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Scientists at Oak Ridge National Laboratory have used their expertise in quantum biology, artificial intelligence and bioengineering to improve how CRISPR Cas9 genome editing tools work on organisms like microbes that can be modified to produce renewable fuels and chemicals.
CRISPR is a powerful tool for bioengineering, used to modify genetic code to improve an organism’s performance or to correct mutations. The CRISPR Cas9 tool relies on a single, unique guide RNA that directs the Cas9 enzyme to bind with and cleave the corresponding targeted site in the genome.
Existing models to computationally predict effective guide RNAs for CRISPR tools were built on data from only a few model species, with weak, inconsistent efficiency when applied to microbes.
UCLA scientists have developed a new method to engineer more powerful immune cells that can potentially be used for “off-the-shelf” cell therapy to treat challenging cancers.
“Off-the-shelf” cell therapy, also known as allogenic therapy, uses immune cells derived from healthy donors instead of patients. The approach can bring cell therapies, like chimeric antigen receptor (CAR) T cell therapy, to more patients in a timelier manner, which is one of the major barriers in getting these life-saving treatments to patients.
“Time is often of the essence when it comes to treating people with advanced cancers,” said Lili Yang, associate professor of microbiology, immunology and molecular genetics and member of the UCLA Health Jonsson Comprehensive Cancer Center. “Currently, these types of therapies need to be tailored to the individual patient. We have to extract white blood cells from a patient, genetically engineer the cells and then re-infuse them back into the patient. This process can take weeks to months and can cost hundreds of thousands of dollars to treat each patient.”
Squamous cell lung cancer is a lung cancer subtype that is particularly difficult to treat. A new study now has revealed a novel genetic alteration that occurs in some cases in this type of tumor and that may expose a weakness of the tumor for therapeutic intervention.
The University of Cologne researchers led by Professor Roman Thomas, director of the Department of Translational Genomics, was able to show that a certain genetic change occurs during tumor formation and that a previously unknown oncogene is produced. Oncogenes are genes that promote the growth of tumors. In some cases, they can be inhibited by targeted drug treatments.
This approach is often accompanied by a higher success rate and lower side effects compared to conventional chemotherapy. The scientists’ discovery could therefore be a first step toward a more successful therapy of this particular type of cancer.
A susceptibility to gain weight may be written into molecular processes of human cells, a Washington State University study indicates.
The proof-of-concept study with a set of 22 twins found an epigenetic signature in buccal or cheek cells appearing only for the twins who were obese compared to their thinner siblings. With more research, the findings could lead to a simple cheek swab test for an obesity biomarker and enable earlier prevention methods for a condition that effects 50% of U.S. adults, the researchers said.
“Obesity appears to be more complex than simple consumption of food. Our work indicates there’s a susceptibility for this disease and molecular markers that are changing for it,” said Michael Skinner, a WSU professor of biology and corresponding author of the study published in the journal Epigenetics.
Equivalent to an 80-year-old human reverting to the age of 26.
A groundbreaking study into anti-aging has reported significant rejuvenation effects using exosomes, tiny particles which can be extracted from biological fluids such as blood plasma.
Old and young rat. Image generated by DALL·E 3
In recent years, the prospect of being able to halt or even reverse aging has begun to seem less like science fiction and more like a scientific milestone that could emerge in the relatively near future.
They look like storm clouds that could fit on the head of a pin: Organoids are three-dimensional cell cultures that play a key role in medical and clinical research. This is thanks to their ability to replicate tissue structures and organ functions in the petri dish. Scientists can use organoids to understand how diseases occur, how organs develop, and how drugs work.
Single-cell technologies allow researchers to drill down to the molecular level of the cells. With spatial transcriptomics, they can observe which genes in the organoids are active and where over time.
The miniature organs are usually derived from stem cells. These are cells that haven’t differentiated at all, or only minimally. They can become any kind of cell, such as heart or kidney cells, muscle cells, or neurons. To make stem cells differentiate, scientists “feed” them with growth factors and embed them in a nutrient solution.
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Engineered vesicular stomatitis virus (VSV) pseudotyping offers an essential method for exploring virus–cell interactions, particularly for viruses that require high biosafety levels. Although this approach has been employed effectively, the current methodologies for virus visualization and labeling can interfere with infectivity and lead to misinterpretation of results. In this study, we introduce an innovative approach combining genetic code expansion (GCE) and click chemistry with pseudotyped VSV to produce highly fluorescent and infectious pseudoviruses (clickVSVs). These clickVSVs enable robust and precise virus–cell interaction studies without compromising the biological function of the viral surface proteins. We evaluated this approach by generating VSVs bearing a unique chemical handle for click labeling and assessing the infectivity in relevant cell lines.
Epigenetics, the chemical mechanisms that controls the activity of genes, allows our cells, tissues and organs to adapt to the changing circumstances of the environment around us. This advantage can become a drawback, though, as this epigenetic regulation can be more easily altered by toxins than the more stable genetic sequence of the DNA.
An article recently published at Science with the collaboration of the groups of Dr. Manel Esteller, Director of the Josep Carreras Leukaemia Research Institute (IJC-CERCA), ICREA Research Professor and Chairman of Genetics at the University of Barcelona, and Dr. Lucas Pontel, Ramon y Cajal Fellow also of the Josep Carreras Institute, demonstrates that the substance called formaldehyde, commonly present in various household and cosmetic products, in polluted air, and widely used in construction, is a powerful modifier of normal epigenetic patterns.
The publication is led by Dr. Christopher J. Chang, of the University of California Berkeley in the United States, whose research group is pioneer in the study of the effects of various chemical products on cell metabolism. The research has focused on investigating the effects of high concentrations of formaldehyde in the body, a substance already been associated with an increased risk of developing cancer (nasopharyngeal tumours and leukaemia), hepatic degeneration due to fatty liver (steatosis) and asthma. Dr. Esteller points out that this is relevant because “formaldehyde enters our body mainly during our breathing and, because it dissolves well in an aqueous medium, it ends up reaching all the cells of our body”.
