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Recently, researchers from Peking University in China published a research paper titled "Transfer of mitochondrial DNA into the nuclear genome during induced DNA breaks" in the journal Nature Communications. Hu Jiazhi's team used PEM-seq, a high-throughput sequencing method they had previously developed for systematic analysis of gene editing products, and found that mitochondrial DNA fragments may be inserted into the targeted site during nuclear genome editing. At the same time, targeted editing of mitochondrial DNA can also cause mitochondrial DNA instability, leading to its insertion into the nuclear genome.
Recently, researchers published a research paper titled "Engineered IscB-ωRNA system with improved base editing efficiency for disease correction via single AAV delivery in mice" in the journal Cell Reports. The study successfully engineered the IscB-ωRNA system, a transposon-related CRISPR ancestral system. The gene knockout and base editing efficiency of IscB-ωRNA were improved, and the feasibility of the optimized IscB-ωRNA system for gene editing therapy was verified in a mouse metabolic disease model. The optimized micro-IscB-ωRNA system can be delivered via a single adeno-associated virus (AAV) vector, and has great application potential in gene editing therapy.
Imagine if there was a technology that could directly modify our DNA to cure or prevent genetic diseases that are currently untreatable. This is no longer a plot in science fiction, but a reality with gene editing therapy. By precisely editing the genome, we can correct or eliminate problematic genes and provide long-lasting treatments for genetic diseases.
Pleural mesothelioma is a rare and highly malignant tumor that originates from mesothelial cells on the surface of the pleura and is often closely related to asbestos exposure. Although immunotherapy such as immune checkpoint inhibitors can improve the survival of patients to a certain extent, the overall efficacy is limited. The median overall survival of patients is only about 18 months, and the prognosis is not ideal. Therefore, it is urgent to further explore and develop new strategies for the treatment of pleural mesothelioma.
Programmed cell death 1 (PD-1) is the primary cancer drug target for immune checkpoint blockade (ICB). Since PD-1 receptor inhibition activates tumor-specific T cell immunity, researchers have mainly focused on the expression of PD-1 on T cells and its immunobiological characteristics. In contrast, researchers currently do not know what the mechanism behind the functional regulation of PD-1 in cancer cells is.
PARP inhibitors can improve the survival of breast cancer patients with BRAC1/2 mutations, but the drugs will eventually stop working and the cancer will recur. Recently, in a research report titled "FLT1 activation in cancer cells promotes PARP-inhibitor resistance in breast cancer" published in the international journal EMBO Molecular Medicine, scientists from Columbia University and other institutions discovered a new cancer drug that can prevent or slow the recurrence of cancer by studying cancer-bearing mice.
The selective metastasis of cancer cells to specific organs is a complex process that is influenced not only by anatomical factors but also by biological and organ-specific microenvironmental factors. The pre-metastatic niche refers to soluble factors and extracellular vesicles (EVs) produced by cells at the primary tumor site, which can modify the microenvironment of distant organs to accommodate migrating cancer cells and promote their growth. In addition, disseminated tumor cells (DTCs) can enter a dormant state in the circulation and in the new tissue environment, evade immune surveillance, and interact with the tissue microenvironment to awaken from dormancy. Finally, metastatic colonization requires multiple biological processes. These processes rely on the intrinsic properties of cancer cells and the permissive tumor microenvironment provided by cells in the target organ.
Recently, the team led by Professor Yilai Shu from the Affiliated Eye, Ear, Nose and Throat Hospital of Fudan University in China published a research paper titled "A base editor for the long-term restoration of auditory function in mice with recessive profound deafness" in the journal Nature Biomedical Engineering. The study used adenine base editor (ABE)-mediated gene editing therapy to effectively repair the Otof pathogenic mutation in the deaf mouse model and restore the expression level of otoferlin in 88% of the inner hair cells of the inner ear. At the same time, it improved the synaptic exocytosis function of the inner hair cells of the inner ear and restored hearing to a level close to the wild type for up to 1.5 years without obvious off-target effects. It is reported that this is the longest-observed effective result in the field of gene therapy for deafness in animal models to date.
Type I interferon (IFN-I) and IFN-γ can promote anti-tumor immunity by promoting the body's T cell response. Paradoxically, IFN-γ can promote T cell exhaustion by activating immune checkpoints, and the downstream regulatory mechanisms of these different responses are still unclear to researchers. Recently, in a research report entitled "Opposing tumor-cell-intrinsic and -extrinsic roles of the IRF1 transcription factor in antitumor immunity" published in the international journal Cell Reports, scientists from the David Geffen School of Medicine at the University of California and other institutions revealed the role and details of a special protein called interferon regulatory factor (IRF1) in cancer progression and response to therapy, which is expected to provide new insights to help improve the efficacy of cancer immunotherapy.
In a new study, researchers from the Institute of Biochemistry at the University of Kiel have found a way to inhibit the function of the cancer-causing protein MYC. This could be used to develop new drugs. The relevant research results were recently published in the journal Gut, with the title of the paper "Targeting MYC effector functions in pancreatic cancer by inhibiting the ATPase RUVBL1/2".
