Jun 4 2024Washington State University Importantly, the researchers also found that inhibiting CDK7 could help enhance the medication's cancer-killing capability.
Doxorubicin remains the mainstay treatment for certain cancer types for which targeted therapies or other better treatments are not available." The researchers found that CDK7 activated CDK2, which set off the chain of molecular signals that eventually led to heart cell death. They also showed that mice that lacked the CDK7 gene were protected from doxorubicin-induced heart toxicity. Next, they used a CDK7 inhibitor drug known as THZ1 to block the protein's activity and examine the impact on heart health and cancer growth.
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