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Breast Cancer Drug Curbs Heart Disease.

aking trastuzumab should consider any treatment change, Spector said. However, it may be important to conduct well-controlled clinical trials to answer this question.

In addition to its association with breast cancer, HER2 is also essential for the early development and later sustenance of heart muscle cells. It appears that trastuzumabs mechanism for blocking HER2 is different.

We found that lapatinib activates a critical pathway that protects heart cells from committing suicide as a result of stress, Spector continued. Heart muscle cells require a tremendous amount of energy to function properly and are therefore extremely sensitive to energy deprivation as a consequence of reduced oxygen or nutrient supply. In addition, heart muscle cells appear to be sensitive to the death promoting effects of inflammation.

Our experiments in isolated human heart muscle cells indicate that lapatinib activates a pathway that protects cardiac muscle cells from the death-promoting effects of mediators of inflammation, which are activated in cancer patients, particularly those who have received chemotherapies that damage heart tissue, Spector said. In contrast, trastuzumab does not activate this protective pathway.

With clinical trials currently investigating the combination of lapatinib with trastuzumab, there is a possibility that the effects of lapatinib in cardiac muscle cells might protect the heart against potential toxicity associated with trastuzumab, Spector added.

More broadly, Spector said that these findings of how lapatinib bestows cardiovascular protection during times of stress whether from chemotherapy or heart muscle cells deprived of oxygen during a heart attack -- could be used in other situations.

Using this system, we could theoretically screen drugs that are in the development phase to see what their effects may be on heart muscle cells, Spector said. We may be able to select the drug candidates
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