Dr R Sean Morrison from Mount Sinai Medical Center, New York, gave an important and thought-provoking talk on the sensitive topic of palliative medicine – care aimed at relieving and preventing symptoms without having a curative effect on disease.
People are living longer – by 2030 the number of people over 80 will have doubled in the UK. Within this ageing population comes a huge swathe of older men and women with diseases like cancer who may need palliative care.
Dr Morrison drew attention to the 6.5 million caregivers in the UK who look after relatives and friends with illness, and how palliative care should focus not just on the patient but on the people who help them cope too.
His impassioned plea was that we think more carefully about what we mean by ‘palliative care’ and that it should not be synonymous with end-of-life care. It should be part of a more holistic package of care offered early to patients and their families alongside their treatment to try to cure disease.
To underline his point, he showed how people with advanced lung cancer who were given earlier palliative care (which included help with symptoms such as sleep disturbance, pain and anxiety) had an improved quality of life, fewer depressive symptoms and received fewer burdensome treatments.
But even more important, people who received the early palliative care lived, on average, three months longer than those who did not. Dr Morrison said that cancer drugs with such life-extending effects are routinely approved, so palliative care needs to be given the focus it deserves.
When it comes to developing more effective ways to treat cancer, it’s not always possible or ethical to carry out experiments with patients, so scientists turn to animal models. And while a lot of cancer research is done using simple organisms such as fruit flies or zebra fish, sometimes only a mouse will help yield the information we need. Yet finding ways to accurately mimic human cancers and their response to treatments in mice is a challenge.
In a fascinating session looking at the very latest developments in this field, Dr Louis Chesler’s talk stood out. He spoke about progress at The Institute of Cancer Research in developing a more accurate mouse model of neuroblastoma – a devastating but rare type of childhood cancer.
Often, children with neuroblastoma are initially treated successfully, but the cancer can come back. Thanks to this model, scientists have been able to test new approaches for treating these children, which are now being taken forward into clinical trials to help save lives in the future.
Dr Ton Schumacher from the Netherlands Cancer Institute opened a fascinating session on immunotherapy – treatments that harness the body’s own defence mechanisms to fight cancer. The buzz around immunotherapy has been building in recent years, and this was a good chance to see some of the recent research in this area.
Dr Schumacher has been studying whether the immune system can be re-programmed to recognise faulty molecules on the tumour cells based on its genetic mistakes, leaving healthy cells alone. Early results from lab models of melanoma showed that boosting the immune cells that can spot and target these tumour molecules dramatically slowed its growth.
Dr Stanley Riddell from the USA followed with a presentation on the development of genetically engineered white blood cells. The specialised cells, called T cells, can be modified to target molecules on the surface of tumours. Dr Riddell’s work has teased apart the specific types of T cells that are most effective, and clinical trials for people with lymphoma who don’t respond to chemotherapy are looking promising.
And Dr Doug Fearon from Cambridge took an in depth look at why immunotherapies have not yet benefitted patients with pancreatic cancer. He described a type of cell called a fibroblast in the tissue around the tumour that protects the tumour by barricading the white blood cells from getting in. In mice studies, blocking molecules made by the fibroblasts reversed the barrier and made immunotherapies like ipilimumab more effective.
This approach could lead to new treatments for pancreatic cancer, a disease that is notoriously difficult to treat.
Cancer cell migration is a major problem. It leads to metastasis that results in the death of many cancer patients. And yet we don’t understand very much about it. Dr Eric Sahai from our London Research Institute introduced a session to bring us all up to speed with the latest developments in this area of research.
One of the challenges in understanding cell movement is the problem of heterogenetity, which we often hear about in a genetic context from researchers like Professor Charlie Swanton. But it happens in cell migration too. Cancer cells will adapt to their environment and use a variety of methods to get from one place to another and create problems. And multiple mechanisms of getting about can all happen in the same piece of tumour at the same time.
We need to understand how cells move in the 3D environment of the tumour to truly understand this process. Professor Sahai has developed a computer model of a cancer cell that he can challenge with different environments and see how it responds. He’s created “a virtual cell that seems to be behaving in a reasonable manner”, meaning that it’s doing pretty much what real cancer cells do.
Dr Ewa Paluch from University College London then talked about how cancer cells can very quickly – in seconds – switch from one way of moving to another – which she beautifully exemplified with stunning films of cell movement. This makes them very good at adapting to their environment. People in Dr Paluch’s lab are even going so far as to create lab-based obstacle courses for cancer cells, to see how they cope.
Finally, Dr Peter Friedl spoke about his work to understand how tumour cells move through real tissues. We used to think that tissues created some sort of barriers to movement. But in fact tumour cells are very good at adapting to spaces and wedging their way through. Dr Friedl described tissues as being like complex cities such as Liverpool or London. There are impenetrable areas so built up you can’t simply walk through them. But there are also tracks you can move along – like pavements and alleyways.
These tracks in tissue allow tumour cells to begin invading nearby tissue in a non-destructive way that is very hard to spot. The more we understand about this process, the more we can block it and cut off the tracks used by cancer.
The final talk of the conference came from Professor Nazneen Rahman, from the The Institute of Cancer Research, who gave us an engaging overview of the hunt for cancer predisposition genes . Perhaps the most famous examples – thanks to Angelina Jolie – are the BRCA genes (BRCA1 and BRCA2), linked to breast, ovarian and prostate cancer.
More than 100 of these genes have been found so far, and inheriting a faulty version of one of them significantly increases cancer risk. And tests for around half of them are already available on the NHS, helping people and their families, as well as their doctors, to make decisions about prevention, screening and cancer treatment.
Professor Rahman outlined how she and her team are searching for predisposition genes in families affected by many cases of breast and ovarian cancer, making some unusual and intriguing findings in the process. She also highlighted some of the benefits, challenges and potential pitfalls of dealing with these genes, particularly when it comes to translating genetic information into clinical decisions about cancer prevention and treatment.
Wrapping up the whole event, our chief executive Dr Harpal Kumar, this year’s chair of the NCRI, reiterated the purpose of the conference – to bring people together across the whole cancer research community to share new ideas and push forward progress in beating the disease.
We agree with his summary that it’s been the best conference so far, with a real buzz in the air. We left feeling exhausted but also elated at the tremendous progress being made in our understanding of cancer.