ISTOCK, MELETIOSVERRASCRISPR doesn’t work very well in human cells whose DNA-damage response is working normally. Instead, the genome-editing method selects for cells with a faulty response—one tied to cancer, according to two studies published today (June 11) in Nature Medicine.
“It’s something we need to pay attention to, especially as CRISPR expands to more diseases,” Sam Kulkarni, the CEO of CRISPR Therapeutics, which was not involved with either study, tells STAT News. “We need to do the work and make sure edited cells returned to patients don’t become cancerous.”
In one study, researchers found that the inhibition of p53, which organizes a DNA damage response, made CRISPR more efficient in a human cell line. “However, inhibition of p53 leaves the cell transiently vulnerable to the introduction of chromosomal rearrangements and other tumorigenic mutations,” they write in their report. This means that the cells in which CRISPR worked may have a compromised p53 pathway, which would in turn make them vulnerable to becoming cancerous.
Separate experiments ...
