By Inflame 
Stanford Medicine researchers have identified a genetic factor contributing to heart cell damage caused by the chemotherapy drug doxorubicin, offering hope for mitigating its toxic effects. While highly effective against cancer, doxorubicin can lead to severe heart complications, such as irregular rhythms, cell death, and even heart failure, limiting its long-term use.
Using a CRISPR-based genetic screening tool, the team pinpointed a gene, CA12, as a key player in heart toxicity. By targeting this gene, researchers found a way to protect heart cells. A drug called indisulam, currently under investigation as a cancer treatment, showed promising results in both lab-grown heart cells and mice, reducing doxorubicin-induced heart damage and preserving heart function.
This breakthrough not only sheds light on the genetic mechanisms of chemotherapy-related toxicity but also opens doors to broader applications of the screening tool in studying other diseases.