SCOTS scientists have discovered genetic "brakes" which could slow down or stop diseases such as multiple sclerosis and cancer, it was announced yesterday.
In what has been hailed as a "big step" towards answering one of medical science's great questions, the findings of researchers at the Roslin Institute could lead to new treatments and even cures for illnesses which affect the immune system.
It was previously thought that a select group of "master" genes was responsible for controlling the growth of cells that can cause the conditions.
But the study discovered that there are actually hundreds of genes which interact with each other in a way that is much more complicated than previously thought.
MS, a disease in which the immune system mistakenly attacks and damages sheaths that protect nerve cells, can cause symptoms ranging from vague tingling to blindness and paralysis. It affects one in every 500 people in Scotland – the highest proportion in the world – and nearly 100,000 across the UK.
Professor David Hume, the director of the University of Edinburgh's Roslin Institute, said a whole new field of scientific research had been opened up, which would dramatically alter the way in which vaccines were used and drugs were tested.
MS charities last night welcomed the findings which, they said, highlighted Scotland's leading role in research into the illness, while cancer specialists described the breakthrough as "exciting".
Professor Hume said: "This research provides an incredible resource for the study of immunity and disease in humans and animals. This study has effectively shown us where the brakes are which could slow down or stop diseases like cancer and multiple sclerosis. We believe that this could lead to treatments and cures for many diseases of the immune system."
The scientists said they believed that variations in this network explained why people could develop diseases in different ways.
The team hopes that, by identifying weak spots in the gene structure, they will be able to stop the growth of tumours, enabling the growth of healthy cells.
They also hope the new research could lead to treatments for the likes of myeloid leukaemia and arthritis.
The researchers said the findings offered up previously hidden information about the immune system and could ultimately help doctors understand why some cancer patients responded to immunotherapies while others did not.
Professor Hume, who carried out the three-year study as part of a team of international researchers, focused on the immune system and examined the genes involved with white blood cells called macrophages.
When healthy, these cells cleanse the body of viruses and bacteria, but if they grow uncontrollably, they can turn against the body's own tissue to cause conditions such as MS, arthritis and emphysema.
It was previously thought that such cell-growth processes were managed by a select group of master, or regulator, genes that give instructions to many other genes.
However, the research makes clear that there are, in fact, hundreds of regulator genes which all interact with each other to control cell development and growth. Scientists say it helps to explain why people can develop the same disease in different ways, because of variations in different parts of their genetic networks.
By identifying the weak spots in these networks, it is hoped it will soon be possible to stop the growth of tumours, or enable the growth of healthy cells.
Prof Hume, recognised as an international authority in genome sciences, said last night the study was akin to discovering the function of every single part of a car, whereas before only eight or nine were known.
He added: "The traditional way we have carried out research in this area is to look at one gene at a time. We thought processes like cells growing or dying were controlled by a very small number of master genes, but in fact it's an entire environment that creates the changes, with around 20,000 different elements.
"It means we have a much better understanding of how tumours develop.
"There are literally thousands of different ways of developing a tumour, and every one is likely to be different. That represents a serious challenge for us, but it gives us hope that, depending on how the tumour arises, we can know what therapies will be useful."
He said: "We will be able to understand why different people have different responses to pathogens. If you infect a large number of people with influenza, only a few would get sick – we now know why, and how to prevent it from happening. It will make a significant difference to the way vaccines are used and the way drugs are tested, as we will be able to establish likely side-effects to therapies."
Dr Lesley Walker, director of cancer information at Cancer Research UK, said: "This exciting research reveals just how complex the development of our immune system is – areas of the genome that we thought were dormant may actually play an important role in guiding its evolution."
She added: "The studies may eventually help to explain why some people respond to immunotherapies and others don't."
A spokesman for the Multiple Sclerosis Society Scotland, the charity of which JK Rowling served until recently as patron, said: "Every day, researchers are learning more about the genetic make-up of MS, and anything that helps put the pieces of this complex puzzle together must be a good thing.
"This study also highlights the important role that research in Scotland is playing in developing our understanding of MS and other autoimmune conditions," the spokesman added.
Dr Mark Matfield, scientific adviser for the St Andrews-based Association for International Cancer Research, said: "This is a really powerful new study of how cells work. It shows us the mechanisms controlling how cells change are much more complicated than we thought. It may go some way to explain why it has been so difficult to understand these mechanisms.
"This study only looks at white blood cells, and we'll need to find out if this is generally true in other types of cells," he said. "However, this clearly takes us one big step closer to understanding the way cells grow and change – one of the great questions of medical science."
The discovery is regarded as an important breakthrough for the Roslin Institute, which formed a multi-million-pound partnership with the University of Edinburgh last year. Scientists intend to extend the project with funding from the Biotechnology and Biological Sciences Research Council to look at the way genes communicate to control immunity in livestock animals.
The study was conducted as part of the Functional Annotation of the Mammalian cDNA (FANTOM], a consortium comprising scientists at the Roslin Institute, the RIKEN Yokohama Institute in Japan, and researchers from the US, Canada, Australia, Switzerland, Norway, South Africa, Sweden, Denmark, Italy, Germany, and Singapore.
It was previously thought that a select group of "master" genes was responsible for controlling the growth of cells that can cause the conditions.
But the study discovered that there are actually hundreds of genes which interact with each other in a way that is much more complicated than previously thought.
MS, a disease in which the immune system mistakenly attacks and damages sheaths that protect nerve cells, can cause symptoms ranging from vague tingling to blindness and paralysis. It affects one in every 500 people in Scotland – the highest proportion in the world – and nearly 100,000 across the UK.
Professor David Hume, the director of the University of Edinburgh's Roslin Institute, said a whole new field of scientific research had been opened up, which would dramatically alter the way in which vaccines were used and drugs were tested.
MS charities last night welcomed the findings which, they said, highlighted Scotland's leading role in research into the illness, while cancer specialists described the breakthrough as "exciting".
Professor Hume said: "This research provides an incredible resource for the study of immunity and disease in humans and animals. This study has effectively shown us where the brakes are which could slow down or stop diseases like cancer and multiple sclerosis. We believe that this could lead to treatments and cures for many diseases of the immune system."
The scientists said they believed that variations in this network explained why people could develop diseases in different ways.
The team hopes that, by identifying weak spots in the gene structure, they will be able to stop the growth of tumours, enabling the growth of healthy cells.
They also hope the new research could lead to treatments for the likes of myeloid leukaemia and arthritis.
The researchers said the findings offered up previously hidden information about the immune system and could ultimately help doctors understand why some cancer patients responded to immunotherapies while others did not.
Professor Hume, who carried out the three-year study as part of a team of international researchers, focused on the immune system and examined the genes involved with white blood cells called macrophages.
When healthy, these cells cleanse the body of viruses and bacteria, but if they grow uncontrollably, they can turn against the body's own tissue to cause conditions such as MS, arthritis and emphysema.
It was previously thought that such cell-growth processes were managed by a select group of master, or regulator, genes that give instructions to many other genes.
However, the research makes clear that there are, in fact, hundreds of regulator genes which all interact with each other to control cell development and growth. Scientists say it helps to explain why people can develop the same disease in different ways, because of variations in different parts of their genetic networks.
By identifying the weak spots in these networks, it is hoped it will soon be possible to stop the growth of tumours, or enable the growth of healthy cells.
Prof Hume, recognised as an international authority in genome sciences, said last night the study was akin to discovering the function of every single part of a car, whereas before only eight or nine were known.
He added: "The traditional way we have carried out research in this area is to look at one gene at a time. We thought processes like cells growing or dying were controlled by a very small number of master genes, but in fact it's an entire environment that creates the changes, with around 20,000 different elements.
"It means we have a much better understanding of how tumours develop.
"There are literally thousands of different ways of developing a tumour, and every one is likely to be different. That represents a serious challenge for us, but it gives us hope that, depending on how the tumour arises, we can know what therapies will be useful."
He said: "We will be able to understand why different people have different responses to pathogens. If you infect a large number of people with influenza, only a few would get sick – we now know why, and how to prevent it from happening. It will make a significant difference to the way vaccines are used and the way drugs are tested, as we will be able to establish likely side-effects to therapies."
Dr Lesley Walker, director of cancer information at Cancer Research UK, said: "This exciting research reveals just how complex the development of our immune system is – areas of the genome that we thought were dormant may actually play an important role in guiding its evolution."
She added: "The studies may eventually help to explain why some people respond to immunotherapies and others don't."
A spokesman for the Multiple Sclerosis Society Scotland, the charity of which JK Rowling served until recently as patron, said: "Every day, researchers are learning more about the genetic make-up of MS, and anything that helps put the pieces of this complex puzzle together must be a good thing.
"This study also highlights the important role that research in Scotland is playing in developing our understanding of MS and other autoimmune conditions," the spokesman added.
Dr Mark Matfield, scientific adviser for the St Andrews-based Association for International Cancer Research, said: "This is a really powerful new study of how cells work. It shows us the mechanisms controlling how cells change are much more complicated than we thought. It may go some way to explain why it has been so difficult to understand these mechanisms.
"This study only looks at white blood cells, and we'll need to find out if this is generally true in other types of cells," he said. "However, this clearly takes us one big step closer to understanding the way cells grow and change – one of the great questions of medical science."
The discovery is regarded as an important breakthrough for the Roslin Institute, which formed a multi-million-pound partnership with the University of Edinburgh last year. Scientists intend to extend the project with funding from the Biotechnology and Biological Sciences Research Council to look at the way genes communicate to control immunity in livestock animals.
The study was conducted as part of the Functional Annotation of the Mammalian cDNA (FANTOM], a consortium comprising scientists at the Roslin Institute, the RIKEN Yokohama Institute in Japan, and researchers from the US, Canada, Australia, Switzerland, Norway, South Africa, Sweden, Denmark, Italy, Germany, and Singapore.
The Scotsman, 20th April 2009
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