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Chimeric antigen receptor (CAR) T cell therapy is a promising cancer treatment, but how to enhance its efficacy has always been a mystery. Recently, in a research report titled "Cullin-5 deficiency promotes chimeric antigen receptor T cell effector functions potentially via the modulation of JAK/STAT signaling pathway" published in the international journal Nature Communications, researchers from Nagoya University and other institutions in Japan have discovered a way to improve the effectiveness of this potential cancer therapy. By modifying a specific gene, the ability of immune cells to fight cancer can be enhanced for a long time, which may reduce the chance of cancer recurrence.
In the field of cancer treatment, proteolysis targeting chimeras (PROTACs) are gradually emerging as a new generation of drugs. This type of drug can accurately target and degrade proteins closely related to cancer growth, bringing hope for conquering those "undruggable" targets that are difficult to deal with with traditional drugs, and also opening up new treatment pathways for many diseases that have no effective treatment options. However, the intracellular transport mechanism of PROTACs, especially what factors affect its therapeutic effect in cancer cells, has always been a mystery that researchers are eager to solve.
In the field of medical research, ACE2 has attracted much attention as a receptor for SARS-CoV-2. It is also of great significance during pregnancy. The circulating level of ACE2 in pregnant women is higher than that in non-pregnant women, and the expression and genetic variation of ACE2 are closely related to various pregnancy diseases such as preeclampsia and fetal growth restriction. Recently, a research article titled "Genetically edited human placental organoids cast new light on the role of ACE2" published in Cell Death Dis constructed a placental organoid model through gene editing technology, and deeply explored the mechanism of action of ACE2 in placental development.
In 2010, Sonia Vallabh witnessed her 52-year-old mother develop a rapidly progressive, mysterious, and undiagnosed dementia, and soon died from it. A year later, she learned that her mother had a hereditary prion disease, fatal familial insomnia. After undergoing genetic testing, Sonia learned that she also carried the disease-causing gene mutation, which meant that she herself was likely to suffer from this prion disease. More importantly, this fatal disease usually develops around the age of 50 and quickly leads to death, and there is no cure.
Dysfunction of DNA repair is a key driver of cancer. Understanding the molecular mechanisms behind dysfunctional DNA repair in cancer cells is crucial for the occurrence of cancer and the development of new therapies. Recently, in a research report titled "EZH2 directly methylates PARP1 and regulates its activity in cancer" published in the international journal Science Advances, scientists from Northwestern University and other institutions discovered a new molecular mechanism behind dysfunctional DNA repair in prostate cancer cells through research. This research finding is expected to guide scientists to develop new targeted therapies to treat prostate cancer patients who are resistant to current standard therapies.
CRISPR-Cas9 has long been likened to a pair of genetic scissors because of its ability to elegantly and precisely snip any desired DNA fragment. But it turns out that the CRISPR system has more than just one strategy in its toolbox. CRISPR is a mechanism originally discovered in bacteria, and it has been operating for centuries as an adaptive immune system. Certain single-celled organisms naturally use CRISPR to protect themselves from viruses (called bacteriophages) and other foreign genetic fragments.
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.
