Harnessing the body’s own immune system to fight against cancer is a tantalising prospect, and one which our own scientists are working hard on.
The field of immunotherapy has gathered pace in recent years, even attracting the esteemed journal Science’s “Breakthrough of the Year” award in 2013.
So it’s no surprise that new research arriving hot out of the lab attracts media attention.
This is understandable given the somewhat overenthusiastic press release in which the researchers describe their work as potentially leading to a ‘pill’ that could stop cancer spreading
As one of our own experts commented, the science is genuinely fascinating, but it’s a long way off being a ‘pill’ that could be given to people.
Putting the ‘brakes’ on cancer spread
This latest research focussed on a particular type of immune officer called a natural killer (NK) cell.
NK cells provide a rapid response, killing off cells infected by viruses along with many other foreign invaders that can target the body.
The authors of this study – based at the Institute of Molecular Biotechnology in Austria – investigated the potential for turning NK cells focus towards cancer.
The immune system has the potential to eliminate tumours, but it can be stopped in its track by a number of different ‘molecular brakes.’
The Austrian research team identified one of these brakes – a molecule called Cbl-b – and showed both skin cancer and breast cancer were less able to spread in mice that were engineered to no longer produce Cbl-b.
This finding was a little confused in some of the media coverage, which stated that the researchers have “identified the Cbl-b molecule which stops tumour metastasis, or the spreading of cancer from one organ to an adjacent part.”
It’s actually the other way round.
Based on their experiments in mice, the researchers conclude that Cbl-b is actually helping these cancers spread.
‘Awakening’ the immune system
The researchers go on to show that blocking how Cbl-b works kick starts NK cells to dampen the spread of cancer.
Digging even deeper, the scientists showed that Cbl works via another set of molecules from a family called the TAM receptors.
They developed an experimental chemical compound that blocks the TAM receptors and mirrors the effects they saw when Cbl-b was blocked.
In essence the chemical compound was ‘awakening’ the immune system’s NK cells and slowing the spread of cancer.
This was another finding that became confused in the media coverage that stated the chemical “awakens the immune system’s TAM-receptors to kill this type of cancer.”
This type of chemical is known as a ‘kinase inhibitor’ and as the name suggests it actually blocks the molecules it targets.
A long road
These are promising results, but the experimental compound is a long way off being a ‘pill’ that could be given to patients.
This is early stage research and we don’t yet know whether this ‘brake’ will be a useful target in human cancers.
And the compound may cause side effects that are not apparent in this study.
The potential is there though.
The success of drugs such as ipilumimab that target the ‘brakes’ in another type of immune cell, the T cell, shows the potential power of this type of therapy.
But claims that a ‘pill’ has been developed – or even that it’s “on the horizon” – is misleading to patients and can give false hope when the long road of drug development is not made clear.
- Paolino M., et al. (2014). The E3 ligase Cbl-b and TAM receptors regulate cancer metastasis via natural killer cells., Nature, PMID: 24553136
Image from Wikimedia Commons.