New Molecule Prevents Heart Disease Caused By Toxic Breast Cancer Drugs

New Molecule Prevents Heart Disease Caused By Toxic Breast Cancer Drugs

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According to Dr. Patrizio Lancellotti, professor and chair of the ESC EACVI/HFA Cardiac Oncology Toxicity Registry, patients with some types of breast cancer have greater odds of dying because of heart disease instead of cancer.

Dr. Alessandra Ghigo, a research fellow in the Department of Molecular Biotechnology and Health Sciences at University of Torino in Italy and first author of a new paper on Cardio-Oncology added, “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 percent of them could die of heart disease caused by their treatment. This has led to a new field of medicine called cardio-oncology.”

There are several treatments for breast cancer, including the chemotherapeutic drugs doxorubicin and trastuzumab (perception), which contain anthracyclines — substances that are extremely toxic to the heart. “Radiation therapy can make anthracyclines even more cardiotoxic, as can the sequence of anthracylines followed by trastuzumab. The latter combination for metastatic breast cancer can cause severe heart failure in up to 27% of patients,” Dr. Lancellotti explained.

“Not beyond us” was the theme for World Cancer Day 2015, and new research outcomes were presented during the Heart Failure Winter Research Meeting, demonstrating solutions for cancer drugs’ cardiotoxicity.

Dr. Ghigo’s research focused on the enzyme phosphoinositide 3-kinase gamma (PI3K gamma) that regulates heart function, demonstrating that mice with hypertension were protected from heart failure through inhibition of  PI3K gamma’s activity. In this specific study, Dr. Ghigo used mice expressing an inactive form of PI3Kgamma to simulate an enzyme inhibitor. Researchers observed that mice treated with anthracycline doxorubicin survived longer when compared to normal mice, and their heart function was fully preserved. Mice with an active form of PI3K gamma had severe heart failure after 2 months of doxorubicin treatment.

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Dr. Ghigo added: “The PI3K? 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? to both protect the heart from doxorubicin and prevent tumour growth. Our research shows that inhibiting PI3K? stops inflammation in the tumour and kills the tumour.”

The researcher explained that one of the main issues concerning the cardiotoxicity caused by chemotherapy is linked to the fact that anticancer regimens require adjustment; this means that lower doses of agents might be required to prevent cardiotoxicity or, in more extreme situations, treatment cessation. Using PI3K gamma inhibitors combined with chemotherapy drugs provides a wider and safer use of anticancer therapies, as one can bypass the need to lower therapeutic dosages or treatment modification.

Dr. Ghigo 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? could be a novel way to prevent heart failure caused by cancer drugs while also helping to kill the tumour itself.”

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