Thursday, 19 July 2012

An Anti-Cancer Polypill

The big health news story of the day is on the report that adoption of the 'polypill' - the proposed pill that combines a statin with three common blood pressure drugs. According to the authors of the study, rolling this polypill out to all over 50s will save tens of thousands of lives (I've seen different numbers in different reports, but they all agree it's a significant fugure). The rationale of the pill is that by taking these relatively cheap and non-toxic drugs lives will be saved by reducing the number of heart attacks and strokes. However, the effect should, in theory, extend to lives saved by preventing cancer. There's pre-clinical evidence that at least two of the drugs - simvastatin and losartan - have cancer prevention properties.

The idea of a polypill is one that I'll be exploring later in the year when it comes to cancer, and specifically for Li Fraumeni Syndrome and other hereditary cancer syndromes. An anti-cancer polypill would take simvastatin and losartan - one half of the current polypill - and add two additional drugs - aspirin and metformin. I believe that such an anti-cancer polypill has huge potential, both for the over 50s and also for people at high risk of cancer, including those who've been treated for the disease and are in remission.

As I said, this is an area that I'll be exploring in more detail in the future, so watch this space...

Friday, 13 July 2012

Dr Helen Hanson

Congratulations to Dr Helen Hanson, who is acting as the medical advisor to the George Pantziarka TP53 Trust. She has been appointed to a post of Consultant at the Royal Marsden Hospital, in London. One of Dr Hanson's plans is to start a specialist TP53 clinic at the hospital. This is a development we'll be following closely, and we'll report back as things develop in the future.

Wednesday, 4 July 2012

Biomarkers for Osteosarcoma Response to Chemo

Clinical advances in the treatment of osteosarcoma are rare, and as I have highlighted in the past (here, for example), there are no signs of improvements in outcomes in recent years. The standard treatment for osteosarcoma is neo-adjuvant chemotherapy (using multiple chemo drugs) to shrink the tumours and then surgery to remove them. One of the things that we do know about osteosarcoma is that good response to chemotherapy (defined as greater than 90% tumour cell death), is associated improved chances overall survival. In other words the more the tumour is killed by the chemo the more chance there is that the surgery removes it all and that there is a lower risk that it will have metastasised. However, assessing the rate of tumour kill is hard to do - at the moment you actually need to remove a sample of the tumour to analyse it. Unlike some other forms of cancer, there are no generally recognised bio-markers that you can use as a way of assessing the success rate during the chemotherapy treatment protocol. Nor is there any way of establishing which patients will respond well to chemotherapy and those that won't.

A just published study has looked at the relationship between the expression of the p16 gene in osteosarcoma and response to chemotherapy. The results were clear - loss of p16 expression in tumours is strongly correlated with a worse response to chemotherapy. This backs up previous work which looked at the relationship between p16 and survival in osteosarcoma. This new study now provides the link to explain this relationship. Lower p16 expression causes less sensitivity to chemotherapy, leading to less tumour cell necrosis and ultimately leading to worse outcomes.

This means that p16 expression can be checked at initial diagnosis and treatment options adjusted accordingly. For patients with high levels of p16 expression then the standard treatments will have more chance of success. For those with little or no p16 expression, other options will need to be considered.

Details of this new study are here: