Day 7. Cardiff

'Croeso i Gymru. Fynd am dro braf.'

The forecast was rain. Beefy and his crew left Bristol for an hours drive to the Welsh capital.

As the crowds gathered at the City Hall, true to form, the skies cleared and the sun shone. Yet again, the weather had been kind to us. Today's Local Hero, Seren, was looking forward to the day.

Welsh rugby star Tom Shanklin looked nervous at the start. 'I have heard all about the pace he goes at. Is it really that fast?'.

The collections in the city centre were amazing as the walk made its way towards the Millennium Stadium before heading out onto the Bay. We were greeted by stunning scenery bathed in Welsh sunshine. What a start to the day! 

Beefys walk crew are, in his words, 'essential to the success of every walk we do.'

It is made up of family and friends and has changed very little since the first walk back in 1985.

We shall all be raising a glass this evening to absent friends, especially Chris 'Crash' Lander and Bill 'The 'Highwayman' Rumsan who both played a part in shaping the walks from day 1,  25 years ago.

The walk today finishes with a stroll (at 4.5 mph) down the Taff Trail. Meeting us at the Stadium was Jamie Roberts (Wales & British Lions star). Another great day. Thanks for your support Doc.

The long drive to Norwich awaits. Except for Beefy who takes a helicopter - as you do.

Thank you Wales.

Big Gaz.  

Survival rates for cancer in the UK are not as good as in some other countries.

One of the reasons for this is poorer outcomes among certain groups and including older patients aged 75 years and over. An international research study by the National Cancer Equality Initiative (NCEI) has now shown that in several countries older people are often not offered the treatment most likely to benefit them.

The study (www.dh.gov.uk/health/2012/02/age-oncology)  explored the extent to which age influences treatment decisions across a range of cancers: breast cancer (non-HER2-positive); chronic myeloid leukaemia (CML); colorectal cancer (bowel cancer); non-Hodgkin lymphoma; and renal cell carcinoma (kidney cancer).

The findings revealed that while clinicians believe they do not discriminate against older people, there is a tendency for less intensive treatments to be prescribed according to the chronological age of the patient rather than their biological age. This means that more robust older patients are potentially denied potentially curative or life prolonging treatments.

Older people may also unwittingly collude in the process as they often have preconceptions about the side effects of chemotherapy or not report symptoms accurately or quickly enough.

Part of the problem is that clinical trials tend not to include older patients. Increased trial activity in this age group would provide clinicians with the information they need to better determine what approach is best for their patients.

Our Research Director Professor Chris Bunce says: “It’s time to revisit the options for older cancer patients. The advent of novel therapies and better care together with an increased understanding of these diseases is extending the opportunities for meaningful anticancer treatments over and above palliative care”.

The National Cancer Equality Initiative (NCEI) and the Pharmaceutical Oncology Initiative (POI) collaborated on this study, supported by the Department of Health.

The NCEI says more work needs to be done to provide guidance for clinicians so that they have accurate information about an older person’s ability to benefit from cancer treatment rather than making assumptions on the basis of age.

Sally Clark – Science Communications Team

Cancer ‘stem cells’ are something of a hot topic in research circles at the moment. Despite decades of research and clinical trials, advanced cancers, especially once they spread in the body, are notoriously difficult to control or eradicate. Professor Mel Greaves at the Institute of Cancer Research argues this month in Nature that the genetic makeup of cancer stem cells may help explain how patients become resistant to drugs.

When designing new drugs, cancer stem cells have been widely regarded as the ‘bull’s-eye’ in the target. Recent research by Prof Greaves’ team into the most common form of childhood cancer, acute lymphoblastic leukaemia (ALL), reveals that the crucial stem cells that drive the cancer have, within individual patients, many different sets of mutations. 

This work, funded by Leukaemia & Lymphoma Research, suggests that there is no single ‘bull’s-eye’ but rather multiple targets that are diverse and constantly shifting. It vividly confirms that, as long suspected, cancer clones evolve in a Darwinian fashion by genetic ‘natural selection’ in the body.

“This Darwinian perspective has important implications for leukaemia and cancer therapy,” says Professor Greaves. “Our research may help explain why advanced cancers remain so difficult to eradicate. A massive investment is being made in developing new drugs for advanced cancer that target the tumours’ specific genetic mutations as potential ‘Achilles heels’. Whilst some of the new drugs show considerable promise, it is important to recognise that these genetic mutations are constantly evolving, which has the potential to create lethal resistance.”

A cancer stem cell is created when a single healthy stem cell becomes genetically mutated. These mutated stem cells then go on to clone multiple copies of themselves, driving and sustaining the cancer. It had been assumed that leukaemia developed in a ‘linear model’, with leukaemia stem cells acquiring additional genetic mutations with successive divisions. Variations in the combinations of genetic abnormalities found within different cancer stem cells were thought to represent earlier versions of the cancer stem cell in its development.

Professor Greaves has in fact shown that in the very early stages of the disease the original cancer stem cell produces distinct ‘sub-clones’ of itself. Each of these sub-clones contains different combinations of genetic mutations and will go on to develop further sub-clones independently of each other, like branches. While some sub-clones will be destroyed by drugs, other branches may be resistant to treatment and become dominant, driving the cancer forward.

While thankfully over 90% of children now survive childhood ALL, the long term survival rates for children who relapse remain tragically much lower. The ‘Darwinian’ model of cancer development offers a convincing explanation of why children might relapse. It seems clear that developing a deeper knowledge of how leukaemia stem cells operate and how some may evade treatment is vital to making sure that all children survive in the future.

Henry Winter - Science Communications Team