Yesterday I awoke bright and early, on my way to the University of Leeds for the British Neuro Oncology Society’s (BNOS) annual conference. This particular conference is titled; ‘Trials, Technologies and T Cells.’ I will be attending for the duration, 3 days, whereby I will hear from a number of influential speakers in the field.
I feel I am in a fortunate position to be able to peer beyond that no so transparent screen between the patient and scientist understanding and experience of this disease. Bridging that gap and relaying important information and experiences to and from both sides is of great importance to me. I feel a great sense of responsibility to represent these patients as best I can and vice versa.
I had been looking forward to seeing some of the latest research developments, particularly relating to recent developments in immunotherapy, novel new imaging techniques, and also the latest research from Imperial College London (with whom I am travelling) on the ketogenic diet studied in vitro using ketone esters. I will be in their research lab very soon to test some of my own theories barring any possible restrictions I may encounter.
The main objective of BNOS is to ‘promote research and education in Neuro-Oncology and to improve treatment of patients with tumours of the central nervous system.’
I was very much looking forward to hearing presentations from speakers coming to Leeds from around the world. The conference themes are:
– Glioma Biology
– Imaging Radiotherapy and Surgical Technologies
– Novel Technologies
– Brain Metastases
– Clinical Studies
I will try to update as much as I can through my blog and social media as the conference progresses with new information I take in along with my thoughts.
I had been especially interested in hearing from Dr. Bernhard Radlwimmer and his presentation on Glioblastoma Epigenetics and Metabolism
In 2013 Dr. Radlwimmer wrote a paper of interest to me entitled:
‘Brain Cancer: Hunger for amino acids makes it more aggressive’.
The paper is so important because it explains why the IDH1 gene is so important as a prognostic factor for brain cancer patients and why managing the disease metabolically is much more complicated than simply starving a tumour of glucose and ramping up the blood ketones. I would advise brain cancer patients to ask about this gene mutation to determine what treatment strategy they wish to pursue and to empower them with the knowledge required to make a truly informed decision, dictating a clearer path forward in typically murky, clear as mud times.
Dr. Radlwimmer has previously established that, ‘An enzyme that facilitates the breakdown of specific amino acids (IDH1) makes brain cancers particularly aggressive. Scientists have discovered this in an attempt to find new targets for therapies against the dangerous disease.’
DH1 encodes cytosolic isocitrate dehydrogenase 1, which is involved in the control of oxidative cellular damage. Mutation of IDH1 appears to be a very strong prognostic factor in diffuse gliomas, whatever the grade. (Laubessiere et al., 2010)
|Roles of IDH1/IDH2 in cellular resistance to apoptosis, oxidative stress and anticancer treatments. http://theoncologist.alphamedpress.org/content/15/2/196.short|
I asked him his opinion on efficacy of the ketogenic diet keeping in mind his paper on how amino acids, particularly glutamine, can fuel the disease.
Following the talk I asked Dr. Radlwimmer if he thought IDH1 status of the tumour could potentially predict responsiveness to the ketogenic diet and if so, could an adapted version of the diet improve efficacy for these patients in theory. I had wondered if more therapeutic ketosis (or exogenous ketones) in itself can change expression of the IDH1 gene or if nutrient deprivation via protein restriction and/or periodic fasting can bypass this potential contraindication for individuals who do not express this enzyme.
The answer to my reasonable hypotheses is that he simply didn’t have enough information to commit to any theories on this. I suspected he may of course have alternative ways of exploiting the metabolic characteristics discussed but this was not established. It seems logical that my theory may be valid and as yet I see no reason at present to question that. I am open to challenging these beliefs however.
I then had the pleasure of learning about new developments in immunotherapy, as well as novel imaging techniques. There are three main classes of novel immunotherapeutics specific to brain cancer. Here are a few pictures from these talks that grabbed me.
I found it particularly interesting how tumours treated with certain methods of immunotherapy actually can double in size before they eventually shrink, however this was no complete surprise to me, being part of the immune response where T cells seek to hunt down the cancerous cells, now recognised as a foreign body. In simple terms the T cells become activated, dividing rapidly and secreting small proteins called cytokines that regulate and active this immune response, ‘attacking’ the tumour for want of a better expression. The body reacts with an inflammatory response (pseudoprogression, short term tumour enlargement), and the patient can often experience flu like symptoms, before the tumour starts to shrink relatively rapidly.
I enjoyed the talk on novel imaging techniques having had first hand experience with MR Spectroscopy for my own tumour. My last scan was the first to show no detectable disease as well as no visible disease. I remain cautious and somewhat skeptical of my own methods. I feel it is a good idea to constantly question yourself. Although I feel I have done better than expected and my seizure control without medication for so long has been truly liberating I remain cautious and vigilant.
Today I look forward to Professor Nicola Sibson’s presentation on targeting inflammatory response and biomarkers of the disease. A huge target and so very important! It is a great pleasure to be hear, to share my own story, and to learn from the many dedicated professionals who make this their life’s work.