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Sent: Tuesday, March 15, 2005 7:10 PM
Subject: Scientists put cancer cells in permanent 'coma'
http://www.mariecurie.org.uk/news/


Dear Docs & science friends,

http://www.mariecurie.org.uk/news/
http://www.mariecurie.org.uk/news_view/late_scientists-put-cancer-cells-in-perma\
nent-coma.html

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News : Scientists put cancer cells in permanent 'coma'
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An unexpected discovery by scientists at the Marie Curie Research Institute
could point the way to a completely new approach to treating cancer.


Current treatments are based on cutting out or killing cancer cells. Now
scientists think their work could lead to a third way of dealing with them. They
have successfully put cancer cells into a permanent 'coma' by reactivating a
natural self-defence mechanism which responds to dangerous mutations by putting
the cell into a state called senescence - meaning that it cannot divide any
more.

Continued >>



Scientists put cancer cells in permanent 'coma'
An unexpected discovery by scientists at the Marie Curie Research Institute
could point the way to a completely new approach to treating cancer.


Current treatments are based on cutting out or killing cancer cells. Now
scientists think their work could lead to a third way of dealing with them. They
have successfully put cancer cells into a permanent 'coma' by reactivating a
natural self-defence mechanism which responds to dangerous mutations by putting
the cell into a state called senescence - meaning that it cannot divide any
more.

In cancers this safeguarding mechanism is bypassed, enabling cell division to
run out of control. Scientists previously thought that in cancers it was damaged
beyond repair.

This new work by the Marie Curie Cancer Care scientists and published today
shows that they can switch back on the mechanism that triggers senescence in
cells for the deadly skin cancer malignant melanoma. The cells stop dividing -
and never divide again.

Dr Colin Goding, Leader of the Signalling and Development Group, who led the
research, explained: "When certain genes called oncogenes are activated by
mutation, they cause cancer to develop. Many oncogenes control cell growth or
cell division.

"When these are mutated, it's like the accelerator in a car being jammed on -
the cell is continuously getting instructions to divide.

"In our lifetime of 70 years or so, we get mutations in these genes all the
time, but may only get cancer once. That is partly because we are protected by
the senescence mechanism.

"Normal cells sense that something is wrong - that the accelerator is jammed on
- and they put on this brake on cell division called senescence, which means the
cell will never divide again. It's in a coma - permanently.

"We thought that when normal cells became melanomas, it wasn't possible to
switch on senescence - these are cancer cells, so by definition, they've
overcome this braking mechanism.

"We were looking at a gene called Tbx2, which is too active in melanoma and
other cancers, and wanted to know exactly what it did and how it did it. It
turned out to be linked to a mechanism that repressed senescence.

"What really surprised us was that when we inhibited Tbx2 in melanoma cells,
they senesced and stopped dividing. This means we have potentially a new way of
stopping cancer cells dividing.

"Now we want to find out in what proportion of melanomas and other cancers we
can induce senescence. We are not sure whether this will be effective against
all melanomas or just some.

"Being able to design drugs that reactivate senescence would be a great boon.
The beauty of it is that this natural mechanism would automatically target cells
which have the accelerator jammed on - it would hit the cancer cells, but not
normal cells."

The scientists carried out their work on human cells in culture. While the
discovery potentially opens up a new route for tackling cancer, drug development
is a long process. It will be at least ten years before the benefits of this
work are seen in the clinic; no clinical trials are planned at this stage.

Dr Goding has been working on malignant melanoma for the past 16 years. His
group started investigating Tbx2 six years ago, and the scientists have focussed
on senescence for three years.

Skin cancer specialist Dr Tim Eisen, Senior Lecturer at the Royal Marsden
Hospital, London, has one of the largest practices dealing with skin cancer in
the UK. He is a member of the National Cancer Research Institute Melanoma
Clinical Studies Group. He said: "My colleagues and I see around 150
newly-referred patients with malignant melanoma every year.

"Understanding how melanomas develop and survive will be crucial to developing
effective treatment for this dangerous condition. At present, we do not have
very effective treatment for melanoma once it has spread to other parts of the
body. "Dr Colin Goding's discovery is an important contribution to this exciting
field. It suggests new ways of tackling melanoma - although much work remains to
be done."

The work of Dr Goding's team work is funded in part by the Association for
International Cancer Research (AICR), which is based in Scotland. Dr Mark
Matfield, the AICR's Scientific Consultant believes the research could open up a
whole new approach to treating cancer in the future.

He said: "Malignant melanoma is a particularly fast growing cancer and we don't
have any really effective treatments for advanced cases.

"This work will excite the scientific community because of the possibility that
this protective self-defence mechanism could form the basis of a potential
treatment, not only for melanomas but also for other fast-growing cancers like
breast, prostate and pancreatic cancer, which between them kill more than 30,000
people in the UK every year."

Pictured: Senescent melanoma cells before and after Tbx2 is switched off.
Senescent cells are blue. Images by permission of Cancer Research.


a.. The team's work was published in Cancer Research, March 15, 2005.65(6):
Vance, K., Carreira, S., Brosch, G.. and Goding, C.R. Tbx2 is overexpressed and
plays an important role in maintaining proliferation and suppression of
senescence in melanomas.
b.. In 2003, malignant melanoma killed 1,766 Britons. If detected early
enough, malignant melanoma is relatively easy to treat as it can simply be
removed from the skin. However, melanoma is a highly aggressive cancer and if it
spreads to other parts of the body, it is very difficult to deal with: current
treatments are largely ineffective.
c.. Scientists at the Marie Curie Research Institute, in Oxted, Surrey,
investigate the causes and treatment of cancer. They focus on how the cells of
our bodies should normally operate; what causes many of the complicated
processes in cells to go wrong, leading to cancer; and how better treatment can
be developed through in-depth knowledge. For more details see
www.mariecurie.org.uk/help/mcri.html
d.. The Association for International Cancer Research (AICR) is a totally
independent charity based in Scotland. It has no commercial ties, no links with
any particular research institutions, and no commitment to follow any particular
line of research. It funds what it considers to be the best researchers and the
most valuable studies wherever they are in the world. This innovative approach
to funding research has enabled AICR to contribute significantly to furthering
man's understanding of cancer.
e.. With Compliments from: Dr. BHUDIA : Science Group Of INDIA.
http://uk.groups.yahoo.com/group/venustransit_2004/
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Founder :"Kutch Amateurs Astronomers Club - Bhuj - Kutch".
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