Jan-Feb 2014 ASCB Newsletter - page 8-9

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The science of life, the life of science
Do you want to
of ataxin-1 amyloid oligomers correlates with
disease progression. Additionally the researchers
found that these mutant ataxin-1 oligomers
propagate, although it’s not yet clear how that
spreading correlates with disease. However,
targeting these ataxin-1 oligomers with passive
immunotherapy rescues motor defects in mice
with a disease phenotype.
Speaking on Tuesday at the session entitled
Tumor Microenvironment as a Driver and
Target in Cancer Progression, Johanna Joyce, a
cancer biologist at Memorial Sloan-Kettering
Cancer Center, said that in looking for new
strategies to treat glioblastoma, her lab turned
to non-tumor cells that are part of the glioma
microenvironment, the cancer’s cellular
neighbors. In particular, her lab zeroed in on
tumor-associated macrophages (TAMs). TAMs
are normally the brain’s front-line immune cells,
and they depend on colony-stimulating factor-1
(CSF-1) for differentiation and survival. When
the Joyce lab used an inhibitor of the CSF-
1 receptor to target TAMs in a mouse model
of glioblastoma multiforme, the treated mice
survived many months beyond the control
At the final Minisymposium in the medicine
thread, Cancer Cell Biology, Sarah Hymowitz
of Genentech showed how the BRAF-MEK
complex reveals diverse mechanisms of pathway
dysregulation. Growth factor receptor pathways
drive many cancers, she said. The BRAF
V600E mutation is found in more than 60%
of melanomas and promotes MEK signaling.
BRAF and MEK form a stable complex in vitro,
and Hymowitz and colleagues determined the
crystal structure of the complex. They then used
conformation-specific BRAF inhibitors and
showed that the interaction between BRAF and
MEK can lead to changes in pathway activation.
At the same session, Mikala Egeblad from
Cold Spring Harbor Laboratory told the
audience how the neutrophil extracellular traps
(NETS) that capture and kill bacteria can also
serve to enhance cancer metastasis. Egeblad
described how metastatic tumor cells can recruit
neutrophils and trigger neutrophils in their
vicinity to “cast” NETs. And this, she found,
enhances the ability of tumors to invade and
spread through the activity of the digestive
enzymes in the NETs. Most intriguingly, her
team used DNase to digest the DNA scaffold of
the NETs. The effect was to reduce the ability
of the tumor cells to form metastases in mice.
Since DNase was shown in animals to counter
metastasis, there is the prospect, says Egeblad,
that the enzyme might have a role in human
cancer therapy.
While the scientific outlook at the 2013
Annual Meeting was bright and sunny, a cloud
of pessimism about science funding, especially
in the United States, hung over many of the
participants, including 2013 Nobel Prize
winner James Rothman, who told a special
plenary session that shortsighted federal support
cutbacks were “crushing” basic science. But 2013
ASCB President Don Cleveland saw the bright
lining in the thunder cloud—exciting science
is always its best demonstration of value. “Basic
science is the way to do translational research,”
Cleveland said.
—Christina Szalinski
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—Thea Clarke
Science Highlights, continued from p.6
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