The American Association for Cancer Research (AACR) annual meeting is by far the largest conference in the world dedicated to cancer research.
Raj Mehta, from our technology transfer arm Cancer Research Technology, is at the conference and will be giving us a flavour of what’s been going on.
The annual AACR conference, here in sunny Washington DC, is both daunting and inspiring.
Daunting because of the sheer scale of the event – at any one time there may be up to 10 different presentations going on, so it’s difficult to shake the feeling that you’re missing a great talk while sitting in another. It’s also daunting because it gives us an opportunity to glimpse the true scale of the problem that is cancer.
Throughout the conference we’ve heard about many different types of cancer, each with a number of sub-types, and each sub-type driven by different genetic faults. All these various biological permutations need different approaches to treat cancer,while some cancers will become resistant to those treatments in different ways.
But this conference is also deeply inspiring, shown by the dedication of the researchers searching for causes and cures, as well as the great progress we are now making in our understanding of the disease and how to treat it.
A couple of sessions particularly caught my eye, starting with one looking at how cancer cells grow and spread. This is the first time I’ve come across the term “Gompertzian growth curve“, which describes a rate of growth that’s faster at the beginning and slows down as time goes on.
It appears that the commonly-held belief that cancer cells grow exponentially (i.e. one cell becomes two, which become four, then eight and so on) may not be accurate. Tumours grow faster when they are small and slow down as they become larger – a discovery that might have profound effects on the treatment and needs more in-depth investigation.
Another fascinating session discussed how to arm our body’s immune system to fight cancer, focusing on specific ‘killer’ white blood cells known as cytotoxic T lymphocytes (CTLs). If you imagine our immune system is like an army fighting invading bacteria and viruses, then CTLs would be tanks – capable of blasting infected cells to prevent infections from spreading.
CTLs, like the rest of our immune system, are very carefully controlled so that they don’t kill normal, uninfected cells. But they also don’t attack cancer cells, as these ‘look’ too similar to healthy tissue.
Encouragingly, we heard about a new approach for persuading CTLs to attack tumour cells, which has had highly encouraging responses in small clinical trials. The process involves harvesting CTLs from patients and ‘retraining’ them to recognise certain molecules found only on the surface of cancer cells, using specially engineered proteins known as “chimeric antigen receptors”. Once instructed, the CTLs are then returned back into the patient’s bloodstream where they can go into battle, homing in on cancer cells and killing them.
But while the concept sounds great, there are a few drawbacks. Firstly, there are very few proteins that are exclusively produced by cancer cells and not by healthy cells, so there’s a risk that these potent killing machines could attack normal cells that carry even small amounts of the target molecule.
It’s also a very complex therapy that needs to be tailor-made for every single patient, so it’s not currently practical or affordable on a larger scale. But it’s certainly an exciting field of research, with the potential for big breakthroughs in the future.
Raj Mehta is a business development executive at Cancer Research Technology