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Breast cancer research in 2016 – what did we learn?

Understanding risks

We know the causes of breast cancer are a complex mix of our genetics, our lifestyle and the environment, and in 2016 some more of that complexity was pulled apart.

Firstly, the Breast Cancer Now Generations Study released two major papers looking at the evidence linking breast cancer to stress and to Hormone Replacement Therapy (HRT).

The researchers found that for combined HRT (that’s version that contain oestrogen and a progestogen) the risk of breast cancer may be higher than previously thought. Some women may find this useful when considering taking HRT, but for all women who are on or considering HRT we would recommend that anyone with concerns about HRT talks about the risks and benefits with their doctors.

The Generations Study also showed that there is unlikely to be a link between stress and breast cancer, specifically day-to-day psychological stress and adverse life events like a loss in the family.

Outside of the Generations Study, a huge review of evidence on working night shifts and breast cancer found that shift-work is unlikely to increase breast cancer risk.

Completing our gene directory

Moving from external factors to genes inside of breast cancer, this year we hit a milestone when researchers announced that we may now have a definitive list of the genes that can go wrong and cause cancer to develop – the most complete map of the breast cancer landscape to date.

Researchers led by Professor Sir Mike Stratton at the Sanger Institute in Cambridge found that 93 genes contain the vast majority, if not all, of mutations that occur in breast cancer. Having this list will help direct research into new treatments that target those mutated genes and help us learn more about the causes of breast cancer.

Giving hormone-driven cancer a harder time

Some of those mutations will cause the 80% of breast cancer cases that are driven to grow by hormones, and Breast Cancer Now scientists led by Dr Lesley-Ann Martin want to know how to better treat those cancers. This year they found that cancers which normally depend on hormones to grow could instead be switching their “fuel source” to molecules made from cholesterol to avoid the effects of anti-hormone treatment. This finding raises the possibility that statins, drugs that lower cholesterol in the blood, could be used to treat breast cancer, but more research is needed to explore this.

In other big news for hormone-driven breast cancer, trial results this year suggested that taking aromatase inhibitors for ten years rather than five could help reduce the chances of a breast cancer recurrence. Whilst this is important, we still need to see evidence on how this ten-year course affects survival and quality of life.

Turning the tide on triple negative

There was also some positive news on tackling triple negative breast cancer this year, as Dr Alan McIntyre and colleagues in Nottingham found a potential new approach to stop it spreading. The team discovered that when starved of oxygen (as often happens in rapidly growing tumours) breast cancers can undergo a molecular change that helps them spread – but also makes them susceptible to a drug called JQ1.

Currently, a group of drugs similar to JQ1 are being investigated in clinical trials for use in several different types of cancer. If these trials are successful, and with the added weight of Dr McIntyre’s lab findings, clinical trials of JQ1 for triple negative breast cancer could begin in a few years.

Another type of drug that’s already being trialled for other cancers are PIM-inhibitors. Results published by Breast Cancer Now-funded scientists only a few months ago showed that these could be used to push triple negative breast cancer cells – but not normal cells – closer to the ‘cliff-edge of death’. This is an exciting prospect for a group of breast cancers that are badly in need of targeted treatments – clinical trials to investigate whether PIM-inhibitors could be effective for people triple negative breast cancer could start in the next couple of years.

Stifling secondary breast cancer

This year our scientists have had a number of successes in finding out how breast cancer manages to spread from the breast and how it manages to grow in other sites in the body.

Professor Clare Isacke’s team at our Research Centre identified two ways that non-cancer cells might help breast cancer spread. First, she revealed how breast tumours “radicalise” surrounding cells called fibroblasts to help them spread, and secondly, how cells that wrap around blood vessels are convinced to help breast cancer cells enter the bloodstream in order to spread around the body.

These discoveries could lead to tests that better predict a woman’s risk of their disease spreading, and so who might need more intensive treatment. Furthermore, while this is early research, this could direct the development of new drugs that stop the spread of breast cancer in its tracks.

Another new approach for stopping secondary breast was suggested by Dr Andy Reynolds, who released papers this year showing how secondary tumours from breast and other cancers get their blood supply – by piggy-backing on patients’ existing blood vessels, instead of always growing their own as was previously thought.

This finding not only gives us a new approach to starve secondary breast cancer but reveals why some drugs that stop the growth of new blood vessels haven’t worked as well as hoped, and how we could combine those drugs with new ones to get better results for patients.

Roll on 2017

It may have been a turbulent year in the celebrity and political world, but for breast cancer research, 2016 has been a great year of steady progress. We’re looking forward to 2017 and the discoveries that will bring closer the day when everyone survives breast cancer.

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