Summary:
As you watch the video, think about the importance of the following:
Captions:
Dr Nikki Verrillis: Basically today what I’m going to do is hopefully give you bit of an idea of how we as medical researchers
use our biology, basically, but really biochemistry I suppose as well, to try and understand human diseases.
In my particular research interest is in cancer.
But how we use that knowledge to try and understand a disease
and then to try and develop treatments for that particular disease.
I’m from the University of Newcastle just a couple of hours up the road and I also work in association with
the Hunter Medical Research Institute up in Newcastle and that’s basically a collaboration between
the University of Newcastle and all of the hospitals within the Hunter region.
So we work closely with oncologists and doctors at the hospital.
We work closely with the patients to find out what it is that we need to do improve their outcome
and their survival and of course we work closely with researchers and students at the university.
Summary:
Listen to Nikki as she talks about cancer research:
Captions:
Really just to give you an overview of cancer in terms of statistics, I don’t always put this sort of slide in,
because we all know someone who’s been affected by cancer
either individually or themselves or a family or a close friend.
We’ve all been, and if you haven’t been, we will be affected by cancer at some stage in our life.
So we know it’s important and we know we want to find a cure.
But just to give you a bit of an idea in terms of Australian statistics
there’s over hundred thousand new cases of cancer diagnosed every year.
So it really is a highly prevalent disease
and obviously an important disease that we need to understand.
The most common cancers are in men are prostrate cancer.
In both men and women – are colo-rectal or bowel cancer and in women breast cancer.
Melanoma, particularly in Australia: Australia has the highest rate of skin cancer and melanoma
and lung cancer is still extremely prevalent.
And of course it’s important to note that with at least these last two we know
what the risk factors are for these cancers.
We know, what for the most part causes these cancers and we can prevent it if we do the right thing.
It doesn’t necessarily mean we always do.
What I think is also important to note is that while there’s around a hundred thousand new cancers
diagnosed every year
there’s around thirty nine thousand people die from cancer.
Now while this only around about a third, so we can cure around sixty to sixty- five,
seventy percent of patients, obviously too many people are dying of this disease so we need to understand it,
and we need to try and find ways to fight it.
Another interesting thing is that while these are the most common cancers in this order,
the most common cancer causing death is actually lung cancer. So this is a really malignant disease,
it’s often not detected until quite late on in the development of cancer
and unfortunately therapies for this cancer for the most part are not brilliant.
Breast cancer is number five and this has really dropped in the last ten years
and this is because of medical research
this is because we understand it there’s been a lot of funding being put into breast cancer
and we now understand it a lot better and we’ve come up with newer therapies,
we’re still not there but we’re getting there.
So, overall, a lot of people ask me: is the number, is the incidence of cancer increasing?
Because it seems we all know someone with cancer. And if you just look at the actual numbers, yes it is.
It definitely is, over the last ten years it’s increased quite dramatically
but what’s also increased is the amount of time that we live,
so we’re living for much longer now. We’re not dying of other diseases that we’ve found cures for,
so we do actually see a higher incidence of cancer but this is age related.
And so in terms of risk of developing cancer throughout life by the time you’re aged eighty-five
if you’re a male you’ve got one in two chance,
if you’re a female one in three chance of developing some sort of cancer.
As I said the incidence of cancer is increasing with age but what I think is really important,
and I mention this particularly for breast cancer,
is the rate of death from cancer is reducing and this continues to reduce.
So overall it’s reduced about twelve percent in the ten year period from 1993 to 2003.
And this really is because we understand it a lot more and we’re developing new therapies.
Summary:
As you watch the video, consider what Nikki has to say and answer the following questions:
Captions:
Basically what I am going to do is to give you a bit of an overview from a biological point of view
what cancer is, how we’re currently treating cancer and why sometimes this treatment fails
too often this treatment fails.
I’ll then give you a bit of an overview of the type of research that I do up in Newcastle.
And really what we’re trying to ask there is what goes wrong in a cancer cell compared to a normal cell?
And if we can understand that can we develop therapies specific for that cancer cell
that won’t affect the normal cells?
We’re also asking questions like,
Why do some patients respond really well to a chemotherapy and others don’t?
So, we have around a third of patients who will die from cancer.
Why do those patients not respond and others do?
What can we figure out from the differences in those different patients
to work out how to treat them better?
And obviously the ultimate question:
can we develop specific therapies and new therapies to treat these patients?
So basically the easy answer to what is cancer? Is it’s uncontrolled cell growth. So obviously what’s a cell?
I know most of you girls will have a fair idea of this but just to remind you
basically our body is made up of trillions and trillions of tiny, tiny little cells.
Now you can have a look at an example here, just a one centimetre square on a piece of skin.
Each of these individual blocks here is an individual cell.
And we’ve got lots of different types of cells if you look at this area of skin.
So, on the outside we’ve got dead skin cells and these are constantly being sloughed off from your skin
as you rub against things so we have to keep making more cells to replenish those.
Underneath we’ve got what we call these epidermal cells and the blue you can see in the middle is the nucleus
where the DNA is stored. And we’ve got a whole bunch of different cells and basically
as I said the body’s made up of trillions and trillions of these cells
and depending on the role that a cell needs to play
or whereabouts in the body it is it will be a different type of cell.
So it can be a skin cell or it can be a liver cell or a lung cell
and that’s pre-programmed so when a cell is first originated
it knows what type of function it’s got to have and where abouts in the body it’s got to go to.
So we’ve got his sort of architecture making up our body of all these cells
but each of those individual cells also has a really highly complex architecture within that.
And really all we need to point out here is, as I mentioned, those in the centre we have a nucleus,
every cell has got a nucleus and within that we’ve got our DNA – our genetic material.
So, this DNA codes for all the proteins, everything that goes on in that cell
and all the genes within the nucleus code for what we refer to really as workers. They’re the proteins.
They’re the things within the cell and on the outside of the cell that actually do the function that do the work.
And it’s really these proteins I’m particularly interested in. But we look at the genes and proteins within cells
and we look at those in normal cells and compare them to cancer cells to try to figure out what’s going on.
Summary:
As you watch the video, listen to what Nikki has to say about:
Captions:
Now we know what a cell is, basically we can get back to the question of, what is cancer?.
Well as I’ve said it’s uncontrolled cell growth.
Now cells normally have to divide, have to grow so if we start off with one individual cell.
This will go through a process called mitosis, cell division where we now end up with two daughter cells
each of those two cells can divide into two cells so we get four cells and we get this exponential cell growth.
But what happens in the normal situation in the normal body with our cells is that at a certain period of time,
and this will depend on the type of cell, so for example our skin cells are constantly coming off every few days
we need to generate more skin cells, so what the body does is it goes back to our stem cells
which you’ll have heard a lot about, mostly residing in our bone marrow and as stem cells
have this amazing ability of being able to generate any type of cell within the body.
So the body goes back to these stem cells and says we need to make more skin cells.
So we go back to here and start going through the cell division.
Similarly, if you look at a blood cell they last around three months
and then the body’s got to go back and start again.
But what happens is once it gets to that limited life span is basically a traffic light comes on
and tells these cells right you’ve divided enough times,
you’ve gone through all the cell divisions that you’re allowed
it’s now time for you to stop growing and to die and we’ll go back to our stem cells.
This is totally normal and this is what we want to happen. What happens in cancer is this gets out of control.
So quite often there’ll be some kind of genetic damage. Could be quite early on at this stage in the cell division
or it could be further down the track. But some kind of damage occurs to that cell,
to the genes of that cell that causes changes in that particular cell.
Sometimes we know what this damage is,
it could be UV light damage caused by skin or it could be a carcinogen say from cigarette smoking.
Many times, unfortunately, we don’t know what that change is
and there’s a lot of research going on around the world
trying to figure out what causes these initial changes and how can we detect it at the one cell level
before it gets into a bigger tumour?
But basically we start off with this cell that’s under gone some type of damage and in the initial stages
we get the same sort of cell division. Each of these cells can divide into two, then into two again
but when we get to this stage instead of the red light coming on
and telling these cells it’s time for you to stop growing
the green light comes on and the cells can continue to grow.
And this is where we start getting expediential growth of cells and this can become a tumour mass.
Once it gets to a certain size it’s almost becoming like a small organ
and you actually the tumour will have to develop
its own blood supply so that it can get nutrients and oxygen into those cells so that it can continue to divide.
Now for most cancers this type of tumour is not necessarily what causes the ultimate death of a patient.
The problem is that when one or more of these cells breaks away from the initial tumour it can get into our blood system
or into our lymphatic system and can move to another site in the body
and obviously if this is on a major organ an essential organ then this is where problems start to occur.
Summary:
As you watch the video, listen to what Nikki has to say about:
Captions:
That’s basically what cancer is. How are we currently fighting it?
Well first of all as I said earlier on there’s a lot of research going on
trying to work out what this initial damage is to the cell.
And if we can figure out what the damage is, can we avoid it?
So identifying and avoiding risk factors. I mentioned a couple of risk factors we know are UV light exposure
so being out in the sun too often and cigarette smoking are two of the major issues that we know about.
The next stage, and this is really where my research comes in,
is trying to identify what those signals are that turn from red to green.
So trying to figure out what changes in those cells to cause them
to continue to grow and continue to divide indefinitely.
And if we can figure out what that switch is from red to green
then hopefully we can develop drugs to block that switch and that’s really where my interest lies.
There’s also a lot of researchers around the world trying to block the blood supply to the tumour.
So if we can stop the blood supply getting to the tumour then the cells will go on to die
because they can’t get oxygen and nutrients.
And if this change causes this particular cell to not respond to that chemotherapy treatment
well then of course that cell will survive.
One cell? Probably not a problem. The problem is this cell still has the capacity to divide and to grow.
And so this is where we start getting growth of a new tumour and basically relapse of a patient.
And the problem is because this has started from a cell that was resistant to the chemotherapy drugs
this patient will no longer respond to that particular chemotherapy drug so we need a different
type of treatment to be able to get a positive outcome for those patients.
So basically the cells have sort of altered their internal architecture
to be able to, to avoid being killed by the chemotherapy drugs.
So a lot of my research is involved in trying to figure out what this particular change is.
What changes in these cells that make them not respond to the drug
and can we use that change to our advantage?
Can we come along with a different drug that particularly targets that changed cell
and treat that in the relapse patients?
Summary:
Listen to Nikki’s traffic light analogy and think about the following questions:
Captions:
Basically my research, one of the major things that we are particularly interested up in Newcastle,
is what are the signalling genes or genes that encode for the proteins
that turn those traffic lights from red to green
and allow the cells to continue to grow and divide?
And can we use those changes as a target for new therapeutic drugs?
And the other question that I won’t go into too much detail today but is what is the mechanisms
giving rise to the resistance to chemotherapy drugs?
So what are the changes that occur in that particular cell that makes it resistant to chemotherapy drugs?
And can we detect that change really early? Can we say to a patient when they come in they’re diagnosed
we can see that you’ve this particular type of change in your cancer cell,
we know that you’re not going to respond long term to drug A so let’s give you drug B to start with.
Can we predict the outcome? And this is a really important question that we’re trying to follow up.
How early can we predict how well a patient will respond to a particular type of therapy
and if they’re not going to respond to that therapy let’s give them something else.