5 things overheard at the NCRI cancer conference
All of the stories below were heard at the National Cancer Research Institute annual conference 2017 in Liverpool.
‘Sugar’ sponges for brain tumours
We often say that the genetic and molecular properties of cancer are really important. But we shouldn’t forget that cancer is a physical disease and the physical properties play a part in how it can be treated. One odd thing about cancer is that as the disease progresses the tumour tissue becomes stiffer. Professor Val Weaver told us that there are a lot of complex cellular things going on that cause this stiffness. Her group recently found that a sugary protein produced by cells, called galectin-1, plays a key role in the stiffness of brain tumours. Studies in mice with cancer revealed that removing galectin-1 reduced stiffness and allowed the mice to live longer. Weaver then let us in on a secret – that her team are working on developing ‘sponges’ that can be injected into the brain tumour site to mop up galectin-1 in patients.
Chasing cancer down blind alleys
Professor Steve Jackson, a pioneering researcher in the many molecular tricks cells use to repair damage to their DNA, believes that the future for cancer therapy will be one where clinicians are able to back cancer into a corner and pin it into submission with a variety of treatments.
Using his inside knowledge, gathered over a quarter of a century of research, Jackson explained that they are starting to understand how using drugs to block one molecular trick can force the cell to use another and ultimately lead to the cell overcoming the effects of the treatment. The good news is that this also reveals weaknesses in the cancer. By understanding and predicting what the next trick to be used by the cancer cell will be it might be possible to keep hitting the cancer with a different treatment as the cells adapt. Professor Jackson said that doctors could end up “chasing cancer down blind alleys” – leaving the disease with no route to escape.
How cells get their energy is really complicated
If you studied biochemistry at university then you might remember the hours put in trying to remember all those chemical equations that describe cell metabolism (the processes that cells use to get energy). If you didn’t then the crux of it is that cell metabolism is really complicated (see this horrifying diagram if you don’t believe me). One thing I learnt from the conference is that, when it comes to cancer cells, metabolism is even more complex.
An interesting concept I picked up in a session led by Dr Christian Frezza was that cancer cells ‘rewire’ their circuitry for producing energy over time as the disease progresses. Frezza called this the ‘metabolic evolution of cancer’ and explained that it runs in parallel to the classic genetic evolution of cancer (genetic mutations that enable cancer cells to survive are selected and passed on to the next generation of cancer cells). This idea raises lots of questions about what the ‘wiring’ diagrams of cell metabolism look like at different times during the disease and how can differences in the wiring compared to normal cells be used to develop targeted treatments.
Anti-psychotic drugs might be bad news for cancer
Finding new uses for drugs that already exist is always good because a lot of the hard work is already done. Professor Jim Norman let us in on some of his most recent research which has revealed a potential new way to reduce the spread of breast cancer to the lungs – in mice at least. His teams work uncovered a new molecular mechanism that breast cancer cells use to become invasive – that is to push away from the tumour into nearby tissue and ultimately spread around the body. Interestingly, one of the proteins that drives this mechanism can be inhibited using drugs that were originally developed as anti-psychotics. Further research in this area could find a new use for these drugs to stop breast cancer spreading – the stage of the disease that is often lethal.
Olaparib might work on brain tumours
One of the big pieces of clinical news from this year’s conference was that the ovarian cancer drug, olaparib, seems to be able to infiltrate brain tumours. Olaparib is already approved for ovarian cancer and is being tested in clinical trials for several other caner types, but this is the first bit of evidence suggesting it might be worth pursuing trials in brain cancer.
In the study, they found that olaparib was found in brain tumour samples of patients who were given the drug. This is a significant step because the brain is protected by a barrier that blocks many drug molecules (and other things) from reaching the brain. This makes brain tumours notoriously hard to treat so the fact that this drug can get there means it might be worth testing further to see if it works as an effective treatment.