Together we will beat cancer


Chocolate, biscuits, crisps and ice cream; just some of our guilty pleasures, particularly at this time of year. But a raft of headlines today warn that these high fat foods could make cancer more aggressive.

So, is there any truth in it? The science says maybe.

As it stands, cutting out the odd chunk of chocolate won’t stop cancer from spreading. But if you dig a little deeper, the research behind today’s news is a lot more complex, and far more interesting, than the headlines make out.

The story is based on a study published in the journal Nature by a group of scientists in Barcelona. The researchers were studying the processes that allow cancer cells to break away from a tumour and spread, or metastasise, around the body.

They focused on a molecule called CD36, which helps cells take up fats from the blood.

But what role, if any, does fat play in how cancers spread?

This research provides an intriguing glimpse into the potential role of the CD36 molecule in cancer spread. And it could point to a potential new approach for treating cancer, although that’s a long way off.

But it’s very far from providing evidence that the odd bar of chocolate will make cancer more aggressive.

Let’s take a look what the researchers actually uncovered.

What did the scientists find?

The researchers were studying mice with mouth cancer, and they homed in on a small group of cancer cells that break free from the tumour and spread, forming new tumours in other tissues.

The team’s goal was to understand more about these aggressive cancer cells and what makes them tick. When they analysed genes inside these cells they noticed that lots of genes involved in fat uptake and fat processing were unusually active.

At the top of the list was CD36.

Fat in the diet clearly plays a role in this study, but the mice were fed a diet excessively high in fat, not a normal diet at all

– Professor John Marshall

“Scientists have been interested in CD36 for a long time,” says Professor John Marshall, a Cancer Research UK scientist from Barts Cancer Institute in London. “It’s a type of molecule called a scavenger receptor. The first connection between CD36 and fat was made in 1999, when scientists genetically engineered a mouse with no CD36.”

Fats are essential to the normal running of our bodies. For example, a thin layer of fat forms the outside of cells giving them shape, fats form the basis of many hormones which allow our organs to communicate with each other, and fats are an essential and rich source of fuel for cells.

The CD36 molecule helps cells take up certain fat molecules from the blood so they can use them as energy for building new cells.

And in this study, the team revealed for the first time that CD36 and certain types of fat play an important role in cancer spreading.

Because the scientists were studying cells in mice, they could use genetic engineering to make mouth cancer cells that had high or low levels of CD36. And they saw that, in line with their theory, the amount of CD36 in the cancer cells was linked to how aggressively the cancer spread.

But was this effect linked to the uptake of fat, or was the molecule playing another role?

To answer this, the scientists compared mice given a very high-fat diet with those on a normal diet. And they found that the most aggressive cancers were in mice with high levels of CD36 on the cancer cells combined with a high fat diet, suggesting that CD36 was driving cancer spread by fat uptake.

“Fat in the diet clearly plays a role in this study,” says Marshall, “but the mice were fed a diet excessively high in fat, not a normal diet at all.”

Where could this research lead?

It’s an interesting discovery, but does the same thing happen in people? And could this help scientists develop ways to stop cancer spreading by stopping CD36 doing its job?

Early experiments in this study indicate this could be a possibility. The researchers treated the mice with molecules that stick to CD36 and stop it transporting fat into cells.

They found that although these mice still developed mouth tumours, the drug completely stopped the cancer spreading to other organs. In contrast, the cancer spread in all of the mice that weren’t given the treatment.

According to Marshall, it’s a really exciting discovery: “Not only did targeting CD36 completely stop cancer metastasising in the mice, but it also reduced the size of tumours that had already grown in distant sites.”

What about CD36 in people?

The discovery of the role CD36 plays in mice with mouth cancer is intriguing. But people, and their cancers, are genetically a lot more complex than mice.

To try and determine if CD36 might be important in cancer in people, the researchers analysed big databases of genetic information from cancer samples taken from patients. And they found that for certain types of cancer – small cell lung, bladder, or a common type of breast cancer – survival was poorer for people who had high CD36 levels in their cancer cells.

This is far from concrete proof, but it suggests that the research might hold true for some forms of cancer in people too. “This could have huge potential,” says Marshall.

This is a really interesting piece of research, and the good news is that it could lead to new drugs that block CD36, similar to the treatment the mice were given.

“The most exciting thing about this study is that, as far as I’m aware, it’s the first metastasis-promoting molecule that is on the surface of cancer cells and therefore accessible to drugs,” says Marshall.

Of course, there’s still a way to go before this approach would be available for patients. Any new treatment would need further research and rigorous safety checks before being tested in people.

And the next exciting piece of the puzzle will be further research into just how CD36 is fuelling cancer spread. “This is a beautiful study, but the next thing we need to find out is the mechanism by which CD36 regulation of certain types of fat molecules is driving metastasis,” says Marshall.

Interestingly, obesity increases the risk of 13 types of cancer.

But the biology behind how it does this isn’t fully understood – something we’ve covered before. So this latest study could also offer important clues about how obesity causes cancer, as well as ways to tackle it once a tumour has developed.

Take-home message: should patients avoid a high fat diet?

While this is an exciting piece of research, it’s far from providing any kind of proof that patients should cut out fat from their diet.

Firstly, this study worked with mice. There’s no direct evidence that patients with cancer who drastically reduce fat consumption see any improvement in their chances of surviving.

Our diets are very complex, much more varied than a lab mouse’s diet, and foods usually contain a mixture of different fats that have a huge variety of roles in our bodies. We don’t know what potential harms might be caused by dramatically reducing dietary fat, or whether cutting out a single type of fat would be effective.

For cancer patients undergoing cancer treatment, it’s important that they consume enough calories to cope with the physical burden of therapy.

And for anyone who has completed treatment and concerned about their diet or weight, we recommend talking to your doctor or a qualified dietician before making any radical changes to your diet, just to make sure it won’t negatively affect your health.


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Emma January 11, 2017

Hi Neville,
There’s no good evidence that cutting sugar out of your diet is helpful for cancer patients – more information can be found in this blog post. It’s true that cancer cells use ‘sugar’ (or glucose, the molecule that sugars and carbohydrates are broken down into) at a faster rate than healthy cells tend to – this is because they are multiplying rapidly. It’s a fascinating area of research, and scientists are looking into abnormalities in the way cancer cells take up and use glucose with the aim of developing drugs that cut off their energy supply without harming healthy cells. But this isn’t evidence that sugary foods support the growth of cancer, or that cutting out these foods will stop cancer cells multiplying. Our advice to people getting treatment for cancer is to try and stick to a healthy balanced diet (more here) and most importantly eating enough to help cope with the physical toll some therapies can take.
Best wishes,
Emma, Cancer Research UK

Neville January 9, 2017

One dietary approach to possibly “controlling” or limiting cancer cell growth is a low carbohydrate/ high fat diet (LCHF and could be a ketogenic diet) which attempts to prevent high sugar spikes in the blood (“cancer cells love sugar”). This is of course quite a different approach to the one possibly suggested here.

We need clarity and evidence! This is a vitally important issue to many people!

Ana January 5, 2017

@ Angeli – If you read carefully you’ll find that the article is actually highlighting the fact that inhibiting the activity of this specific molecule will result in cancer not spreading which would make a huge difference to cancer patients.
Additionally, we should be a bit more encouraging of anything that could potentially save lives because unless you have a better way of going about this, science has always been about trial and error before getting to confirmed facts.

Angeli December 30, 2016

This still sounds like guesssing rather than scientific fact. Yes, these are facts in themselves but when you take a step back into common sense, I know too many slim people on healthy diets who developed and died of cancer, including the main obesity-attributed cancers (ovarian, breast). Not to mention the vast amount of obese, middle aged people who have survived on terrible diets, smoking and drinking!

Surely we should be looking at experiments on how damaged cells lead to cancer, through smoking, through certain occupations like the building and engineering trades (lung and other organs affected by materials and processes like radiation). What about what our bodies have to filter through our food and leave residues via our blood and lymphatic systems in cancer prone organs or glands?

And then there are the attributable inherited genes…..