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| Heidelberg,
Sunday 4 September 2005 |
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| A new link between stem cells and tumors |
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| Emmanuel Caussinus |
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| Cayetano González |
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| Left: Normal dividing neuroblasts create a large new cell and a smaller cell destined to become part of a nerve. Right: If molecules aren't put in the right places, this asymmetric division doesn't occur and a tumor develops. |
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Press
Release 4 September 2005 [PDF]
Scientists at the European Molecular Biology Laboratory
[EMBL] in Heidelberg and the Institute of Biomedical
Research of the Parc Científic de Barcelona
[IRB-PCB] have now added key evidence to claims
that some types of cancer originate with defects
in stem cells. The study, reported this week in
the on-line edition of Nature Genetics [September
4] shows that if key molecules aren't placed in
the right locations within stem cells before they
divide, the result can be deadly tumors.
Cells in the very early embryo are interchangeable and
undergo rapid division. Soon, however, they begin
differentiating into more specific types, finally becoming
specialized cells like neurons, blood, or muscle. As they
differentiate, they should stop dividing and usually
become embedded in particular tissues. Some tumor cells
are more like stem cells because they are identical, they
divide quickly, and in the worst case Ð metastasize Ð they
wander through the body and implant themselves in new
tissues.
Specialized cells may die through age or injuries, so the
body keeps stocks of stem cells on hand to generate
replacements. Usually the stem cell divides into two types:
one that is just like the parent, which is kept to maintain
the stock, and another that differentiates. This is what
happens with neuroblasts. Cell division creates one large
neuroblast and a smaller cell that can become part of a
nerve. This process is controlled by events that happen
prior to division. The parent cell becomes asymmetrical: it
collects a set of special molecules, including Prospero and
other proteins, in the area that will bud off and become the
specialized cell.
"This asymmetry provides the new cell with molecules
it needs to launch new genetic programs that tell
it what to become," says Cayetano González,
whose group began the project at EMBL and has continued
the work as they moved to the IRB-PCB. "The current
study investigates what happens when the process
of localizing these molecules is disturbed."
Whether Prospero and its partners get to the right place
depends on the activity of specific genes in the stem cell.
EMBL PhD student Emmanuel Caussinus from
González's group created neuroblasts in which these
genes were disrupted. "We no longer had normal
neuroblasts and daughter cells capable of becoming part
of a nerve," Caussinus says. "Instead, we had a tumor."
When these altered cells were transplanted into
flies, the results were swift and dramatic. The
tissue containing the altered cells grew to 100
times its initial size; cells invaded other tissues,
and death followed. The growing tumor became "immortal",
Caussinus says; cells could be retransplanted into
new hosts for years, generation after generation,
with similar effects.
The study proves that specific
genes in stem cells – those which control the fates
of daughter cells – are crucial. If such genes are
disrupted, the new cells may no longer be able to
control their reproduction, and this could lead
to cancer. "It puts the focus on the events that
create asymmetrical collections of molecules inside
stem cells," González says. "This suggests new lines
of investigation into the relationship between stem
cells and tumors in other model organisms and humans."
Source article
Induction of tumor growth by altered stem-cell
asymmetric division in Drosophila melanogaster
E. Caussinus and C. González
Nature Genetics, 4 September 2005 [online
publication]
Press contact
Sarah Sherwood
EMBL Information Officer, European Molecular Biology Laboratory,
Meyerhofstrasse 1, 69117 Heidelberg, Germany
Tel: +49 [0] 6221 387125
E-mail: sarah.sherwood@embl.de |
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