Giant touchscreen helping in the battle against cancer

A giant touchscreen computer for junior doctors and medical students to study tumours in fine detail is the latest weapon in the battle against cancer for Oxford University Hospitals NHS Foundation Trust.

Cancer Research UK Oxford Centre has funded the 55-inch wide screen for the teaching of histopathology speciality trainees and medical students from the University of Oxford and the 500 researchers and clinicians that make up the Oxford Centre.

It allows users to “pinch and pull images” to identify the features of tumours that could predict their prognosis.

Until now, junior doctors and medical students have had to use microscopes linked to other microscopes used by teachers.

With the new technology, users can manipulate images – which are sent to the hospital pathology department – by zooming in and out and moving and rotating the images.

It is hoped the technology will improve the teaching of junior doctors and medical students so they can provide the best possible cancer diagnosis to patients.

The £25,780 computer has been funded by the Cancer Research UK Oxford Centre and draws on more than 400 scanned images from Oxford University Hospitals NHS Foundation Trust patients.

The first session took place on February 23 for urological pathology to prepare histopathology registrars for upcoming fellowship of the Royal College of Pathologists’ exams.

Dr Clare Verrill, Senior University Lecturer in Pathology, who taught the first session: “Having this digital screen, enables a new and exciting way of teaching where learners and teachers are able to interact with the images and makes for stimulating and interesting discussions .

With an increasing trend for use of digital pathology images for routine diagnostics as well as research, histopathology registrars will be better equipped for modern pathology practice.

Histopathology speciality trainee Dr Andrew Smith said: “Histopathology training is driven by practical experience – you have to look at a lot of cases to learn how to recognise tumours for what they are.

“Having access to cases digitally and in high resolution means you can learn from a case even when the slides for that case are not available in the department.

“I think using interactive technology in this way also makes the subject more accessible. Hopefully it will inspire more medical students and junior doctors to pursue a career in histopathology.”

Dr Claire Bloomfield, Strategic Planning Lead at the Cancer Research UK Oxford Centre, said: “Supporting our future leaders in cancer diagnostic is a key aim for the Cancer Research UK Oxford Centre.

“Effective, detailed diagnosis is a key foundation in our vision of making cancer therapies more targeted to individual patients.”

Dr Áine McCarthy, Cancer Research UK’s science information officer, said: “This technology offers a unique way for junior doctors and medical students to study the art of histopathology, a hugely important area of medicine.

“By using state of the art technology, we’re offering these doctors and students better training which will benefit both them and patients in the future.”

If you’re an Oxford Centre member interested in using this resource, please email


The future of cancer treatment

1 in 3 people born after 1960 in the UK will be diagnosed with some form of cancer in their lifetime, and each year, 4th February marked World Cancer Day, to raise awareness and encourage individuals and governments to fight the disease.

The Cancer Research UK Oxford Centre has many research groups working at the cutting edge of the fight against cancer, and Charvy Narain of Oxford Science Blog spoke to one such researcher, Professor Colin Goding from Ludwig Cancer Research at the Nuffield Department of Medicine, about what cancer treatments might look like in the future.


Oxford Science Blog: Why is cancer of interest to scientists?

Colin Goding: We have something like 14 million million cells in our body, but only one in three of us, and over many years, gets cancer (defined by the uncontrolled division of cells which grow to form tumour). At the cellular level, cancer is extremely rare, and this is because we have mechanisms that block mutated cells progressing towards disease.

We study these mechanisms in melanomas, which are cancers that begin in melanocytes – the cells the produce the pigment melanin, which colours skin, hair and eyes. So melanomas are usually (but not always) skin cancers.

Melanoma are a good ‘model’ for cancer because we can see all stages of the disease: completely normal pigment cells, but also moles that have an activated cancer-causing gene that puts its foot on the ‘accelerator’ pushing cells to divide, counterbalanced by a very strong anti-cancer mechanism (present in all cells) that cuts the fuel to the engine so cells stop dividing.

We can also see melanomas that progress to spread across the surface of the skin, or those that start to invade and spread to other parts of the body. We’re particularly interested in how these state changes happen.

OSB: Given the rarity of the cellular events that lead to cancer, how does it ever take hold?

CG: It is a complicated process, but to get a cancer, you need to inactivate the ‘brake’ that stops uncontrolled cell division, and there is more than one cellular braking system. On top of this, the genes encoding the ‘accelerator’ for cell division have to be turned on.

If these mutations occur in the wrong order, the engine stalls: there is no cancer. To get cancer, the mutations need to happen in the correct order: you lose the ‘brakes’, the cell machinery gets put in gear, and then the ‘accelerator’ mutations happen.  Only then will the cancer progress.

OSB: Why are you particularly interested in melanomas?

CG: The advantage of studying melanomas is that, as a skin cancer, we can see all of these disease stages – in lung cancer, for example, by the time a patient comes in with symptoms, the cancer has usually already moved to quite a late stage.

Another advantage of studying melanomas is that we understand a lot about the genetics of pigment cells, and many of the genes that have gone wrong in melanoma are the ones involved in the normal development of pigment cells. So we have a pretty good understanding of the genetic basis of this form of cancer: we know that the ‘accelerator’ genes are, for example, and we understand the braking mechanisms too.

Melanoma is also a form of cancer that affects many people: there are over 13,000 new cases of melanoma every year. The measure that correlates best with disease rates is childhood sunburn and cases of melanoma have been doubling every 10 years for the last 40 years. This is partially because there is about a 30 year lag between people becoming aware of the dangers of UV exposure from the sun and a change in disease rates.

And it is still the case that if you go to a park on a hot sunny day, or the beach, there are still people who are getting burnt. So there is still work to do in educating the public about the dangers of excessive sun exposure.

OSB: How has the treatment for melanoma changed over these decades?

CG: For 50 years, there was very little progress in treatments for melanoma: surgery to cut out early lesions before they started to spread is still a very effective therapy, but that was pretty much it.

But the realization that certain genes act as the accelerator pedal to push melanoma formation has led to drugs that target this mechanism. We now know which cancer gene responds to which particular drug. The response in patients whose cancer stems from these sorts of mutations is very good, but if the patient does not have the specific gene targeted by that drug, treatment with that drug might actually make things worse. So patients are now increasingly being tested for particular mutations before being treated with specific drugs.

The real problem, however, is that even if a drug works, for most patients, it is almost inevitable that resistance to that drug also appears some months later: the drug stops working, and the cancer carries on growing and spreading, eventually killing the patient.

A huge amount of work over the last 50 years or so has also gone into  understanding the mechanisms cells use to block immune cells from infiltrating and attacking a developing tumour. Many of these mechanisms have now been identified, and the consequence is that there are now new drugs in the clinic that will help reactivate the immune system, enabling it to attack the cancer.

These drugs have also been very effective in many patients, but again, not all patients respond, there are many side-effects, and in some cases, resistance sets in after a while.

Essentially, resistance seems almost unavoidable for any one single kind of drug.

OSB: What can be done to combat this resistance?

CG: The first mechanism for cancer drug resistance is genetic:  unless the disease is at a very early stage, within all the cancer cells in a patient’s body there is likely to be at least one that has another mutation that confers resistance to a particular drug or therapy. So when that drug is used, all of the other cells die, but the one with the mutation survives – and it then repopulates the tumour. This turns out to be quite a common mechanism for resistance to so-called targeted therapies that hit a key molecule.

The only way to really deal with this mechanism of resistance is to treat the patient early, and when the treatment is successful, to monitor the patient very carefully, with tools that are more sensitive that those we currently have, to track the cancer coming back.

This is because it’s a numbers game for genetic resistance – the chances of resistance developing are proportional to the number of cancer cells in the body. The greater the number of these cells, the greater the likelihood that some cells will be resistant to the drug being used. So even if you have a second drug that can kill cancer cells that survive the first drug, giving the second drug at a later stage, when there are many more cancer cells, means that it is again almost inevitable that a few cells will be resistant to the second drug too.

So treating as early as possible, when there are as few cancer cells in the body as possible, is the best way of overcoming genetic resistance.

OSB: How does your own work approach these treatment failures?

CG: We work on the second mechanism for cancer resistance, one based on the cancer cells in a tumour adopting different states.

We and others have found that in different circumstances, cancer cells can adopt different ‘personalities’ that can be more or less resistant to a particular treatment. The adoption of these different states is influenced by the microenvironment surrounding each cell, which includes factors like oxygen or nutrient levels, or signals from infiltrating immune cells.

All of these factors combine to induce the tumour cells to adopt different states. One of these states might be a drug-resistant state, another might be an invasive state, where cells start to move away from the primary tumour and spread throughout the body to form metastases.

For example, we now know, from the work that we’ve done on melanomas, that movement away from the primary tumour to seed these metastasis is primarily driven by the cancer cells’ microenvironment.

The interesting thing is that the cancer cell states are dynamic and reversible, and these micro-environmental influences can potentially be modulated by drugs. This isn’t quite the case for the genetic mutations, which are pretty much irreversible – you can target the altered protein made by the mutation, or you can try and kill the mutated cells when their numbers are low, but that’s the only way you can deal with the genetic issue in cancer.

But by understanding cancer cell states, we can perhaps turn a drug-resistant population of cells to a drug-sensitive one.

OSB: How could you bring about this change in state?

CG: We could do this by changing the micro-environment, or by finding drugs that drive cells to adopt a particular state. We’ve done this quite successfully for a drug called methotrexate – this was already in use for psoriasis and rheumatoid arthritis, but we found out a couple of years ago that this drug switches on one of the genes that stops melanoma cells spreading to other parts of the body. Working in collaboration with another group, we also found that methotrexate also sensitized cancer cells to another drug, and so we’re currently working on ways to drive cancer cells into states responsive to different drugs.

We think many drugs designed for other diseases and not currently used to treat cancer might turn out to be useful for targeting some of these mechanisms which can switch cancer cells from one state to another.

OSB: How do you think cancer therapies need to change in the future?

CG: Cancer therapies need two things: first, we need to identify relapse (the cancer coming back) way ahead of when we do now, so that drugs that can bypass resistance to the first therapy can be given before resistance to the second therapy arises. This is similar to what we already do for bacterial infections: we don’t use the same antibiotic again when a first dose leaves resistant bacteria, and we ideally give a second antibiotic before the infection becomes re-established.

The second approach needs us to really understand the mechanisms by which cancer cells adopt inter-convertible states with different drug sensitivities. Then, we can use drug combinations, so that drug A sensitizes a tumour to drug B.  We need to be really clever about how to do this and get the timing right. This requires quite a lot of work to understand fully the processes involved, but we’re getting there!


Read more about world-leading Oxford science on the Oxford Science Blog here

Oxford researcher secures funding for powerful imaging technique in pancreatic cancer

Pancreatic Cancer Research Fund (PCRF) is funding six new research projects with a total of £1 million – bringing the charity’s support for research into the UK’s most lethal cancer to over £8 million. This is the third year that PCRF has invested £1 million in a single funding round. In total, the charity has funded 40 cutting edge research projects across the UK and Ireland, worth over £6 million.

Oxford researcher Dr Bart Cornelissen will be leading one of the six newly funded projects. Dr Cornelissen aims to use powerful imaging techniques to diagnose early stage pancreatic cancer. His team has already developed an imaging agent that attaches to a protein known as claudin-4 which is expressed in the early stages of the disease. This project will develop the agent so that this protein can be rapidly detected and monitored using PET scanners, which are increasingly common in hospitals. Dr Cornelissen is part of the Cancer Research UK Oxford Centre Pancreatic Cancer working group, and the early stages of this project were supported by an Oxford Centre Development Fund award.

Projects at Imperial College London, University of Liverpool, Swansea University, Cancer Research UK Manchester Institute and Queen Mary University of London, will also receive funding.

These new grants are in addition to the £2 million committed to the Pancreatic Cancer Research Fund Tissue Bank, which launched in January 2016 and will accelerate research progress. The Tissue Bank is the world’s first nationally co-ordinated pancreas tissue bank and has already been hailed as “one of the most important developments in resourcing UK pancreatic cancer research in a generation”.

Says PCRF’s founder and CEO, Maggie Blanks: “In the charity’s early years, we had to focus on basic research to help understand pancreatic cancer and its mechanisms, with the knowledge that this would be a springboard for future research progress. More recently – typified by this year’s grants – we’ve been able to focus on projects that are closer to patients. These include innovative ways of making current treatments much more effective, developing ‘personalised medicine’ approaches and finding ways to diagnose the disease in its earliest stages.

“We’re committed to beating this disease and thanks to our loyal supporters whose fundraising enables us to fund all these projects and initiatives, we’re making real progress towards this goal.”

Oxford charities come together for World Cancer Day

The Lord Mayor of Oxford is joining forces with a cancer patient, who received life-saving treatment in Oxford’s Early Phase Clinical Trials Unit, to unite the community on World Cancer Day.

Cancer Research UK Oxford Centre and Oxford City Council are being supported by five local charities – Macmillan, Sue Ryder, International Network for Cancer Treatment and Research, Cochrane and the Oxfordshire Prostate Cancer Support Group – to help raise money and awareness, and represent cancer patients in Oxford on February 4.

They include Susan Cakebread, who was told she may have only eighteen months to live after being diagnosed with cancer, but is now free from signs of the disease after taking a trial drug for almost three years.

Susan, who will celebrate her 69th birthday on World Cancer Day, received her pioneering treatment at the Early Phase Clinical Trials Unit at the city’s Churchill Hospital which aims to discover new treatments for the future.

The Lord Mayor, Councillor Rae Humberstone, will host a programme of events which start with doctors, scientists and patients joining members of the public in Bonn Square to form a human chain to mark the day.

They will wear Unity Bands™ to show their support for Susan and others affected by cancer. The Unity Bands – made of two parts and knotted together to symbolise the power of what can be achieved when people come together – will be available for a suggested £2 donation on the day. The charities hope people in Oxford will pick up a Unity Band and wear it with pride on February 4.

Experts will later be on hand in the Town Hall to share the most up to date research in Oxford where Cancer Research UK spends around £22 million every year. Representatives from local charities will give short talks about their work and throughout the day there will be several lab tours at the Cancer Research UK Oxford Centre.

World Cancer Day celebrations will culminate with a Gala Concert in the evening.

The Lord Mayor said: “Along with doctors, health workers and representatives of the many cancer charities, I am helping to launch Oxford’s contribution to World Cancer Day. Many of us have had, or will have, a more than passing acquaintance with cancer. “It may be through a family connection, a friend or work colleague, or a personal experience of “The Big C”. My wife successfully fought breast cancer in 2006 and I had a brush with skin cancer in 2012.

“Highlighting cancer awareness is as important as welcoming new forms of treatment, if we are to finally beat this terrible disease. Therefore, I hope people in Oxford will do their bit to promote that awareness and also show support for those who are, in many different ways, currently affected by cancer. Whether by making a £2 donation for a Unity Band or joining the human chain in Bonn Square, all support is most welcome. Thank you”.

Tara Clarke, Research Engagement Manager in Oxford who organised the event, said: “World Cancer Day is a unique opportunity for people in our region and beyond, to unite for one day and show that together we can do something about cancer. So many of us have been affected by the disease, which is why on February 4 we are calling on the people of Oxford to join together and wear their Unity Band with pride. Success stories like Susan’s would not be possible without the commitment of our amazing supporters, who fund each charity’s individual work into the prevention, detection, treatment and support of those with cancer.

“So whatever the motivation – to remember a loved one, celebrate people who have overcome the disease, or to rally in support of those going through treatment – World Cancer Day is a chance to get involved and help reduce the impact of cancer on future generations.”

This year for the first time, three leading national cancer charities – Breast Cancer Care, Anthony Nolan and the Movember Foundation – have joined forces with Cancer Research UK to galvanise the whole nation to support World Cancer Day and help transform the lives of millions of people affected by cancer.

Each charity has Unity Bands available in their own colours and all money raised from the Unity Bands will go towards the charities’ individual research projects and support services.

Money raised will fund breakthroughs in scientific research; save and improve the lives of people with blood cancers; provide high quality care, support and information for people with breast cancer, and fund research and support services to tackle prostate and testicular cancer.

For more information on the partnership and to get a Unity Band, go to