Please wait while the transcript is being prepared...
0:00
My name is Jude Fitzgibbon.
I am a Professor
in Personalized Cancer Medicine
at the Barts Cancer Institute.
It's part of
Queen Mary University of London.
My lecture today
is on the Molecular Genetics
of Non-Hodgkin Lymphoma.
I am going to be using
an indolent B-cell malignancy
called follicular lymphoma
as an example.
0:19
I think it's important to preset
that cancer represents
almost
the perfect genetic disease
where it's radicalized
maybe 10-20 genes
to actually shift
the balance from a normalcy
to a malignant phenotype.
And so we need to think of these
genes as individuals
but also how they kind of
work together to cooperate
to actually drive this change
in phenotype.
And it's helpful
to think of a formula
in relationship to cancer
and indeed B-cell malignancy
in relationship to the genetics
and the microenvironment
working together
to give rise to cancer.
0:55
The technology
has improved fantastically.
When I started my PhD
in the late '80s, you know,
I did my first polymerase
chain reaction,
my first PCRs using
three water baths set
at different temperatures,
a stopwatch, and a tweezers
to actually move the chews
from one place to another.
Now we've got the opportunity
to actually sample all genes,
all DNA in one single experiment
and monitor their expression
at the same time.
1:23
So I think what we should do
is we should try
and get a very clear picture
of what the human genome is.
So if we can imagine
the human genome as a stadium
of 25,000 spectators,
that corresponds
to 25,000 genes.
We know where each spectator,
where each gene lies.
We know the location
and the position,
and then we know exactly
what they look like
because
that's their DNA sequence.
And how they sound
because that's the sequence
of their messenger RNA.
We've now the tools
to define the DNA
and the mRNA profiles
of every cancerous cell
in single experiments
where we can focus
in on the whole genome,
that's the three billion base
pairs of sequence.
If we're just interested
in looking at
the coding sequence,
which is less than 2 percent
of the genome,
we can
focus in on 50 mega bases.
But what's ideal is when we know
the key genes
that we know to be important,
we can focus in on those
using other different
technologies.
Now what's also key is to preset
that we're not just
looking at genes here
because
these are not just genes,
they're genes with clothes on.
So you can see the spectators
have specific clothes on.
And it's that combination
of the gene sequence itself,
but also
the control of gene expression
and gene function
via epigenetics.
That's key in this shift
from normalcy
to the tumor phenotype.
