Don’t believe the hype – 10 persistent cancer myths debunked

Google ‘cancer’ and you’ll be faced with millions of web pages. And the number of YouTube videos you find if you look up ‘cancer cure’ is similarly vast.
The problem is that much of the information out there is at best inaccurate, or at worst dangerously misleading. There are plenty of evidence-based, easy to understand pages about cancer, but there are just as many, if not more, pages spreading myths.
And it can be hard to distinguish fact from fiction, as much of the inaccurate information looks and sounds perfectly plausible. But if you scratch the surface and look at the evidence, many continually perpetuated ‘truths’ become unstuck.
In this post, we want to set the record straight on 10 cancer myths we regularly encounter. Driven by the evidence, not by rhetoric or anecdote, we describe what the reality of research actually shows to be true.

• Myth 1: Cancer is a man-made, modern disease
• Myth 2: Superfoods prevent cancer
• Myth 3: ‘Acidic’ diets cause cancer
• Myth 4: Cancer has a sweet tooth
• Myth 5: Cancer is a fungus – and sodium bicarbonate is the cure
• Myth 6: There’s a miracle cancer cure…
• Myth 7: …And Big Pharma are suppressing it
• Myth 8: Cancer treatment kills more than it cures
• Myth 9: We’ve made no progress in fighting cancer
• Myth 10: Sharks don’t get cancer

Myth 1: Cancer is a man-made, modern disease

It might be more prominent in the public consciousness now than in times gone by, but cancer isn’t just a ‘modern’, man-made disease of Western society. Cancer has existed as long as humans have. It was described thousands of years ago by Egyptian and Greek physicians, and researchers have discovered tell-tale signs of cancer in a 3,000-year-old skeleton.
While it’s certainly true that global lifestyle-related diseases like cancer are on the rise, the biggest risk factor for cancer is age.
The simple fact is that more people are living long enough to develop cancer because of our success in tackling infectious diseases and other historical causes of death such as malnutrition. It’s perfectly normal for DNA damage in our cells to build up as we age, and such damage can lead to cancer developing.
We’re also now able to diagnose cancers more accurately, thanks to advances in screening, imaging and pathology.
Yes, lifestyle, diet and other things like air pollution collectively have a huge impact on our risk of cancer – smoking for instance is behind a quarter of all cancer deaths in the UK – but that’s not the same as saying it’s entirely a modern, man-made disease. There are plenty of natural causes of cancer – for example, one in six worldwide cancers is caused by viruses and bacteria.

Myth 2: Superfoods prevent cancer

Blueberries, beetroot, broccoli, garlic, green tea… the list goes on. Despite thousands of websites claiming otherwise, there’s no such thing as a ‘superfood’. It’s a marketing term used to sell products and has no scientific basis.

That’s not to say you shouldn’t think about what you eat. Some foods are clearly healthier than others. The odd blueberry or mug of green tea certainly could be part of a healthy, balanced diet. Stocking up on fruits and veg is a great idea, and eating a range of different veg is helpful too, but the specific vegetables you choose doesn’t really matter.
Our bodies are complex and cancer is too, so it’s gross oversimplification to say that any one food, on its own, could have a major influence over your chance of developing cancer.

The steady accumulation of evidence over several decades points to a simple, but not very newsworthy fact that the best way to reduce your risk of cancer is by a series of long-term healthy behaviours such as not smoking, keeping active, keeping a healthy body weight and cutting back on alcohol.

Myth 3: ‘Acidic’ diets cause cancer

Some myths about cancer are surprisingly persistent, despite flying in the face of basic biology. One such idea is that overly ‘acidic’ diets cause your blood to become ‘too acidic’, which can increase your risk of cancer. Their proposed answer: increase your intake of healthier ‘alkaline’ foods like green vegetables and fruits (including, paradoxically, lemons).
This is biological nonsense. True, cancer cells can’t live in an overly alkaline environment, but neither can any of the other cells in your body.
Blood is usually slightly alkaline. This is tightly regulated by the kidneys within a very narrow and perfectly healthy range. It can’t be changed for any meaningful amount of time by what you eat. And while eating green veg is certainly healthy, that’s not because of any effect on how acid or alkaline your body is.
There is something called acidosis. This is a physiological condition that happens when your kidneys and lungs can’t keep your body’s pH (a measure of acidity) in balance. It is often the result of serious illness or poisoning. It can be life-threatening and needs urgent medical attention, but it’s not down to overly acidic diets.
We know that the immediate environment around cancer cells (the microenvironment) can become acidic. This is due to differences in the way that tumours create energy and use oxygen compared with healthy tissue. Researchers are working hard to understand how this happens, in order to develop more effective cancer treatments.
But there’s no good evidence to prove that diet can manipulate whole body pH, or that it has an impact on cancer.

Myth 4: Cancer has a sweet tooth

Another idea we see a lot is that sugar apparently ‘feeds cancer cells’, suggesting that it should be completely banished from a patient’s diet.
This is an unhelpful oversimplification of a highly complex area that we’re only just starting to understand.
‘Sugar’ is a catch-all term. It refers to a range of molecules including simple sugars found in plants, glucose and fructose. The white stuff in the bowl on your table is called sucrose and is made from glucose and fructose stuck together. All sugars are carbohydrates, commonly known as carbs – molecules made from carbon, hydrogen and oxygen.
Carbs – whether from cake or a carrot – get broken down in our digestive system to release glucose and fructose. These get absorbed into the bloodstream to provide energy for us to live.
All our cells, cancerous or not, use glucose for energy. Because cancer cells are usually growing very fast compared with healthy cells, they have a particularly high demand for this fuel. There’s also evidence that they use glucose and produce energy in a different way from healthy cells.
Researchers are working to understand the differences in energy usage in cancers compared with healthy cells, and trying to exploit them to develop better treatments (including the interesting but far from proven drug DCA).
But all this doesn’t mean that sugar from cakes, sweets and other sugary foods specifically feeds cancer cells, as opposed to any other type of carbohydrate. Our body doesn’t pick and choose which cells get what fuel. It converts pretty much all the carbs we eat to glucose, fructose and other simple sugars, and they get taken up by tissues when they need energy.
While it’s very sensible to limit sugary foods as part of an overall healthy diet and to avoid putting on weight, that’s a far cry from saying that sugary foods specifically feed cancer cells.
Both the ‘acidic diet’ and ‘sugar feeds cancer’ myths distort sensible dietary advice – of course, nobody is saying that eating a healthy diet doesn’t matter when it comes to cancer. You can read about the scientific evidence on diet and cancer on our website.
But dietary advice must be based on nutritional and scientific fact. When it comes to offering diet tips to reduce cancer risk, research shows that the same boring healthy eating advice still holds true. Fruit, vegetables, fibre, white meat and fish are good. Too much fat, salt, sugar, red or processed meat and alcohol are less so.
Also, this post, “What should you eat while you’re being treated for cancer“, is packed with links to evidence-based advice from our CancerHelp UK website. And this post, from the Junkfood Science blog, explores the science behind sugar and cancer in more detail.
[Edited to add more information and links KA 28/03/14]

Myth 5: Cancer is a fungus – and sodium bicarbonate is the cure

This ‘theory’ comes from the not-very-observant observation that “cancer is always white”.
One obvious problem with this idea – apart from the fact that cancer cells are clearly not fungal in origin – is that cancer isn’t always white. Some tumours are. But some aren’t. Ask any pathologist or cancer surgeon, or have a look on Google Image search (but maybe not after lunch…).
Proponents of this theory say that cancer is caused by infection by the fungus candida, and that tumours are actually the body’s attempt at protecting itself from this infection.
But there’s no evidence to show that this is true.
Furthermore, plenty of perfectly healthy people can be infected with candida – it’s part of the very normal array of microbes that live in (and on) all of us. Usually our immune system keeps candida in check, but infections can get more serious in people with compromised immune systems, such as those who are HIV-positive.
The ‘simple solution’ is apparently to inject tumours with baking soda (sodium bicarbonate). This isn’t even the treatment used to treat proven fungal infections, let alone cancer. On the contrary, there’s good evidence that high doses of sodium bicarbonate can lead to serious – even fatal – consequences.
Some studies suggest that sodium bicarbonate can affect cancers transplanted into mice or cells grown in the lab, by neutralising the acidity in the microenvironment immediately around a tumour. And researchers in the US are running a small clinical trial investigating whether sodium bicarbonate capsules can help to reduce cancer pain and to find the maximum dose that can be tolerated, rather than testing whether it has any effect on tumours.
As far as we are aware, there have been no published clinical trials of sodium bicarbonate as a treatment for cancer.
It’s also worth pointing out that it’s not clear whether it’s possible to give doses of sodium bicarbonate that can achieve any kind of meaningful effect on cancer in humans, although it’s something that researchers are investigating.
Because the body strongly resists attempts to change its pH, usually by getting rid of bicarbonate through the kidneys, there’s a risk that doses large enough to significantly affect the pH around a tumour might cause a serious condition known as alkalosis.

One estimate suggests that a dose of around 12 grams of baking soda per day (based on a 65 kg adult) would only be able to counteract the acid produced by a tumour roughly one cubic millimetre in size. But doses of more than about 30 grams per day are likely to cause severe health problems – you do the maths.

Myth 6: There’s a miracle cancer cure…

From cannabis to coffee enemas, the internet is awash with videos and personal anecdotes about ‘natural’ ‘miracle’ cures for cancer.
But extraordinary claims require extraordinary evidence – YouTube videos and Facebook posts are emphatically not scientific evidence and aren’t the same as good-quality, peer-reviewed evidence.
In many cases it’s impossible to tell whether patients featured in such anecdotal sources have been ‘cured’ by any particular alternative treatment or not. We know nothing about their medical diagnosis, stage of disease or outlook, or even if they actually had cancer in the first place. For instance, we don’t know what other cancer treatments they had.
And we only hear about the success stories – what about the people who have tried it and have not survived? The dead can’t speak, and often people who make bold claims for ‘miracle’ cures only pick their best cases, without presenting the full picture.
This highlights the importance of publishing data from peer-reviewed, scientifically rigorous lab research and clinical trials. Firstly, because conducting proper clinical studies enables researchers to prove that a prospective cancer treatment is safe and effective. And secondly, because publishing these data allows doctors around the world to judge for themselves and use it for the benefit of their patients.
This is the standard to which all cancer treatments should be held.
That’s not to say the natural world isn’t a source of potential treatments, from aspirin (willow bark) to penicillin (mould). For example, the cancer drug taxol was first extracted from the bark and needles of the Pacific Yew tree.
But that’s a far cry from saying you should chew bark to combat a tumour. It’s an effective treatment because the active ingredient has been purified and tested in clinical trials. So we know that it’s safe and effective, and what dose to prescribe.
Of course people with cancer want to beat their disease by any means possible. And it’s completely understandable to be searching high and low for potential cures. But our advice is to be wary of anything labelled a ‘miracle cure’, especially if people are trying to sell it to you.
Wikipedia has this excellent list of ineffective cancer treatments that are often touted as miracle cures, which is worth a browse.
If you want to know about the scientific evidence about cannabis, cannabinoids and cancer – a topic we’re often asked about – please take a look at our extensive blog post on the subject, including information about the clinical trials we’re helping to fund.
And if you’ve seen links to article about scientists in Canada “curing cancer but nobody notices”, these refer to an interesting but currently unproven drug called DCA, which we’ve also written about before.

Myth 7: … and Big Pharma are suppressing it

Hand in hand with the idea that there is a cornucopia of ‘miracle cures’ is the idea that governments, the pharmaceutical industry and even charities are colluding to hide the cure for cancer because they make so much money out of existing treatments.
Whatever the particular ‘cure’ being touted, the logic is usually the same: it’s readily available, cheap and can’t be patented, so the medical establishment is suppressing it in order to line its own pockets. But, as we’ve written before, there’s no conspiracy – sometimes it just doesn’t work.
There’s no doubt that the pharmaceutical industry has a number of issues with transparency and clinical trials that it needs to address (the book Bad Pharma by Ben Goldacre is a handy primer). We push regulators and pharmaceutical companies hard to make sure that effective drugs are made available at a fair price to the NHS – although it’s important to remember that developing and trialling new drugs costs a lot of money, which companies need to recoup.
Problems with conventional medicine don’t automatically prove that alternative ‘cures’ work. To use a metaphor, just because cars sometimes crash doesn’t mean that flying carpets are a viable transport option.
It simply doesn’t make sense that pharmaceutical companies would want to suppress a potential cure. Finding a highly effective therapy would guarantee huge worldwide sales.
And the argument that treatments can’t be patented doesn’t hold up. Pharma companies are not stupid, and they are quick to jump on promising avenues for effective therapies. There are always ways to repackage and patent molecules, which would give them a return on the investment required to develop and test them in clinical trials (a cost that can run into many millions) if the treatment turns out to work.
It’s also worth pointing out that charities such as Cancer Research UK and government-funded scientists are free to investigate promising treatments without a profit motive. And it’s hard to understand why NHS doctors – who often prescribe generic, off-patent drugs – wouldn’t use cheap treatments if they’d been shown to be effective in clinical trials.
For example, we’re funding large-scale trials of aspirin – a drug first made in 1897, and now one of the most widely-used off-patent drugs in the world. We’re researching whether it can prevent bowel cancer in people at high risk, reduce the side effects of chemotherapy, and even prevent cancer coming back and improve survival.
Finally, it’s worth remembering that we are all human – even politicians and Big Pharma executives – and cancer can affect anyone. People in pharmaceutical companies, governments, charities and the wider ‘medical establishment’ all can and do die of cancer too.
Here at Cancer Research UK we have seen loved ones and colleagues go through cancer. Many of them have survived. Many have not. To suggest that we are – collectively and individually – hiding ‘the cure’ is not only absurd, it’s offensive to the global community of dedicated scientists, to the staff and supporters of cancer research organisations such as Cancer Research UK and, most importantly, to cancer patients and their families.

Myth 8: Cancer treatment kills more than it cures

Let’s be clear, cancer treatment – whether chemotherapy, radiotherapy or surgery – is no walk in the park. The side effects can be tough. After all, treatments that are designed to kill cancer cells will inevitably affect healthy cells too.
And sometimes, sadly, treatment doesn’t work. We know that it’s very difficult to treat late-stage cancer that has spread throughout the body, and while treatment can provide relief from symptoms and prolong life, it’s not going to be a cure for very advanced cancers.
Surgery is still the most effective treatment we have for cancer, provided it’s diagnosed early enough for an operation to be done. And radiotherapy helps cure more people than cancer drugs. Yet chemotherapy and other cancer drugs have a very important part to play in cancer treatment – in some cases helping to cure the disease, and in others helping to prolong survival.
The claims on the internet that chemotherapy is “only 3 per cent effective” are highly misleading and outdated, and are explored in more depth in these two posts from the Science Based Medicine blog.
It important to point out that in an increasing number of cases, the drugs do work. For example, more than 96 per cent of all men are now cured of testicular cancer, compared to fewer than 70 per cent in the 1970s thanks in part to a drug we helped to develop called cisplatin. And three-quarters of children with cancer are now cured, compared with around a quarter in the late 1960s – most of them are alive today directly thanks to chemotherapy.
We know that we still have a long way to go until we have effective, kinder treatments for all types of cancer. And it’s important that doctors, patients and their families are realistic and honest about the best options for treatment, especially when cancer is very advanced.
It may be better to opt for treatment aimed at reducing pain and symptoms rather than attempting to cure the disease (palliative care). Balancing quality and quantity of life is always going to be an issue in cancer treatment, and it’s one that each patient must decide for themselves.

Myth 9: We’ve made no progress in fighting cancer

This simply isn’t true. Thanks to advances in research, survival from cancer has doubled in the UK over the past 40 years, and death rates have fallen by 10 per cent over the past decade alone. In fact, half of all patients now survive at least ten years.
This article by our chief clinician, Professor Peter Johnson, outlines some of the key facts.
By definition, these figures relate to people treated at least 10 years ago. It’s likely that the patients being diagnosed and treated today have an even better chance of survival.
To see how the picture has changed, make yourself a cuppa and settle down to watch this hour-long documentary we helped to make – The Enemy Within: 50 years of fighting cancer. From the early days of chemotherapy in the 50s and 60s to the latest ‘smart’ drugs and pinpoint-accurate radiotherapy, it highlights how far we’ve come over the years.
There’s still a long way to go. There are some cancers where progress has been much slower – such as lung, brain, pancreatic and oesophageal cancers. And when you lose someone you love to cancer, it can feel as though no progress has been made at all.
That’s why we’re working so hard to beat cancer sooner, to make sure that nobody loses their life prematurely to the disease.

Myth 10: Sharks don’t get cancer

Yes they do.

Cannabis, cannabinoids and cancer – the evidence so far

What are cannabinoids and how do they work?

“Cannabinoids” is a blanket term covering a family of complex chemicals (both natural and man-made) that lock on to cannabinoid receptors – protein molecules on the surface of cells.
Humans have been using cannabis plants for medicinal and recreational purposes for thousands of years, but cannabinoids themselves were first purified from cannabis plants in the 1940s. The structure of the main active ingredient of cannabis plants – delta-9 tetrahydrocannabinol (THC) – was discovered in the 60s. It wasn’t until the late 1980s that researchers found the first cannabinoid receptor, followed shortly by the discovery that we create cannabinoid-like chemicals within our own bodies, known as endocannabinoids.

The CB1 and CB2 receptors. 

We have two different types of cannabinoid receptor, CB1 and CB2, which are found in different locations and do different things. CB1 is mostly found on cells in the nervous system, including certain areas of the brain and the ends of nerves throughout the body, while CB2 receptors are mostly found in cells from the immune system. Because of their location in the brain, it’s thought that CB1 receptors are responsible for the infamous ‘high’ (known as psychoactive effects) resulting from using cannabis.
Over the past couple of decades scientists have found that endocannabinoids and cannabinoid receptors are involved in a vast array of functions in our bodies, including helping to control brain and nerve activity (including memory and pain), energy metabolism, heart function, the immune system and even reproduction. Because of this molecular multitasking, they’re implicated in a huge range of illnesses, from cancer to neurodegenerative diseases.

Can cannabinoids treat cancer?

There is no doubt that cannabinoids – both natural and synthetic – are interesting biological molecules. Hundreds of scientists around the world are investigating their potential in cancer and other diseases – as well as the harms they can cause – brought together under the blanket organisation The International Cannabinoid Research Society.
Researchers first looked at the anticancer properties of cannabinoids back in the 1970s, and many hundreds of scientific papers looking at cannabinoids and cancer have been published since then. This Wellcome Witness seminar is also fascinating reading for aficionados of the history of medical cannabis, including the scientific, political and legal twists.
But claims that this body of preclinical research is solid “proof” that cannabis or cannabinoids can cure cancer is highly misleading to patients and their families, and builds a false picture of the state of progress in this area.
Let’s take a closer look at the evidence.

Lab research

Virtually all the scientific research investigating whether cannabinoids can treat cancer has been done using cancer cells grown in the lab or animal models. It’s important to be cautious when extrapolating these results up to real live patients, who tend to be a lot more complex than a Petri dish or a mouse.

Virtually all the research into cannabinoids and cancer so far has been done in the lab.

Through many detailed experiments, handily summarised in this recent article in the journal Nature Reviews Cancer, scientists have discovered that various cannabinoids (both natural and synthetic) have a wide range of effects in the lab, including:

• Triggering cell death, through a mechanism called apoptosis
• Stopping cells from dividing
• Preventing new blood vessels from growing into tumours
• Reducing the chances of cancer cells spreading through the body, by stopping cells from moving or invading neighbouring tissue
• Speeding up the cell’s internal ‘waste disposal machine’ – a process known as autophagy – which can lead to cell death

All these effects are thought to be caused by cannabinoids locking onto the CB1 and CB2 cannabinoid receptors. It also looks like cannabinoids can exert effects on cancer cells that don’t involve cannabinoid receptors, although it isn’t yet clear exactly what’s going on there.
So far, the best results in the lab or animal models have come from using a combination of highly purified THC and cannabidiol (CBD), a cannabinoid found in cannabis plants that counteracts the psychoactive effects of THC. But researchers have also found positive results using synthetic cannabinoids, such as a molecule called JWH-133.
It’s not all good news though, as there’s also evidence that cannabinoids may also have undesirable effects on cancer.
For example, some researchers have found that although high doses of THC can kill cancer cells, they also harm crucial blood vessel cells, although this may help their anti-cancer effect by preventing blood vessels growing into a tumour. And under some circumstances, cannabinoids can actually encourage cancer cells to grow, or have different effects depending on the dosage and levels of cannabinoid receptors present on the cancer cells.

Others have discovered that activating CB2 receptors may actually interfere with the ability of the immune system to recognise and destroy tumour cells, although some scientists have found that certain synthetic cannabinoids may enhance immune defences against cancer.
Furthermore, cancer cells can develop resistance to cannabinoids and start growing again, although this can be got round by blocking a certain molecular pathway in the cells known as ALK.
And yet more research suggests that combining cannabinoids with other chemotherapy drugs may be a much more effective approach. This idea is supported by lab experiments combining cannabinoids with other drugs including gemcitabine and temozolomide.

Clinical research

But that’s the lab – what about clinical research involving people with cancer? Results have been published from only one clinical trial testing whether cannabinoids can treat cancer in patients, led by Dr Manuel Guzman and his team in Spain. Nine people with advanced, terminal glioblastoma multiforme – an aggressive brain tumour – were given highly purified THC through a tube directly into their brain.
Eight people’s cancers showed some kind of response to the treatment, and one didn’t respond at all. All the patients died within a year, as might be expected for people with cancer this advanced.
The results from this study show that THC given in this way is safe and doesn’t seem to cause significant side effects. But because this was an early stage trial, without a control group, it’s impossible to say whether THC helped to extend their lives. And while it’s certainly not a cure,  the trial results suggest that cannabinoids are worth pursuing in clinical trials.
There is also a published case report of a 14-year old girl from Canada who was treated with cannabis extracts (also referred to as “hemp oil”), but there is limited information that can be obtained from a single case treated with a varied mixture of cannabinoids. More published examples with detailed data are needed in order to draw a fuller picture of what’s going on. [Updated 26/03/14, KA]
A handful of other clinical trials of cannabinoids are currently being set up. We are helping to support the only two UK trials of cannabinoids for treating cancer, through our Experimental Cancer Medicine Centre (ECMC) Network funded by Cancer Research UK and the devolved Departments of Health. One early-stage trial is testing a synthetic cannabinoid called dexanabinol in patients with advanced cancer, and the other is an early-stage trial testing a cannabis extract called Sativex for treating people with glioblastoma multiforme brain tumours.

Unanswered questions

There are still a lot of unanswered questions around the potential for using cannabinoids to treat cancer.

An antique bottle of cannabis extract.

The biggest issue is that there isn’t enough evidence to show that they can treat cancer in people, although research is still ongoing around the world.
And it’s not clear which type of cannabinoid – either natural or synthetic – might be most effective, what kind of doses might be needed, or which types of cancer might respond best to them. So far there have been intriguing results from lab experiments with prostate, breast, lung cancer, skin, bone and pancreatic cancers, glioma brain tumours and lymphoma. But the take-home message is that different cannabinoids seem to have different effects on various cancer types, so they are far from being a ‘universal’ treatment.
Most research has been focused on THC, which occurs naturally in cannabis plants, but researchers have found that different cannabinoids seem to work better or worse different types of cancer cells. Lab experiments have shown promising results with THC on brain tumour and prostate cancer cells, while CBD seems to work well on breast cancer cells.
Then there’s the problem of the psychoactive effects of THC, particularly at high doses, although this can be counteracted by giving it together with CBD. Because of this problem, synthetic cannabinoids that don’t have these effects might be more useful in the long term.
There are also big questions around the best way to actually get the drugs into tumours. Because of their chemical makeup, cannabinoids don’t dissolve easily in water and don’t travel very far in our tissues. This makes it hard to get them deep into a tumour, or even just deliver them into the bloodstream in consistently high enough doses to have an effect.
The clinical trial led by Dr Guzman in Spain involved directly injecting cannabinoids into patients’ brains through a small tube. This isn’t an ideal method as it’s very invasive and carries a risk of infection, so researchers are investigating other delivery methods such as tablets, oil injections, mouth sprays or even microspheres.
We also don’t know whether cannabinoids will help to boost or counteract the effects of chemotherapy, nor which combinations of drugs might be good to try. And there are currently no biological markers to help doctors identify who might benefit from cannabinoids and who might not – remember that one patient on the brain tumour trial failed to respond to THC at all.
None of these issues are deal-breakers, but these questions need answering if there’s any hope of using cannabinoids to effectively and safely treat cancer patients.
It’s worth remembering that there are hundreds of exciting potential cancer drugs being developed and tested in university, charity and industry labs all over the world – cannabinoids are merely a small part of a much larger picture.
Most of these compounds will never make it into the clinic to treat patients for a huge range of reasons including toxicity, lack of effectiveness, unacceptable side effects, or difficulty of delivering the drug to tumours.
Without doing rigorous scientific research, we will never sift the ‘hits’ from the ‘misses’. If cannabinoids are ever to get into clinical use, they need to overcome these hurdles and prove they have benefits over existing cancer treatments.

Can cannabis prevent or cause cancer?

So that’s a brief look at cannabinoids to treat cancer. But can they stop the disease from developing? Or could they play a role in causing cancer?

There’s controversy around the health risks of cannabis. 

In experiments with mice, animals given very high doses of purified THC seemed to have a lower risk of developing cancer, and there has been some research suggesting that endocannabinoids (cannabinoids produced by the body) can suppress tumour growth. But there’s no solid scientific evidence at the moment to show that cannabinoids or cannabis can cut the risk of cancer in people.
When it comes to finding out whether cannabis can cause cancer, the evidence is a lot murkier. This is mainly because most people who use cannabis smoke it mixed with tobacco, a substance that definitely does cause cancer.
This complex issue recently hit the headlines when the British Lung Foundation released a study suggesting that the cancer risks of cannabis had been underestimated, although this has been questioned by some experts including Professor David Nutt.

What about controlling cancer symptoms such as pain or sickness?

Although there’s a lack of data showing that cannabinoids can effectively treat cancer, there is good evidence that these molecules may be beneficial in other ways.
As far back as the 1980s, cannabinoid-based drugs – including dronabinol (synthetic THC) and nabilone – were used to help reduce nausea and vomiting caused by chemotherapy. But there are now safer and more effective alternatives and cannabinoids tend to only be used where other approaches fail.
In some parts of the world – including the Netherlands – medical use of marijuana has been legalised for palliative use (relieving pain and symptoms), including cancer pain. For example, Dutch patients can obtain standardised, medicinal-grade cannabis from their doctor, and medicinal cannabis is available in many states in the US.
But one of the problems of using herbal cannabis is about dosage – smoking it or taking it in the form of tea often provides a variable dose, which may make it difficult for patients to monitor their intake. So researchers are turning to alternative dosing methods, such as mouth sprays, which deliver a reliable and regulated dose.
Large-scale clinical trials are currently running in the UK testing whether a mouth spray called Sativex (nabiximols) – a highly purified pharmaceutical-grade extract of cannabis containing THC and CDB – can help to control severe cancer pain that doesn’t respond to other drugs.
There may also be potential for the use of cannabinoids in combating the loss of appetite and wasting experienced by some people with cancer, although a clinical trial comparing appetite in groups of cancer patients given cannabis extract, THC and a placebo didn’t find a difference between the treatments.

Science Snaps: designer drugs

They may look like pictures from a strange forest on another planet, but these illustrations depict a key process in all our cells that dictates when a cell will grow, divide or move.
It’s tightly regulated, but if faults arise then cells can grow and divide out of control – a hallmark of cancer.
In this guest post, Emily Burns and Jeroen Claus – PhD students from our London Research Institute – explore this molecular wilderness revealing the science behind the illustrations and how it’s being translated into the targeted cancer treatments of the future.
‘Personalised’ or ‘precision’ medicine is a hot topic in cancer treatment.
It holds the potential to specifically target the cancer-causing molecules driving each patient’s tumour.
Rather than using a single therapy across the board, each patient could receive a treatment tailored to their cancer – even allowing us to target more than one molecule at the same time.
In our research we study the intricate shapes of these potentially cancer-causing proteins, looking for new ways to spot the weaknesses that could be exploited by the targeted treatments of the future.

How it all begins

Each one of our cells is covered with molecules known as protein receptors. These receptors receive signals from outside the cell and relay the messages inside.
Their messages are diverse, including instructions such as “Grow”, “Multiply”, or “Move that way”.
The recipe for these cell surface receptors – along with every other protein in our body – lies in our genes, encoded within our DNA. But mistakes in the DNA code, known as genetic mutations, can lead to errors in these receptors: there can be far too many of them, or they can become constantly active.
Imagine a person holding a megaphone, shouting instructions. Now imagine there are 1000 times more of them: that message is going to be a lot louder.
This is shown in the illustrations below, and is exactly what can happen on some cancer cells.

On the left is what the surface of a healthy cell might look like – the number of blue receptor molecules is tightly controlled. But on the right is what happens on some cancer cells – the receptors are produced in huge excess, resulting in much louder messages being sent inside the cells.
And louder messages result in more cells multiplying, which lead to uncontrolled growth. This is how a tumour develops.
It’s the same for faulty receptors becoming constantly active: the message is no longer switched off, so it continuously tells cells to grow.

It’s in the detail

Scientists now have an increasingly better idea of the types of receptor that can become mutated. One receptor that we’re particularly interested in is called HER2 – the blue ‘trees’ in our images.
In about one in five breast cancer patients there are far too many HER2 receptors, constantly telling the cells to multiply. In order to target HER2 specifically, we need to know what it looks like, so that a drug can be designed to mute the signals it is sending into the cell.
Scientists are able to look at the unique details of HER2 on an incredibly intricate molecular level, using a technique called X-ray crystallography. In doing so, they can create a snapshot of the active part of the protein and tailor-make a drug that will sit within it, preventing the receptor from working.
One such drug is called lapatinib. It acts as a molecular plug, sitting deep within the active region of the receptor. Lapatinib is just one of the drugs available in the growing arsenal of precision treatments, which target specific cancer-causing proteins.
Drugs that work along similar lines are also used to treat people with particular types of leukaemia, lung cancer, bowel cancer and skin cancer.

Testing the treatments of the future

A big challenge is finding out who will and who won’t benefit from these types of treatment.
It is now possible to extract DNA from a patient’s tumour and find out which receptors have been mutated. This can give doctors very specific information about a particular patient’s disease, and can reveal if there is a targeted drug available that may be suited to their tumour.
Yesterday Cancer Research UK launched the latest stage of its Stratified Medicine Programme with an ambitious clinical trial to link this kind of molecular diagnosis with potential new treatments for late stage lung cancer patients.
But in many cases this isn’t straightforward.
We now know that different regions of the same tumour can carry different genetic faults, making the process of identifying which drugs to use very difficult.
And tumours can adapt, becoming resistant to these more personalised treatments. Scientists are working hard to understand how this happens by spotting the tricks these proteins play to avoid our designer drugs.
By refining the design we hope that more patients can be treated with drugs tailored to their disease in the future, increasing survival and bringing cures closer.

Mapping cancer risks – what can (and can’t) it tell us

For centuries humans have used maps to chart the world around us. As well as capturing the planet’s geography, they can also help us make sense of the lives of the people that inhabit it.
Maps tracking diseases such as the Black Death go back to the Middle Ages, and John Snow’s depiction of the 1854 Broad Street cholera outbreak has a special place in the hearts of medical mappers.
Information about who gets what illnesses and where they live is vital when it comes to understanding and researching health risks, and planning public services. Today we have more data about health and disease than ever before, yet no-one but the most hardened statistician would want to trawl through endless spreadsheets to pull out meaningful patterns.
So it’s not surprising that researchers are using computer software to help process and display this kind of data, making it easier to navigate and understand. One example is our own Local Cancer Statistics portal, which we launched last year to enable politicians, healthcare providers and the public to access understandable data about cancer diagnosis and treatment in their area.

Today, the Small Area  Health Statistics Unit (SAHSU) at Imperial College London launches their Environment and Health Atlas – a new set of high-resolution maps displaying data about diseases such as cancer alongside environmental risk factors including pollution and pesticides.
Users can zoom into neighbourhoods and flip between different health outcomes and local environmental factors. But while it’s tempting to pop your postcode into the site and start scaring yourself silly, it’s important to step back and look at what these maps can – and can’t – tell us.

What is it?

The atlas details the distribution of 14 health conditions, including lung cancer, breast cancer, heart disease and leukaemia, across England and Wales. Alongside sit maps revealing local variations of certain environmental agents such as air pollution, sunshine and pesticides.
This is the first time that this kind of map has been created at such high granularity, drilling down to local neighbourhoods made up of 3,000 to 6,000 people. The online portal is accompanied by a hefty print version packed with extra detail – a perfect gift for the statistician in your life, perhaps?
It’s also the first UK atlas of its kind to adjust for age and social deprivation, revealing underlying health risks that aren’t just the result of ageing populations or poverty.

What can – and can’t – it tell us?

The most important thing to know about these maps is that they reflect overall health risks and trends in different areas, rather than an individual person’s risk of getting any particular disease. They also show relative rather than absolute risks, which can be difficult to understand in the absence of wider context.
Relative risks compare outcomes between different groups – for example, saying that people living in one town are 20 per cent more likely to get a particular type of cancer than those in another when the overall risk might still be relatively low. Whereas absolute risks make more definitive “You have a 15 per cent chance of getting disease X if you live here”-type statements.
To focus particularly on cancer, there are many different factors that influence a person’s risk, including their age and sex, genetic makeup and lifestyle (such as smoking, diet and physical activity). As an example, if you have a strong family history of breast cancer, moving to an area with a lower risk on the map is unlikely to make a difference.
But, like our own Local Cancer Statistics portal, the maps reveal patterns and trends that will be of vital importance to regional healthcare planners and policy-makers. For example, there are higher health risks across the board in parts of the North West, Yorkshire and South Wales, highlighting the need for further research into why this is happening and what can be done about it.

Correlation or causation?

It’s also important to note that the maps can’t tell us if there is a direct link between a particular environmental factor and a disease. This is because, as any good statistician will tell you, correlation does not equal causation.
Correlations can easily be drawn between all kinds of trends, but they don’t necessarily prove that one thing causes the other. A country’s chocolate consumption reflects its number of Nobel prizewinners, the falling German birthrate appears to be due to a decline in the stork population, and the performance of the Welsh rugby team can be linked to dead Popes.  None of these are true causal relationships.
In contrast, the maps show that respiratory problems, such as lung cancer and chronic pulmonary disease are worse in urban areas, which fits with what we know about the evidence from large-scale studies of a link between the two.

Related to the story we released earlier this week about increasing melanoma rates and UV exposure from the sun and sunbeds, the atlas also shows that skin cancer risk is highest in the South West. However, sunshine duration is highest in southeast England.

News digest – Chantler review on standard packs, revolutionary bowel cancer trial, laser popped ‘nanoballoons’ and more

• This week’s big news was the release of Sir Cyril Chantler’s independent review on the evidence for standardised cigarette packaging. Following support for the review the Government will now push on with the introduction of plain packs. The BBC were among the many media outlets to cover the announcement and we outlined the key points from the review and what comes next in this blog post.
• We launched our revolutionary FOCUS4 clinical trial for advanced bowel cancer that offers targeted treatments to different groups of patients based on combinations of ‘biomarkers’ found in their tumour.
• New Scientist covered a review of breast screening in the US which, like the recent UK Independent Breast Screening Review, tried to estimate how many lives are saved by breast screening, compared to the number of women who are diagnosed with a cancer that would never have harmed them. Clear and balanced information, such as the new leaflet sent out with screening invitations, can help women decide whether to take up screening or not.
• And the Telegraph covered an editorial in the British Medical Journal questioning the value of regular breast self-examination. We advise women to be breast aware – know what’s normal for you, so it’s easier to notice changes. The same goes for men knowing their testicles. You can read more on our Spot Cancer Early pages.
• We held our first conference to tackle the challenges of ‘big data’ in research. See our press release for more info.
• The benefits of a healthy diet full of fruit and vegetables was reinforced by research showing that the more fruit and veg your diet contains, the lower your risk of dying from any cause, including cancer. The BBC and the Mail Online were among the many media outlets to cover the research and NHS Choices took and in depth look at the findings.
• New research showed that poor oral health and irregular dental checks could increase the chance of developing mouth and throat cancers. The BBC covered this, but the study is too small to confirm whether excessive use of mouthwash also increases the risk as some media outlets are reporting. The best advice for reducing the risk of mouth and throat cancers is to stop smoking, cut down on alcohol and visit your dentist for regular checkups.
• The Mail Online covered new research highlighting the potential benefits of aspirin for some bowel cancer patients. But bigger studies are needed to work out what the correct dose might be for these patients and how long to take it for. It’s important to stress that aspirin can cause serious side effects and any patients thinking of taking it should speak to their doctor first.
• UK scientists discovered that faults in a gene called POT1 could point towards people at greater risk of developing malignant melanoma – the most dangerous form of skin cancer – due to their family history. The BBC has more info.
• And the Telegraph covered an interesting Swedish study suggesting men who live alone are at higher risk of dying from malignant melanoma. As this NHS Choices article points out, single men being diagnosed later may help to explain the finding – so it’s a good idea for everyone to keep an eye on their skin and tell their GP if they notice any changes to a mole or normal patch of skin. Don’t forget about the bits that are harder to see – a mirror or a friend can help.
• New research from Wales revealed the origins of different types of breast cancer in mice and provides important clues about what drives diversity in the disease. The BBC and our news story have more details.
• A £4.5 million injection of funding from the Government is being used to streamline the process of approving clinical trials and research in the NHS. PharmaTimes covered this and we explored what’s changing in this blog post.

And finally

• With mentions of ‘Lasers’ and ‘nanoballoons that pop’ this fascinating early stage research that could provide new ways to deliver anti-cancer drugs to tumours caught our eye. It’s still very early stages, but finding new ways to deliver drugs directly to cancer cells – saving normal cells from potential damage – is a fascinating area of research and one to keep an eye on.

When muscle turns to bone – clues for treating deadly childhood brain tumours

Imagine each time you injured yourself – whether a simple cut, or a broken limb – your body’s natural healing mechanisms turned damaged muscle into bone.
It sounds like science fiction, but this cruel twist on recovery is real.
It’s a rare genetic condition known as fibrodysplasia ossificans progressiva (FOP) – sometimes referred to as Stone Man Syndrome – that locks people in a second skeleton as they age.
Yesterday, a team of our researchers based at The Institute of Cancer Research (ICR) in London revealed a remarkable genetic link between FOP and a devastating type of childhood brain tumour, publishing their findings in the journal Nature Genetics.
And the discovery could offer new ways to treat children with the disease, which up until now has proved incurable.

Harry Eastlack and the frozen skeleton

FOP traps patients in a second skeleton as they age

The story starts in Philadelphia in the US back in 1938, when five year old Harry Eastlack broke his leg.
Suffering problems during his recovery, Harry’s knee and hip stiffened as bone began to form on his thigh muscles.
As he grew the condition spread around his body, freezing up his muscles and joints.
Attempts to remove the excess bone only made it worse, growing back quicker and stronger than before.
Harry had FOP and sadly died just shy of his 40th birthday, but his legacy lives on through research.
He donated his overgrown skeleton to medical research and it can be seen on display at the Mütter Museum in Philadelphia.
Studying rare diseases – including rare forms of cancer – can be tough. Funding can be scarce and with only a handful of people affected around the world, accessing samples for research and enrolling enough people in clinical trials can be a struggle.
But interest in Harry’s skeleton kick-started research into FOP.
And it’s through that research that our scientific stories align today – research that could now benefit children with a rare and devastating type of brain tumour called diffuse intrinsic pontine glioma, or DIPG for short.

From bones to brains

Dr Chris Jones and his team are finding the key gene faults driving childhood cancers

Dr Chris Jones and his team at the ICR are scanning reams of genetic data that could provide new ways to target a variety of childhood cancers.
Among these is DIPG, which affects between 20 and 30 children in the UK each year. It develops from early ‘precursor cells’ that during normal development would go on to form specialised brain cells, called ‘glial cells’.
Due to their location in the brain, these tumours cannot be removed by surgery, meaning the outlook for patients with DIPG is poor. On average, children with DIPG survive for less than a year and there are no effective treatments to target the disease.
That’s why Dr Jones and his team are focussed on learning more about DIPG and translating this into potential new ways to treat it.
Their latest study, which is part of our Genomics Initiative and is funded through our Catalyst Club – a pioneering venture to raise £10 million to aid research into personalising cancer treatment – is starting to piece together the genetic puzzle of DIPG.
By finding the key gene faults driving the disease, Dr Jones hopes to lay the foundations for future cures.

A surprising genetic crossover

The team scoured the DNA code of 26 unique samples from children with DIPG.

“Finding that the same few spelling mistakes are shared between two rare and drastically different diseases is remarkable” - Dr Chris Jones

They found that in just over a quarter of these samples a cluster of genetic faults were cropping up in a precise portion of a particular gene that had not previously been linked to DIPG.
In fact, when they ran these faults through a vast database of known cancer-linked errors they saw that no other tumour type carried these faults with the same high frequency.
This was a striking result.
“Less than one per cent of the many thousands of samples present in the database matched the faults we saw so frequently in these DIPG patients,” said Dr Jones.
“It really shows how important these faults could be in pinpointing a subset of patients that could benefit from treatments in the future,” he added.
But even more striking was the discovery that these same genetic faults matched those responsible for FOP.
“When you think that the human genome – the complete set of genetic information found in our cells – is over 3 billion letters in length, finding that the same few spelling mistakes are shared between two rare and drastically different diseases is remarkable,” Dr Jones said.

Turning stone into treatments

From reams of genetic data a surprising link emerges

The gene Dr Jones and his team identified is known as ACVR1 and it produces a key protein in cells called ALK2.
If the faulty gene is present in all cells at birth then that child will develop FOP. But it’s extremely rare, affecting just one in two million people.
And now it would seem it’s possible that if the faulty gene is present only in the early precursors to the specialised glial cells then this could lead to DIPG.
The faulty version of ACVR1 produces a hyperactive form of ALK2 that permanently switches on a set of signals in cells.
In FOP these signals seem to be responsible for the tell-tale bone growths characteristic of the condition.
The precise role these signals play in DIPG is not yet known, and more research will be needed to pin down the molecular miswiring that may be responsible for the disease.
But thanks to research into FOP there are potential drugs already being developed that target the faults in ACVR1. And these could be repurposed as a new treatment for children with DIPG in the future.
It’s early days, but when Dr Jones took a selection of DIPG cells that carry the faulty ACVR1 gene and treated them with one of these promising compounds in the lab he saw that it was effective at killing the cells.
“These compounds aren’t quite at the stage of being ‘drugs’ we could give to people. But our first sets of experiments have shown promising early results,” Dr Jones said.
“The big challenge will be turning these into compounds suitable for treating DIPG patients.
“This will require some complicated chemistry to find ways of getting these potential drugs into the brain, which can be a real challenge and has been one of the major stumbling blocks when developing treatments for DIPG – and other brain tumours – in the past.”

Research feeds research

This study is a fascinating example of how two drastically different, but equally devastating, diseases can be brought together by the genetic events that fuel them.
And how two research communities, previously unknown to each other, can now work together to widen the benefit of their research for the patients who rely on it.
Whether peering at Harry Eastlack’s overgrown skeleton, or decoding vast swathes of data from childhood tumour samples, genes are genes.
And whether research like this is aiming to stop muscle turning to bone or improve the outlook for children with brain cancer, it’s all adding to our understanding of biology and underpinning the treatments of the future.

Epstein-Barr virus and the immune system – are cures in sight?

EBV can hide away in immune cells to avoid detection

In this post we take a look at how scientists untangled the complicated relationship between EBV and our immune system and what happens when the virus goes unchecked. We’ll then delve into how this foundation of knowledge is building towards new ways to tackle EBV-driven cancers.
 

Stealth tactics

The remarkable thing about EBV, as a virus, is its understated success. Around nine out of 10 adults carry the virus, making it one of the commonest human viral infections around.
If caught as a child, EBV normally causes no symptoms at all. Catching it later in life can also be symptom-free, although some people get quite ill for a short while with glandular fever before the immune system kicks into action.
But the virus has a card up its sleeve.
Unlike most infections, it isn’t conquered by the immune response. Instead it waves a white flag and retreats into hiding, lurking inside B cells – a type of white blood cell in the immune system.
This works to the virus’s advantage in the long run. As long as our immune defences are intact, the virus quietly persists under the radar, spreading from person to person, without us even knowing it’s there.
But there’s a darker side to EBV infection. There are an estimated 200,000 cancers caused by the virus across the world every year, including lymphomas, nasopharyngeal cancers, and some stomach cancers.
After many years of detailed research, scientists are starting to understand why EBV causes cancer in only a small minority of the vast number of infected people, and how it leads to different types of cancers and affects different age groups and populations across the world.
Understanding the way our immune system responds to EBV and keeps the virus at bay has turned out to be a crucial piece of the puzzle, and it’s leading to new ways to tackle these cancers.
And just as the story of the discovery of EBV had a hefty dose of serendipity, a couple of chance medical observations revealed the battle ground between EBV and our immune system.

When our defences are breached

EBV erupting from an infected B cell

One of the first clues came from some of the earliest people to receive human organ transplants, which became commonplace in the 1960s.
A decade later, doctors noticed that there were a worrying number of patients developing cancer after their transplant – primarily skin cancers, but commonly lymphomas too (coined post-transplant lymphoma).
The link to EBV was founded on a chance encounter in a lift. EBV expert, Dorothy Crawford, overheard a conversation between transplant surgeons discussing how to treat one of their patients who had developed post-transplant lymphoma.
She suspected EBV may be playing a role in the lymphomas and had been searching for samples to test, and suddenly the opportunity fell into her lap. The surgeons agreed to send her a sample from their patient – and, sure enough, all of the tumour cells tested positive for EBV.
Soon more samples were examined, and the link between EBV and post-transplantation lymphomas was confirmed.
The next intriguing piece of the puzzle turned up in the 80s, from within the gay community in San Francisco.
A new sexually transmitted infection had broken out, which we now know to be HIV, leading to AIDS. Many young men were hospitalised with infections such as pneumonia, but some had certain types of cancer including lymphomas that resembled ‘post transplant’ lymphomas.
These cancers were nearly all positive when tested for EBV too.
The discoveries raised big questions. Why were EBV-positive lymphomas so frequently affecting patients receiving organ transplants and young adults with AIDS? And what did these groups of people have in common?
The answer is a huge loss in the strength of their immune system. In the case of people receiving donor organs, they are given powerful drugs to suppress their immune reactions to stop them rejecting the organs.
Patients with AIDS lose a crucial part of their immune system, as the HIV virus destroys important white blood cells called T cells.

The pieces fall into place

Highly magnified view of EBV virus particles

Around the same time, scientists in Cambridge made a huge breakthrough.
In 1984 they published the complete DNA sequence of EBV. This meant scientists were able to identify the key proteins made by the virus that pushed B cells to grow out of control and become cancerous.
Combining this knowledge with the new understanding of the role played by our immune system helped untangle the complicated relationships.
EBV-linked cancers develop due to a combination of factors but they share one thing in common – a swing in the delicate balance between the body and the virus. We now know that the ability of our immune defences to keep the virus in check is one of the crucial barriers stopping cancers forming.
The lack of a robust immune defence against EBV (caused by drugs, disease, or small variations in genes that mean immune cells are less able to spot EBV) allows the normally timid virus to run riot. Then the proteins made by the virus instruct cells to keep dividing – the principle cause of cancer.

From knowledge comes treatments

Gathering interesting scientific knowledge is all very well, but what patients want are cures. The next step was to turn this information into new treatments for people with EBV-related cancers.
The idea seemed simple – if gaps in the immune system were causing the cancer to develop, could we turn the tables and use the immune system to strike back at the cancers?
In 1995, pioneering scientist Cliona Rooney working in the US showed that this approach held promise, while she was working at a clinic giving children with leukaemia life-saving bone marrow transplants.
To stop the donor’s bone marrow attacking the child’s tissue, the doctors removed T cells first.

A healthy human T cell

But while the treatment helped to cure their leukaemia, it left the children at high risk of developing EBV-related lymphoma.
To bridge the gap, Rooney and her team rescued the T cells removed from the donor marrow and separated out the ones that could specifically attack EBV. They then grew these ‘EBV killer T cells’ in the lab until they had sufficient numbers to inject into the children following their transplant.
The results were remarkable.
The 10 children she initially treated responded well – none had any problems caused by the donor’s T cells, and the three children whose EBV levels had shot up regained control of their infections.
One child had already developed a post-transplant lymphoma, but the EBV killer cells attacked and destroyed the tumour without needing any other treatment.
As with many early experimental therapies, Rooney’s new treatment had practical drawbacks, principally that it took a lot of time and money to make personalised EBV killer T cells from every individual donor.
The next step came from Cancer Research UK-funded scientist Dorothy Crawford, who first linked EBV with post-transplant lymphomas back in 1980.
She set up a large bank of EBV killer T cells taken from people donating blood and began a large clinical trial matching them to post-transplant patients to see if they could treat the lymphomas caused by EBV. The results were published in 2007, showing that more than half of patients who had developed lymphomas were completely cured.
This pioneering technique is now available for post-transplant patients with EBV-linked lymphomas.
Most patients are successfully treated by lowering the dose of immune suppressing drugs or a therapy that destroys B cells called rituximab. But for those who don’t respond the EBV killer T cells are a crucial avenue of treatment.

There’s much more to come

Following Rooney and Crawford’s ground-breaking research, scientists and doctors are now exploring whether the EBV killer T cells could also be manipulated to treat people with other EBV-linked cancers, such as nasopharyngeal cancer and lymphomas.
And there is another exciting approach in the pipeline – vaccines, both as a treatment and a preventive measure.

A vaccine against EBV could prevent and treat cancers linked to the infection

Our researchers in Birmingham are leading a clinical trial to find out whether a vaccine designed to boost the anti-EBV immune response of patients with nasopharyngeal cancer is an effective treatment.
The vaccine acts as a sharp reminder to the immune cells that the cancer cells infected with EBV are dangerous and should be destroyed.
So far, early results show that the vaccine is safe and can stimulate the patients’ white blood cells to attack their tumours, so the trial is continuing to the next stage. If it proves successful, the vaccine could also be used to treat people with other types of EBV-linked cancers.
Other Cancer Research UK scientists in Birmingham are working hard in the lab to find out whether a vaccine could be developed as a preventative measure to stop people catching EBV. Vaccinating people at high risk from EBV-linked cancers, such as children in sub-Saharan Africa, to stop them becoming infected in the first place could make a big impact on cancer rates around the world.
Professor Alan Rickinson, a leading expert in EBV research and one of our pioneering team in Birmingham, has seen much of the progress unfold and is optimistic we are working towards cures.
“Looking back over 50 years of research, one thing that really stands out for me is the journey we’ve come on,” he said. “From people’s scepticism of Epstein’s initial discovery that there was a link to Burkitt’s lymphoma, to where we are now – the realisation that EBV plays a key role in several cancers and an understanding of how the virus does this.”
“Thanks to all this research, we’re now moving towards the ultimate goal of being able to prevent EBV infection, potentially stopping many children and adults around the world from developing cancer.”
Despite all the work that’s gone on, the EBV story is far from finished, and we look forward to seeing the fruits of this groundbreaking research making a difference to patients for the next 50 years and more.