My name is Ali Shalati.
I'm going to share with you the
recent stories from the laboratory
and the function of enhancer in
regulation of promoter activity,
and how malfunction
of human cancer.
For over 20 years now, the
burning question in my laboratory
has been why chromosomal
translocation involving the MLL
gene results in pathogenesis
of hematological malignancies.
MLL gene which encoded by about
4,000 amino acid containing protein
undergoes frequent translocation
with large number of translocation
partners as shown here
on the right hand side.
And translocation of MLL to many
of these translocation partners
result in pathogenesis of
As shown in the bottom here,
there are several examples
of MLL translocation, an 11-4
translocation on the left hand side
of the screen and a couple
of 11-19 translocations
on the right hand
side of the screens.
And most of these
translocations are detected
in children upon cytogenetics.
And analysis of blood from the kids
shows that there's a high level
of white blood cell
exist in these patients.
Normally, we have about 1% of
white blood cells in our system.
Looking at blood analysis
from leukemic patients,
some of these patients have
over 80% of white blood cells
in their system, which
complications of infiltration
of these white blood cells
in many tissues and organs
result death for these children.
MLL translocations mostly
afflicts young adults,
early adolescents and infants.
And very little is known about
why these translocation causes
So a true understanding
of molecular properties
of MLL translocational leukemia
is going to be very important
for development of
My laboratory for over 20 years
now has been taking advantage
of genetic and biochemistry
multiple model system including
Saccharomyces cerevisiae, Drosophila
melanogaster, mouse, and also
tissue sample and human cell
lines that we have been working
in the laboratory in the hope of
understanding why translocations
of MLL results in
There will be a little emblem on
the bottom that tells you what model
system I'm talking
about in a given slide,
and our work rapidly moves between
model system trying to define
the role of the
factors that Ive been
studying in leukemic pathogenesis.