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European Society of Cardiology

Clinical Articles, News & Views

Protecting hearts in oncology

The solution to the cardiotoxicity of cancer drugs may lie in the enzyme phosphoinositide 3-kinase gamma (PI3K(s)), according to research presented for the first time at the Heart Failure Association Winter Research Meeting in Les Diablerets, Switzerland.

The study used genetically modified mice expressing an inactive form of PI3K(s) to mimic the use of an enzyme inhibitor. When the mice were treated with the anthracycline doxorubicin, they survived more than normal mice and their heart function was completely preserved. Normal mice, who had the active form of PI3K(s), developed severe heart failure within two months of beginning treatment with doxorubicin.

To see if the findings could be applied to humans the next step was to treat normal nice with doxorubicin plus a drug to inhibit the activity of PI3K(s). The inhibitor was able to completely protect the mice from developing heart failure after doxorubicin treatment, according to the authors.

The same experiment was then performed on mice with breast cancer to ensure that the PI3K(s) inhibitor did not interfere with the anticancer activity of doxorubicin. Again the mice were treated with both doxorubicin and the PI3K(s) inhibitor.

First author Dr Alessandra Ghigo (University of Torino, Italy) said: “Cardiotoxicity of cancer drugs has become an increasing problem in the last decade due to the increasing success of anticancer therapy and aggressive use of these drugs. More people are now surviving cancer but it is estimated that 32% of them could die of heart disease caused by their treatment. This has led to a new field of medicine called cardio-oncology.”

“The PI3K(s) inhibitor protected the mice from developing heart failure. Importantly, the inhibitor was able to synergise with the doxorubicin and help to delay tumour growth. This means we could use an inhibitor of PI3K(s)  to both protect the heart from doxorubicin and prevent tumour growth. Our research shows that inhibiting PI3K(s) stops inflammation in the tumour and kills the tumour,” Dr Ghigo added.

She concluded: “The mechanisms underlying heart failure induced by anticancer therapies are different to those underlying heart failure from other causes such as hypertension. For this reason there are no effective drugs on the market to prevent this new kind of heart failure. Our study shows that PI3K(s) could be a novel way to prevent heart failure caused by cancer drugs while also helping to kill the tumour itself.”

Published on: February 25, 2015

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