The incredible reason your heart never develops cancer

The heart is the only organ that appears to be largely protected from cancer – and until recently scientists were unsure why.
Now not only do they think they have the answer, their findings could pave the way for radical new treatments for a wide range of cancers – including applying external pressure to tumour cells to stop them growing.
Primary cancer of the heart (where the tumour develops in heart tissue, rather than spreading there from elsewhere) is so rare it’s thought to affect only 0.02 per cent of the UK population.
Even then, the majority of those tumours – up to 90 per cent – are benign, meaning they are highly unlikely to spread to other organs or tissue (they can still be fatal if they grow so big they block blood flow).
But what is it that protects the heart against a disease that can so easily infiltrate all other tissues?
It’s long been known that the heart lacks one of the key characteristics that makes other major organs susceptible to cancer – frequent cell division.
Cells in most of our tissues and organs are constantly dividing in order to replace old or damaged ones. And the more they divide, the greater the risk of DNA errors – or mutations – that can lead to cancer.
The constant battering from the heart’s pumping action stops tumour cells growing before they get a chance to become established
However, heart muscle cells – or cardiomyocytes – mostly stop dividing shortly after birth and instead grow in size as we move into adulthood.
‘Dying heart cells are not replaced – unlike the lining of the bowel, for example, which reproduces every five to ten days, which is one of the reasons why bowel cancer is very common,’ explains Dr Klaus Witte, a consultant cardiologist at the Leeds Institute of Cardiovascular and Metabolic Medicine.
But now scientists at the University of Trieste in Italy have found another possible reason why heart cancer is so rare.
Their research suggests that cancer cells simply cannot survive the huge mechanical force that rains down on them in an organ that contracts and expands up to 100,000 times a day.
The constant battering from the heart’s pumping action stops tumour cells growing before they get a chance to become established.
To test the theory, the team in Trieste injected human cancer cells into mice with hearts genetically engineered to pump at a fraction of the normal rate.
The results, recently published in the journal Science, showed that when the heart’s mechanical load – or pumping rate – was dialled right down, cancer cells started to proliferate. When the heart worked normally, they died off again.
But it’s not simply a question of cancer cells being ‘squashed’ in this way.
The pumping action appears to turn on another mechanism
within any cancer cells that do develop in the heart that stops them proliferating.
It stimulates the production of a protein called Nesprin-2, which transmits a signal to the nucleus of a cancer cell, telling it to stop reproducing as the environment is not suitable. But when the heart stopped pumping – or pumped at a much lower rate – this protein was not produced.
Research leader Serena Zacchigna, a professor of molecular biology, said: ‘This suggests the cardiac environment is unfavourable to tumour cells, partly because its continuous mechanical activity physically limits their expansion.’
Now the team are investigating the development of a wearable medical device to treat other cancers – such as skin or breast cancers – by exerting a similar mechanical load on the tumour site to try to suppress malignant cell growth.
Other teams are also focusing on the idea of using external pressure to treat tumours – a field known as mechanotherapy.
Researchers at the University of Galway recently carried out a study where they used AI to study what happens to cancer cells when put under external pressure from being squashed by surrounding tissue.
Results published in the Proceedings of the National Academy of Sciences earlier this year revealed the pressure stops the tumour cell from drawing in the water it needs to grow to a size where it can then split in two – halting proliferation.
Dr Eoin McEvoy, an associate professor of biomedical engineering who was involved in the study, said while applying external pressure to tumours might halt cell growth by activating certain proteins, it comes with risks.
He told Good Health: ‘It’s possible that external compression of, for example, a malignant melanoma [the most dangerous type of skin cancer] could slow down growth but it’s also widely reported that compression of tumours in certain tissues can actually encourage cancer cells to spread. It’s a double-edged sword.’
Instead, the Galway team suggest a better option is to develop drugs designed to act on proteins, such as Nesprin-2, and make cancer cells susceptible to lower levels of pressure in the body, preventing them from growing and dividing.
Commenting on this new heart-led approach to cancer, Dr Witte said: ‘This is a very interesting concept. It’s possible that some kind of wearable device could exert enough force on cancer cells to stop them growing, or that there’s a way to produce proteins – such as Nesprin-2 – that tells the cancer cell this is not a suitable environment for it be in.’
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