刚快速看了一下Nature medicine今天发的这篇文章，文章主要说的观点是CRISPR/Cas引起的DNA双链断裂（DSB）会导致p53通路激活，从而引发暂时的细胞生长抑制，进而降低同源重组效率。作者建议，如果要增加同源重组效率，可以考虑抑制DNA修复通路，但这杨会增加致癌风险。文章并没有说CRISPR会致癌，媒体明显解读不当，看看市场怎么消化吧。

"We report here that genome editing by Cas9 in p53-proficient cells results in a DNA damage response, which causes a growth disadvantage/arrest, and decreases efficiency of precision genome editing. The observed effect is dependent on p53, its direct target p21 and on pRB, which mediates the G1 cell cycle arrest in response to p21. "

“Our results show that inhibiting DNA damage signaling can improve the efficiency of precision genome editing in normal, untransformed cells. However, inhibition of p53 leaves the cell transiently vulnerable to the introduction of chromosomal rearrangements and other tumorigenic mutations.”

$CRISPR Therapeutics AG(CRSP)$ $Editas Medicine, Inc.(EDIT)$ $Intellia Therapeutics, Inc.(NTLA)$