Cancer Research UK’s Run 10k launches ‘Take 5 challenge’ to help busy people train for the events

THE economic downturn is having a detrimental effect on the health, fitness and wellbeing of the nation, according to a new survey released today by Cancer Research UK to launch its Run 10k series.

The findings reveal that a quarter of people (25 per cent) are spending more hours at work compared to this time last year and over half of those that are currently working (56 per cent) admit that work affects the level of exercise they do. Worryingly, a quarter of those currently working (26 per cent) admit they don’t regularly exercise.

In light of these findings, Cancer Research UK has launched the ‘Take 5 Challenge’ - five easy steps designed to help people incorporate exercise and fitness into their busy lives, redress work/life balance issues and provide great preparation for a Run 10k event this autumn.

The survey shows how job cuts and a looming fear of redundancy are affecting people’s lifestyles. Over half (56 per cent) of those who are clocking up extra hours have an increased workload, while a third (34 per cent) say they are over stretched staff-wise and a quarter (25 per cent) are worried about their job security. More than a third (38 per cent) of workers are unhappy with their work/life balance as they are working too much.

In terms of nutrition, 82 per cent of workers say that being busy at work affects their diet, with 41 per cent of workers going for speed over health when choosing food options. Four out of five (81 per cent) of all adults admit they do not get their five portions of fruit and vegetables every day.

The ‘Take 5 Challenge’ easy-to-follow steps, which include tips on extra activity, stretching and hydration, have been designed to help people improve their general health and fitness and get them in the right mind set to take part in a Run 10k. With 43 events taking place across the UK this autumn, Cancer Research UK’s Run 10k series offers people the opportunity to feel good, do something positive and raise money for a great cause.

Cancer Research UK has worked closely with celebrity fitness expert Steve Halsall to create the step-by-step plans, which can be viewed and downloaded at http://www.Run 10k.org/take5challenge. A plan for the less experienced jogger, as well as an in-depth plan for the more seasoned runner keen to beat their personal best, can be downloaded from the site.

Steve Halsall said of Cancer Research UK’s Take 5 Challenge: “Doing the ‘Take 5 Challenge’ and making five small changes to your everyday routine, which require little or no extra time, can have a huge beneficial effect on your fitness levels and general well-being, and even show you how easy it is to take that next step and sign-up for a Run 10k this year. Taking part in a Run 10k will also give you that feel-good factor and sense of achievement that is second-to-none!”

Birmingham City Football Club MD Karen Brady, who is backing the ‘Take 5 Challenge’ adds: “Encouraging a good work/life balance is crucial in keeping morale high and increasing motivation, commitment and engagement. Cancer Research UK’s Run 10k ‘Take 5 Challenge’ encourages people to incorporate health and fitness into their busy lives, which is a great way for workers and their bosses to boost their sense of wellbeing. And by signing up to a Run 10k this year, people will be raising money for a fantastic cause at the same time.”

To view and download the ‘Take 5 Challenge’ plans, please go to http://www.Run 10k.org/take5challenge

*All figures, unless otherwise stated, are from YouGov Plc. Total sample size was 2030 adults. Fieldwork was undertaken between 19th - 22nd June 2009. The survey was carried out online. The figures have been weighted and are representative of all GB adults (aged 18+).

About the ‘Take 5 Challenge’

The Take 5 Challenge offers a beginners plan: available for the less-experienced runner, alongside an advanced plan for the more developed runner. Each plan covers five easy steps to improve general health and well-being:

- Commitment
- Stretching
- Activity
- Hydration
- Attitude

To view or download the ‘Take 5 Challenge’ plans visit http://www.Run 10k.org/take5challenge

About Run 10k

- Run 10k for Cancer Research UK, supported by Tesco, is a series of 43 events held in stunning and unique locations through the UK this autumn.
- This year we hope 60,000 men and women will come together to raise just over £6m to help fund Cancer Research UK’s life saving work.
- For further information about the Run 10K series or details of event locations please visit Run 10k

Source
Cancer Research UK

A UCLA study has identified a way to turn off a key signaling pathway involved in physiological processes that can also stimulate the development of cancer and other diseases. The findings may lead to new treatments and targeted drugs using this approach.

In the study, which is currently available in the online edition of the journal Molecular Endocrinology, scientists found that by activating a receptor in cells called the liver X receptor (LXR), they were able to inhibit the hedgehog (Hh) signaling pathway, which is involved in the maintenance of tissue integrity and stem cell generation. When stimulated in an unregulated manner, however, the Hh pathway can also cause cancers of the brain, lung, blood, prostate, skin and other tissues.

Blocking such unregulated stimulation of the Hh pathway had previously been shown in animal studies to prevent cancers, according to the researchers. How LXR was able to inhibit tumor cell growth by impeding the Hh pathway was previously unknown.

“Our finding shows that activation of LXR signaling is a novel strategy for inhibiting Hh pathway activity and for targeting various cell types, including cancer cells, which may provide important clues as to how we might be able to intervene with tumor formation,” said Farhad Parhami, a professor of medicine at the David Geffen School of Medicine at UCLA and the study’s principal investigator.

During the study, researchers performed various tests activating LXR receptors in cells and found that specific gene expression induced by the Hh pathway could be inhibited. This finding was also confirmed in mice.

“Since Hh signaling plays a major role in other physiological and pathological processes, we may be able to impact other diseases as well,” Parhami said.

Dr. William Matsui of Johns Hopkins Medical Institute, an expert on Hh signaling in cancer development, noted the importance of the UCLA study and its significance for the next stages of research - finding a pharmaceutical drug or substance molecule to act as an agonist, which would stimulate LXR activity to inhibit aberrant Hh signaling.

“The hedgehog Hh signaling pathway is an important regulator of tumor formation, and these findings suggest that LXR agonists may be novel treatments for a wide variety of human cancers,” Matsui said.

According to researchers, utilizing this new treatment pathway could have broad applications in the cancer field.

“This discovery identifies an entirely new and unexpected mechanism of hedgehog pathway modulation,” said study author Dr. James A. Waschek, an expert on Hh signaling in brain tumor development and a professor of psychiatry and biobehavioral sciences at the David Geffen School of Medicine at UCLA. “This has great potential in offering other options, because current hedgehog pathway inhibitors have severe side effects which preclude their use in many cancer patients, especially children.”

Waschek also noted that this discovery may reveal new details on how Hh signals within the cell, which is currently poorly understood.

The next stage of the research will focus on activating the LXR pathway using various pharmacological molecules to inhibit tumor formation. Matsui will be a collaborator in this follow-up research.

In addition, the team has started a medicinal chemistry program to design and test small molecules that activate the LXR pathway while avoiding the adverse effects that may be caused when LXR is activated in tissues such as the liver.

The study was funded by the National Institutes of Health and the American Heart Association.

Other authors include Woo-Kyun Kim and Vicente Meliton from the UCLA Department of Medicine; Peter Tontonoz from the UCLA Department of Pathology and Laboratory Medicine and the Howard Hughes Medical Institute; Kye Won Park from the department of food science and biotechnology at Korea’s Sungkyunkwan University; Cynthia Hong from the Howard Hughes Medical Institute and the David Geffen School of Medicine at UCLA; Pawel Niewiadomski from the UCLA Department of Psychiatry; and Sotirios Tetradis from the UCLA School of Dentistry.

Source:
Rachel Champeau

University of California - Los Angeles

The role of a protein called XIAP in the regulation of cell death has been identified by Walter and Eliza Hall Institute researchers and has led them to recommend caution when drugs called IAP inhibitors are used to treat cancer patients with underlying liver conditions.

A team led by Professor Andreas Strasser from the institute’s Molecular Genetics of Cancer division has found that XIAP (X-chromosome-linked inhibitor of apoptosis protein) is the critical factor that determines which of two pathways will be followed to culminate in a cell’s death.

Programmed cell death (also called apoptosis) removes unwanted and dangerous cells from our bodies, protecting us against cancer development and diseases where the immune system attacks the body’s own tissues, such as in insulin-dependent diabetes.

This cell death process is activated by proteins on the surface of cells. The most prominent of these cell surface proteins is FAS, but curiously it does not always activate apoptosis the same way, Professor Strasser said. “One of the things that’s very curious about FAS is that, depending on the cell type, the way the killing of the cell happens is substantially different,” he said.

“In so-called type I cells, such as lymphocytes (white blood cells involved in the immune response), the killing is very direct. When FAS is activated a protein-destroying enzyme called caspase-8 is recruited and activated, leading to activation of other enzymes (effector caspases) and rapid cell demolition,” Professor Strasser said.

“But in so-called type II cells, which include hepatocytes (liver cells) and pancreatic ?-cells (the cells that produce insulin), that direct pathway is not sufficient to kill the cells; amplification of the apoptosis signalling pathway is required.”

Professor Strasser, with Drs Philipp Jost and Thomas Kaufmann (a former post-doctoral researcher from the institute who is now running his own lab in Bern, Switzerland) as well as with colleagues from St Vincent’s Institute of Medical Research, LaTrobe University and the Institute of Molecular Medicine and Cell Research in Germany, has found that the protein XIAP is the discriminating factor between type I and type II FAS-induced cell death signaling.

The research has been published today in the international journal Nature.

For death to occur in type II cells, caspase-8 must activate the death-promoting protein called BID. Without this activation of BID the cells don’t die.

But the experiments of Professor Strasser’s team revealed that when the gene that produces XIAP is turned off or if the XIAP protein is pharmacologically blocked, hepatocytes or pancreatic ?-cells (both type II cells) will die in a type I manner; that is: independent of the presence of BID.

Professor Strasser said that the finding had implications for cancer patients with underlying liver conditions who were being treated with IAP inhibitors. These inhibitors would block the production of XIAP, thereby interfering with the normal cell death pathway for liver cells and increasing the likelihood of healthy liver cells being killed, he said.

The research would also be of interest to gastroenterologists as in several chronic liver diseases activation of FAS is thought to contribute to cell destruction, he said.

Source:
Penny Fannin

Walter and Eliza Hall Institute