Clockwise from top left: Dr Alessandro Vannini, Dr Simona Parinello, Dr Igor Vivanco, Dr Ivan Ahel, Dr Stephen Tait and Dr Stuart McDonald
We’d like to introduce you to our new leaders at Cancer Research UK. They’re spearheading their own research teams for the first time and setting out to tackle some of the biggest questions we need to answer to help more people survive cancer.
Killing cancer cells – Dr Stephen Tait
Dr Stephen Tait, who works at our Beatson Institute in Glasgow, has found that treating cancer isn’t just about killing cancer cells – it’s also about how you kill them.
Most cancer treatments interfere with vital cell processes, which causes distress to the cells and makes them self-destruct. But the team has found that if you directly press the self-destruct button by blocking a protein called Bcl2, not only do some cancer cells die, it also helps the immune system recognise the rest of the cancer cells.
“We found that if you kill cancer cells in a certain way in the lab, it can make cells of the immune system better at recognising them,” explains Tait.
We need to find out what’s going on in people.
–Dr Stephen Tait, Cancer Research UK
“We want to see if this could help engage the immune system to kill the rest of the cancer cells.”
And Tait believes if the immune system is armed against the tumour, combining this way of killing cancer cells with immunotherapy drugs could be a really effective way to kill cancer cells.
“We’re excited by what we are seeing in the lab, but we have more work to do. The biggest challenge will be to take these findings from the lab into humans. We need to find out what’s going on in people.”
Cancers’ master switch – Dr Alessandro Vannini
At The Institute of Cancer Research, London, Dr Alessandro Vannini is looking at a ‘master switch’ that affects how cancer cells read and interpret their DNA, an important step in making new proteins.
This ‘switch’ helps healthy cells sense harsh conditions, causing them to die. But in cancer cells the ‘master switch’ – called Brf2 – is rewired allowing them to survive, and even thrive in damaging conditions.
“Cancer cells are able to survive conditions that would kill a healthy cell, and the way the cell reads its DNA is important in this survival,” says Vannini.
To do this, cancer cells use Brf2 as a chemical ‘sensor’. And Vannini’s team think this may override the cell’s normal response to harsh conditions.
This provides a potential target for Vannini and his team. They are trying to understand how this ‘master switch’ works and they hope to be able to develop drugs to target Brf2, and stop cancer cells surviving conditions that should kill them.
“The biggest challenge now is how to specifically target this ‘master switch’,” says Vannini. “And personally, I like to be challenged.”
Targeting cancers’ ‘addictions’ – Dr Igor Vivanco
Dr Igor Vivanco, also based at The Institute of Cancer Research, London, is trying to exploit certain cancers’ ‘addiction’ to a molecule called AKT.
While healthy cells also have AKT – which controls a range of cell processes from growth to death and how cells move – they aren’t totally reliant on the molecule to keep doing all these tasks.
But some cancer cells become reliant, or ‘addicted’, to a faulty version of AKT, making it a hot target for cancer drugs.
“Scientists have tried to target AKT before,” says Vivanco. “But a lot of those drugs failed in clinical trials. We want to understand more about this protein so that we can develop better treatments.”
Armed with knowledge about AKT, Vivanco hopes to develop new drugs that target and block this protein better than before. And he hopes this will make them better potential cancer drugs.
But Vivanco isn’t just focussing on AKT. He wants to expand his work, using what he learns from this project and applying it to other faulty molecules.
“I’m hoping that in the future this work will open the door to helping study other proteins,” he says.
So this could lead to a range of new drug targets.
Reducing unnecessary tests – Dr Stuart McDonald
Every 2 to 3 years, patients with Barrett’s have an endoscopy, which involves a tube with a small camera being inserted into their throat, to look for any signs of cancer.
“Most of these patients won’t get cancer,” explains McDonald. “But because oesophageal cancer is so difficult to treat, especially in the later stages, we don’t want to miss any Barrett’s patient who’s showing signs of cancer.”
The challenge is there’s not yet a good way of telling apart the people with Barrett’s who would benefit from a regular endoscopy from those that won’t.
McDonald hopes to tackle this.
“We want to design a way to split patients with Barrett’s into two groups – those with a high risk of developing oesophageal cancer and those with a low risk. That way we can offer more resources to high risk patients,” he says.
And this will be beneficial for low risk patients too.
“If you have a low risk of developing oesophageal cancer, then being able to avoid an endoscopy is a good thing. We want to avoid subjecting patients to the stress of the procedure that they will not benefit from,” McDonald explains. He also says it will avoid unnecessary use of NHS resources.
But finding a way to split the patients is no mean feat.
According to McDonald, the key to determining high versus low cancer risk patients is hidden within the samples they collect from Barrett’s patients. He hopes by studying how the condition evolves, he can to develop tools that can be used by doctors to reliably tell these patients apart. This would be a major advance in how we treat patients with Barrett’s.
On the hunt for new drugs – Dr Ivan Ahel
At the University of Oxford, Dr Ivan Ahel is finding out what role 2 recently discovered molecules, called MACROD1 and MACROD2, play in how breast and prostate cancers develop.
“We don’t know much about these molecules yet,” explains Ahel. “But we have found that they work overtime in breast and prostate tumours, and are thought to be associated with a worse patient outcome,”
And he has a hunch they may also play a role in drug resistance in these cancers.
There’s a lot to be discovered.
– Dr Ivan Ahel, Cancer Research UK
Through his work, Ahel aims to get a better understanding of the role these proteins play in the way cancer cells become resistant to treatment.
He also hopes that the molecules may be a marker for these cancers, to help diagnose the disease, as well as a target to hit with drugs.
“We have a team of several researchers who will be looking at this from several different angles, to help us understand more about these proteins, how they work and what their role is in these cancers.”
“We’re beginning to understand the role of these proteins in cells, but now we need to look in the body. There’s a lot to be discovered.”
Tackling hard to treat brain tumours – Dr Simona Parrinello
Glioblastoma is the most common type of brain tumour. It’s also the hardest to treat. One of the reasons for this is its ability to spread.
At the London Institute for Medical Sciences, Imperial College London, Dr Simona Parrinello is studying how healthy cells and glioblastoma cells communicate with each other to help the cancer cells escape a tumour via blood vessels.
Parrinello has already identified a molecule called Ephrin as an important factor in this process, allowing the cancer cells to use the blood vessels as a highway to the rest of the brain. But she thinks there may be other molecules involved too.
“We’ve found some important interactions between cancer cells and blood vessels in these tumours,” Parrinello explains. “But we need to know more about the other molecules and cells that are involved in glioblastoma so that we can target the disease better.”
“It’s complicated work, so we need to invest more time, money and effort into figuring it out.”
By understanding more about these interactions in gliobastoma tumours, Parinello hopes to identify new treatments that can prevent the disease from spreading, and help more people survive.
- These projects were funded through our Programme Foundation Award. If you’re a researcher you can find out more about this award on our website.