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)