Our Head of Research, Phil Hexley, outlines what happened at SNO: the 22nd Annual Meeting and Education Day of the Society for Neuro-Oncology
The Society held its 22nd annual meeting in November and we were there in force to learn about the latest progress and build relationships with the world leaders in neuro-oncology.
Professor Alfred Yung, Keynote Presentation
Professor Yung spoke about the landscape of neuro-oncology, highlighting the major gaps that need to be addressed. A hot topic for discussion is understanding tumour heterogeneity - this is where different cells in a tumour have different biological characteristics, for example cells in the middle of the tumour may grow and respond very different to cells on the surrounding edges.
It is this heterogeneity that makes killing the entire tumour difficult as treatments may kill some cells but other cells could survive and grow.
Understanding the issues of drugs not reaching the tumour through the blood-brain barrier (BBB) was another key area Professor Yung spoke about. The BBB are the cells which help protect the brain from harmful things in the blood.
Even when drugs can kill tumour cells they are often unable to pass through the BBB in sufficient levels to kill the tumour cells. Increasing the level of drugs in the body may not be the solution as it can increase unwanted side-effects too.
So, even though we need to find new drugs we also need to make sure these drugs are reaching the tumour cells in sufficient levels to be effective.
Closing his keynote presentation Professor Yung spoke about how he thinks the neuro-oncology researchers should proceed, stating we should:
“Unleash the power of data, be patient-centric, improve lives, move the needle for patient care"
This was an inspiring talk from a distinguished researcher and clinician, providing focus on patients and highlighting the areas that need to be addressed, setting the tone for the conference ahead.
Tumour heterogeneity and resistance
If we are ever going to find a cure it won't do to just kill one of the tumour cell types, we have to target all of them. Before we can understand how cells grow and differ across the tumour, we first have to identify the different cells. This is quite a difficult task because infiltrating tumour cells look the same as normal brain cells.
Mr Stuart Smith, a Neurosurgeon and Clinical Associate Professor at The University of Nottingham, has developed a new way of identifying these invasive glioblastoma cells using 5-ALA, the pink drink. Invasive glioblastoma cells can be separated from surrounding brain tissue because the tumour cells glow under fluorescent light. These invasive cells can then be analysed to see what about the invasive cells are different from other parts of the tumour.
As methods are developed to understand heterogeneity, Dr Paul Mischel gave a great talk on how tumour cells develop this diversity in the first place.
The more we understand how heterogeneity develops and spreads in tumours, the better-equipped we are to identify how to stop it. Dr Mischel noticed how quickly different tumour cells can develop such variety of growth and survival processes – the normal way we believe cells divide and pass on their DNA just didn't seem to match up with the speed diversity develops across the tumour.
Dr Mischel's group identified ring structures of extra-chromosomal DNA in glioblastoma cells. These ring structures look similar to plasmids – the ringed DNA system found in bacteria.
We know bacterial plasmids helps with rapid adaptations to the environment, and plays a role in the heterogeneity seen in bacterial populations.
This is early days but an exciting discovery that these ringed structures of extra-chromosomal DNA may be how tumour cells develop this heterogeneity, and might lead to new ways of tackling tumour resistance.