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UK: Scientists Find Secrets Of Cell Death

LONDON, April 10, 2004 (UPI) -- Medical researchers in England say they have a new insight into the biological
processes of cell death, which could lead to a new treatment for cancer.

The Medical Research Council Toxicology Unit team at Leicester University hopes their work will eventually lead to a
new treatment for a range of diseases by manipulating the complex interactions that lead to a cell's death, but which
often go wrong in diseases.

The research is published in the journal Molecular Cell, the BBC reported.

Cells in the human body continually die off to be replaced by new cells. Most cells kill themselves by a programmed
death reaction, known as apoptosis.

Failure of the normal apoptosis process can play a part in diseases such a cancer, certain neurodegenerative disorders
such as Parkinson's and auto-immune diseases such as lupus.

The Leicester researchers hope that uncovering details of apoptosis will enable scientists to find ways to manipulate
it for treating disease.

One hope would be to amplify the apoptosis process to stop cancer, which often thrives because of a failure of cells to
die off at the end of their natural life.

SOURCE: Washington Times, DC
http://washingtontimes.com/upi-breaking/20040410-064328-7283r.htm

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UK: Secrets Of How Cells Die Revealed
BBC News, UK
Last Updated: Saturday, 10 April, 2004, 00:26 GMT 01:26 UK

Scientists have taken an important step towards understanding the biological processes involved when cells die.

The Medical Research Council Toxicology Unit team hopes the work will eventually led to new treatment for a range of
diseases, including cancer.

They believe it should be possible to manipulate the complex interactions within a cell that lead to its death - and
which often go wrong in disease.

The research is published in the journal Molecular Cell.

Cells in the human body are continually dying and most of these cells kill themselves by a programmed form of cell
death, known as apoptosis.

In a healthy body, the number of cells stays constant. Millions of new cells are produced every second, and millions of
others are lost or kill themselves.

Failure of the normal apoptosis process plays a role in different diseases including cancer, certain neurodegenerative
disorders such as Parkinson's and auto-immune diseases, such as lupus.

Previous research has shown that the life cycle of a cell is regulated by a complex cellular machine called the
proteasome.

This works by controlling the delicate balance of proteins in a cell. Proteins which are no longer needed are tagged,
and targeted for destruction by the proteasome.

Killer proteins

However, during apoptosis, the part of the proteasome which is able to spot the tags is effectively disabled by the
release of enzymes called caspases.

This allows for the build up of proteins within the cell which can ultimately trigger its death.

The Leicester team hope that pinpointing this procedure will enable scientists to find ways to manipulate it to treat
disease.

For instance, amplifying the apoptosis process could potentially stop cancer, which often results from a failure of
cells to die off at the end of their natural life.

Lead researcher Professor Gerald Cohen, who is based at Leicester University, said: "This new research takes us a step
closer to understanding how cells die.

"The challenge now is to use this knowledge to work towards finding new drugs and treatments for the many common
diseases and conditions which occur when cell death goes wrong."

Dr Julie Sharp, science information manager at Cancer Research UK, said: "In the future scientists may be able to use
this information to design treatments that switch cell death back on, stopping cancer cells in their tracks."

Linda Kelly, chief executive of the Parkinson's Disease Society, said: "The society welcomes this new advance which
will take us closer to understanding why cells die.

"We look forward to future work in this important area of research."

SOURCE: BBC News, UK
http://news.bbc.co.uk/1/hi/health/3610677.stm

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