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Hello. I'm Peter Gallant from
the University of
Wurzburg in Germany.
I'm going to tell you about
the function of the Myc
protein in Drosophila.
In particular its role
in controlling growth.
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Two research interests
converge on the Myc gene,
on one hand, the wish to
understand and treat
human cancers.
On the other hand, the
desire for describing
the mechanisms that control
animal size during development.
However, it was the connection
of Myc to tumors that
led to the identification
of the Drosophila Myc gene.
In the 1960s,
several retroviruses
were isolated
that caused tumors in chickens.
The advent of molecular
cloning later allowed
the isolation of the
transforming principle
in these viruses.
A gene that was dubbed
viral myelocytomatosis gene
or v-Myc. Subsequently related
genes were identified
in the human genome.
The first of these were called
C-Myc and N-Myc and L-Myc.
Most interestingly, these
genes were found to
be overexpressed in
many human tumors,
often as a consequence of
gene amplifications
or rearrangements.
For example, virtually
all cases of
Burkitt's lymphoma
carry translocations
of the C-Myc locus
that juxtaposed the
protein-coding sequences to
the strong regulatory regions
of immunoglobulin genes.
In other tumors, Myc levels
are increased transcriptional or
post-translational
as a consequence
of the activation of
other oncogenic lesions,
such as the Wnt
signaling pathway.
Altogether, it is estimated that
up to 70 percent of
human tumors contain
elevated amounts of Myc.
These increased Myc
levels indeed played
a causal role in transformation,
as was shown in many
different mouse models,
such as the famous E
mu-myc mouse that was
generated by Gerry Adams
a quarter-century ago.
In these animals, C-Myc
is expressed under
the control of the
immunoglobulin mu enhancer,
which leads to the
development of lymphomas.
How then, to make
proteins achieve
