Lifeboat Foundation

One question for Brad Ringeisen, a chemist and executive director of the Innovative Genomics Institute. Founded by Nobel Prize-winning biochemist Jennifer Doudna, it aims to bridge revolutionary gene-editing tool development to affordable and accessible solutions in human health and climate.

Will CRISPR cure cancer?

We’re always thinking about: What are those targets in the future? Cancer is one of those things. The biggest impact is going to be what’s called systemic delivery, or in vivo delivery. There’s been one example of this in the community right now—to treat a liver disease. Intellia Therapeutics, a biotech company, has shown that you can actually intravenously apply CRISPR-Cas9 treatment. (CRISPR is the guide RNA, the targeting molecule, and Cas9 is the cutting molecule that edits DNA.) It can go to the liver and target the liver cells, and make edits at a high enough efficacy to treat genetic liver disease. The problem is that the liver is the easiest. It’s like the garbage can of the body. Pretty much anything that you put into the body is ultimately going to find its way to the liver. So that’s absolutely the easiest tissue to deliver to. But trying to deliver to a solid tumor, or to the brain, is much more difficult.

An artificial intelligence program may enable the first simple production of customizable proteins called zinc fingers to treat diseases by turning genes on and off.

The researchers at NYU Grossman School of Medicine and the University of Toronto who designed the tool say it promises to accelerate the development of gene therapies on a large scale.

Illnesses including cystic fibrosis, Tay-Sachs disease, and sickle cell anemia are caused by errors in the order of DNA letters that encode the operating instructions for every human cell. Scientists can in some cases correct these mistakes with gene editing methods that rearrange these letters.

An exploration of the structure of deoxyribonucleic acid, or DNA. If you want to learn more, join our free MITx #700x Introduction to Biology course (http://bit.ly/700xBio) or our #703x Genetics (https://bit.ly/GeneticsPart1) Also try #705x Biochemistry. (http://bit.ly/705xBiochem) or our advanced #728x Molecular Biology course (http://bit.ly/MITx7281x). Learn more about our work: http://web.mit.edu/mitxbio/courses.html.

This video was created for MITx 7.28.1x Molecular Biology: DNA Replication & Repair, offered on edX.

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Amount of toxin present in wheat, which is carcinogenic when heated, can be reduced and grown, new field study confirms Toast could soon be healthier after scientists grew a field of wheat genetically-edited to remove a cancer-causing chemical. Bread, when baked, produces a dangerous toxin called acrylamide, which is believed to be carcinogenic and when toasted is even more lethal.

CRISPR has started moving out of university research laboratories and into the world of human clinical trials.

We are about to see the emergence of a new medical technology, genetic vaccines.

Enhancers change rapidly during evolution, but the mechanisms by which new enhancers originate in the genome are mostly unknown. Not all regions of the genome evolve at the same rate and mutations are elevated at late DNA replication time. To understand the role played by mutational processes in enhancer evolution, we leveraged changes in mutation rates across the genome. By examining enhancer turnover in matched healthy and tumor samples in human individuals, we find while enhancers are most common in early replicating regions, new enhancers emerged more often at late replicating regions. Somatic mutations in cancer are consistently elevated in enhancers that have experienced turnover compared to those that are maintained. A similar relationship with DNA replication time is observed in enhancers across mammalian species and in multiple tissue-types. New enhancers appeared almost twice as often in late compared to early replicating regions, independent of transposable elements. We trained a deep learning model to show that new enhancers are enriched for mutations that modify transcription factor (TF) binding. New enhancers are also typically neutrally evolving, enriched in eQTLs, and are more tissue-specific than evolutionarily conserved enhancers. Accordingly, transcription factors that bind to these enhancers, inferred by their binding sequences, are also more recently evolved and more tissue-specific in gene expression. These results demonstrate a relationship between mutation rate, DNA replication time and enhancer evolution across multiple time scales, suggesting these observations are time-invariant principles of genome evolution.

The authors have declared no competing interest.

Genome-wide studies have identified 27 risk loci associated with attention-deficit hyperactivity disorder and shown its genetic link with other psychiatric conditions.

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When it comes to DNA, one pesky mosquito turns out to be a rebel among species.

Researchers at Rice University’s Center for Theoretical Biological Physics (CTBP) are among the pioneers of a new approach to studying DNA. Instead of focusing on chromosomes as linear sequences of genetic code, they’re looking for clues on how their folded 3D shapes might determine gene expression and regulation.

For most living things, their threadlike chromosomes fold to fit inside the nuclei of cells in one of two ways. But the chromosomes of the Aedes aegypti mosquito—which is responsible for the transmission of tropical diseases such as dengue, chikungunya, Zika, mayaro and yellow fever—defy this dichotomy, taking researchers at the CTBP by surprise.