November 27, 2023 • 29 mins
A tumour is often thought of as a kind of chaotic tissue – cancer cells multiplying without control or reason, wreaking havoc in the body with devastating outcomes. In this episode we speak to Professor Alex Swarbrick who is charting an ‘atlas’ through that chaos, using cutting-edge genomic technologies to reveal the intricate inner workings of breast cancer.
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Episode Transcript
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Dr Viviane Richter (00:01):
A tumour is often thought of as a kind of chaotic tissue:
cancer cells multiplying without control or reason, wreaking havoc in
the body with devastating outcomes. But today we speak to
a remarkable researcher who is charting an atlas through that chaos,
(00:22):
using cutting-edge genomic technologies to reveal the intricate inner workings
of breast cancer. You're listening to Medical Minds. The podcast
that takes you inside the labs at the Garvan Institute
of Medical Research. I'm your host, Dr Viviane Richter. And
I'm here with Professor Alexander Swarbrick, Head of the Tumour
(00:42):
Progression Lab at Garvan. Welcome, Alex.
Prof Alex Swarbrick (00:45):
Hi, Viviane. It's a pleasure to be here.
Dr Viviane Richter (00:48):
Alex, before we talk about your research into breast cancer,
can you tell us how you were first exposed to science?
Prof Alex Swarbrick (00:55):
Yeah, sure. My dad was a geologist. And so I
guess I always had science in the family with him,
he would always be bringing rocks and minerals home. My
brother was an engineer as well. So you know someone
else kind of thinking in that quantitative kind of space,
so I wouldn't say I was always destined to be
a scientist, but there was always lots of science and
(01:18):
inquisitive kind of thought around the house.
Dr Viviane Richter (01:21):
How would you say your dad as a geologist influenced
your love for science?
Prof Alex Swarbrick (01:26):
So he did a lot of fieldwork when he when
I was young, and so he actually took me on
some of those trips. I guess this was before satellite
imaging became as kind of detailed as it is now.
And so he would actually go out into the field
and need to pick up chunks of rock and put
them in the bag and label the bag. So I
was kind of his field hand. But he'd also sometimes
bring the the geology home, which was kind of crazy.
(01:48):
So he was a uranium minerals explorer for a time,
and so he would sometimes play like, find the yellowcake
with the Geiger counter, and so we'd be running around
kinda click, click, click, click. Oh, it's in the cupboard.
You know, which was great. I'm sure it was perfectly
safe as well.
Dr Viviane Richter (02:08):
Literally exposed to science. That, honestly sounds like the origin
story of a marvel superhero. Did you know at that
point that you wanted to get into research?
Prof Alex Swarbrick (02:19):
I think so. Yeah, it wasn't... I'm not sure it had kind of
crystallised in my mind exactly what that looked like. I
wasn't great at school, so, you know, I guess I
hadn't formulated the idea very well, but it seemed like
I was pretty predestined to do it. And certainly by
the end of high school, I was, you know, I
knew that I wanted to go and do a science degree.
Dr Viviane Richter (02:38):
So what did you end up doing?
Prof Alex Swarbrick (02:40):
Yeah. So I enrolled in chemical engineering and industrial chemistry
in my first year, which I didn't love. I wasn't
really a chemistry prodigy, let's say, and it was also
I think I'd misunderstood what it was about. You know,
we had our first field trip to the dog food factory,
studying the physics of how the food moves around the
(03:00):
pipes in the factory. And I thought, alright, no, this
is not really what I thought I was signing up for.
I then kind of shifted into a more straight chemistry degree.
Analytical chemistry, mostly. So testing things, detecting the levels of contaminants,
that kind of stuff. It still didn't really connect with me.
And – but I think what really got me was the
(03:20):
development of molecular biology and biochemistry, and it was around
this time that two massive changes shook the field. The
first was the development of PCR, which I think everyone
knows the acronym now after COVID, right? Because that's what everyone,
that's where your nasal swab goes with PCR. And essentially,
(03:42):
PCR is polymerase chain reaction. So it's a way to
take a really tiny bit of DNA and amplify it
up to a huge amplification and lets you then kind
of measure it and test it. So that's why we
use it for COVID testing, to detect a tiny bit
of virus in your nostrils. But it can also then
enable you to do anything and work with any kind
(04:03):
of DNA. And the application that really connected with me
was the cloning of insulin, which was going on at
the same time, interestingly, by one of the ex Directors
of the Garvan Institute, John Shine. And so he was
in San Francisco. They were cloning insulin, which really revolutionised
the lives of diabetics because it went from needing to
(04:25):
extract the insulin from animal cadavers, for example, to being
able to synthesise it, make it synthetically and so to me,
that was just so exciting, and I didn't look back.
Dr Viviane Richter (04:36):
So what does a PCR machine actually do?
Prof Alex Swarbrick (04:38):
So PCR is actually like many great discoveries. It's quite
elegant and simple. It's comprised of three stages, three steps
with three different enzymes. So the first one is, you take
your DNA that you want to amplify. You heat it up,
and the two strands of the DNA fall apart because
DNA is double stranded, so you heat it, they start
(04:59):
to shake and separate. You then – there's a second step
where you add a kind of a – what we would
call a primer, I guess it's like a starting point
to each of those two strands of DNA. And then
the third step is you add in an enzyme that
can make new DNA together with all the individual bits
that you need the A, G, T and C. And that
(05:22):
enzyme then essentially starts to assemble the replicate strand of
DNA on the two copies that you've separated previously. And
so you control that just by cycling temperatures. For those
three different steps and so essentially a PCR machine is
like a thermal cycler. It just goes through those steps
and it does it 3040 times every time you double
(05:45):
what you started with. So first cycle you get two
times as much, then four times and eight, then 16
and 32. So you end up with something like a
million fold amplification. But back when I, I guess, first
saw PCR in action, instead of being the kind of
smooth boxes with a single button on the front that
they are now, it was, you know, literally three water
(06:07):
baths with this hacked kind of little crane moving tubes
between each of them. And it would take about a
day to run because they were basically homemade. But nonetheless,
it was really intriguing, and today's machines work in essentially
the same way.
Dr Viviane Richter (06:23):
So, Alex, what were some of the first projects that
you worked on in the lab?
Prof Alex Swarbrick (06:27):
So I did my honours in molecular biology at UNSW,
and the project I did was to sequence a couple
of genes from the giardia parasite. Some people might remember
giardia from the water contamination scare we had way back,
and so the idea was to try to understand different
species of giardia by finding differences in their DNA sequence.
(06:49):
And so I was in a fortunate position where I'd
previously done some training with a federal government testing lab,
which is in Pymble, and I convinced them to buy
what was probably one of the first DNA sequencers in
the country and for me to work between UNSW and
the site in Pymble. And so I got to get
(07:11):
this machine in, set it up, using PCR to do
the sequencing. And, you know, I think in the course
of my honours, which was about nine months, I probably
sequenced about three genes and read about 800 what we
call nucleotides, which is the building block of DNA, the AGCT.
So that's three times 800 – about 2400 nucleotides, and I
(07:34):
did that. It took me about nine months of absolute grind.
But of course, the technology of DNA sequencing is probably,
I think certainly has grown faster than any other technology
humanity has ever created. So in terms of the scale,
growth in scale and decline in cost, we've gone from
(07:57):
that project.
You know, 2400 nucleotides, I read, probably cost us $20,000.
You can now sequence billions of nucleotides in a day
for a few $1000 so it's just kind of mind
boggling where things have come just in that period of time.
So now you can sequence whole human genomes in the
snap of your fingers.
Dr Viviane Richter (08:18):
So after your honours, where did you embark on a PhD?
Prof Alex Swarbrick (08:23):
So I came to Garvan actually, focusing on hormonal control
of breast cancer. Many breast cancers are hormonally controlled by estrogen,
by progesterone and by other hormones as well. And so
we were really just beginning to understand how that worked
at a molecular level. So again, bringing those tools of
molecular biology to try to explain the clinical observations that
(08:45):
we've been making for decades and put them into kind
of a molecular framework.
Dr Viviane Richter (08:51):
After your PhD, like many researchers, you went overseas.
Prof Alex Swarbrick (08:55):
One of the advantages of medical research is that you
can travel. Your qualifications are generally accepted everywhere, and because
of the global nature of research, it's the normal thing
to do, particularly in Australia. In fact, it's kind of
it's unusual maybe to not go overseas. And so that
was a great opportunity.
Looked at a few different places to go, interviewed in
(09:16):
New York, which was, you know, fantastic. Interviewed in San
Francisco and interviewed in Mexico, which was a bit of
a lifestyle choice. But in the end went for San Francisco. And,
you know, I'm so glad I did. It was an
incredible time. We spent 3.5 years there. I was fortunate
to go into the lab of a Nobel laureate who
was the chancellor of the uni at the time. And
(09:38):
it was the lab in which oncogenes were discovered. So
the genes that drive cancer – it was his discovery. Mike
Bishop with Harold Varmus, where they discovered that in fact,
the genes that make cancers go are actually our own genes,
but they get corrupted. So that's what an oncogene is.
(09:58):
And so that was a you know, a fantastic amazing
environment to work in. University of California, San Francisco, UCSF,
really one of the world's greatest research institutes. Massive scale
compared to where I'd come from, you know, Australian science
was still pretty small, not very well resourced. And so
that was absolutely mindblowing to go there. And so I
(10:19):
learned so much about research and collaboration and was really yeah,
so lucky to have the chance. And then my wife
and I, we had our first child there. And so, yeah,
it was time to come back to Sydney.
Dr Viviane Richter (10:31):
UCSF, that's where John Shine cloned insulin.
Prof Alex Swarbrick (10:35):
Yeah that's right. So it was UCSF the the very same
place where so much interesting stuff was going on. And
it was it was from UCSF and actually around those
same discoveries that the drug company Genentech was also born. So,
so much kind of going on in that bay area
at that time.
Dr Viviane Richter (10:52):
So how did you find your way into the lab of
a Nobel laureate?
Prof Alex Swarbrick (10:56):
Like a lot of kind of branch points in my life,
there was a bit of luck involved in this. I
saw Mike's recent publications. He seemed to be doing some
pretty good research. It was in a city that I'd
always wanted to live in. And he looked like a
nice guy on the website. You know, that seemed important.
And really it was only when I got there that
I realised he was a Nobel laureate, realised he was
(11:17):
the chancellor of the university, and I just kind of
bumbled my way into this situation. But I guess he
could see my commitment and interest. And so, yeah, I
think it was just hugely fortunate, a great bit of
luck that I kind of followed my nose and ended
up in this in this lab that then really kind
of transformed my career.
Dr Viviane Richter (11:39):
So tell me about that. Tell me about following your nose.
Prof Alex Swarbrick (11:43):
Yeah, I think it's interesting. I guess some people, some
people's perception of science is that it's a very dry,
calculated existence, very quantitative. And of course, that's an absolute
pillar of scientific method. Right? You have to get your
data and make it believable and reproducible and reliable. But
it's also a creative pursuit, it really is. And the
(12:03):
way people kind of achieve that creativity, I guess, is
in various ways and for me I feel it's sometimes
kind of following my intuition, and I don't know what
intuition is, but I think it's, you know, I feel
like it's your mind in the background, integrating 100 or
1000 little facts or pieces of information that you've collected
(12:27):
over your life and turning it into something you don't
know how you got there and how it became that.
But it makes sense, and I gotta say, that's kind
of served me pretty well. So in, in addition to
I guess that very structured process that you need to
use to do science, I think there is also quite
a fluid, intuitive component. And often that's where, where some
(12:48):
of the best things that I've discovered have come from.
Dr Viviane Richter (12:51):
Let's talk about some of those discoveries, Alex. What did
you do after your postdoc?
Prof Alex Swarbrick (12:57):
Well, I spent about 3.5 years in San Francisco, and
as I mentioned, we had our daughter there, and so
that the clock was kind of ticking to get back
home to the support of our families. During my time
in Mike's lab, I'd worked mostly on the function of oncogenes,
as I mentioned earlier, these are the genes that get
corrupted that drive cancer. But what we were learning was
(13:19):
that cancer isn't just the product of one oncogene. It
takes a series of mutations to become a cancer. You know,
if you look at your skin and you have a mole.
A mole is actually melanocytes, so skin cells that have
acquired one, two, maybe three oncogenic mutations. But that's not enough
to become a melanoma. And so I became really interested in, well,
(13:42):
what are those second hits we call them, second, like,
offences that drive the cell closer and closer to the
brink of becoming full blown cancer. And so, moving from
studying one oncogene in Mike's lab and then came back,
I was fortunate to get a position back at Garvan.
That was partly a consequence of a travelling fellowship I
(14:04):
had from the federal government that tried to bring Australians
back from overseas. And so I set up then in
my lab experiments to understand what we called oncogene cooperation.
You know, why is it that when you get the
first gene Mick is your first oncogenic hit? Why do
you often then get a mutation in rats as the
(14:25):
second hit? How do they work together? How does that
then affect the behaviour of the cancer, those kind of things.
Dr Viviane Richter (14:32):
And what technology supported that work?
Prof Alex Swarbrick (14:35):
So we were mostly doing work in cell culture and
sometimes with animal models. A lot of genetics again, a
lot of molecular biology and essentially kind of introducing these
different combinations of oncogenic mutations and looking at the resulting phenotype.
But one of the things that frustrated us was that
we'd constantly observe, instead of a really predictable, homogeneous outcome,
(14:59):
if that makes sense, all the same, you'd get these
tumours that were really quite variable. They'd have different appearances
under the microscope. They'd be composed of different cells like
immune cells and fibroblasts. And it led us to more
and more appreciate that we were trying to, you know,
trying to simplify human disease, which is wildly complicated. And so, yeah,
(15:20):
we were frustrated sometimes by these experiments, we didn't feel
we had the tools to study them appropriately and again,
maybe by luck or, um, intuition, a new technology was emerging,
called single-cell genomics that allowed you to do the kind
of studies we'd always done, but at the level of
(15:40):
the single cell. So previously, genetics and genomics, we needed
to take a million cells or a billion cells, mash
them all up and collect them, and then study that
just so you had enough material to study and through
incredible engineering and biotechnology, people had managed to miniaturise this
down to the level of the cell. And this to
(16:01):
us was revolutionary. And it's actually turned out to be revolutionary.
This really was a turning point in biomedical research. And
of course, this technology now is very mainstream. And so
we jumped on it. We saw that coming, and we
were fortunate that Garvan acquired one of the instruments that
you need to do this at about that time. The
machine was actually designed for a different purpose. But people
(16:24):
quickly figured out you could hack it to do this
single-cell genomics. And in fact, it was never once used
for the purpose it was bought for. It was entirely
used for the single-cell genomics, and so that was an
absolute turning point for us. We recognised the opportunity that
that brought the potential for it, and I really kind
of put all my chips on on single-cell genomics, and
(16:45):
it's turned out to be really fantastic. The insights it
gives us and its ability to address some of those
problems that we saw.
Dr Viviane Richter (16:53):
Alex you lead the Breast Cancer Cell Atlas. Now, when
I think of an atlas, I think of a big
reference book that primary school kids might use. Tell us,
what does the breast cancer cell atlas do?
Prof Alex Swarbrick (17:08):
Yeah, it's an interesting analogy, isn't it? The kind of
using the word atlas. And I think to us the
intention is to generate a map that helps us define
the cellular makeup of a tumour. So you know a
cancer is made of cells. Some of those cells are
the cancer cells that get those oncogenic mutations that we
(17:29):
talked about earlier. But a lot of the cells in
there aren't cancer cells. There are other cell types. They're
immune cells, they're fibroblasts, for example, the cells that make
collagen and all sorts of other cells mixed in there.
And there's this increasing appreciation that a cancer isn't just
a random mess of cancer cells dividing and dividing like
(17:52):
a bacteria might do. But rather it's kind of a
broken tissue. And so, just like a normal tissue, like
your skin or your eye retina or something, cells are
organised into performing particular roles and cells interact with one another.
And so there's an increasing awareness that we have to
understand all the cells, what we call the ecosystem, the
(18:14):
cellular ecosystem of a tumour, to properly understand the behaviour
of a tumour and ultimately predict its behaviour. Because that's
what we need to be able to do is understand
who's gonna have a great outcome, who's not gonna have
a good outcome and how we can intervene in that.
And so the atlas is really the first step in
deeply mapping all the cells that make up all the
(18:37):
many types of breast cancers that you can see in
the community.
Dr Viviane Richter (18:41):
So tell us about these ecosystems. What do they look like?
How do the cells talk to each other?
Prof Alex Swarbrick (18:48):
Yeah, it's an interesting question. So cells organise into distinct
architectures you could call it, you could call it a neighbourhood.
That's another term we use. So they kind of collect
around each other. And instead of that being random, as
we do this work, we're learning more and more that
there are repeating patterns that this type of fibroblast very
(19:10):
frequently is found with this type of immune cell. And
not only that, when they're found together, the immune cell
has a particular behaviour. In one example of work we're
doing now, we found that a certain type of fibroblast
that 10 years ago, we would have said, was a
passenger in the cancer irrelevant to the patient. Now what
we know is it's actually secreting molecules from its surface.
(19:35):
Next to these T cells, the T cells take up
those molecules, and it changes their behaviour. And this is
important because those T cells are actually the killer cells
of the immune system. What they're meant to be doing
is going and killing the cancer cells to eradicate your disease.
But instead they become inactivated through this interaction with the fibroblasts.
(19:55):
So it's almost like a poisoned soil in which these
T cells are planted. And so the question then becomes well, firstly,
can we use that as a way to predict patients'
disease progression? If we find this this interaction, can we
use that as a way to tailor their treatment? But secondly,
can we stop the fibroblast doing this to the T cell?
(20:17):
Can we figure out the language of that interaction? What
are the molecules that are being produced and block them
and thereby wake up the T cell again.
Dr Viviane Richter (20:25):
Has some of this research already had impact in patients?
Prof Alex Swarbrick (20:29):
It has, it's early days, and really, there's a huge
gulf from fundamental research to clinical impact. There's a lot
you have to do because we have to get it right.
You don't wanna start a clinical trial with some half-baked idea,
and firstly because and most importantly, because that can, you
know you're putting a patient potentially at risk of a
(20:49):
new treatment that's utile. But also it's massively wasteful and
just gets us there more slowly. But there are some
great examples, many great examples now, which is really fantastic.
We ran one project ourselves a few years ago. We
found a different type of fibroblast. Now, actually, in a
subset of these nasty breast cancers called triple-negative breast cancers,
(21:13):
these tumours are naturally aggressive. They divide quickly. They grow quickly,
they invade, they spread through the body. But we also
don't have very good treatments for them. Those patients still
essentially get surgery, radiotherapy, chemotherapy, like we were doing 50
years ago. And so what we find is that in
a subset of those patients, their cancer cells set up
(21:33):
this conversation with type of fibroblasts, and in this case,
the fibroblasts actually make a fertile soil for the cancer
cells to grow. More importantly, the fibroblasts set up a
fertile soil for the cancer cells to be more aggressive
and more drug resistant. So we proposed. Well, what if
(21:57):
we could block that signal that interaction with the fibroblasts?
Might the cancer cells become more sensitive to chemotherapy? And
in experimental models, we could show that to be true.
And so we ran a phase 1 trial, and so a
clinical trial. They come in different phases. The first one
when you're trying a new treatment. The objective is really
(22:19):
to ask. Is this safe? Can you give this to
people safely? That's the first thing. But at the same time,
we were able to ask, can we also see any
evidence that it's maybe helping? And so we enrolled 12
women with really nasty, aggressive, metastatic, triple-negative breast cancer. It
had already spread to distant organs from their breast. They'd
(22:41):
already failed every line of treatment that was available to them.
They were really out of options. And so we gave
them combination therapy to block this conversation – and I gotta
digress – the name of the molecule that the cancer cells
use to signal to the fibroblasts is hedgehog. And this
is what happens when you let, like biology geeks name genes. Anyway.
(23:05):
So we gave one drug to block hedgehog, and another
drug was the chemotherapy that these patients were failing to
respond to. Now the most important thing was this was
well tolerated. It wasn't particularly toxic, no more than the chemotherapy.
But more importantly, three patients showed clinical benefit, and one
of them actually had a complete response to the drug.
(23:25):
Now these are really early days. It's what we call
a single arm trial. We didn't have a comparison group,
patients who only got chemotherapy, for example, so it doesn't
prove that the combination worked. But it's nonetheless really provocative,
really exciting and gives us reason to now want to
progress to further lines of clinical trial, to directly test
(23:46):
the value, the benefit to patients. For this.
Dr Viviane Richter (23:48):
That's incredible. It must be so motivating to see that effect
in patients.
Prof Alex Swarbrick (23:53):
Yeah, it it really is. I mean, even if it's
just one person getting clinical benefit for I don't know,
a few months, we don't really know. But nonetheless, it's
an incredible feeling, so motivating and makes the, you know,
four or five years of slog for all the students
and postdocs in the lab worth it.
Dr Viviane Richter (24:12):
So much has been invested in finding a cure for
breast cancer. Do you think we'll get them?
Prof Alex Swarbrick (24:18):
I think we already are. I think it depends how
you think about it. Whether we will cure every breast cancer
is a pretty massive goal, and I think that's a
long way off to be realistic with you. But at
the same time, you know, you can think of an
analogy of we're picking off the low lying fruit in
a way, if you think of the tree and some
(24:39):
cancers are easy to treat, they are relatively non-aggressive, and
we have incredible treatments for them now. And so we
we cure a majority of patients with breast cancer that
come in with a diagnosis. They're cured. They will not
die from breast cancer in their lifetime. And gradually, that
proportion of people who are cured is increasing year on
year on year. And in fact, there have been phenomenal
(25:00):
new developments in the last few years that are not
just microscopically turning the dial but really changing things for patients.
But I think we need to be realistic that at
least in my lifetime, there will be cancers that we
can't cure. Exactly why? It's a multitude of reasons. It's
partly probably based on the individual properties of the person
(25:24):
who has the disease. We know now that your immune
system is an essential component to responding to many therapies,
and we're all different in that way. But also it's
probably a lot to do with the features of the
cancer itself. The combination of oncogenes, for example, that this
cancer has acquired determines its aggressiveness. So I think there
(25:45):
are always gonna be, at least in the foreseeable future,
classes of cases that are beyond our reach. But I
think what really drives us on is that we are
still making really major game changing insights into how to
treat breast cancer. And when I say we, I mean
the global breast cancer research community, we're nowhere near levelling out.
(26:07):
It's not mission accomplished by any means. There are still
so many patients in need, but I think so many
opportunities for us to change their lives.
Dr Viviane Richter (26:17):
Alright, Alex, we've already learned a lot about you, but
it's time we dug a little deeper. It's time for
the fast five. What do you do in your downtime?
Prof Alex Swarbrick (26:27):
Well, I have two kids. Two teenage kids love to
spend time with them when they will agree to spend
time with me. Otherwise, love seeing my friends play a
bit of guitar. I'm not really so inspired by the
kind of computer music anymore. Rather, I just torture people
with some guitar playing.
Dr Viviane Richter (26:44):
Lovely. Any favourite tunes that you like to bust out?
Prof Alex Swarbrick (26:47):
I like campfire repertoire is kind of what I hit.
So I'd say probably Jeff Buckley Hallelujah. You know, great example.
Dr Viviane Richter (26:56):
Classic! Any secret skills?
Prof Alex Swarbrick (26:57):
Oh, love cooking, couldn't really claim to be fantastic at it.
Make an unbelievable salad dressing, though.
Dr Viviane Richter (27:04):
Favourite holiday?
Prof Alex Swarbrick (27:05):
Would have to be around the world trip with my
wife in our twenties, we went through Central, South America, USA, Europe.
Just fantastic. Living on noodles every day. Wonderful.
Dr Viviane Richter (27:18):
Are you reading anything interesting at the moment?
Prof Alex Swarbrick (27:20):
I've just finished All the Light We Cannot See, which
is a really beautiful book set in World War II, story
of two kids kind of surviving. But then they find
each other in the rubble of Europe. It's really beautiful.
Dr Viviane Richter (27:36):
Who do you admire?
Prof Alex Swarbrick (27:38):
I think my colleagues Elgene Lim, for example. He's a medical oncologist
that I work with. He is just such an energetic, kind,
giving person. He is super inspiring. Similarly, my colleague Sandra O'Toole,
who's a pathologist, she works at RPA. She's an absolute powerhouse,
somehow just makes it all work and is kind and
(28:01):
funny at the same time. So I'm so lucky to
be surrounded by people that I really think are fantastic.
Dr Viviane Richter (28:08):
Is there anything you're afraid of?
Prof Alex Swarbrick (28:10):
Yeah, many things. I'm terrified of spiders. If there's a
spider in the house, I run. Thankfully, my wife is
like a ninja spider hunter, and she'll just catch them.
Chuck them outside.
Dr Viviane Richter (28:21):
Do you play any sports?
Prof Alex Swarbrick (28:22):
Yes, I love playing tennis. That's my thing.
Dr Viviane Richter (28:25):
Who's your favourite tennis player?
Prof Alex Swarbrick (28:27):
I would have to say Alcaraz, the Spanish player. He
is just an absolute phenomenon. Has every shot in the
book and he's 19 or something? So yeah, just I
don't know. You could have got the sense that tennis
was would never improve any further past, you know, the the greats.
But he's come along and just changed the game again.
Dr Viviane Richter (28:49):
Professor Alex Swarbrick. Thank you so much for joining us
on Medical Minds.
Prof Alex Swarbrick (28:53):
Oh, thanks so much for having me. It's been great fun.
Dr Viviane Richter (28:56):
If you'd like to know more about Alex's research or
the work we do at Garvan, head to garvan.org.au. And
if you've enjoyed this podcast, please leave a review and
share with other podcast lovers. I'm Dr Viviane Richter. Thanks
for listening. This podcast was recorded on the traditional country
(29:17):
of the Gadigal people of the Eora Nation. We recognise
their continuing connection to land, waters and community. We pay
our respects to Aboriginal and Torres Strait Islander cultures and
Elders past, present and emerging.
A tumour is often thought of as a kind of chaotic tissue:
cancer cells multiplying without control or reason, wreaking havoc in
the body with devastating outcomes. But today we speak to
a remarkable researcher who is charting an atlas through that chaos,
(00:22):
using cutting-edge genomic technologies to reveal the intricate inner workings
of breast cancer. You're listening to Medical Minds. The podcast
that takes you inside the labs at the Garvan Institute
of Medical Research. I'm your host, Dr Viviane Richter. And
I'm here with Professor Alexander Swarbrick, Head of the Tumour
(00:42):
Progression Lab at Garvan. Welcome, Alex.
Prof Alex Swarbrick (00:45):
Hi, Viviane. It's a pleasure to be here.
Dr Viviane Richter (00:48):
Alex, before we talk about your research into breast cancer,
can you tell us how you were first exposed to science?
Prof Alex Swarbrick (00:55):
Yeah, sure. My dad was a geologist. And so I
guess I always had science in the family with him,
he would always be bringing rocks and minerals home. My
brother was an engineer as well. So you know someone
else kind of thinking in that quantitative kind of space,
so I wouldn't say I was always destined to be
a scientist, but there was always lots of science and
(01:18):
inquisitive kind of thought around the house.
Dr Viviane Richter (01:21):
How would you say your dad as a geologist influenced
your love for science?
Prof Alex Swarbrick (01:26):
So he did a lot of fieldwork when he when
I was young, and so he actually took me on
some of those trips. I guess this was before satellite
imaging became as kind of detailed as it is now.
And so he would actually go out into the field
and need to pick up chunks of rock and put
them in the bag and label the bag. So I
was kind of his field hand. But he'd also sometimes
bring the the geology home, which was kind of crazy.
(01:48):
So he was a uranium minerals explorer for a time,
and so he would sometimes play like, find the yellowcake
with the Geiger counter, and so we'd be running around
kinda click, click, click, click. Oh, it's in the cupboard.
You know, which was great. I'm sure it was perfectly
safe as well.
Dr Viviane Richter (02:08):
Literally exposed to science. That, honestly sounds like the origin
story of a marvel superhero. Did you know at that
point that you wanted to get into research?
Prof Alex Swarbrick (02:19):
I think so. Yeah, it wasn't... I'm not sure it had kind of
crystallised in my mind exactly what that looked like. I
wasn't great at school, so, you know, I guess I
hadn't formulated the idea very well, but it seemed like
I was pretty predestined to do it. And certainly by
the end of high school, I was, you know, I
knew that I wanted to go and do a science degree.
Dr Viviane Richter (02:38):
So what did you end up doing?
Prof Alex Swarbrick (02:40):
Yeah. So I enrolled in chemical engineering and industrial chemistry
in my first year, which I didn't love. I wasn't
really a chemistry prodigy, let's say, and it was also
I think I'd misunderstood what it was about. You know,
we had our first field trip to the dog food factory,
studying the physics of how the food moves around the
(03:00):
pipes in the factory. And I thought, alright, no, this
is not really what I thought I was signing up for.
I then kind of shifted into a more straight chemistry degree.
Analytical chemistry, mostly. So testing things, detecting the levels of contaminants,
that kind of stuff. It still didn't really connect with me.
And – but I think what really got me was the
(03:20):
development of molecular biology and biochemistry, and it was around
this time that two massive changes shook the field. The
first was the development of PCR, which I think everyone
knows the acronym now after COVID, right? Because that's what everyone,
that's where your nasal swab goes with PCR. And essentially,
(03:42):
PCR is polymerase chain reaction. So it's a way to
take a really tiny bit of DNA and amplify it
up to a huge amplification and lets you then kind
of measure it and test it. So that's why we
use it for COVID testing, to detect a tiny bit
of virus in your nostrils. But it can also then
enable you to do anything and work with any kind
(04:03):
of DNA. And the application that really connected with me
was the cloning of insulin, which was going on at
the same time, interestingly, by one of the ex Directors
of the Garvan Institute, John Shine. And so he was
in San Francisco. They were cloning insulin, which really revolutionised
the lives of diabetics because it went from needing to
(04:25):
extract the insulin from animal cadavers, for example, to being
able to synthesise it, make it synthetically and so to me,
that was just so exciting, and I didn't look back.
Dr Viviane Richter (04:36):
So what does a PCR machine actually do?
Prof Alex Swarbrick (04:38):
So PCR is actually like many great discoveries. It's quite
elegant and simple. It's comprised of three stages, three steps
with three different enzymes. So the first one is, you take
your DNA that you want to amplify. You heat it up,
and the two strands of the DNA fall apart because
DNA is double stranded, so you heat it, they start
(04:59):
to shake and separate. You then – there's a second step
where you add a kind of a – what we would
call a primer, I guess it's like a starting point
to each of those two strands of DNA. And then
the third step is you add in an enzyme that
can make new DNA together with all the individual bits
that you need the A, G, T and C. And that
(05:22):
enzyme then essentially starts to assemble the replicate strand of
DNA on the two copies that you've separated previously. And
so you control that just by cycling temperatures. For those
three different steps and so essentially a PCR machine is
like a thermal cycler. It just goes through those steps
and it does it 3040 times every time you double
(05:45):
what you started with. So first cycle you get two
times as much, then four times and eight, then 16
and 32. So you end up with something like a
million fold amplification. But back when I, I guess, first
saw PCR in action, instead of being the kind of
smooth boxes with a single button on the front that
they are now, it was, you know, literally three water
(06:07):
baths with this hacked kind of little crane moving tubes
between each of them. And it would take about a
day to run because they were basically homemade. But nonetheless,
it was really intriguing, and today's machines work in essentially
the same way.
Dr Viviane Richter (06:23):
So, Alex, what were some of the first projects that
you worked on in the lab?
Prof Alex Swarbrick (06:27):
So I did my honours in molecular biology at UNSW,
and the project I did was to sequence a couple
of genes from the giardia parasite. Some people might remember
giardia from the water contamination scare we had way back,
and so the idea was to try to understand different
species of giardia by finding differences in their DNA sequence.
(06:49):
And so I was in a fortunate position where I'd
previously done some training with a federal government testing lab,
which is in Pymble, and I convinced them to buy
what was probably one of the first DNA sequencers in
the country and for me to work between UNSW and
the site in Pymble. And so I got to get
(07:11):
this machine in, set it up, using PCR to do
the sequencing. And, you know, I think in the course
of my honours, which was about nine months, I probably
sequenced about three genes and read about 800 what we
call nucleotides, which is the building block of DNA, the AGCT.
So that's three times 800 – about 2400 nucleotides, and I
(07:34):
did that. It took me about nine months of absolute grind.
But of course, the technology of DNA sequencing is probably,
I think certainly has grown faster than any other technology
humanity has ever created. So in terms of the scale,
growth in scale and decline in cost, we've gone from
(07:57):
that project.
You know, 2400 nucleotides, I read, probably cost us $20,000.
You can now sequence billions of nucleotides in a day
for a few $1000 so it's just kind of mind
boggling where things have come just in that period of time.
So now you can sequence whole human genomes in the
snap of your fingers.
Dr Viviane Richter (08:18):
So after your honours, where did you embark on a PhD?
Prof Alex Swarbrick (08:23):
So I came to Garvan actually, focusing on hormonal control
of breast cancer. Many breast cancers are hormonally controlled by estrogen,
by progesterone and by other hormones as well. And so
we were really just beginning to understand how that worked
at a molecular level. So again, bringing those tools of
molecular biology to try to explain the clinical observations that
(08:45):
we've been making for decades and put them into kind
of a molecular framework.
Dr Viviane Richter (08:51):
After your PhD, like many researchers, you went overseas.
Prof Alex Swarbrick (08:55):
One of the advantages of medical research is that you
can travel. Your qualifications are generally accepted everywhere, and because
of the global nature of research, it's the normal thing
to do, particularly in Australia. In fact, it's kind of
it's unusual maybe to not go overseas. And so that
was a great opportunity.
Looked at a few different places to go, interviewed in
(09:16):
New York, which was, you know, fantastic. Interviewed in San
Francisco and interviewed in Mexico, which was a bit of
a lifestyle choice. But in the end went for San Francisco. And,
you know, I'm so glad I did. It was an
incredible time. We spent 3.5 years there. I was fortunate
to go into the lab of a Nobel laureate who
was the chancellor of the uni at the time. And
(09:38):
it was the lab in which oncogenes were discovered. So
the genes that drive cancer – it was his discovery. Mike
Bishop with Harold Varmus, where they discovered that in fact,
the genes that make cancers go are actually our own genes,
but they get corrupted. So that's what an oncogene is.
(09:58):
And so that was a you know, a fantastic amazing
environment to work in. University of California, San Francisco, UCSF,
really one of the world's greatest research institutes. Massive scale
compared to where I'd come from, you know, Australian science
was still pretty small, not very well resourced. And so
that was absolutely mindblowing to go there. And so I
(10:19):
learned so much about research and collaboration and was really yeah,
so lucky to have the chance. And then my wife
and I, we had our first child there. And so, yeah,
it was time to come back to Sydney.
Dr Viviane Richter (10:31):
UCSF, that's where John Shine cloned insulin.
Prof Alex Swarbrick (10:35):
Yeah that's right. So it was UCSF the the very same
place where so much interesting stuff was going on. And
it was it was from UCSF and actually around those
same discoveries that the drug company Genentech was also born. So,
so much kind of going on in that bay area
at that time.
Dr Viviane Richter (10:52):
So how did you find your way into the lab of
a Nobel laureate?
Prof Alex Swarbrick (10:56):
Like a lot of kind of branch points in my life,
there was a bit of luck involved in this. I
saw Mike's recent publications. He seemed to be doing some
pretty good research. It was in a city that I'd
always wanted to live in. And he looked like a
nice guy on the website. You know, that seemed important.
And really it was only when I got there that
I realised he was a Nobel laureate, realised he was
(11:17):
the chancellor of the university, and I just kind of
bumbled my way into this situation. But I guess he
could see my commitment and interest. And so, yeah, I
think it was just hugely fortunate, a great bit of
luck that I kind of followed my nose and ended
up in this in this lab that then really kind
of transformed my career.
Dr Viviane Richter (11:39):
So tell me about that. Tell me about following your nose.
Prof Alex Swarbrick (11:43):
Yeah, I think it's interesting. I guess some people, some
people's perception of science is that it's a very dry,
calculated existence, very quantitative. And of course, that's an absolute
pillar of scientific method. Right? You have to get your
data and make it believable and reproducible and reliable. But
it's also a creative pursuit, it really is. And the
(12:03):
way people kind of achieve that creativity, I guess, is
in various ways and for me I feel it's sometimes
kind of following my intuition, and I don't know what
intuition is, but I think it's, you know, I feel
like it's your mind in the background, integrating 100 or
1000 little facts or pieces of information that you've collected
(12:27):
over your life and turning it into something you don't
know how you got there and how it became that.
But it makes sense, and I gotta say, that's kind
of served me pretty well. So in, in addition to
I guess that very structured process that you need to
use to do science, I think there is also quite
a fluid, intuitive component. And often that's where, where some
(12:48):
of the best things that I've discovered have come from.
Dr Viviane Richter (12:51):
Let's talk about some of those discoveries, Alex. What did
you do after your postdoc?
Prof Alex Swarbrick (12:57):
Well, I spent about 3.5 years in San Francisco, and
as I mentioned, we had our daughter there, and so
that the clock was kind of ticking to get back
home to the support of our families. During my time
in Mike's lab, I'd worked mostly on the function of oncogenes,
as I mentioned earlier, these are the genes that get
corrupted that drive cancer. But what we were learning was
(13:19):
that cancer isn't just the product of one oncogene. It
takes a series of mutations to become a cancer. You know,
if you look at your skin and you have a mole.
A mole is actually melanocytes, so skin cells that have
acquired one, two, maybe three oncogenic mutations. But that's not enough
to become a melanoma. And so I became really interested in, well,
(13:42):
what are those second hits we call them, second, like,
offences that drive the cell closer and closer to the
brink of becoming full blown cancer. And so, moving from
studying one oncogene in Mike's lab and then came back,
I was fortunate to get a position back at Garvan.
That was partly a consequence of a travelling fellowship I
(14:04):
had from the federal government that tried to bring Australians
back from overseas. And so I set up then in
my lab experiments to understand what we called oncogene cooperation.
You know, why is it that when you get the
first gene Mick is your first oncogenic hit? Why do
you often then get a mutation in rats as the
(14:25):
second hit? How do they work together? How does that
then affect the behaviour of the cancer, those kind of things.
Dr Viviane Richter (14:32):
And what technology supported that work?
Prof Alex Swarbrick (14:35):
So we were mostly doing work in cell culture and
sometimes with animal models. A lot of genetics again, a
lot of molecular biology and essentially kind of introducing these
different combinations of oncogenic mutations and looking at the resulting phenotype.
But one of the things that frustrated us was that
we'd constantly observe, instead of a really predictable, homogeneous outcome,
(14:59):
if that makes sense, all the same, you'd get these
tumours that were really quite variable. They'd have different appearances
under the microscope. They'd be composed of different cells like
immune cells and fibroblasts. And it led us to more
and more appreciate that we were trying to, you know,
trying to simplify human disease, which is wildly complicated. And so, yeah,
(15:20):
we were frustrated sometimes by these experiments, we didn't feel
we had the tools to study them appropriately and again,
maybe by luck or, um, intuition, a new technology was emerging,
called single-cell genomics that allowed you to do the kind
of studies we'd always done, but at the level of
(15:40):
the single cell. So previously, genetics and genomics, we needed
to take a million cells or a billion cells, mash
them all up and collect them, and then study that
just so you had enough material to study and through
incredible engineering and biotechnology, people had managed to miniaturise this
down to the level of the cell. And this to
(16:01):
us was revolutionary. And it's actually turned out to be revolutionary.
This really was a turning point in biomedical research. And
of course, this technology now is very mainstream. And so
we jumped on it. We saw that coming, and we
were fortunate that Garvan acquired one of the instruments that
you need to do this at about that time. The
machine was actually designed for a different purpose. But people
(16:24):
quickly figured out you could hack it to do this
single-cell genomics. And in fact, it was never once used
for the purpose it was bought for. It was entirely
used for the single-cell genomics, and so that was an
absolute turning point for us. We recognised the opportunity that
that brought the potential for it, and I really kind
of put all my chips on on single-cell genomics, and
(16:45):
it's turned out to be really fantastic. The insights it
gives us and its ability to address some of those
problems that we saw.
Dr Viviane Richter (16:53):
Alex you lead the Breast Cancer Cell Atlas. Now, when
I think of an atlas, I think of a big
reference book that primary school kids might use. Tell us,
what does the breast cancer cell atlas do?
Prof Alex Swarbrick (17:08):
Yeah, it's an interesting analogy, isn't it? The kind of
using the word atlas. And I think to us the
intention is to generate a map that helps us define
the cellular makeup of a tumour. So you know a
cancer is made of cells. Some of those cells are
the cancer cells that get those oncogenic mutations that we
(17:29):
talked about earlier. But a lot of the cells in
there aren't cancer cells. There are other cell types. They're
immune cells, they're fibroblasts, for example, the cells that make
collagen and all sorts of other cells mixed in there.
And there's this increasing appreciation that a cancer isn't just
a random mess of cancer cells dividing and dividing like
(17:52):
a bacteria might do. But rather it's kind of a
broken tissue. And so, just like a normal tissue, like
your skin or your eye retina or something, cells are
organised into performing particular roles and cells interact with one another.
And so there's an increasing awareness that we have to
understand all the cells, what we call the ecosystem, the
(18:14):
cellular ecosystem of a tumour, to properly understand the behaviour
of a tumour and ultimately predict its behaviour. Because that's
what we need to be able to do is understand
who's gonna have a great outcome, who's not gonna have
a good outcome and how we can intervene in that.
And so the atlas is really the first step in
deeply mapping all the cells that make up all the
(18:37):
many types of breast cancers that you can see in
the community.
Dr Viviane Richter (18:41):
So tell us about these ecosystems. What do they look like?
How do the cells talk to each other?
Prof Alex Swarbrick (18:48):
Yeah, it's an interesting question. So cells organise into distinct
architectures you could call it, you could call it a neighbourhood.
That's another term we use. So they kind of collect
around each other. And instead of that being random, as
we do this work, we're learning more and more that
there are repeating patterns that this type of fibroblast very
(19:10):
frequently is found with this type of immune cell. And
not only that, when they're found together, the immune cell
has a particular behaviour. In one example of work we're
doing now, we found that a certain type of fibroblast
that 10 years ago, we would have said, was a
passenger in the cancer irrelevant to the patient. Now what
we know is it's actually secreting molecules from its surface.
(19:35):
Next to these T cells, the T cells take up
those molecules, and it changes their behaviour. And this is
important because those T cells are actually the killer cells
of the immune system. What they're meant to be doing
is going and killing the cancer cells to eradicate your disease.
But instead they become inactivated through this interaction with the fibroblasts.
(19:55):
So it's almost like a poisoned soil in which these
T cells are planted. And so the question then becomes well, firstly,
can we use that as a way to predict patients'
disease progression? If we find this this interaction, can we
use that as a way to tailor their treatment? But secondly,
can we stop the fibroblast doing this to the T cell?
(20:17):
Can we figure out the language of that interaction? What
are the molecules that are being produced and block them
and thereby wake up the T cell again.
Dr Viviane Richter (20:25):
Has some of this research already had impact in patients?
Prof Alex Swarbrick (20:29):
It has, it's early days, and really, there's a huge
gulf from fundamental research to clinical impact. There's a lot
you have to do because we have to get it right.
You don't wanna start a clinical trial with some half-baked idea,
and firstly because and most importantly, because that can, you
know you're putting a patient potentially at risk of a
(20:49):
new treatment that's utile. But also it's massively wasteful and
just gets us there more slowly. But there are some
great examples, many great examples now, which is really fantastic.
We ran one project ourselves a few years ago. We
found a different type of fibroblast. Now, actually, in a
subset of these nasty breast cancers called triple-negative breast cancers,
(21:13):
these tumours are naturally aggressive. They divide quickly. They grow quickly,
they invade, they spread through the body. But we also
don't have very good treatments for them. Those patients still
essentially get surgery, radiotherapy, chemotherapy, like we were doing 50
years ago. And so what we find is that in
a subset of those patients, their cancer cells set up
(21:33):
this conversation with type of fibroblasts, and in this case,
the fibroblasts actually make a fertile soil for the cancer
cells to grow. More importantly, the fibroblasts set up a
fertile soil for the cancer cells to be more aggressive
and more drug resistant. So we proposed. Well, what if
(21:57):
we could block that signal that interaction with the fibroblasts?
Might the cancer cells become more sensitive to chemotherapy? And
in experimental models, we could show that to be true.
And so we ran a phase 1 trial, and so a
clinical trial. They come in different phases. The first one
when you're trying a new treatment. The objective is really
(22:19):
to ask. Is this safe? Can you give this to
people safely? That's the first thing. But at the same time,
we were able to ask, can we also see any
evidence that it's maybe helping? And so we enrolled 12
women with really nasty, aggressive, metastatic, triple-negative breast cancer. It
had already spread to distant organs from their breast. They'd
(22:41):
already failed every line of treatment that was available to them.
They were really out of options. And so we gave
them combination therapy to block this conversation – and I gotta
digress – the name of the molecule that the cancer cells
use to signal to the fibroblasts is hedgehog. And this
is what happens when you let, like biology geeks name genes. Anyway.
(23:05):
So we gave one drug to block hedgehog, and another
drug was the chemotherapy that these patients were failing to
respond to. Now the most important thing was this was
well tolerated. It wasn't particularly toxic, no more than the chemotherapy.
But more importantly, three patients showed clinical benefit, and one
of them actually had a complete response to the drug.
(23:25):
Now these are really early days. It's what we call
a single arm trial. We didn't have a comparison group,
patients who only got chemotherapy, for example, so it doesn't
prove that the combination worked. But it's nonetheless really provocative,
really exciting and gives us reason to now want to
progress to further lines of clinical trial, to directly test
(23:46):
the value, the benefit to patients. For this.
Dr Viviane Richter (23:48):
That's incredible. It must be so motivating to see that effect
in patients.
Prof Alex Swarbrick (23:53):
Yeah, it it really is. I mean, even if it's
just one person getting clinical benefit for I don't know,
a few months, we don't really know. But nonetheless, it's
an incredible feeling, so motivating and makes the, you know,
four or five years of slog for all the students
and postdocs in the lab worth it.
Dr Viviane Richter (24:12):
So much has been invested in finding a cure for
breast cancer. Do you think we'll get them?
Prof Alex Swarbrick (24:18):
I think we already are. I think it depends how
you think about it. Whether we will cure every breast cancer
is a pretty massive goal, and I think that's a
long way off to be realistic with you. But at
the same time, you know, you can think of an
analogy of we're picking off the low lying fruit in
a way, if you think of the tree and some
(24:39):
cancers are easy to treat, they are relatively non-aggressive, and
we have incredible treatments for them now. And so we
we cure a majority of patients with breast cancer that
come in with a diagnosis. They're cured. They will not
die from breast cancer in their lifetime. And gradually, that
proportion of people who are cured is increasing year on
year on year. And in fact, there have been phenomenal
(25:00):
new developments in the last few years that are not
just microscopically turning the dial but really changing things for patients.
But I think we need to be realistic that at
least in my lifetime, there will be cancers that we
can't cure. Exactly why? It's a multitude of reasons. It's
partly probably based on the individual properties of the person
(25:24):
who has the disease. We know now that your immune
system is an essential component to responding to many therapies,
and we're all different in that way. But also it's
probably a lot to do with the features of the
cancer itself. The combination of oncogenes, for example, that this
cancer has acquired determines its aggressiveness. So I think there
(25:45):
are always gonna be, at least in the foreseeable future,
classes of cases that are beyond our reach. But I
think what really drives us on is that we are
still making really major game changing insights into how to
treat breast cancer. And when I say we, I mean
the global breast cancer research community, we're nowhere near levelling out.
(26:07):
It's not mission accomplished by any means. There are still
so many patients in need, but I think so many
opportunities for us to change their lives.
Dr Viviane Richter (26:17):
Alright, Alex, we've already learned a lot about you, but
it's time we dug a little deeper. It's time for
the fast five. What do you do in your downtime?
Prof Alex Swarbrick (26:27):
Well, I have two kids. Two teenage kids love to
spend time with them when they will agree to spend
time with me. Otherwise, love seeing my friends play a
bit of guitar. I'm not really so inspired by the
kind of computer music anymore. Rather, I just torture people
with some guitar playing.
Dr Viviane Richter (26:44):
Lovely. Any favourite tunes that you like to bust out?
Prof Alex Swarbrick (26:47):
I like campfire repertoire is kind of what I hit.
So I'd say probably Jeff Buckley Hallelujah. You know, great example.
Dr Viviane Richter (26:56):
Classic! Any secret skills?
Prof Alex Swarbrick (26:57):
Oh, love cooking, couldn't really claim to be fantastic at it.
Make an unbelievable salad dressing, though.
Dr Viviane Richter (27:04):
Favourite holiday?
Prof Alex Swarbrick (27:05):
Would have to be around the world trip with my
wife in our twenties, we went through Central, South America, USA, Europe.
Just fantastic. Living on noodles every day. Wonderful.
Dr Viviane Richter (27:18):
Are you reading anything interesting at the moment?
Prof Alex Swarbrick (27:20):
I've just finished All the Light We Cannot See, which
is a really beautiful book set in World War II, story
of two kids kind of surviving. But then they find
each other in the rubble of Europe. It's really beautiful.
Dr Viviane Richter (27:36):
Who do you admire?
Prof Alex Swarbrick (27:38):
I think my colleagues Elgene Lim, for example. He's a medical oncologist
that I work with. He is just such an energetic, kind,
giving person. He is super inspiring. Similarly, my colleague Sandra O'Toole,
who's a pathologist, she works at RPA. She's an absolute powerhouse,
somehow just makes it all work and is kind and
(28:01):
funny at the same time. So I'm so lucky to
be surrounded by people that I really think are fantastic.
Dr Viviane Richter (28:08):
Is there anything you're afraid of?
Prof Alex Swarbrick (28:10):
Yeah, many things. I'm terrified of spiders. If there's a
spider in the house, I run. Thankfully, my wife is
like a ninja spider hunter, and she'll just catch them.
Chuck them outside.
Dr Viviane Richter (28:21):
Do you play any sports?
Prof Alex Swarbrick (28:22):
Yes, I love playing tennis. That's my thing.
Dr Viviane Richter (28:25):
Who's your favourite tennis player?
Prof Alex Swarbrick (28:27):
I would have to say Alcaraz, the Spanish player. He
is just an absolute phenomenon. Has every shot in the
book and he's 19 or something? So yeah, just I
don't know. You could have got the sense that tennis
was would never improve any further past, you know, the the greats.
But he's come along and just changed the game again.
Dr Viviane Richter (28:49):
Professor Alex Swarbrick. Thank you so much for joining us
on Medical Minds.
Prof Alex Swarbrick (28:53):
Oh, thanks so much for having me. It's been great fun.
Dr Viviane Richter (28:56):
If you'd like to know more about Alex's research or
the work we do at Garvan, head to garvan.org.au. And
if you've enjoyed this podcast, please leave a review and
share with other podcast lovers. I'm Dr Viviane Richter. Thanks
for listening. This podcast was recorded on the traditional country
(29:17):
of the Gadigal people of the Eora Nation. We recognise
their continuing connection to land, waters and community. We pay
our respects to Aboriginal and Torres Strait Islander cultures and
Elders past, present and emerging.
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