Whenever someone makes some claim or other about ‘curing cancer’, your bullshit-filters should be set to maximum. Few maladies in modern times attract so many conspiracy theories, quack claims, charlatanry and outright bullshit as cancer. Whether it’s nutters raving that it’s all a Big Pharma con, or a snake-oil salesman-cum-stoner mumbling that weed, like, totally cures cancer, man, the horse-dookey is as high as an elephant’s eye.
For the a patient cured is a patient lost to Big Pharma! conspiracy theorists, it’s worth pointing out that death rates from cancers have plummeted in the last half-century. If Big Pharma are trying to stop people surviving cancers, they’re doing a shit job at it. As for the ‘X cures cancer’ hucksters, recall that ‘cancer’ isn’t a single disease with a single cure: it’s a class of many different diseases, with different treatments. Some with remarkable survival probabilities, others much less so.
But a recent study makes a remarkable claim that isn’t ‘curing cancer’. Instead, it’s that a simple and extremely common drug may be able to stop cancers spreading. Metastasis, as it’s called, is when some type of cancers rapidly spread from their original site, and set new cancers sprouting elsewhere in the body.
If doctors could stop that dreadful process, survival rates from many cancers could possibly vastly improve.
Scientists have uncovered the mechanism behind how aspirin could reduce the metastasis of some cancers by stimulating the immune system, in a new study primarily funded by the Medical Research Council.
In the study, published in Nature, the scientists say that discovering the mechanism will support ongoing clinical trials, and could lead to the targeted use of aspirin to prevent the spread of susceptible types of cancer, and to the development of more effective drugs to prevent cancer metastasis.
For all its ubiquity, of course, aspirin is not without side effects. Nothing is. For most people, the risks from taking the occasional aspirin are extremely low. But for others, and for prolonged usage, the risks can be much higher.
The scientists caution that, in some people, aspirin can have serious side-effects and clinical trials are underway to determine how to use it safely and effectively to prevent cancer spread, so people should consult their doctor before starting to take it.
That aspirin can reduce the spread of some cancers has been known for a while. What was missing was a mechanism for how it worked. The new study may have found it.
In this study, led by researchers at the University of Cambridge, the scientists say their discovery of how aspirin reduces cancer metastasis was serendipitous.
They were investigating the process of metastasis, because, while cancer starts out in one location, 90 per cent of cancer deaths occur when cancer spreads to other parts of the body.
The scientists wanted to better understand how the immune system responds to metastasis, because when individual cancer cells break away from their originating tumour and spread to another part of the body they are particularly vulnerable to immune attack. The immune system can recognise and kill these lone cancer cells more effectively than cancer cells within larger originating tumours, which have often developed an environment that suppresses the immune system.
Unsurprisingly, the answer lies in the genes.
The researchers previously screened 810 genes in mice and found 15 that had an effect on cancer metastasis. In particular, they found that mice lacking a gene which produces a protein called ARHGEF1 had less metastasis of various primary cancers to the lungs and liver.
The researchers determined that ARHGEF1 suppresses a type of immune cell called a T cell, which can recognise and kill metastatic cancer cells.
To develop treatments to take advantage of this discovery, they needed to find a way for drugs to target it. The scientists traced signals in the cell to determine that ARHGEF1 is switched on when T cells are exposed to a clotting factor called thromboxane A2 (TXA2).
This was an unexpected revelation for the scientists, because TXA2 is already well-known and linked to how aspirin works.
TXA2 is produced by the cells in our blood called platelets. Normally, this is helpful: clotting is what stops wounds from bleeding forever. Occasionally, it goes awry, though, causing heart attacks and strokes. In the case of cancers, TXA2 suppresses the T cells that would attack wandering cancer cells.
Aspirin’s ability to prevent heart attacks and strokes is linked to its suppression of TXA2 production. This same mechanism also releases T cells from suppression.
Professor Rahul Roychoudhuri, from the University of Cambridge, who led the study, said: “Despite advances in cancer treatment, many patients with early stage cancers receive treatments, such as surgical removal of the tumour, which have the potential to be curative, but later relapse due to the eventual growth of micrometastases – cancer cells that have seeded other parts of the body but remain in a latent state.
“Most immunotherapies are developed to treat patients with established metastatic cancer, but when cancer first spreads there’s a unique therapeutic window of opportunity when cancer cells are particularly vulnerable to immune attack. We hope that therapies that target this window of vulnerability will have tremendous scope in preventing recurrence in patients with early cancer at risk of recurrence.”
Dr Jie Yang, who carried out the research, at the University of Cambridge, said: “It was a Eureka moment when we found TXA2 was the molecular signal that activates this suppressive effect on T cells. Before this, we had not been aware of the implication of our findings in understanding the anti-metastatic activity of aspirin. It was an entirely unexpected finding which sent us down quite a different path of enquiry than we had anticipated.”
Further research is planned, to determine how to adapt the discovery into clinical practice.
