• Adenovirus Service • AAV Service • Lentivirus Service • Retrovirus Service
The homologous recombination (HR) pathway repairs DNA damage, such as double-strand breaks (DSBs), by copying sequence information from a homologous donor DNA template (typically the sister chromatid) to the damaged site. During HR in mammals, the RAD51 (radiation-sensitive protein 51) recombinase forms a nucleoprotein filament around the resected single-stranded DNA (ssDNA) generated during DSB end processing at the DSB site, known as the presynaptic filament. Subsequently, the presynaptic filament scans the genome for a suitable homologous DNA donor through a process called homology search. However, how this homology search occurs in the context of the three-dimensional (3D) genome remains largely unexplored.
In a new study, scientists from the Max Planck Institute for Evolutionary Anthropology analyzed the effects of over 2,000 clinically approved drugs on DNA repair and CRISPR genome editing outcomes. They discovered compounds that could be used to improve genome editing, molecules that can selectively kill cultured cancer cells, and further identified two proteins with novel functions in DNA repair.
During the global COVID-19 pandemic, mRNA vaccines gained worldwide recognition for their high efficiency and safety, showcasing the tremendous potential of mRNA technology. However, the applications of mRNA extend far beyond vaccines. In treating complex diseases like cancer, precisely delivering drugs to diseased cells while avoiding damage to healthy tissues has long been a major challenge in the medical field. Currently, although technologies like lipid nanoparticles (LNP) are widely used for mRNA delivery, their targeting capabilities remain limited, often leading to drug accumulation in non-target organs like the liver, causing potential side effects.
If breast cancer poses a significant threat to women's health, then triple-negative breast cancer (TNBC) is the most cunning and stubborn type among them. It grows rapidly, is prone to early metastasis, and more problematically, it lacks estrogen receptors, progesterone receptors, and HER2 protein-these three targets are the "sights" for many effective anti-cancer drugs. Therefore, TNBC has limited treatment options, chemotherapy remains the primary approach, and it easily develops drug resistance, often returning more aggressively after recurrence.
Artificial intelligence (AI) is driving advancements in genome editing, from predictive modeling to generative design. Emerging generative AI tools such as RFdiffusion, AlphaFold 3, and ESM now facilitate the de novo design of linkers, inhibitors, and enzymes. Recently, a commentary article titled "Expansion of artificial intelligence for genome editing" published in Nature Structural & Molecular Biology reviewed the recent work by Lu et al., who utilized AI to improve the precision of mitochondrial cytosine base editors.
The potential of mRNA therapy in vaccines, immunotherapy, protein replacement therapy, and gene editing has been clinically validated. However, the precise delivery of mRNA to target cells remains a critical bottleneck limiting its efficacy and safety. Recently, a team from Ghent University in Belgium published a study titled "Cell-specific mRNA delivery via nanobody-functionalized lipid nanoparticles" in the Journal of Controlled Release, proposing a novel lipid nanoparticle (mRNA-LNP) solution. This approach targets aminopeptidase N (APN) on the surface of intestinal epithelial cells using nanobody-functionalized LNPs, addressing both the issue of cell-specific mRNA delivery and overcoming the intestinal epithelial barrier.
Tumor cells exhibit remarkable adaptive capabilities under therapeutic pressure, a phenomenon scientifically termed cellular plasticity. Without relying on genetic mutations, they can alter their differentiation states to evade drug attacks and regain vitality. This survival strategy appears prominently in colorectal cancer treatment. Combined KRAS and EGFR inhibitor therapy has been regarded as a key approach to combat KRAS-mutant colorectal cancer. However, tumor cells still develop escape mechanisms to resist this dual suppression.
From CRISPR-Cas9 to prime editing, gene therapy has become increasingly precise. However, this precision has also introduced a paradox of "excessive specificity": to treat over 200,000 different pathogenic mutations, we would need to develop thousands of distinct drugs, a nearly insurmountable cost. Is there a universal strategy that could treat thousands of different genetic diseases with just one "drug component"?
Chimeric antigen receptor (CAR)-T cell therapy has revolutionized the treatment landscape for patients with hematological malignancies. However, its widespread application remains constrained by labor-intensive manufacturing processes, limited production capacity, and inconsistent clinical efficacy. In vivo CAR-T cell engineering, which generates CAR-T cells directly within the patient's body, eliminates the need for ex vivo cell processing and complex logistics while enhancing clinical outcomes, thereby addressing these challenges.
Recently, researchers have successfully developed an innovative big data platform called the "Cancer Immunology Data Engine (CIDE)." This platform integrates clinical outcomes from 5,957 cancer patients worldwide who received immunotherapy, covering a comprehensive multi-omics dataset of 17 cancer types and containing 8,575 tumor samples. The study has been published in the journal Cell.
