Building an artificial tumour in the lab

Professor Fran Balkwill

Fran Balkwill plans to build the world’s first artificial tumour

In 2000, a team of archaeologists in the ancient Egyptian city of Thebes uncovered the mummified remains of a young woman called Tabaketenmut. The big toe of her right foot was missing. In its place was a wood and leather contraption tied to the limb with string, which researchers believe to be the earliest example of a prosthetic body part.

This rudimentary device – developed more than 2,000 years ago to help a woman walk – is often cited as one of the first and most primitive examples of bioengineering, the use of artificial components to replace damaged or absent parts of the body.

Today the term has a much broader meaning and includes disciplines such as materials science, biology, mathematics, engineering and computing. And we’ve come an incredibly long way since – thanks to primitive bioengineering – Tabaketenmut walked the earth.

Just last month, we heard the astonishing news that scientists have been able to grow a functioning kidney in the lab. And researchers in the US have developed a high-tech ‘lung on a chip’ to help them study infections and other diseases.

Now Cancer Research UK scientist Professor Fran Balkwill is looking to make a similarly monumental step forward in cancer biology by bioengineering the first ever three-dimensional artificial tumour.

She hopes the work will underpin the development of new treatments that attack the interactions between cancer cells and healthy tissues that unwittingly support them, known as the microenvironment.

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I want to break free – the microenvironment and metastasis

This entry is part 4 of 4 in our Microenvironment series
Cancer spread is a huge challenge for patients, doctors and researchers.

Cancer spread is a huge challenge for patients, doctors and researchers.

No man is an island, and the same can be said of tumour cells. Previous posts in our ‘microenvironment’ series have discussed how the cells and structures around a tumour – known collectively as its microenvironment – are crucial to its survival.

In this article we explore how tumours draft in these surrounding cells to break free and spread to other parts of the body.

This process of cancer spread (or metastasis) is a huge problem for cancer patients and their doctors; most deaths from cancer are caused by the disease spreading around the body. So understanding how cancer cells break free from the confines of the primary tumour and move around the body is a crucial question for scientists.

And the more we learn, the more we realise that developing the ability to spread is no easy feat for tumours – they wouldn’t get anywhere without a helping hand. So here, we’ll learn about how their healthy neighbours send them on their way.

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Feeling the heat – the link between inflammation and cancer

This entry is part 3 of 4 in our Microenvironment series
Fire_from_loppings

Inflammation is crucial for cancer development

Regular readers will know that the infrastructure supporting a tumour – its ‘microenvironment’ – is a hot topic in cancer research at the moment. In our previous post in this series, we looked at how otherwise healthy cells collude to form the blood vessels nourishing the tumour. Today, we’ll tell a story that began in 1863, when a German pathologist called Rudolf Virchow peered down his microscope.

Our body’s immune system forms a defensive shield that any fighting force would be proud of. One of its most powerful weapons is inflammation, a carefully orchestrated manoeuvre designed to eliminate enemies such as bacteria, injured cells and chemical irritants. Without it, we probably wouldn’t survive beyond infancy.

But inflammation has a split personality – one that can wreak havoc for those unfortunate enough to experience it. And we now know that inflammation’s dark side is a powerful force in cancer development, where it aids and abets tumour growth and spread around the body.

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Getting to the root of tumour blood vessels

This entry is part 2 of 4 in our Microenvironment series
Plant roots

Blood vessels are the ‘roots’ of a tumour. Image source: Wikimedia Commons

In the first of this series we explained how the ‘neighbourhood’, or microenvironment, around a cancer affects how it grows and spreads.

In this next post we’re taking a look at how blood vessels grow into, and feed, a tumour.

Angiogenesis

As we’ve said before, a tumour can be thought of as a ‘rogue organ’ in the body – not one that is useful to us, but one that has the same requirements as any other. This includes a network of blood vessels (vasculature), supplying the cancer cells with oxygen and nutrients, and removing waste products. And, in the case of cancer, enabling it to survive, grow, and spread around the body.

But while the blood supply feeding our healthy tissues grows as we develop in the womb, a tumour has to ‘plumb in’ its own blood supply from nearby blood vessels – a process known as angiogenesis.

And because angiogenesis is so fundamental to how cancers grow and spread, it’s an exciting focus for cancer researchers all over the world.

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Getting to know the neighbours – the tumour microenvironment

This entry is part 1 of 4 in our Microenvironment series
Pancreatic cancer cells

Tumour cells don’t live in isolation

Despite the huge progress that has been made over recent decades, more than 150,000 people lose their lives to cancer every year in the UK, usually because the disease has spread through their body.

Understanding why this happens – and how we can treat tumours once they have spread – is crucial if we are to beat cancer.

Cancer is not just one but hundreds of different diseases, depending on where in the body it started and the underlying molecular faults that drive it.

Over the years, many researchers have poured their efforts into understanding individual types of cancer -  such as the recent work from Cancer Research UK’s Professor Carlos Caldas showing that breast cancer can be divided into ten distinct types – as well as searching for the fundamental characteristics of cancer cells (for example, our very own Sir Paul Nurse and Sir Tim Hunt’s Nobel prize-winning work on understanding how all cells divide).

Much of the effort in developing new cancer treatments has focused on identifying and targeting specific molecules in cancer cells – good examples of this approach in action are revolutionary ‘targeted’ drugs like breast cancer drug trastuzumab (better known as Herceptin) and leukaemia drug imatinib (also called Glivec).

But as well as this focus on cancer cells themselves, it’s becoming increasingly clear that tumours are more than just collections of rogue cells. Blood vessels, immune cells and other healthy tissues are hijacked to support a tumour, helping it grow, spread and resist treatment.

Researchers are increasingly turning their attention to this ‘bad neighbourhood’ around a around a tumour, to understand how it can be brought back under control to treat cancer more effectively.

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Notes from the NCRI conference (day 3)

Jacco van Rheenen

It was another day of fascinating talks

It’s been another packed day at the NCRI conference, full of interesting discussion and debate (as were yesterday’s and Sunday’s sessions).

But before we get stuck into the day’s events, it’s worth flagging the overnight media coverage from the meeting, with OnMedica covering this story on prostate screening, while the BBC was one of several news outlets to cover a promising potential method to detect cancer.

And now to the main event.

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Notes from the NCRI conference (day 1)

Joan Massague at the NCRI 2012

Professor Joan Massague speaking at the 2012 NCRI Cancer Conference

It’s November, which means we’re in Liverpool again for the annual NCRI Cancer Conference.

Researchers from around the world will be spending the next three days in the BT Convention Centre on the River Mersey, discussing the latest and greatest developments in cancer research.

Tomorrow the conference really gets going, with a packed agenda planned – but we’ve heard several interesting talks this afternoon already.

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