Overview
- The team at Wageningen University & Research and Van Andel Institute, in a Nature paper on Wednesday, showed that ThermoCas9 cut DNA in cultured tumor cells but left healthy cells untouched.
- ThermoCas9 reads a short DNA tag called a PAM that overlaps a common human methylation site, and a methyl group at that spot blocks the enzyme from latching on and prevents cutting.
- The authors report this is the first CRISPR enzyme shown to respond to the most abundant type of DNA methylation in human cells, enabling targeting based on a chemical mark rather than a letter change in DNA.
- The study did not show tumor cell death or effects in animals, and the next step is to raise DNA damage in tumor cells enough to trigger killing while assessing delivery and safety.
- Because many diseases alter methylation patterns, the approach could one day help flag other diseased cells such as in some childhood cancers or autoimmune disorders if future studies bear it out.