Hi, I'm Dr. Malcolm Brock and I'm Associate Professor of
Surgery and Oncology here at the Johns Hopkins hospital.
And my team and I are working on a very exciting new promising
way of treating cancer.
[MUSIC]
Genetics is the hardware, the actual DNA sequence to
describe and tell us how cancer works.
Epigenetics is the software,
it's how these genes function and work together.
To explain how we're gonna fight cancer using epigenetics,
let's go to the toy box.
[MUSIC]
In the toy box here,
this young little fellow represents a cancer cell.
And we're gonna put him right here because he's well
protected, as all cancer cells are.
You can see all the cancer cells here they all have armor.
Very, very difficult for us to kill these guys.
And let's take out of the tool box this.
This represents chemotherapy.
And what we presently do is we try to kill these cancer cells.
So we use our chemotherapy and we go bam, bam, bam.
And sometimes we kill them, but then what we realize is that as
soon as we do that other cancer cells quickly come up.
And they're even more protected.
They've got their shield, they've got their armor,
they're on horses.
They actually change a little bit and
you can see now that they're even more fortified.
We take the chemotherapy and
we try to get at them and we can't really affect them.
They become resistant.
What was known was that epigenetic therapy did work for
liquid tumors, cancers like leukemia.
But what we found here at Johns Hopkins
that hadn't been shown before was that epigenetic therapy
could actually be used with the big cancers such as lung cancer.
The solid tumors.
What we found when we tested the epigenetic therapy in humans was
that, interestingly, it worked in three different ways.
So let's go back to the toy box.
Here's our chemotherapeutic agent we had before.
And if epigenetic therapy, they actually,
this represents two different drugs.
One was a chemotherapeutic agent that was old.
And the other, was a relatively new drug.
We put them together.
And, we put them together at very low doses so
that it no longer acted like a chemotherapeutic agent.
And instead, at a very low dose,
we try not to kill the cancer cell because remember before
when we kill the cancer cell, the others would rush in and
the more fortified ones would even be harder to kill.
And what we found that as he takes up this drug more and
more, the genes change.
And genes that were silent all of a sudden come back to life
and the cancer cell changes,
from a cancer cell to a more normal cell.
He starts to look more normal.
And as soon as that happens you can see that he can become
more vulnerable to all sorts of things.
Just by him taking off all of his armor very quickly
he would just die.
The second way that epigenetic therapy works, is that again,
we sprinkle on some of the sand, and we found that again,
the genes that were silenced come back on.
And the armor starts to come off but
it wasn't enough to kill the cell.
But then we gave good old chemotherapy, and
the chemotherapy, bam, killed the cell.
And it even worked better than if it would have worked before
the epigenetic therapy was given.
Another way we saw that this worked is that,
just like these cells became more and more normal, and
defenseless, we would give them immune therapy.
Here represented by a white blood cell and
we found that the immune therapy also had that added punch
where your own immune system all of a sudden would go ahead and
take care of defeating the cancer.
As you can see,
cancer is a formidable foe, much like a full army.
We need a lot of different ways to treat it.
We know from our previous clinical trials that epigenetic
therapy works with lung cancer.
But which particular lung cancers, and
in which patients will it work the best?
That is our next frontier.
[MUSIC]