiltrate, and even when they do manage to enter, they are rapidly rendered dysfunctional.
Recently, a study published in the Journal of Extracellular Vesicles unraveled a previously unknown intercellular communication axis spanning tumors, extracellular vesicles, and platelets. The researchers showed that tumor cells selectively package endogenousdouble-stranded RNA (dsRNA)into extracellular vesicles (EVs), which then activate the innate immune OAS–RNASEL pathway in blood platelets, triggering targeted degradation of ribosomal proteinmRNAs(RP mRNAs).
The clinical success ofchimeric antigen receptor (CAR) T-celltherapy highlights the need for scalable, non-invasive strategies to engineer T cells directly in vivo. AlthoughmRNA deliveryoffers a promising alternative,lipid nanoparticle-based carriersgenerally exhibit limited T-cell transfection efficiency in vivo and often require antibody conjugation.
Evolution is constantly writing new biological innovations within genomes. Exploring this vast design space holds the potential to unlock transformative biotechnology functions; however, even the simplest genomes are immensely complex, where a single nucleotide mutation can render an organism non-viable. Consequently, most advances in biological engineering have remained restricted to individual genes or genetic circuits, while whole-genome-scale de novo design has long been deemed an elusive goal.
Pathological myocardial hypertrophy serves as a critical harbinger of heart failure (HF) and can be triggered by external stimuli such as pressure overload or heightened sympathetic nervous activity. Although liquid-liquid phase separation (LLPS) represents a fundamental cellular stress-response mechanism implicated in diverse disease etiologies, its precise role in heart failure has remained elusive. Of particular interest are paraspeckles—membrane-less nuclear organelles formed via LLPS driven by the long non-coding RNA Neat1.
CRISPR-Cas9serves as the ultimate "Swiss Army knife" ofgenome editing, yet it suffers from a fundamental flaw: it cleaves both strands of the DNA double helix. While double-strand breaks (DSBs) efficiently trigger repair mechanisms, they also unleash a cascade of adverse side effects, including insertion-deletion mutations (indels), chromosomal translocations, large genomic deletions, andoff-targetcleavage. While such unintended genomic events might be tolerable in basic research, they pose severe safety hazards in human gene and cell therapies.
Personalized messenger RNA (mRNA) neoantigen vaccines hold immense potential in cancer immunotherapy. However, their customized manufacturing pipeline typically spans more than three months, which risks missing the optimal therapeutic window for patients. The primary bottleneck causing this delay is that current mRNA vaccine production relies heavily on plasmid fermentation andin vitro transcription (IVT), involving numerous complex steps.
Virus-like particles (VLPs)hold great promise for delivering genome editors; however, VLP-mediated cytosine base editing in vivo has historically suffered from limited efficacy.
Researchers at Weill Cornell Medicine, Cedars-Sinai Medical Center, and Roswell Park Comprehensive Cancer Center have engineered specializedCAR-T cellscapable of specifically targeting and destroying bladder cancer cells. Published in the Journal of Experimental Medicine (JEM), the study demonstrates that delivering these CAR-T cells directly into the bladder via a catheter effectively controls bladder tumors in mice, raising hopes for a similar therapeutic approach in human clinical settings.
Cancer metastasis remains the leading cause of cancer-related mortality worldwide, and metastasizing cancer cells often exhibit physical properties markedly different from those of healthy cells. Recent studies have revealed that metastatic cancer cells are generally softer and more deformable than normal cells. This "softness" is no coincidence—it allows cancer cells to squeeze through blood vessel walls and establish secondary tumors in distant tissues. However, this biomechanical flexibility comes with a crucial side effect: it makes it difficult for natural killer (NK) cells and cytotoxic T lymphocytes (CTLs) within the immune system to effectively engage and attack them. According to World Health Organization estimates, breast cancer ranks as the most commonly diagnosed malignancy among women globally, with approximately 2.3 million new cases in 2022, while the 5-year survival rate for metastatic breast cancer patients remains below 30%.
