The mainstays of cancer treatment remain chemotherapy, surgery and radiotherapy. These are the big three treatment modalities and have, largely, remained in place as the core weapons in the arsenal of oncologists despite the advent of a number of newer treatments. However, there is a class of treatments called ablative therapies that really need to become the fourth big weapon in the anti-cancer arsenal. Ablative therapies include photodynamic therapy (PDT), cryoablation, radio-frequency or microwave ablation and the new kid on the block, irreversible electroporation (which I have previously written about here).
Of these treatments, which all take the approach of directly and physically attacking tumours rather indirectly using drugs or radiation, it is PDT which is the most mature and most widely used. PDT works by injecting a light sensitive drug (called a photosensitiser) into a patient and then letting the drug accumulate in tumour cells – normal cells do not take up the drug to the same extent. Once the drug has been absorbed by the tumour light is applied to it – usually by a surgeon operating to gain access to the tumour and then shining a laser or LED directly on to the tumour. The photosensitive drug in the tumour cells reacts to the light and in the process kills the cell. In this way PDT can be used to destroy solid tumours directly.
While PDT is the most mature of the ablative treatments, it’s still not used widely enough in the UK, and even many oncologists remain unaware that it is available and that it’s a viable treatment option for their patients. This is a treatment that works, can be used against a wide variety of tumour types and does not produce the long-term side-effects of radiotherapy or chemotherapy. If ever there was a treatment that needed to become more widely known and available to more patients it’s this one. And, luckily, there are people around who are actively campaigning to raise awareness of PDT amongst the medical profession, amongst patients and the general public.
One such group is PDT Norfolk (take a visit to their site here: http://www.pdtnorfolk.co.uk/). Recently I travelled up from London to meet with the team at PDT Norfolk to discuss some of the science, some strategy and ways that we could work together. It was a good meeting and I think some very positive ideas came out of it. I think this is a campaign that has the potential to advance research in PDT as well as to raise the profile of the treatment, provide resources for patients and help to bring this treatment to a wider range of patients.
Commentary on cancer research, information on supplements and treatments, relevant book reviews, links to useful sites and other information that cancer sufferers, their families and friends may find useful.
Wednesday, 27 February 2013
Tuesday, 19 February 2013
Of Mice and Men
I’ve written about the state of cancer research on a number
of occasions in the past, in particular focusing on the use of different models
of cancer – for example here: http://www.anticancer.org.uk/2012/05/wrong-models-of-cancer-part-2.html
and here: http://www.anticancer.org.uk/2012/04/standards-in-cancer-research.html
and here: http://www.anticancer.org.uk/2011/11/test-tube-cancer-cells-and-people.html.
So I hope it’s not getting repetitive to raise the subject again in the light
of an important new paper in the Proceedings of the National Academy of
Sciences (PNAS). The paper, Genomic responses in mouse models poorly mimic human inflammatory diseases
is not about cancer as such, but it’s as important and relevant as any paper on
cancer.
The opening line of the paper makes plain why these results are important:
And it’s true enough in most areas of medicine, but none more so than in cancer research, where the mouse model is king. But the only problem is that mouse models don’t always match human disease profiles at all well. In the specific case that this paper outlines, it turns out that mouse models of massive inflammatory responses in critically ill patients are miles apart. To quote from the paper again:
The reason for this divergence turns out to be because the relationship between genes changed in human patients bears little relationship to the genes expressed in the mouse models of the diseases – the relationship is pretty much random. However, for years scientists who have been studying these diseases have focused on drugs that work for mice and then these drugs have subsequently failed in humans. Not only has this cost millions, it also means that much research effort has been wasted in targeting genes that have nothing to do with human diseases. It also means that potentially useful drugs have been abandoned precisely because they failed to do anything in mice.
And it’s not just inflammatory diseases at stake – the same is true in cancer research. We can only speculate on how much money, effort and intellectual energy has been wasted on research that doesn’t apply to people. The reliance on test tubes and mouse models means that much time and effort has been for nothing.
Something needs to change.
The opening line of the paper makes plain why these results are important:
A cornerstone of modern biomedical research is the use of mouse models to explore basic pathophysiological mechanisms, evaluate new therapeutic approaches, and make go or no-go decisions to carry new drug candidates forward into clinical trials.
And it’s true enough in most areas of medicine, but none more so than in cancer research, where the mouse model is king. But the only problem is that mouse models don’t always match human disease profiles at all well. In the specific case that this paper outlines, it turns out that mouse models of massive inflammatory responses in critically ill patients are miles apart. To quote from the paper again:
The success rate is even worse for those trials in the field of inflammation, a condition present in many human diseases. To date, there have been nearly 150 clinical trials testing candidate agents intended to block the inflammatory response in critically ill patients, and every one of these trials failed.
The reason for this divergence turns out to be because the relationship between genes changed in human patients bears little relationship to the genes expressed in the mouse models of the diseases – the relationship is pretty much random. However, for years scientists who have been studying these diseases have focused on drugs that work for mice and then these drugs have subsequently failed in humans. Not only has this cost millions, it also means that much research effort has been wasted in targeting genes that have nothing to do with human diseases. It also means that potentially useful drugs have been abandoned precisely because they failed to do anything in mice.
And it’s not just inflammatory diseases at stake – the same is true in cancer research. We can only speculate on how much money, effort and intellectual energy has been wasted on research that doesn’t apply to people. The reliance on test tubes and mouse models means that much time and effort has been for nothing.
Something needs to change.
Wednesday, 13 February 2013
LFS SIGNIFY Trial Looking for Volunteers
This just in from the people running the SIGNIFY trial for Li Fraumeni Syndrome:
We are conducting a small scale pilot study to investigate the use of whole body magnetic resonance imaging (MRI) in families with Li Fraumeni Syndrome.
We would like to enrol individuals in the trial who are between 18 and 60 years old and are known to have a genetic mutation (alteration) in the P53 gene as well as unrelated people who do not carry the gene mutation whose scan results can be used as controls.
All study participants will undergo a whole body MRI scan at the Royal Marsden Hospital, Sutton, Surrey.
If you are interested please contact SIGNIFY study coordinator Dr Emma Killick or another member of the SIGNIFY team at the Institute of Cancer Research on 0208 661 3375.
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