How cancer cells communicate and how we can slow them down Hasini Jayatilaka
Cancer.
It’s a devastating disease
that takes an enormous emotional toll.
Not only on the patient,
but the patient’s loved ones, as well.
It is a battle that the human race
has been fighting for centuries.
And while we’ve made some advancements,
we still haven’t beaten it.
Two out of five people in the US
will develop cancer in their lifetime.
Of those, 90 percent will succumb
to the disease due to metastases.
Metastasis is a spread of cancer
from a primary site to a distal site,
through the circulatory
or the lymphatic system.
For instance, a female patient
with breast cancer
doesn’t succumb to the disease simply
because she has a mass on her breast.
She succumbs to the disease
because it spreads
to the lungs, liver,
lymph nodes, brain, bone,
where it becomes unresectable
or untreatable.
Metastasis is a complicated process.
One that I’ve studied
for several years now.
And something that my team
and I discovered recently
was that cancer cells are able
to communicate with each other
and coordinate their movement,
based on how closely packed they are
in the tumor microenvironment.
They communicate with each other
through two signaling molecules
called Interleukin-6 and Interleukin-8.
Now, like anything else in nature,
when things get a little too tight,
the signal is enhanced,
causing the cancer cells
to move away faster from the primary site
and spread to a new site.
So, if we block this signal,
using a drug cocktail that we developed,
we can stop the communication
between cancer cells
and slow down the spread of cancer.
Let me pause here for a second
and take you back to when
this all began for me in 2010,
when I was just a sophomore in college.
I had just started working
in Dr Danny Wirtz’s lab
at Johns Hopkins University.
And I’ll be honest: I was a young,
naive, Sri Lankan girl,
(Laughter)
who had no previous research experience.
And I was tasked
to look at how cancer cells move
in a 3D collagen I matrix
that recapsulated, in a dish,
the conditions that cancer cells
are exposed to in our bodies.
This was new and exciting for me,
because previous work had been done
on 2D, flat, plastic dishes
that really weren’t representative
of what the cancer cells
are exposed to in our bodies.
Because, let’s face it,
the cancer cells in our bodies
aren’t stuck onto plastic dishes.
It was during this time
that I attended a seminar
conducted by Dr Bonnie Bassler
from Princeton University,
where she talked about how bacteria cells
communicate with each other,
based on their population density,
and perform a specific action.
It was at this moment that a light bulb
went off in my head, and I thought,
“Wow, I see this
in my cancer cells every day,
when it comes to their movement.”
The idea for my project was thus born.
I hypothesized that cancer cells
are able to communicate with each other
and coordinate their movement,
based on how closely packed they are
in the tumor microenvironment.
I became obsessed with pursuing
this hypothesis.
And fortunately, I work for someone
who is open to running
with my crazy ideas.
So, I threw myself into this project.
However, I couldn’t do it by myself.
I needed help.
I definitely needed help.
So we recruited undergraduate
students, graduate students,
postdoctoral fellows and professors
from different institutions
and multiple disciplines
to come together and work on this idea
that I conceived
as a sophomore in college.
After years of conducting
experiments together
and merging different ideas
and perspectives,
we discovered a new signaling pathway
that controls how cancer cells
communicate with each other and move,
based on their cell density.
Some of you might have heard this,
because most of social media knows it
as the Hasini effect.
(Laughter)
(Applause)
And we weren’t done yet.
We then decided that we wanted
to block this signaling pathway
and see if we could slow down
the spread of cancer.
Which we did, in preclinical
animal models.
We came up with a drug cocktail
consisting of tocilizumab,
which is currently used to treat
rheumatoid arthritis,
and reparixin, which is currently
in clinical trials against breast cancer.
And interestingly, what we found
was that this cocktail of drugs
really had no effect on tumor growth,
but directly targeted metastases.
This was a significant finding,
because currently, there aren’t any
FDA-approved therapeutics
that directly target the spread of cancer.
In fact, the spread of cancer, metastasis,
is thought of as a byproduct
of tumor growth.
Where the idea is, if we can stop
the tumor from growing,
we can stop the tumor from spreading.
However, most of us know
that this is not true.
We, on the other hand,
came up with the drug cocktail
that targets metastasis
not by targeting tumor growth,
but by targeting the complex
mechanisms that govern it,
through the targeting
of the Hasini effect.
(Laughter)
This work was recently published
in “Nature Communications,”
and my team and I received an overwhelming
response from around the world.
Nobody on my team could have predicted
this sort of response.
We seem to have struck a nerve.
Looking back, I am extremely grateful
for the positive response that I received,
not only from academia, but also patients,
and people around the world
affected by this terrible disease.
As I reflect on this success
I’ve encountered with the Hasini effect,
I keep coming back to the people
that I was fortunate enough to work with.
The undergraduate students
who demonstrated superhuman powers
through their hard work and dedication.
The graduate students
and the postdoctoral fellows,
my fellow Avengers,
who taught me new techniques
and always made sure I stayed on track.
The professors, my Yodas
and my Obi-Wan Kenobis,
who brought their expertise into
making this work into what it is today.
The support staff, the friends and family,
people who lifted our spirits,
and never let us give up
on our ambitious endeavors.
The best kind of sidekicks
we could have asked for.
It took a village to help me
study metastasis.
And believe me, without my village,
I wouldn’t be here.
Today, our team has grown,
and we are using the Hasini effect
to develop combination therapies
that will effectively target
tumor growth and metastases.
We are engineering
new anticancer therapeutics,
to limit toxicity and to reduce
drug resistance.
And we are developing
groundbreaking systems
that will help for the development
of better human clinical trials.
It blows my mind to think that all this,
the incredible work that I’m pursuing –
and the fact that I’m standing here,
talking to you today –
all came from this tiny idea
that I had when I was sitting
at the back of a seminar
when I was just 20 years old.
I recognize that right now,
I am on this incredible journey
that allows me to pursue work
that I am extremely passionate about,
and something that feeds
my curiosity on a daily basis.
But I have to say,
my favorite part of all of this –
other than, of course, being here,
talking to you, today –
is the fact that I get to work
with a diverse group of people,
who make my work stronger,
better and just so much more fun.
And because of this, I have to say
that collaboration is my favorite
superhuman power.
And what I love about this power
is that it’s not unique to me.
It’s within all of us.
My work shows that even cancer cells
use collaboration to invade our bodies
and spread their wrath.
For us humans, it is a superpower
that has produced incredible discoveries
in the medical and scientific field.
And it is the superpower
that we can all turn to
to inspire us to create
something bigger than ourselves,
that will help make
the world a better place.
Collaboration is the superpower
that I turn to, to help me fight cancer.
And I am confident
that with the right collaborations,
we will beat this terrible disease.
Thank you.
(Applause)