Behind-the-scenes at Cancer Research UK

We can send a man to the moon, so why can’t we beat cancer?

Just a few years ago, we at last reached the point where half of all people diagnosed with cancer could expect to survive it. Within 20 years, scientists hope that figure will rise even further to 3 in 4 people.

Reaching these milestones does not happen easily. It is the culmination of years of research by thousands of scientists around the world, working in fields as diverse as genetics, pharmacology and biochemistry – as well as medicine.

Much of this research takes place here in Manchester. In fact, cancer is one of The University of Manchester’s five main ‘research beacons’ – priority research areas in which we are world leaders – the others being industrial biotechnology, advanced materials, energy and addressing global inequalities.

Beyond the main university campus, we also have the Cancer Research UK Manchester Institute, situated over the road from the Christie Hospital in Withington, south Manchester. Their brand new £28.5 million building opened its doors last year, and is jointly funded by The University of Manchester, The Christie NHS Foundation Trust and Cancer Research UK.

Cancer Research UK is the world’s largest independent cancer research charity, and funds and conducts research into the prevention, diagnosis and treatment of the disease. Its work is almost entirely funded by donations from the public.

The Christie Hospital is one of Europe’s leading centres for cancer treatment and research, treating over 40,000 patients a year, and around 400 early phase clinical trials are taking place here at any one time. This makes The Christie an ideal next-door-neighbour for the new Cancer Research UK Institute.

Research in places like Manchester has vastly improved our knowledge of cancer and how we can treat it over the past decades. The discovery of epigenetics has shone a new light on the different ways this disease can arise, while genome sequencing has given us new and highly effective methods of diagnosis, allowing us to accurately tailor treatments to each individual’s needs.

There’s still such a long way to go however.

Cancer is not one disease nor one hundred diseases but many thousands, each unique and requiring a different response. Such a diverse assortment of diseases is only possible because the body itself is so diverse.

37 trillion cells, and 10,000,000 components per cell make the body 125 billion times more complicated than the Saturn Rockets that allowed humans to go to the Moon. It is only when we consider this staggering complexity that we can begin to appreciate the immense challenge we face in trying to treat the numerous different types of cancer.

2333main_MM_Image_Feature_19_rs4
© NASA

 

 

Cell division and inflammatory disease link revealed

A ground-breaking study by scientists from the Faculty of Life Sciences and The University of Liverpool scientists has been published in the journal eLife and has identified a new link between inflammation and cell division.

Two of the most important processes in the human body, their accurate control is a holy grail for scientists researching the prevention of infection, inflammatory disease and cancer.

Professor Mike White, who led the BBSRC-funded research and investigates how cells adapt to signals in the body, hit upon the discovery using advanced microscopy and mathematical modelling at the University of Manchester’s world-leading systems microscopy centre and the University of Liverpool’s Centre for Cell Imaging.

“This is an exciting discovery: for the first time we find a link between the system which regulates how cells divide and the basis of some of medicine’s most intractable diseases,” he said.

Inflammatory signals produced by a wound or during an infection can activate a protein called Nuclear Factor-kappaB (NF-κB), which controls the activity of genes that allow cells to adapt to the situation.

Incorrect control of NF-κB is associated with inflammatory diseases, such as Crohn’s disease, psoriasis and rheumatoid arthritis; it has also been linked with ageing and some cancers.

A key way in which human cells adapt to signals in their environment is by dividing to produce new cells through a repeating pattern of events, called the cell cycle. A cell first makes copies of its DNA, in a stage known as the DNA synthesis phase, and then divides into two daughter cells.

The cell cycle is controlled by a family of proteins called E2 factors, which control the start of the new cell’s DNA synthesis phase.

In the eLife study, the team showed that the NF-κB and E2 factors bind to each other in the cell. This controls the level of the NF–κB signal, which is enhanced just before DNA synthesis, but reduced during the DNA synthesis phase.

They also show that signals which activate NF-κB can change the timing of cell division.

The findings suggest that direct interactions between E2 factor proteins and NF-κB enable cells to decide whether to divide and determine how they react in different ways to inflammatory signals.

The work used a set of mathematical equations to make predictions about cell responses, which were then tested by experiments and shown to be correct.

Professor White added:

“We are particularly proud of our combination of maths and experimentation. This is due to the strong support from BBSRC for the area of systems biology and the work of a dedicated team of scientists from different disciplines.”


The paper, Dynamic NF-κB and E2 interactions control the priority and timing of inflammatory signalling and cell proliferation is available. It is available on the eLife website