#crispr

#crispr

The groundbreaking clinical trial, described on 31 October in the American Journal of Human Genetics, will deploy an offshoot of the CRISPR-Cas9 gene-editing technique called base editing, which allows scientists to make precise, single-letter changes to DNA sequences. The study is expected to begin next year, after its organizers spent months negotiating with US regulators over ways to simplify the convoluted path a gene-editing therapy normally has to take before it can enter trials.

Do you think we should genetically modify wildlife? What if we could make seabirds resistant to the flu that has been exterminating them en masse, just by tweaking their DNA a smidgen? Or make fish that can shrug off pollution, or coral that can survive warming waters? Engineer in the sorts of change that could occur naturally, given enough time, if only the wildlife would stop dying already. Thanks to newly emerging methods, such as Crispr, these feats are within reach.

Doctors predicted Wayne Frederick, the president of Howard University, wouldn't live past 8. Now he's 54. Frederick came to the U.S. from Trinidad and Tobago with a dream of finding a cure for his disease, sickle cell anemia, but detoured into higher ed administration. At an event hosted by the American Council on Education at Howard University this week, Frederick said CRISPR gene editing, a technology developed in academia, made his dream a reality.

Known by scientists as 'parthenogenesis', this natural form of asexual reproduction lets healthy offspring develop from a female's unfertilised eggs. Only last month, a female lizard at a zoo near Birmingham gave birth to eight hatchlings, despite never having been in contact with a male. But virgin births have already occurred in a wide range of animals such as sharks, snakes, crocodiles, crustaceans, scorpions and wasps.

CRISPR screening is extremely effective at finding important factors in obesity and metabolism that could become therapeutic targets, showcasing the potential of microproteins.

The MYC oncogene drives tumor growth and resistance in over half of human cancers. MYC inhibitors like MYCi975 show promise in pre-clinical trials.

Large-scale genome-wide association studies have identified many complex trait loci related to autoimmune, metabolic, and infectious diseases, yet assigning function to non-coding variants remains challenging.

CRISPR offers more control than viral carriers do, but typically requires the cutting of DNA - raising the chances of unwanted mutations and incomplete repair.