0:03

Welcome to The Referral. I'm Dr. Curran,

0:05

a surgeon in the NHS, and this is

0:07

your weekly fix for all things health, science

0:10

and actionable tips to improve your life. Today

0:12

I'm going to be discussing the emperor of all

0:15

maladies, cancer. Why do we get

0:17

cancer and will we ever be able to beat cancer?

0:19

Over the past few years, there have been some breakthroughs

0:22

in cancer science and cancer treatment. And today

0:24

I'm fortunate enough to be joined by Professor

0:27

Peter Johnson. He is the cancer

0:29

guy. He's the chief clinician at Cancer

0:31

Research UK and a professor

0:33

of medical oncology at the University of

0:35

Southampton. He's also the clinical director for

0:37

cancer in NHS England. And those

0:39

changes appear to be capable

0:42

of inducing cancers at different rates.

0:44

Why people who live on a predominantly

0:46

fibre-based diet are much less prone to bowel

0:48

cancer than people who live on a high-fat diet.

0:51

Later on, I'll be answering your questions in CrowdScience.

0:54

And remember, if you've got a question you want me

0:56

to answer on this show, get in touch via

0:58

thereferralpod.com. You can hear

1:00

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1:02

about

1:03

your queries in CrowdScience Extra.

1:05

Just visit the referral show page on Apple Podcasts

1:07

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1:09

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1:16

yet asked your own question, get in touch

1:18

via thereferralpod.com.

1:22

Professor Peter Johnson, thank you so

1:25

much for joining me today. You are

1:27

a professor of medical oncology. You

1:29

have dedicated most of your adult life

1:31

to cancer research and cancer

1:34

advancement as well. Tell me a little

1:36

bit about what a daily life looks

1:38

like for you if there exists such a thing.

1:40

So I'm a medical oncologist with a particular

1:43

interest in cancer immunology. And

1:45

I'm a clinical academic. So I divide my

1:47

time between clinical work, looking after people with

1:49

cancer. And in my case, that's a specialization

1:51

in lymphoma.

1:52

As I've gone on, I've become more

1:55

and more narrow in my interests. I used to treat

1:57

lots of different sorts of cancer and more

1:59

recently just...

1:59

lymphoma. And at the same time, we

2:02

run a large program of research in trying

2:04

to understand how the immune system can be taught

2:06

to recognize cancer and how to combat

2:09

it. And whilst that was for

2:12

a large part of my career, a bit

2:14

of a niche specialty and something

2:17

that people thought sounded interesting, but

2:19

they weren't sure if it was ever going to work. In the last decade,

2:21

we've seen an explosion of knowledge

2:24

and application in the clinic, which has been really

2:27

exciting to see. Yeah, I mean, you've

2:29

mentioned their immunotherapy and how it

2:32

was a niche thing. And now almost

2:35

every few weeks, I seem to read

2:37

headlines, sometimes sensationist headlines,

2:40

about a groundbreaking new cancer therapy.

2:43

And it all seems to be based on monoclonal

2:45

antibodies, cancer vaccines,

2:48

and some form of immunomodulation

2:51

to improve either responsiveness

2:53

to cancer therapy or finding a way to

2:56

limit cancer evasion against the immune

2:58

system. What are some of the, you could say,

3:01

groundbreaking things within the last couple of years

3:03

we've seen in immunology that's

3:05

helped with cancer treatment? I mean, if you look

3:07

at the history of medicine and biomedicine,

3:10

I mean, systemic treatment of illnesses,

3:13

there are two things which have enabled

3:15

us to make progress historically. One is small

3:17

chemical entities, drugs, and

3:20

the other is vaccination

3:22

or some means of bringing the immune system to

3:24

bear on an illness. And vaccination, of course, derives

3:26

from the original general experiments

3:29

of using cowpox to prevent people from

3:31

getting smallpox. So the idea that

3:33

you can bring the immune system to bear

3:35

on an illness goes back a very long way.

3:38

And indeed, the idea that you can bring the immune system

3:40

to bear on cancer has a long history as

3:42

well, well over a century. The difficulty

3:44

with modulating immunity is

3:47

that it's an infinitely complex system. So

3:49

one of the things that the COVID pandemic

3:52

has taught everybody is

3:54

an enormous amount about the immune system, everybody

3:56

who's thought about COVID and

3:59

what vaccination is. to prevent virus

4:01

infections might do has heard

4:03

the terms T cells and B cells. So

4:06

our immune system consists largely

4:08

of lymphocytes.

4:10

These are a particular sort of white blood cell. They

4:13

come in two broad strains, the T

4:15

cells, which are very good at recognizing things

4:17

like cells infected with viruses and

4:19

directly killing those cells, and B cells,

4:22

which are the cells in the immune system which go on

4:24

to make antibodies. So when I vaccinate

4:27

you against COVID, two things happen.

4:29

Firstly, you produce T

4:31

cells which recognize the little bit

4:34

of the COVID virus that I vaccinated you

4:36

against. And secondly, you go on to

4:38

produce B cells which make antibodies, which

4:40

stick to cells infected by

4:42

the COVID virus. So the immune

4:44

system is fantastically good and fantastically

4:47

well evolved over millennia for

4:50

us to fight infectious diseases. What

4:52

we can also do is tune the

4:54

immune system to recognize and fight

4:56

cancers. And in exactly the

4:58

same way as a cell infected

5:00

by a virus has little bits of virus

5:03

protein visible on its surface. So

5:05

a cancer cell, which has developed mutations

5:08

in the course of its development from

5:10

being a normal cell in the lining

5:12

of your bowel to being a cancer cell, as it

5:14

develops those mutations, those little mutations

5:16

are expressed as little bits of protein on the cell surface

5:19

as well. So we can use the

5:21

immune system which we've mainly developed

5:24

over the centuries to protect

5:26

us from infectious diseases to also

5:28

attack cancers, which they're not primed

5:31

to do naturally, but we can artificially

5:34

co-opt the immune system into doing

5:36

that. Do you think there's a bit of evolutionary

5:39

game theory at play here, you know, in the same

5:41

way that, for example, populations

5:43

and ecology and animals in the environment

5:45

evolve to avoid or

5:47

get better at killing other, you know, their

5:50

prey in the same way that as

5:52

we evolve our treatment, radiotherapy,

5:54

chemotherapy, immunotherapy against

5:57

cancer cells, they become better at evading the

5:59

immune system. those treatments, but at the

6:01

same time they're in this double bind

6:04

where they become more resistant

6:06

to chemotherapy or radiotherapy,

6:09

but because they are better at evading something

6:11

else, they become worse and they

6:13

expose their Achilles heel at another

6:15

thing, for example immunotherapy,

6:18

which allows many patients to

6:20

be given treatment with two things,

6:22

you know, chemotherapy and immunotherapy

6:24

for example. So people think of

6:26

cancer as one thing, but we have

6:28

lots of different sorts of cancers, they arise in different

6:31

tissues of the body and they grow

6:33

in very different ways, and if I look

6:35

at two cancers from the same organ

6:38

but from two different people, two types of breast cancer,

6:40

and I look at the genetic changes within those

6:43

cancers, they will be unique to each particular

6:45

person. So cancers are very

6:47

individualized things they develop in very individual

6:49

ways, and as the

6:52

cells go from being nice normal well-behaved

6:54

cells which know when to grow, when to divide and

6:56

when to stop, to being this chaotic

7:00

uncontrolled growth spreading around the body,

7:03

going and living in places where they shouldn't live,

7:05

that process of evolving from normal

7:07

to malignant is of course

7:10

all the time under the selection pressure of the immune

7:12

system. So we generate tiny cancers

7:14

all the time or we generate changes in cells

7:17

all the time which might lead on to cancer. Most

7:19

of the time our immune system spots it,

7:22

takes them out and nothing ever happens, they

7:24

never develop. So by

7:26

definition something which has already turned

7:28

into a cancer which is capable of spreading around the

7:30

body has gone out under the radar,

7:32

has escaped that surveillance and

7:35

is able to grow despite the controls

7:37

of the immune system. So it's already evolved

7:40

in a way which has protected it from

7:42

immune oppression and

7:44

our job in trying to treat it is to work out

7:46

how you restore that suppression, how you restore the

7:48

recognition.

7:55

You love Lala Kent on Vanderpump Rules.

7:57

Now get to know her on Give Them Lala.

7:59

so down with dudes giving me pet names

8:02

right off the bat. The second a dude, I first

8:04

meet him and he calls me baby, I'm like, and we're

8:06

done here, goodbye. Really? Yeah,

8:08

don't call me babe, baby, boo, bye.

8:10

Interesting, that's a big red flag. But I can call them boo, because

8:13

I call everybody boo. What if that's their excuse?

8:15

That's funny. No, you don't, you're a man, you move different than

8:17

me. Watch what Lala is talking

8:19

about on YouTube or search for

8:21

Give Them Lala wherever you

8:23

listen.

8:26

Hello listeners of The Referral, it's

8:28

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9:29

Your point about all cancers being different, the biologies

9:31

of even same types of cancer in

9:34

two different people being different, for example, even

9:37

the same type of lobular breast cancer

9:40

in two different patients will be completely different

9:42

on a genetic basis. How

9:46

deep into bespoke cancer

9:48

therapy are we in 2023? Instead

9:52

of just saying, you have this type of chemotherapy

9:54

for both these patients, looking

9:57

into the specific genetic sequence

9:59

of the cancer, of those cancers and almost

10:02

on a genetic level providing treatment

10:04

for that. Are we there yet? So we've

10:07

come a long way in cancer treatment without

10:09

knowing the very specific changes that take

10:11

place in people's cells. Surgeons

10:14

cure enormous numbers of people with early

10:16

cancers by doing essentially the same operation

10:18

that everybody, bowel cancer,

10:20

will get the same sort of operation. Similarly

10:22

chemotherapy and radiotherapy, which are, you

10:25

know, radiotherapy is shining up a

10:27

beam of intense radiation on a cancer in a particular

10:30

place. And again, that doesn't take any account of

10:32

the biological characteristics of the cancer. And

10:35

chemotherapy, similarly, is

10:38

a form of mild poison which stops the

10:40

cells from dividing or kills them in various ways.

10:44

As we've had the explosion of knowledge

10:46

and our ability to see into

10:48

the molecular changes within

10:50

individual cancer cells, so we're

10:52

starting to understand much more about

10:55

what the precise determinants are of success. The

10:58

analogy might be cartography,

11:00

for example. In the Middle Ages we had these

11:03

rather beautiful medieval maps,

11:06

things like the Map of Mundi, where they drew dragons

11:08

around the edge and the geographical

11:10

outlines of the countries were more of

11:12

a vague resemblance to the shape of the country. But

11:15

it was more a work of art than a work of precise

11:17

science. Whereas now you have,

11:19

you know, satellite images which can show you

11:21

whether the garden shed is open or not. So

11:24

the level of gaze and the precision of

11:26

gaze that we've developed through technological changes

11:30

has made an enormous difference to our ability

11:32

to understand cancers at a molecular level.

11:34

And would it be fair to say that not

11:37

necessarily all cancer needs

11:39

to be treated? I mean, it sounds like a controversial

11:41

statement, but a recent long-term study

11:44

looking at active surveillance versus

11:47

more aggressive measures such as radiotherapy

11:49

and surgery in prostate cancer, for

11:51

example, suggested, you know,

11:53

there was no significant difference in mortality

11:56

in several years' follow-up between just watching

11:58

and waiting in close surveillance and

12:00

actually intervening with quite

12:02

intense treatments for prostate cancer, for example.

12:05

This again varies enormously from cancer

12:07

type to cancer type and prostate cancer is

12:09

a very good case in point where there

12:12

are a lot of people who die of prostate cancer, so

12:14

it's not a benign situation.

12:17

It does spread around the body and there are plenty

12:19

of people who die from it. Conversely, there

12:21

are a lot of people who, as we get older, we all of us

12:24

have more and more changes in our cells. There

12:26

are a lot of people who have cancer

12:29

cells within their prostates who will

12:31

die of something else before the prostate cancer

12:33

ever turns into anything nasty. And

12:37

one of the jobs of biology is to try and

12:39

understand how to tell in advance

12:41

which is which so that we can really intervene

12:43

quickly for the people who really need the

12:45

treatment and we can leave alone the people who

12:47

don't. What role do you see

12:50

the microbiome having in

12:52

changing the course of cancer treatment,

12:55

either improving it or making

12:57

someone more resistant to

12:59

a particular type of therapy? I

13:02

think the microbiome is a good case

13:04

in point and it's a long way from my area

13:06

of expertise, but it's

13:09

clear that there are levels of complexity

13:12

over and above what takes place in cancer cells.

13:14

The micro environment, the organismal

13:16

environment, which you should also include

13:18

the microbiome. And certainly we

13:20

can see that changing the diet

13:23

from a very Western diet, rich in saturated

13:25

fats, to a much more fiber based diet, such

13:27

as you might get in Sub-Saharan

13:30

Africa, for example, has an enormous

13:32

effect in a very short space of time on the

13:35

bacterial content of the gut. Not surprisingly,

13:39

if there's a lot of fat for them to live on, then you'll get

13:41

the sort of bacteria that like a lot of fat. If

13:43

there's only fiber for them to live on, you'll get a lot of bacteria

13:45

that are happier in that environment. And

13:48

those changes appear

13:50

to be capable

13:53

of inducing cancers at different rates,

13:55

should I say. And we've wondered

13:58

for a long time about why people who live on the gut, on

14:00

a predominantly fiber-based diet

14:02

are much less prone to bowel cancer than people who live

14:04

on a high-fat diet. And it looks

14:06

like the microbiome is a potential

14:08

determinant of that. We are really

14:10

just at the beginning of our understanding of this.

14:13

When you look at the bacteria

14:16

that live in the gut, there's thousands of them

14:18

in any one person's gut. And you're trying to, again,

14:21

understand all this massive information

14:23

and try and pull some rules out of it so

14:25

that you can really go and not just

14:27

do observational work,

14:30

but actually say, okay, if

14:32

A, then B. That's what

14:34

we haven't got that yet in the study

14:36

of the microbiome. But it's pretty clear that skewing

14:39

of the microbiome certainly has

14:41

an influence on the likelihood of developing

14:44

some types of cancer. And

14:46

the rise of bowel cancer in a much younger

14:48

group of patients than we've seen previously over

14:51

the last decade is potentially related to that.

14:53

Also, if we look at the effects of treatments

14:56

using the immune system to fight cancer, we can

14:58

also see that probably those are affected

15:01

by the microbiome and the

15:03

gut at the same time. And that probably

15:05

has to do with the levels and the particular types

15:07

of immune activation that are existing. And you

15:09

mentioned there that a rise in

15:11

things like bowel cancers in younger people. I read

15:13

a statistic recently that people

15:15

born in the 1990s are

15:18

at double the risk of colorectal cancer

15:21

and quadruple the risk of rectal

15:23

cancer than people born in the 1950s. That

15:26

was a report, I think, from the American

15:28

Cancer Society a couple of years ago. Why

15:31

is that? Is that because of changes

15:33

in dietary factors leading to

15:35

a change in the microbiome, or is

15:38

there some other unseen hidden basis

15:40

for that? Yes. Again,

15:43

not my field specifically. And the straight

15:45

answer is we don't know. You have

15:48

to think that it probably has

15:50

a lot to do with diet and the way that our

15:52

diets have changed over the last 50 years. And

15:55

that seems the most likely culprit and

15:57

the most likely explanation for it, but there's

15:59

a huge amount of that. amount of work going on to try and dissect

16:01

this out at the moment and to try and understand what

16:04

has driven this really

16:06

quite striking increase in bowel cancer at

16:08

a younger age, people under the age of 50, which

16:11

previously was pretty uncommon where we're

16:13

seeing increasing numbers of cases now coming

16:15

through. And obviously with our evolving

16:18

diagnostic tools now compared to 10, 15 years

16:20

ago, over the last few years,

16:22

we've seen a rise in the number of these multi-cancer

16:26

early detection blood tests, for example, the

16:28

Galleri test, which claims to be

16:30

able to detect 50 cancers just

16:33

from a blood test. Now I

16:35

see this as a sort of poison

16:37

chalice. There's obviously

16:39

the blessing there, which is, wow, we can detect these cancers

16:42

early before something happens. But also

16:44

the kind of double-edged sword there is, okay,

16:47

in an asymptomatic person, we detect their

16:49

risk of cancer or potentially early

16:51

cancer, and we then subject them to

16:54

a gauntlet of potentially unnecessary

16:57

investigations, often which may be very invasive.

17:00

And then we get down this slippery slope of

17:02

we find things that we shouldn't

17:04

have found which never would have harmed them. And

17:06

we're now just giving them more tests and more procedures

17:09

just on the base of one single blood

17:11

test, which may not have ever harmed them.

17:14

I think you have

17:16

to recognize that not

17:19

knowing is not going to be helpful. Everything

17:22

may be helpful or unhelpful, but unless

17:24

you have the information, unless you've done

17:26

the experiment and investigated

17:28

what happens to people, you're never going to be positioned

17:30

to change the natural history of these things. Two,

17:33

three hundred years ago, most people

17:35

didn't live long enough to be old

17:37

enough to develop cancer. We've

17:40

changed our population

17:43

in ways through public health, through

17:45

the suppression of infectious diseases, through increasingly

17:47

the suppression of cardiovascular disease, to

17:50

allow us to live long enough to get a whole different pattern

17:52

of diseases to those we saw previously. And we're

17:54

still finding our way into

17:56

which ones are the biggest threat to us and

17:59

which ones can be safely watched. And

18:01

I think we still have a huge

18:03

amount of work to do, even in prostate cancer, which we've been

18:05

investigating for a long time to understand

18:08

which ones are likely to grow fast and which ones can

18:10

safely be observed. And

18:13

only by finding them and observing them and

18:16

working out what their natural history does, we'd be able

18:18

to do this. So I'm not a fan

18:20

of the ignorance's bliss school, I thought.

18:23

At the same time, we have to be super careful

18:25

about medicalising the population

18:28

and turning healthy asymptomatic people

18:30

into subjects of intensive medical investigation.

18:33

So there's a middle course to steer between these two.

18:35

I mean, on that point of trying

18:37

to avoid medicalising a healthy asymptomatic

18:40

population, I recently saw

18:42

this influencer in America, Kim Kardashian,

18:45

who was promoting and doing

18:47

an advert on social media, on

18:49

her social media, to her hundreds of millions of followers,

18:52

about a full-body MRI scan.

18:55

And, you know, she was recommending this as

18:57

a life-saving treatment where you can do

18:59

a full-body MRI scan, okay, full-body

19:01

MOT, and pick up things

19:03

which you wouldn't have picked up. Now, that seems

19:06

to be the steroid version of

19:08

the cancer blood test, where you would

19:10

find things that routinely shouldn't, you

19:12

know, need to be picked up at all. What are your

19:14

thoughts on a routine screening,

19:18

full-body screening, for just an asymptomatic

19:20

population in their 20s or 30s? I

19:22

think it's really important for healthcare

19:24

assistants in general that we go

19:26

on the basis of evidence, and that we do

19:29

things for which there's good evidence of benefit.

19:32

And until there's good evidence of benefit, we should

19:34

do the research, we should work out what

19:36

works. And I wouldn't jump

19:39

into embracing those kinds

19:41

of technologies without some really clear evidence

19:43

that it's helpful to people. I

19:45

can completely understand why people want to

19:47

do that. But at the same time, it's

19:50

really important that we do it in a very measured

19:52

and careful way. And recently I saw,

19:55

you were quoted talking about the seven-minute

19:58

anti-cancer jab, which is all over the head. It's

20:01

gone from being a hospital-based

20:03

intravenous infusion, which would take an hour

20:05

or maybe longer in some patients, to

20:07

now having a subcutaneous

20:10

under-the-skin seven-minute injection.

20:13

How much of an impact can that

20:15

have on cancer services in the UK

20:18

and potentially over the world if it's ever rolled

20:20

out worldwide? So, my total

20:22

antibodies, we've always tended to give

20:24

intravenously because that was how they

20:26

were originally developed and these antibodies

20:29

which stick to the cancer cell surface

20:31

and allow the immune system to recognise and target

20:34

it, which we've been using for 25 years,

20:36

have been transformative in my

20:39

own area of lymphoma and the likelihood

20:41

of surviving lymphoma has gone

20:43

up massively since we introduced actually just one

20:46

antibody targeting B cells, which

20:48

is what most lymphomas in the West are. And

20:50

you can see the point of inflection in the mortality

20:53

curve for the population as a whole with

20:55

the introduction of this one treatment, which is pretty

20:57

remarkable that if you think about

21:00

medicine and mortality and

21:03

we'd seen a continuously rising mortality rate

21:05

for lymphoma until that antibody was

21:07

introduced and then it started to go down again despite

21:09

the fact the incidence has continued to go up as

21:12

our population ages. So, that's pretty

21:14

remarkable for a piece of medical technology. If

21:16

you want to be able to deliver that in out-of-way

21:19

places where you don't have a big specialist

21:21

nurse population where

21:23

you may not have access to all

21:26

the disposables and all the things that you need for

21:28

lots of intravenous treatments, giving it under

21:30

the skin makes complete sense. So, the ability

21:33

to take this sort of

21:35

treatment into remote settings, into

21:37

less economically fortunate settings

21:40

is incredibly important. So, I think

21:43

that was the original motivation behind

21:46

developing subcutaneous treatments

21:48

with non-glide. You get a much more

21:50

smooth absorption. So, if you give an antibody

21:53

intravenously, you get a huge spike of it and then it

21:55

goes off into the tissues. If you give it subcutaneous,

21:57

you don't get that huge spike. area

22:00

under the curve, the same overall exposure

22:02

to the drug. So that's

22:04

proven to be something

22:07

which originally designed for less

22:10

fell off economies, but which has actually been incredibly

22:12

helpful for our service

22:14

where as we have increasing

22:17

numbers of people coming through and we're under

22:19

pressure for capacity to look after them, if

22:21

you can get people to have a subcutaneous

22:24

injection which takes a few minutes rather than sitting on

22:26

attached to a drip for an injection, that's massively

22:28

helpful for being able to treat more people.

22:31

What we'd really like to do is people giving it themselves

22:33

of

22:33

course, which is the next step.

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23:46

One of the things I like to do on this podcast is

23:48

debunk myths. And when it

23:51

comes to cancer, I think there's an endless list

23:53

of myths that people are trying to propagate.

23:55

Now, the myth I hear a lot on social

23:58

media is that Every

24:00

time you hear something like this seven-minute jab

24:02

or the CAR T cell therapy, which was just

24:05

talked about last year, it seems

24:07

to then disappear and no one hears about it. And

24:09

then there's this conspiracy theorist online say,

24:12

big farmer wants to suppress

24:14

any breakthroughs in cancer

24:16

because more money is made from

24:19

treating disease than curing it. What

24:21

are your thoughts on that take from a conspiracy theorist? It

24:24

isn't a worldview that I recognize

24:26

at all. I think if we could find ways to

24:29

really highly effectively treat cancer in a very

24:31

short space of time, we'd all take it. I'd

24:34

be very happy to be not

24:36

having to look after people with very advanced cancer,

24:38

which has gone beyond the point of being creasable. If

24:41

we had more effective treatments, then that

24:43

would be great. And we could all do

24:45

other things with our spare time. The fact

24:47

of the matter is, you know, we have

24:50

as our population gets older and cancer becomes

24:52

more common, an

24:54

enormous number of people who need our help. And

24:57

also, as we're all getting older

24:59

and getting cancer at more advanced

25:01

ages, we have other illnesses as well. So

25:05

treating a lymphoma in somebody

25:07

who's 40 years old and otherwise incredibly

25:09

fit is reasonably straightforward.

25:12

I wouldn't pretend it's easy for the person

25:14

involved, but it's from the medical point of view reasonably

25:16

straightforward. Doing the same thing

25:18

in somebody who's 85, who's got, you

25:21

know, had coronary artery disease and has got

25:23

a bit of chronic bronchitis and might be diabetic

25:26

is a completely different proposition. So

25:28

the other illnesses which we acquire as we

25:31

get older at the same time as our risk of cancer

25:33

goes up has made this enormously

25:35

more complicated than it used to be. So

25:37

this is not about people

25:40

suppressing fantastic treatments. These treatments

25:42

that you hear about go from being the

25:44

latest thing to something we're routinely doing.

25:47

There are tens of, maybe

25:49

even hundreds of thousands of people having subcutaneous

25:52

antibody treatments now as a result of the

25:54

change in the technology to be able to do that. Similarly,

25:57

something like CAR T cells, which is taking

25:59

some... somebody's own T-cells out, putting

26:03

a construct in which allows them to stick

26:05

to something on a cancer cell surface and

26:07

recognize it and kill it, is something

26:10

which we do for thousands of patients a year now

26:12

in the UK. We've been rolling

26:14

that out over the last five

26:17

years or so. And there's no

26:19

doubt there are quite a lot of people alive

26:21

who've had lymphoma in particular, who

26:24

would not have been alive if they hadn't had T-cell

26:26

treatment. I mean, it has been remarkably

26:28

effective for people whose other types

26:31

of treatment have failed them. And another

26:33

common thing I hear, and usually I feel it's

26:35

a result of fear

26:38

and lack of trust in the medical system, and

26:40

it's a lot about you can cure

26:42

cancer or avoid cancer purely

26:45

with dietary changes. If

26:47

only that were the case. I think there's no doubt

26:49

that there are a lot of factors

26:52

in our lifestyle which predispose

26:54

us to get cancer, the far the

26:56

biggest of which is cigarette smoking where we

26:58

know the dominant risk is really very

27:00

high. But dietary

27:02

changes, as we were saying earlier, probably

27:05

have played a role in the increase of some

27:07

types of cancer. And if we can start

27:10

to understand really what those are

27:12

and to move away from the dietary

27:14

features that make us more likely to develop cancer,

27:17

that can also help. Being overweight,

27:19

not taking enough exercise, we know all of those

27:21

things actually contribute to our cancer risk. So

27:24

there's lots of things we can do that

27:26

are in our hands. But at the same

27:28

time, quite a lot of cancer is random

27:31

damage to the genome,

27:33

which comes down to really bad biological

27:35

luck that these cells develop these

27:38

abnormalities, develop more abnormalities,

27:40

get away from our immune systems and evolve

27:42

in such a way that they turn into all those

27:44

malignancies. And not all of

27:46

that is driven by our lifestyles

27:49

or the way we live. Some of that is just the way that

27:51

cells are as they get older and acquire

27:53

more damage. Yeah, I agree. I mean, you know, obviously,

27:55

if you're living a good lifestyle with a high fibre

27:57

diet, activity, good sleep, Clearly

28:00

you would have a significant reduction in

28:02

your risk of cancer, but then again

28:04

I feel that also points

28:07

the finger at people who get cancer

28:09

and then they're blamed for their lifestyle where actually

28:11

they may have been doing everything right but just

28:13

get a cancer because it's sheer bad luck. Exactly.

28:17

And everybody knows

28:19

of people who've lived well into their

28:22

90s despite smoking 20 cigarettes a

28:24

day and equally people

28:26

who get lung cancer at a terribly young age

28:28

despite never having smoked. So this whole

28:30

thing is probabilistic.

28:33

There are things we can do to help and reduce our

28:35

risk but nothing will completely emanate

28:38

it unfortunately. Just before you go you had

28:40

a question for me. Yeah, I mean

28:42

you're training as a surgeon and

28:44

I'm interested to know

28:47

what you think about the march

28:49

of technology and how that's going to change the

28:51

working lives of surgeons for the future. I

28:54

mean we see lots of innovations.

28:56

Physicians have always been really good at thinking of new ways

28:58

of doing things and innovating and we see for example

29:01

robotic surgeries is really taking

29:04

off in certain areas. I think 96%

29:06

of prostate operations are now done by

29:09

robotic surgery. And

29:11

I'm interested to know how you think that's going

29:13

to change the life and the training of

29:15

surgeons in the future. Yeah, it's a really fascinating

29:18

question because you can clearly see

29:20

that the modern surgical

29:23

trainee and I'm talking about maybe

29:25

surgeons who have trained from the years

29:27

of 2000 onwards who

29:31

were in the sort of laparoscopic era

29:33

of training, minimally invasive surgery where most

29:36

of the operations they do whether it's a hernia

29:38

operation, appendix removal, gall bladder operation,

29:41

bowel cancer operations now, mostly

29:43

done laparoscopically. These surgeons,

29:46

the bulk of their cases will be done laparoscopically

29:49

but we can never discount the fact that

29:52

a small percentage of cases if something

29:54

goes wrong or it's just technically

29:56

difficult you will need to do a big

29:58

open surgery. It's very difficult

30:01

to acquire the open surgical

30:03

skills to the same level of proficiency

30:05

as you are with your laparoscopic skills because

30:08

you're just doing that every day. So

30:11

now with robotic surgery and maybe

30:13

a surgeon in 2040 who's done

30:15

all his training only robotically, how

30:18

can then that surgeon,

30:21

if something happens and there's a catastrophic major

30:23

hemorrhage, would they have the skills

30:26

to quickly open and do things? I don't know because

30:28

the sort of older generation surgeons who

30:31

could do a little bit of everything, they're

30:33

now diminishing and we are

30:35

getting to this super specialized surgeon who just

30:37

focuses on one thing. So it's

30:39

worrying in a way, but obviously fantastic

30:41

that we're developing these novel techniques. But I do

30:43

worry about the, you know, retainment

30:46

of broad range of skills. Feels

30:49

like something where we really need and

30:51

I know the College of Surgeons and the

30:54

Surgical Associations are thinking hard about this.

30:57

How do we make sure that we've got enough

31:00

trained surgeons that really can deal

31:02

with not when things go

31:04

well, but when things don't go well. And of course,

31:07

it's not something where you can send for somebody

31:09

from 20 miles away. You need somebody there right

31:11

now. And I think making sure that we retain those

31:13

skills among our surgeons. As

31:16

a medical oncologist, I've always

31:18

had a degree of scalpel envy. Medical

31:21

oncologists are kind of people who would have been

31:23

surgeons if they had the dexterity, but

31:26

still like this kind of therapeutic inclination

31:28

of the way that we work. And I think really

31:31

important that we retain those really

31:33

high level skills that the

31:35

surgeons have and can work

31:38

in ways which keep people safe

31:40

and make sure that not only can we do the

31:42

everyday stuff that goes well, but also deal with emergencies.

31:45

I think, you know, the field in which you're

31:47

in, hopefully at the rate it's expanding,

31:50

eventually you may be able to slowly

31:52

start putting surgeons out of jobs. That's

31:54

the holy grail maybe one day. It

31:56

would be lovely, but I think we're going to

31:58

need surgeons for a very long time. long time to come so I

32:01

think you're safe. Okay, thank you so much

32:03

Professor John for joining me. Just

32:08

before we go we have a listener question and this

32:10

one is from Carly in London. Carly

32:13

asks, I've had quite an emotional time recently

32:15

and I found myself in tears much more

32:17

than I would like for various reasons. My

32:19

question is, do you need to drink more water

32:22

when you've been crying? Does it dehydrate

32:24

you? Secondly, why do you get a

32:26

headache after you've been crying quite intensely?

32:29

So thank you very much for that question Carly. There's

32:31

quite a few bits to unpick here. Number

32:34

one, the amount you cry is

32:36

very, very, very unlikely to dehydrate

32:39

you. The tears serve many purposes.

32:41

You've got different types of tears, you've got

32:44

emotional tears which you're describing, you've

32:46

also got reflexive tears and tears

32:48

which just lubricate your eyeballs and

32:50

this is all part of your bodily

32:53

fluid which it accounts for. Now if you

32:55

are very dehydrated to the point

32:57

where you literally cannot cry,

33:00

you cannot produce tears, you cannot

33:02

produce sweat, then yes, you may need to

33:04

drink more water but it doesn't work the

33:06

other way where you cry so much. You can actually

33:09

dehydrate yourself and lower

33:11

your total fluid content in

33:13

your body. I don't want to say impossible but

33:16

very, very improbable. And your

33:18

second question about getting a headache,

33:20

there's an emotional reason you've been crying intensely

33:23

and that can play a part in giving you a

33:25

headache whether it's stress related, anxiety

33:27

related, there are lots of obvious

33:30

causes for your headache and finally

33:32

if you're crying intensely, you're contorting

33:34

your face, you're closing your eyes, you're scrunching your

33:36

eyes. So all of these muscles around your

33:39

face and head are being contracted

33:41

and this can lead to this type

33:43

of muscular headache. So Carly, I'm really sorry

33:45

that you've been crying for whatever reason but thank

33:48

you for taking the time to ask this question and

33:50

hopefully that can assuage some of

33:52

your queries and conundrums. And in this week's

33:54

episode in Crowd Science Extra, I'm

33:56

also answering a question from Zalhid in

33:58

Nottingham who asked about out getting

34:00

involved in clinical trials, Zahid

34:03

has celiac disease and he's wondering

34:05

how he can get involved in any clinical

34:07

trials to try new medication or

34:09

otherwise. If you want to find out, check out

34:11

the CrowdScience Extra episode! And

34:15

that's a wrap for today's episode but no doubt

34:17

I'll be covering cancer in the future because there is so

34:20

much to talk about and cutting edge science

34:22

to bring to you. Remember to subscribe for

34:24

weekly episodes and hit the notification

34:26

icon so you don't miss next week's juicy

34:29

episode of CineX. I'll catch you next time.