Tumour drug may prevent infertility caused by chemotherapy

A drug used to slow tumour growth may also prevent infertility caused by standard chemotherapy used for breast cancer treatment, according to a study.

The study, conducted on mice, found that the drug everolimus protects ovaries from cyclophosphamide — a chemotherapy used often against breast cancer but known to deplete the supply of egg cells needed to achieve pregnancy.

Female mice treated with everolimus, along with chemotherapy, were found to have more than twice as many offspring afterward as mice treated with the chemotherapy alone.

Such strong results with an available drug may speed the process of applying for permission to test it in premenopausal cancer patients, the researchers said.

“Our results argue that everolimus may represent a fertility-sparing drug treatment to complement the freezing of eggs and embryos, which are valued methods, but time-consuming, costly, less effective with age and not protective of long-term ovarian function,” said lead author Kara Goldman, reproductive endocrinologist at New York University-Langone.

For the study, published in the Proceedings of the National Academy of Sciences, female mice were treated with cyclophosphamide weekly and then randomised to also receive either everolimus, an experimental drug called INK128 against several cancer types, or nothing.

Everolimus and INK128 block the action of the enzyme mTOR, which is part of signalling mechanisms that encourage cell growth.
Thus, everolimus is already approved to slow tumour growth in some forms of kidney cancer and breast cancer, but in a different way than chemotherapies.

The results showed that mice treated with chemotherapy combined with either mTOR inhibitor had more mouse pups on average, than mice treated with chemotherapy alone.

In addition, mice treated with cyclophosphamide alone saw a 64 per cent reduction in their numbers of primordial follicles when compared to control mice, a pattern reversed by mTOR inhibitors.

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Key proteins regulating heart's electrical communication found

Researchers at Cedars-Sinai Heart Institute in Los Angeles have found that six proteins - five more than previously thought - regulate the rapid flow of electrical communication signals, coordinating heart cells to produce a stable heartbeat.

The smallest of these proteins directs the largest in performing its role of coordinating billions of heart cells during each heartbeat.

Together, the proteins synchronise the beating heart, the researchers claimed.

"The findings advance our understanding of cell-to-cell communication at the root of healthy heart function. When there is less cell communication, which occurs in failing hearts, chances are greater of disturbances in heart rhythm that can result in disability or death," said Robin Shaw, senior author of the study.

Till date, scientists had recognised just one protein involved in cell-to-cell communication that occurs through conduits known as 'gap junctions', said the study.

"The finding adds startling diversity to a key biological process whereby, heart cells communicate with each other electrically," said Eduardo Marbán, director of the Cedars-Sinai Heart Institute.

"The implications are major for arrhythmias and heart failure," he added.

The researchers have also determined that a class of drugs known as 'mTOR inhibitors' - those already used for immunosuppression in organ transplants - can be used to prevent erratic and sometimes fatal heart rhythms.

A properly beating heart is necessary to pump blood to the brain, lungs and other organs.

Cell-to-cell communication occurs in all other organs. The same proteins that help heart cells communicate also play a role in brain function, bone development and insulin production in the pancreas, the study said.

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