https://www.sciencedaily.com/releases/2021/11/211111080332.htm

"Our study shows that in many different cell types, CRISPR gene-editing can confer a selective advantage to cells harboring mutations in genes associated with cancer, such as p53 and KRAS," says co-senior author Ani Deshpande, Ph.D., an assistant professor in the NCI-Designated Cancer Center at Sanford Burnham Prebys. "We have shown that when CRISPR-Cas9 is used to edit the genome, cells with cancer-associated mutations are likely to be selected to survive -- and this is more widespread than scientists previously understood."

CRISPR-Cas9 works by creating double-stranded DNA breaks at specific points in a DNA sequence, allowing scientists to target and edit specific genes. However, the p53 gene responds to double-stranded breaks by arresting cell growth, meaning that cells that have undergone CRISPR would grow and divide less effectively. This means that cells with mutations in the p53 gene can continue to grow and divide normally, giving them a competitive advantage.