Three o'clock in the morning, when you can't sleep,
is the very worst time to come down into your office
and start Googling.
HE CHUCKLES
It's when everything looks the bleakest.
The worst thing you can do is - melanoma, images.
Oh, dear.
Oh, my God.
Oh, Christ.
Oh, that's horrendous.
God, that looks like nothing.
That's a melanoma.
I'm George McGavin.
I'm a scientist and broadcaster.
I've led an amazing life of adventure, studying the science
of a natural world.
Now, suddenly, I'm the one under the microscope.
Six months ago I was diagnosed with malignant melanoma -
skin cancer.
It's just impossible to understand that a mutation in one,
single cell in your heel could potentially kill you
in one year. I mean, it just doesn't compute.
But incredibly, as I was diagnosed, a drug was licensed for use
by the NHS that could potentially save my life.
Look at that.
As a scientist, I want to discover all there is to know
about my cancer, and the drugs that could kill me.
We think it is a new way to think about cancer treatment.
That is my tumour there?
This is your tumour.
Oh, look at it!
The question is, will these drugs work?
This is the story of my year living with a life-threatening cancer,
and the extraordinary new science that could save my life,
and the lives of thousands like me.
I want to know everything about it, and I want to know it now.
Hello.
Darling, I suppose the first thing you want is tea?
Yes. I'll put the kettle on.
It's November 2018, and for those around me,
the news of my diagnosis is still sinking in.
Amy's very special to me and I don't want to upset her,
I don't want her to be anxious.
Like any parent, you want to protect anybody who is close to you.
I've told her enough that she has to know.
I haven't told her exactly how I feel about it.
Because Amy will do all the worrying and more without me
helping it along.
I must show you foot, actually.
There's a nice scab now.
Oh, gosh.
It's just hanging off now.
Oh, man, yeah.
It's such a relief that you don't have to have more scooped out.
That's not, that's not sure.
I mean, if there's any trace of the cancer anywhere else
up here or somewhere else...
I mean, I'm assuming it'll be fine.
Yeah, I'm sure it will.
Can I have my sock, please?
We haven't really talked about, kind of, prognosis
and what the future is looking like.
I'm rather afraid to ask, to be honest, cos I'm not sure
I want to hear that I've got a finite amount of time
left with him.
Clever girl.
Three months ago, I had surgery to remove a cancerous tumour
from my heel.
So there was a big, big hole in my foot, took about six weeks
to properly heal up.
Well, this is how it looks now.
So that's 12 weeks post operation.
Cancer, if it stays in the one place, is fine, and you can
generally hack it out and end of story.
Once it starts to spread and move elsewhere,
then you're in a whole new ball game.
Cancer is described in stages from one to four.
Stage one cancer starts when genetic changes or mutations in a single,
normal cell cause it to start dividing uncontrollably,
forming a cell cluster called a tumour.
But it stays within the same tissue.
And once that happens, it's a cancer, that's it and it won't die.
Stage two cancer is a more advanced or aggressive tumour
that has a higher risk of breaking out from the original tissue.
A cancer become stage three when cells from the tumour break
off and get trapped and grow in the lymph nodes.
Lymph nodes are the body's natural filtration system,
trapping and removing toxins and foreign invaders.
Eventually, these mutant cells migrate into the bloodstream,
invading distant organs throughout the body,
forming secondary tumours.
This is stage IV cancer.
Untreated, this is deadly.
As for me, I've recently been told I'm stage III,
which means the cancer has spread to my lymph nodes.
The good news is, only a few weeks ago, pioneering new drugs
were approved by Nice and made available for NHS melanoma
patients like me.
Bye.
It's a big day for me.
I'm on my way to meet the oncologist in charge of my case.
I'm late now.
The drug treatment I'm about to begin is completely different
from what would have been given to people with malignant melanoma
until just a few weeks ago.
Hack, poison and burn, that's what we had to do
with cancer for decades.
I mean you've got to hack it out, you've got to poison it with drugs
that also poison you, or use high energy beams
to fry it out.
Well, all of these things have left people with some horrific side
effects, and have not always been effective.
But we are now on the cusp of a revolution in cancer treatment,
where we've got drugs and techniques available which mean people
with terminal cancer can survive for decades.
Welcome to St Luke's.
My name is Tim Crook, I'm the melanoma physician here.
In other words, my job is to treat melanoma with drugs.
Now, if we were sitting here a couple of years ago,
even a year ago, the orthodoxy is surgery,
surgery, surgery.
And luck. And then luck.
Now, we have actually a number of effective treatments.
I would be very hopeful that we can shrink this disease down.
Right. The treatment consists of taking one of the drugs,
dabrafenib, the actual BRAF inhibitor,
is taken twice a day and the complimentary drug,
the potentiating drug, if you like, trametinib,
is taken once a day.
If I said, that's a black spot, I'm just going to ignore
it completely, how long would you think I would have?
A year.
Whoa!
I was shocked, actually... Right.
..absolutely shocked. I didn't think he'd say that.
It felt a bit like being punched in the stomach, you know?
What?
Yeah.
He's, you know, pressing quite hard there.
He is pressing quite hard.
The drugs I'm going to get have powerful side effects
that can impact the ability of the heart to pump efficiently.
What's that, what's that?
So before I get my eager hands on the drugs, I need a checkup to see
if my heart is strong enough to handle the treatment.
Hey, hon, you've actually seen inside my heart now.
It's not that attractive, actually. What?
All working...
That looks pretty good.
Yes. For a 64-year-old?
Think so. Yeah.
Thank you very much.
And we're off.
With my body given the all clear, it's time to pick up the drugs -
and not a moment too soon.
One week's supply of one of the drugs is £1,000.
I've had very bad luck in having the disease at all,
but of course very good luck in that I've had it now.
The very two drugs that I need are only authorised for NHS use
just a couple of weeks before they were prescribed to me.
I mean, that is, you know, that's the golden ticket.
Oh, no, no.
Oh, dear.
I'm not going to get stressed this time.
No. Come on, you morons.
I'm dying of cancer here, come on.
Not really, well...
Of this one, of the Tafinlar and then you are taking
the dabrafenib and the trametinib, you take one tablet,
once a day. Yeah. Possible side effects...
Nausea, pyrexia, rash and vomiting.
Lovely.
That's the directions.
How much is that lot, I mean how many thousands of pounds?
That's about £7,000.
That's what I thought it was.
It's horrendously expensive, but... it's reassuringly expensive.
Maybe.
They hand you some pills and they say you take five
of these pills over the day, and you keep taking it for three
months and we'll check you after three months,
and that should do the trick.
It's almost like - are you sure?!
Ugh.
This is actually the hard bit.
I have to take the pills on a completely empty stomach.
One of those, two of those.
These two very expensive drugs I'm taking are called
dabrafenib and trametinib.
Luckily for me, these drugs are all free on our wonderful NHS.
Targeted drug therapy is where drugs are engineered to target a gene
problem in a cell.
Normal cells receive signals from the body to say when the cell
should grow and divide, and when it should die.
Sometimes the signal pathway inside the cell goes wrong
as a result of a genetic mutation and the cells divide uncontrollably,
forming a cancerous tumour.
Targeted drug therapy blocks the signals inside the cell,
so the cancer cell dies.
The great advantage of this therapy, is that it has very little effect
on healthy cells.
It's really sweet, so it's not like taking a chemo drug
and going, "This is toxic, guys. Poof!"
You know, It's going to kill you and a few other things as well.
It's going, "Oh, yeah, I can see that's a problem with that protein,
here's the drug - finished."
And that's it, basically.
There's always that little doubt that there could be cells
in there that are going, "Yeah, we are just waiting for you, buddy.
"We are going to hang about until this is all over and then we're going to go - pow!"
Yeah...
..you don't know.
I won't have a coffee for a whole bloody hour until I can switch
the machine on.
I think I'll switch it on a bit early just to warm it up.
Ah, that's almost enough.
Just to... HE SNIFFS
The scientist in me wants to know more about this cancer.
So I'm going to the pathology lab where the tissue from my heel
was originally diagnosed.
This is a bit of a strange day, I mean this is something very few
people will ever get to do, is to come face-to-face
with the tumour that could have killed you,
or it indeed may, I don't know.
People will say, "How can you find your tumour interesting?"
But it is interesting, it is an interesting thing.
Every single day this pathology lab at the Royal Surrey Hospital
is processing and analysing samples from over 350 people,
all nervously waiting for their life-changing results.
And it was here that my tumour was analysed
by Professor Martin Cook.
Don't touch anything. Don't touch a thing.
Wow, this is where it all happens?
Yeah.
So this room is where my tumour and indeed anybody else's
would have come?
Indeed, in this sort of container.
It's a piece of skin, and you can clearly see there is
something abnormal there.
That is a raised tumour.
The pathologist cuts a piece of the tissue and places it
in a small frame filled with paraffin wax, called a block.
This is absolutely fascinating.
Technicians then slice off a three micron thick sample -
that almost 20 times thinner than a human hair.
This is then carefully placed on a glass slide for analysis
under a microscope.
When my tumour was actually cut out, I had to wait two weeks.
Of course, it's a worrying time because you're thinking,
"What's happening, why aren't I hearing anything?"
Well, of course, this is why you are not hearing anything
because it has to be cut, embedded, dried out,
sectioned, stained and only at that point can you get
the expert eye on it to say, "That's what it is."
And everybody here is sectioning bits of humans.
Yeah, yeah. This has been a real eye opener for me, yeah.
Tremendous.
I am desperate to come face-to-face with my adversary.
This is your tumour.
Hold on, that is my tumour, there?
That's your tissue, there.
Oh, look at it, look at it. Embedded in paraffin.
Look at it!
Yeah, it's a bit of an odd feeling staring at your potential killer.
It was small, yeah.
Totally innocuous little mark, bruise, lump.
Yeah.
But it's deadly.
You sneaky little devil.
This was the first biopsy.
You can see the small black bits, these are cells which
shouldn't be there. Oh, yeah, look at that. My goodness, yes.
Those black bits are cancerous melanocyte cells.
These normally produce melanin, that's the pigment in our skin.
The mutated ones are now dividing uncontrollably.
So, you took a look at this and you knew immediately?
Yeah, I knew this was invasive melanoma.
You can probably...
Are you OK? No, I'm... I'm quite...
Tell me if I'm being too...
No, it's fantastic, I'm just a bit...overcome, really.
Acral lentiginous melanoma, which is a form of this disease.
Very rare.
While almost 90% of melanomas are caused by exposure to the sun,
my melanoma isn't linked to the sun at all.
I thought, well, that's something at least.
I don't have a common cancer.
Let's have something really special.
Hmm.
Now, I want to see how this tumour has moved from stage I in my heel
to stage III in my lymph nodes.
James.
The radiologist on my case, James Crawshaw, will show me
a road map, the PET scan.
Is that me? That is you, yeah.
Radioactive you.
Good to put a human face to the scan, actually.
Yes, that's what he looks like. My goodness.
That's quite a beautiful thing, isn't it? Yeah.
This is recognisably me, every detail.
I haven't seen inside myself before, but I have now.
Bit like an airport body scanner.
Yeah, but it's me, all right, absolutely.
My heart, kidney, liver, lungs. Wow.
And what it is, is we're effectively injecting you with some radioactive
sugar, and the tumours also need sugar.
We start down the bottom, actually. This is your foot.
That's it.
Look at that. On this fused image we are looking for purple.
Purple, right. We are coming up the leg, heading towards the groin now.
So we come onto a purple, bright, purple...
That's below it?
That bright thing is a lymph gland that's got too much activity
in it to be normal.
So that's the first one we come to. So that's one node.
Then we are looking how high up they go.
There's another one, yeah.
You are pretty sure it's only here, it hasn't gone further up?
As far as we can tell, it's not gone beyond that.
Why is that, do you think?
Just the timing, really.
In three months' time I will have another PET scan.
By then, I hope that with targeted drug therapy,
my lymph nodes will be clear of any purple spots.
But there is absolutely no guarantee.
When I come for my next PET scan, what would you expect to see?
I'd expect these lymph glands to be cold.
That's what we hope to see with you, is none of these hot spots anywhere.
There are no absolutes in this, all you need is one cell,
one cancer cell to have gone somewhere else,
but at least it's a good indication that I'm not glowing...
..like a Christmas tree.
The cancer cells have now started to move around my body,
away from the original tumour site in my heel.
That means my cancer has metastasised, and if it gets
as far as my vital organs, it could kill me.
As a biologist, I know the process of migrating tumour cells
must be complex, but what actually happens at a microscopic level?
Here at the Institute of Cancer Research in London,
Dr Chris Bakal is pioneering some extraordinary scientific experiments
to help us understand.
That is a mutant melanoma cell. It's a melanoma cell?
A melanoma cell undergoing the process of division.
That's real, that's what was happening in my tumour?
Exactly, that's what's happening in your tumour a lot.
Cancer is really a process of uncontrolled division
where a handful of mutations allow the cell to divide uncontrollably,
on, and on, and on.
This microscope allows us to get up close to your cancer cells,
really see individual cancer cells that are part of the tumour.
So the green cells are the cancer cells.
Those are the ones causing the disease.
That's quite pretty.
Remarkably, Chris has used my own tumour to create these images.
To help see the cancer cells more clearly,
he has engineered them to express green fluorescent protein
on their membranes.
This green cell here is searching its environment,
trying to hunt for food, trying to hunt for oxygen,
because likely it's running out of both, to see
if there is a way to escape.
That's a bit creepy. It is creepy, yeah.
This is quite creepy, so these little cells are going,
"We are going to go, we are going to eat.
"Let's move." They might be trying to find a way out, and that's
how they might, for example, move to another site in your body.
HE SHUDDERS
I mean, this is amazing.
This one here is sort of stuck.
Using a tiny silicon maze, only a tenth of a millimetre long,
Chris has devised a remarkable way to show how malignant melanoma cells
spread through the body.
These... Oh, my goodness.
These are mutant melanoma cells trying to squeeze through tight
little spaces in this maze we've set up.
That one's away, it's off.
The spaces in the maze are minuscule, smaller, in fact,
than the cell's own nucleus.
A normal cell could not possibly squeeze through here.
Melanoma cells are able to completely squeeze themselves,
and squeeze their entire nucleus, their entire genome to squeeze
through this tiny little pore.
So these normal skin cells which have become mutated,
can suddenly get anywhere they want?
Exactly.
These are the world's first microscopic images
that show how melanoma cells spread.
This really looks alien to me.
Chris hopes that they will help him with his next big idea.
By targeting the shape shifting abilities of cancer cells,
could we stop cancer spreading?
Can we think of drugs, can we think of therapies
that block these shape changes, that frees the cancer cells
in one single shape?
If they can't move, they can't spread.
It's a simple idea, in a way.
You can then just simply cut them out easily without there
being any risk of them having spread?
We think it's a new way to think about cancer treatment.
If he can crack this, that will change how we can treat
cancer in an enormous way.
Not just skin cancer, other cancers.
As with all cancers, it's not just me that needs to cope
with this disease.
It impacts my family, as well, especially my wife Lois.
Lois is an incredible individual who has this
somewhat misplaced view of my invincibility.
There's my head.
My foot.
I said to her, "Aren't you worried about me?"
And she goes, "No!
"Nothing is going to happen to you."
I had a sign of cancer there and there.
And there. That's the nodes.
Yeah.
My heel was the bit where it started. Your heel, yeah.
We have 35 billion cells in us, and most of the time it's fine.
There are mechanisms to tweak bits, to kill certain bits
that shouldn't be there, get rid of them, to alter bits
of DNA, repair that.
I mean, it's an amazing bit of machinery.
Very unhappy face.
But, you know, not surprisingly out of 35 billion cells,
one of them might just go a bit rogue, and that's it.
I reckon inside that shape is 35 billion grains of sand.
Yes. And it started in one,
one grain of sand.
One cell.
That was the one that went rogue.
And then it went up my lymph vessels, and my blood vessels
and it got trapped in my lymph nodes, thank goodness.
And in about five minutes that's just going to get cleansed.
Washed away.
This is it.
Oh, no.
Come on, waves.
This one's coming in - yes!
Oh, there it goes. Yes!
It just got you.
It's the one.
These drugs I'm taking are targeting a mutation in the cancer cells
in my body.
But as a scientist, I want to know more.
I want to know what my specific mutation is,
what it does, and how on Earth they discovered drugs to target it.
This is the very hi-tech Wellcome Sanger Institute.
Today I'm meeting its director, Sir Michael Stratton.
Sir Michael. Morning, George.
Very nice to meet you.
Without him, the targeted drugs that I've been taking would not
exist, because he discovered a key mutation in what is called
the BRAF gene.
The BRAF gene is one of the genes in our bodies that regulate cell
growth, turning it on or off.
When we discovered the BRAF gene, the mutations in BRAF were exactly
the sort that stick it in the on position.
And that's what I've got, in my tumour - it's full-on,
foot on the floor, accelerate, divide, divide, divide?
Exactly that.
And so the thought immediately comes to mind,
well, can we get a drug into it that will then switch it off?
I really want to see how this happens.
I've got so many questions for you now, my head
is spinning with questions.
Stratton was looking for a minute change in the DNA
of melanoma patients.
So, in one of 35 billion cells in the human body,
in one chromosome in that cell, and in one strand of DNA,
was the mutation of the BRAF gene.
A simple change in code.
One letter of code.
And that there is what caused my cancer.
To find that minute change, what he needed was the huge
processing power of super powerful computers.
This is our sequencing facility with our fleet of machines.
These sequencing machines are capable of running the billions
of calculations required to analyse the DNA from tumours, and create
a readable code to identify the mutations.
If we compare ourselves to, let's say 20 years ago,
we can sequence DNA approximately a million times faster
and a million times cheaper.
And all you can hear is a little gentle hum.
Together, the machines produce billions of DNA code sequences
in just minutes.
The sequencing helps figure out which gene mutations
cause which cancers.
Understanding how a cancer works leads you to new treatments.
How do we use this information to develop the next generation
of drugs, and the generation after that, and the generation after that?
But we should be optimistic that this will be achieved.
And the first generation of the very drugs that I am on now
produced some startling results.
This is the sort of thing that we're seeing.
On the left-hand side you can see the person with all those lumps
in their skin.
And on the right, the same person a few weeks after...
A few weeks? Yeah.
The cancer, basically, goes to sleep and sort of dissolves away.
We are very pleased, because we saw pictures like this.
You know, this is why we are here.
All of these things are the products of our imagination as human beings
and it's a tribute to the power of the human mind.
BRAF was just one of the cancer-causing mutations
that Michael and his team identified.
They also found two other mutations - one called BRCA2,
that causes some breast cancers, and another called ERBB2,
behind some lung cancers.
The Sanger Institute hope that by analysing even more cancer
genome sequences, they will discover yet more genetic mutations leading
to more targeted drug therapies like mine.
We are able to arrive at the point now, for the first time in human
history, where a collection of allied diseases,
they are now beginning to yield their secrets.
It's very encouraging to see the ground-breaking science
behind the very drugs that I am on.
I've only been on them for a month, and as the year draws to a close,
I still feel very lucky to be on them at all,
because they are so new.
But I'm not out of the woods yet.
In the meantime, though, it's important that life should go on as usual.
I love my family, and although you are having a nice,
jolly party or lunch, there's always that thing
in the back of your mind.
You think, "This might not happen again, this might be one
"of relatively few meals I have."
Look at that.
You very quickly realise that it's not your death that is
at all important, but the effect is on your family.
They are the ones who are going to have to go on without you.
Now, they might be absolutely fine and I hope they are,
if it ever happens.
But that's the sort of thought that begins to crowd in on you...
..after dark, that's, that's...
Have you made a New Year's resolution?
Erm, no.
I have.
Have a guess. Not die of cancer? Correct. Hey!
Not dying of cancer, that's the only one, I think.
That's the one, yeah.
Ah! Ahhh!
I'm absolutely sure...
You naughty girl!
..when I go, they'll be fine, I know it.
There'll be bad times, just like for me in the last year,
there have been very bad times.
And it's at those times you think about this, and you think about
how they'll cope.
I could see them having a Christmas party sometime hence,
say if I died, and they'll be laughing and drinking and saying,
"Wouldn't it be great if George was here,
"he'd have done this, he'd have done that."
And that's what will happen eventually.
It's the end of January.
Only a few weeks of the first cycle of my targeted drug treatment left,
and time for another PET scan.
This is really the big one for me, this is the important one.
Because if these eye-wateringly expensive drugs I've been swallowing
for the last three months are doing their job,
they should see a very much reduced evidence of any cancer cells.
There should be, hopefully none.
I mean, I haven't thought about it.
I don't want to think about it.
I think it'll be all right so I'm just hanging on to that,
I'm just saying yes, it's going to be fine.
It'll be fine.
It'll be fine!
Are you epileptic? Do what?
Epileptic? No.
Claustrophobic? No.
A-1.
PHONE CHIMES Oh, go away.
I really, really hope that this PET scan will show the bits
that were glowing before are not glowing now.
That's the best I could hope for.
Because the scan has to be analysed by my radiologist and then discussed
by my medical team, it will be two weeks
before I hear anything back.
You are going to think thoughts like, "I hope it's not there,
"I hope it's gone away. I hope it's not as big as it was before."
OK, perfect. We are just at your hips.
OK.
I'm now officially ravenous.
As I take my pills, I'm thinking if the scan shows
the targeted drug therapy has not worked and the cancer has spread,
where else can I turn?
Amazingly, there is another relatively new option.
It takes a radical approach, different from anything
that has gone before, with even more astonishing results.
It's called immunotherapy.
A treatment that stimulates the body's immune system
to kill cancer cells.
For a long time, cancer was regarded as being not something
that our immune system could handle.
Because, they argued, it was too much like us,
it was part of us.
So the immune system wouldn't attack it.
But in America, there was a determined molecular biologist
who believed that there had to be a way around this.
So I've come to Houston, Texas to meet the man who,
just weeks before I arrived, was awarded the Nobel prize
for his work, Professor Jim Allison.
It's not every day you get to meet a Nobel prize-winner.
It was almost universally thought that any hope of immunotherapy
was just not going to work.
But he doggedly stuck with it.
He said, "No, it's going to work, it's going to work.
"And the reason, there is something that we are not seeing."
And eventually he found it.
Professor Allison, your ground-breaking research
for the benefit of numerous patients and all humankind.
Jim, can I call you Jim?
Yeah.
Great to meet you, thank you very much.
I have to say, Jim, this is as close I am ever
going to get to a Nobel prize.
Oh, yeah, George C McGavin, great.
When did you first get interested in cancer?
Because of my family history...
..I always had cancer in the back of my mind.
This is the whole family actually, my grandparents there,
then there is my mom. She had cancer?
She died of lymphoma, he died of melanoma,
he died of lung cancer.
He died of prostate cancer.
And you haven't been spared either?
No, no, I haven't.
I'm on my third cancer now.
Your third?
The general view was that immunotherapy wouldn't work
because these cancer cells were basically our cells,
just gone rogue.
But you said no, no.
My feeling was, I'm pretty sure T cells can do something about cancer.
So we probably got about 100 million different T cells in your body.
T cells are part of the immune system.
They travel through the body like a cellular army,
detecting infected or cancerous cells.
When they find them, they destroy them.
So now you've got the army of the immune system?
But you need hundreds of thousands of them,
or millions even, to go deal with the problem.
You've got to get the troops in the field in large numbers.
But what Jim discovered is that cancer cells have a cunning way
to fool the T cells' checkpoints, sending out proteins that say
"We are normal cells, don't kill us."
Jim realised that checkpoint inhibitor drugs, seen here in blue,
could block this process, allowing the T cells to
recognise it as a rogue cell, and go ahead with destroying it.
This was a completely new way of thinking about cancer treatment.
Rather than targeting the cancer itself,
it was unleashing the body's own immune system to do the work
for it, and the first cancer to respond to this radical
new therapy was melanoma.
I mean, that is an amazing breakthrough point.
But anyway, there was a trial, a phase one trial,
and there were three objector responders.
One of them I know, was a woman.
We gave her one injection, and within a few months
all of her tumours went away.
She is 18 years out now from that single injection,
all her tumours went away.
I met her in 2011, and still tumour free.
You know, we were crying and everything.
You can take a melanoma patient who have mutations
in BRAF, this molecule...
That's mine, I've got that one.
..and you can treat that and the tumours will go away.
Yeah, well... For a little while.
Oh, OK. But you're saying that might not work?
It might, but there is a good chance it's going to come back.
At least I've got immunotherapy up my sleeve.
People need to know that, you know, cancer is not a death sentence.
The people that make it three to four years are going to probably
make it for ten, 15, 20, whatever.
That's when we can start thinking about using the C word.
The C word and it's not cancer, it's cure?
Exactly. The C word!
The first drug that was made out of this work was a thing called
ipilimumab, and it had absolutely miraculous results.
I mean, individuals who were terminal, suddenly
the cancers were just vanishing, were just going.
Across campus from Dr Allison, one of his colleagues,
Dr Sharma has been taking his extraordinary theory
to the next level.
Well, we feel that the immune system is very powerful, and if we learn
how it worked we could do a better job of curing patients.
And clearly we are doing that in a small subset of patients.
We need to do it in a larger group of patients.
We're going to start seeing all these different combination
therapies so that we can help raise the tail, the survival tail,
for more and more patients, and more and more tumour types.
These things that have been developed for skin cancer
like I've got, are also applicable to lots of
other cancers, yeah?
Yes, T cells are just soldiers of the immune system.
So when you target those T cells and you unleash them,
they can go and do their job, so they can do their job
in a melanoma patient, they can do their job in a kidney
cancer patient, for example.
So Dewey Stringer, he is one of those patients
who had stage four kidney cancer.
Well, that's bad? That's very bad. That's the very end of the line?
Yes.
How are the toxicities? I know you've had some
with the immune checkpoint therapy agent?
I'm still here. That's great.
And because of immunotherapy treatments now, Dewey
has had four years plus in terms of survival, and the last year,
he's had no disease on his scans, really.
It's clear to me now that immunotherapy is a very powerful,
pioneering new treatment that is going to be applied
to lots of other cancers.
Not just skin cancer.
HONKING Let me in.
In the wrong lane.
There was something Jim said that actually makes
me slightly worried.
They basically said, yes, it's good that you are on these
drugs, George, but it could come back.
But at least I now know that if it comes back in the future,
I've got immunotherapy.
Immunotherapy, it's certainly doing incredible things and some people
may indeed be cured.
The thing about cancer is, it can do pretty much anything
it wants to do.
We have certainly opened the door, certainly opened the door.
You know, it's easy when you are in places
like this to forget you've even got cancer.
I've just forgotten all about it, this is just...
..so breathtaking.
Back in the UK, the shock waves of Dr Allison's extraordinary
discoveries are also being felt by a unique group of melanoma
patients at my very own hospital here at the Royal Surrey.
You've all had that moment when you suddenly have the dawning,
or the realisation.
What was your first thought?
Everyone here has been diagnosed with stage IV melanoma,
that's a stage further than me.
There cancer has spread to their vital organs,
which until very recently, was a terminal diagnosis.
Yet, amazingly, all the patients here have had extraordinary
responses to Dr Allison's drugs.
I had a PET scan, and I was kind of glowing like a Christmas tree,
and then went on to ipilimumab straight away, immunotherapy.
A support group like this would never have happened before.
Because if you were stage IV, you would be dead.
That means that the drugs are working.
You had a stage IV?
So, like, in your brain as well?
Brain, lungs, erm, breast.
You were a stage IV?
This is it, you know.
Were you told - there isn't anything...?
Yes, five minutes after I was told, I was with my wife...
We have tissues.
I found that hard.
Because, at that point, it's in the family, it's not just you,
it's everybody involved.
Before I made this film, I would have rather pooh-poohed
support groups, actually.
But it's very, very true - a problem shared is very much
a problem halved, or reduced.
But look at where I'm... Look at where I am now.
Just under one year ago, Lisa Roberts was diagnosed
with a melanoma that had spread to multiple organs,
including her brain.
Even, you know, you'd have those days at work where everything
was stressful and you could get caught up in that.
Now I don't. I think I take a step back and just think,
"It's just today, things will be better tomorrow."
When I first got diagnosed, I wasn't really interested
in a group, I didn't really like talking about it.
I didn't want to talk about it.
At the beginning I was on immunotherapy...
Ipi Nivo, right? Yeah, Ipi Nivo and everything was swelling.
This was a couple of weeks, and I had a lump on my arm.
That's a huge red lump.
And that was me celebrating that it was shrinking.
So you had lumps in the brain, your shoulder, intercostal muscles,
the lungs, the liver, pancreas, thigh.
That's a lot to put up with?
Yeah. Being positive for yourself, at least...
It doesn't necessarily fight the cancer, but I'm very sporty
and very competitive, and for me, I had to say, this is a battle
and I'm going to win and I'm very determined.
That's just the way I cope with it.
I think everyone's different, some people will just say,
"Right, let the science take over and heal me."
But then they believe, again, that through that they believe
it's going to happen, because they're believing in the medicine.
Lisa still has one small tumour remaining in her brain
and her treatment is ongoing.
But there is a long road ahead.
You know, when you get a cold or you get ill,
you recover in a week or two and you are just so used to that,
that illnesses don't last a long time.
So I really struggled with the fact that it's coming up to a year
and I still have the disease.
Ten years ago, there was absolutely nothing that could be done.
If you got that disease, malignant melanoma,
they would just say,
"Well, we're very sorry, there's nothing more we can do."
And that is, that's my hope for the research that's being done
and there's some fantastic research which will go on, and on, and on.
My hope is that they will never...
..have to say that again.
It's the end of three months of drug therapy, and today I will find out
if these pills have put my cancer into remission, and potentially
save my life.
This is, this is quite an important day.
This is the one where I will get the results of the PET scan.
I'm just a bit nervous about it all.
Yeah, I just want to find out what the results were.
If these drugs have worked really, really well, then all the cancer
will be gone. That's the best possible outcome.
This is all the very latest in treatment,
so success with these new drugs in my case could be yet another huge
step forward for the future treatment of others.
The whole team meets - the surgeon, the pathologist,
the oncologist, everybody involved in my case meet and they discuss me,
and of course, I'm not able to be there.
I could find out something that will change my life completely today.
Worst case scenario, it could be in my lungs or in my other
organs or my brain.
Morning, team. Welcome.
So, at MTT today we are discussing George McGavin.
Ralph, you first met this gentleman.
He presented in July with a black nodule on the back of his right heel
and he had a biopsy, followed by removal of the lump.
And that came back confirming a melanoma of
2.5 millimetre thickness.
This is the first excision from the foot,
because the thick keratin layer.
And it's quite large, it's conformed.
The PET scan, got a bit of uptake in his right heel.
He's also got at least groin nodes.
I think the highest most node is this one here,
just anterior to the vessels.
Classically we have operated in situations like this, and at
the moment, we are really trying to decide a way forward, aren't we,
that's best for the patient? That's right.
And are you seeing him today to talk to him about his results?
Yeah, that's been a big part of the treatment decision here,
what George wanted.
Hello. Tim, hi. Welcome back to the clinic, George.
Good to see you. Thank you very much.
Please come in and have a seat. Thank you.
How are you doing? Well.
"George, how are you?"
"Well, we've looked at it..."
Just tell me!
You've had a scan, as you know, which tells us
how well you've done.
So, I'm really pleased to give you some good news,
which is that you've had what we call in the trade
a metabolic complete response.
Which is that all the lymph nodes, they've all returned
to a normal appearance.
Now this is a very, very encouraging initial response, well done.
That's as good as you could do.
There's lots to talk about, but from my perspective,
you've done the hard part, which is to get into what can only
be called a complete remission.
There is no metabolically active disease left.
That... That's almost unbelievable.
So, what... What next for me?
Orthodoxy says you should stay on the tablets,
or consider surgery. Can I stay on the tablets?
You can. But - normal life. Thank you so much.
Great stuff, well done.
I'll see you in a month, yeah?
Thank you so much. Brilliant, brilliant.
PHONE RINGING
Don't go to answer phone.
PHONE RINGING
Hello. Hi, darling.
Hi, how are you?
Very, very good, the results are fantastic.
Oh, my God. Yeah.
Valentine's Day, happy Valentine's Day,
I forgot to buy you a card. Yeah, happy Valentine's Day.
Don't be daft. But I think this is better than a card.
I think this is much, much, much more exciting news.
THEY LAUGH
Spring has arrived early for me.
Oh, George, that's really good news.
I'm in the clear.
Gone, absolutely gone.
When I reported this, I knew you'd be over the moon.
Yeah, incredible.
Wow!
That's it, you can't get any better than that.
Hello. Hello, it's me.
Yeah, I'm here. Brilliant news, I'm in the clear.
The best.
Oh, Daddy, I'm so pleased.
That's just fantastic, it's the best news I could hear.
Don't start crying because I'll start.
It's fine, it's all good.
Over the past 12 months, I have been diagnosed with cancer,
had a tumour removed, been told that my cancer had spread
to a stage that, left untreated, could have killed me within a year.
I've consulted with scientists behind the new targeted drugs
and I've met the man responsible for the greatest breakthrough
in cancer research in a century.
Those are cured. Those people are cured.
And now I'm back on a familiar trip to the hospital.
Once again, early in the morning, but this time I'm going
to a nice scan.
Isn't that an amazing sound?
Head.
Look, we got a fantastic headshot there.
Come on, small fry.
By the time this child is your age, and almost certainly by the time
it's my age, the sorts of cancers today which are now
a death sentence, won't be. It'll be, "Yeah, we can fix this."
It's moving so fast.
I'm in the clear. It's the best news I could possibly have had.
Cos to know that I can, you know, head off and have this little one
and not be worrying about you, and know that you are going to be fine,
and you're going to be here. Yeah, for a while.
Everyone has to go sometime. Well, everyone has to go sometime.
Love you.
All right.
Yeah.
I think when you have cancer, it's like you've been in these dark
woods, and suddenly after a drug treatment or a trial or something,
you're in a clearing in the woods, and all the trees have gone back
and you are going, "Oh, yeah. Yeah, yeah this is OK."
And then you might head on again and the trees might close in.
So currently, I am in a nice, sunlit clearing in the woods.
I've been very, very lucky.
I've had the benefit of the latest science at an incredible time
in the evolution of cancer research.
But when my cancer comes back, if it comes back, he says it will,
there'll be something else. There will be something else.
I am going to die at some point,
but it's not going to be of skin cancer.
Of that, I am pretty sure.