(modern electronic music)
- I'd like to introduce you to two incredible professors.
Professor Luda Bard and Dr. Kathryn Jones.
Professor Luda Bard received her undergraduate degree
in Chemistry and Biochemistry
from the University of Maryland, Baltimore County,
and earned a master's degree in Applied Molecular Biology.
Following graduation, she worked at John Hopkins University
in the Psychiatry Department studying schizophrenia.
She started teaching at HCC in 2003
and became a full-time faculty member in 2007.
She currently teaches and is Course Coordinator
for a number of courses,
including Fundamentals of Microbiology, Genetics,
Genetics Lab, Cell Biology,
Biology for Engineers, and Computational Biology.
She currently is co-chair
of the Council for Curriculum Integrity.
Dr. Kathryn Jones received her undergraduate degree
in Biology from the University of Pennsylvania,
and earned a master's and Ph.D in Genetics
from Albert Einstein College of Medicine.
She then worked for 30 years as a scientist,
doing basic research on HIV and related viruses.
Spending the last 20 years as a Principal Scientist
at National Cancer Institute, she joined HCC
as an adjunct professor five years ago,
and is currently teaching Genetics, Genetics Lab,
and Cell Biology.
She also consults for BioInteractive,
a not-for-profit organization which provides materials
that help educators teach Biology.
Now can you please give me a round of applause
for these professors?
(audience applauding)
- [Luda] Thank you, Amanda.
- Welcome, everyone.
Welcome to our nice, SET, beautiful building.
Tonight I'm gonna be talking to you
about some exciting advances that have happened
over the last 15 years in Genetics.
And in particular, I'm gonna talk to you
about some new genetic tests
and how they're changing medicine,
and also can provide you with more information
about who your ancestors are.
So, wait a second, who are you?
- Hi, everybody!
I am from the future!
I actually teach in this classroom in 2068.
And, you know, I was teaching Genetics,
and my students asked me about genome sequencing,
and I figured, oh, you know,
I might as well come here in 2018, right?
So I used this Musk's time machine
(audience laughing)
and you know, here I am.
- Wow, 2068, that's 50 years from now!
What's HCC like in 50 years?
- Ah, you know, same old.
(audience laughing)
I guess, I'm not wearing them,
but bell-bottoms came back.
Patti Turner is still our dean!
(audience laughing and clapping)
And Trump is still the president.
Oh yeah, and the students are much younger than you guys.
- No, these aren't actually our, nevermind, okay, so.
Since you're here from the future,
I was just gonna tell them about DNA and genes
and how they provide the instruction manual for life.
But since you're here from the future,
why don't you start off?
- Okay, here is the molecule of DNA.
And this is your blueprint, and really,
an instructional manual for all of your cells.
You have this instructional manual in all of your cells
and all of the living organisms have DNA inside.
And it starts with your mother's egg,
that is joined by your father's sperm.
And then you have a fertilized egg,
that has DNA molecule in it.
And when the cell goes through celllular divisions,
which is basically like making copies,
making exact copies of the cell,
they also replicate the exact copy of your DNA.
So, at the end of this, you have many cells.
Each cell will contain the same instruction manual.
And then, eventually, and you have to wait for it,
nine months...
You will have a baby!
And so, inside of this baby you have cells,
inside of all of those cells, instruction manual
that gives instructions for the cell.
So, for example, the instruction manual
inside of all of your cells will give you instructions
for your heart to beat, for your eyes to see,
and send a message to your brain,
for your ears to receive signals,
and then they will go also into your brain.
So all of that is done via DNA.
All right, so the fancy term that we going to use
for the collection of all of the DNA is going to be genome.
Can you guys say genome?
- [Audience] Genome.
- Excellent, you guys a great audience, all right.
So, and usually DNA molecules are found on chromosomes.
So, I will not make you repeat that.
You did well with genome.
Okay, so, just like any instruction manual
is composed of letters, in English language we have 26.
I'm from Russia, how many letters are in Russian alphabet?
- [Kathryn] Oh, good.
- [Luda] How many?
- [Audience Member] 33.
- 33, you got my last machine!
(audience laughing)
Yay, very nice, good job.
All right, so, in the language of DNA,
we have only four, A, T, C, and G.
And to just give you a little bit of perspective,
in our genome, we have three billion of those letters.
And again, to just put it in perspective,
it's like counting all of the letters
in Harry Potter series, and multiplying it times 800.
And this slide of course came from Dr. Jones,
because in 2068, there are many more Harry Potter books.
(audience laughing)
So, okay, how do we do all of this?
Well, in DNA, we have segments that we call genes.
And the segments will code for specific molecules
that actually do some work inside of the cells.
And those molecules are called proteins.
So, the proteins
are being made by reading the sequence of those letters.
And then based on the sequence of letters,
we will put amino acids that are going to build a protein.
And once the protein is made,
just like a long thread of amino acids,
they don't stay like this,
they actually do fold and form very specific,
three-dimensional structure.
And this three-dimensional structure comes
from the sequence of those amino acids.
And it's very, very specific, depending on the letters
inside of the genes.
So, for every gene there will be a protein
with specific shape and size.
And of course, that shape and size
will determine the function.
Okay, so based on how you guys look,
I'll try to make it a little bit easier.
So, you guys know Legos, right?
We still play them, right?
Yeah, in 2068, too.
Kids are crazy about them.
Anyway, so the Lego, the instructions for the Legos.
You follow the instructions,
you take a specific Lego piece, it's a certain color.
You put it in a certain order, and then you have a truck.
Okay, the same way we read a gene.
Based on what we read,
we going to take amino acid of specific type,
we going to put it into the thread of amino acids,
and then, at the end of this all,
we going to get a protein.
Now, you could imagine
that if you don't follow instructions well,
or there's something wrong with the instructions,
for example, instead of the wheels,
if I were to place these brown thingies,
then your truck is no longer functional.
The same way, if you put a wrong amino acid
in your protein because you have a wrong A, T, C, or G
in your DNA, you will not get the shape
that you really need for the properly functional protein.
So, a classic example of this is hemoglobin.
Hemoglobin is a protein that carries oxygen
throughout the blood.
And one of the parts of the hemoglobin is beta-globin.
And this is a protein that is very important
for hemoglobin to function.
So if there is a change in the letters,
you can see the highlighted area,
you see that there is A in the mutant beta-globin,
the mistake, where there's supposed to be a T.
So if that mistake was made,
the protein is no longer folded correctly.
And when the protein is no longer folded correctly,
cannot function.
And if you have two copies of those variants,
you don't have a properly functioning hemoglobin,
and your red blood cells look like sickles.
This is sickle cell disease.
In 2068, we fixed it all before babies are born.
Okay, so don't worry, bright future there.
- So, for about 75 years,
we've already known what you spoke of before.
That DNA consists of A, T, Cs, and Gs.
And we knew that it had a code and it could make proteins.
And that proteins made who we are.
But until recently, we didn't have any way to read it.
When we looked at a piece of DNA,
we didn't know what it said.
About 1980, a technique was developed called sequencing.
When you have sequencing, you can take a little piece of DNA
and look at it, and using a special machine,
you can read A, T, G, G, C.
And then you can decode it and know
what kind of protein is encoded by those genes.
That was about 1980.
About five, eight years after that,
a group at the National Institutes of Health
nearby here in Bethesda decided to start
on an ambitious project
to sequence all of the three billion bases
in the human genome, to read all those letters.
Now, for a biologist, this was our version
of trying to get a man on the moon.
It was a huge, ambitious project
that we barely had the tools for,
but we were gonna try to do.
And so what these guys did,
was they called it the Human Genome Project,
and they got literally thousands of scientists
around the world to help them with this huge project,
and went to 20 different institutions
at six different countries,
and they had people to start to sequence the genome.
The first problem they had was they could only sequence
a few hundred base pairs at a time.
And the genome is three billion base pairs.
So the first thing they had to do was chop it up
into about a hundred million pieces.
And not only that, they had to know like a jigsaw puzzle,
how to put the pieces back together when they were finished.
That took about five years,
and then they started to actually sequence
all of those hundred million little pieces.
So around this time, there was another man,
a man by the name of Craig Venter,
who was a businessman and scientist,
who thought that he might be able to finish the job,
since the National Institutes of Health and the consortium
had published this data to the world.
He thought, since he'd done the hard part, sort of,
that he might be able to beat them and get credit for,
with his company, for sequencing the human genome.
So there started this huge race, and in 2003,
the Human Genome Project published the first sequence
of the entire human genome.
And the next day, Craig Venter and Celera Genomics,
his company, published it as well.
So both men, does anyone remember this?
It was a big pretty deal at the time, right?
You guys remember this?
And so not only did they get their faces
on the cover of Time Magazine,
but they were invited to the White House to celebrate.
And they shared the fame.
So you may be wondering who was the first person
to get their genome sequenced?
So, the first person for the Human Genome Project
was James Watson.
Anyone heard of Watson and Crick, right?
So, James Watson was one of the co-discoverers
of the double helix of DNA.
And Celera Genomics,
their first person sequenced was the CEO. (laughing)
So, now you might be wondering,
Professor Bard and anyone,
if we've known how to sequence
the sequence of the human genome for 15 years,
why are you just starting to hear about genetic tests
in the last few years?
The reason for that, like so many things in life, is cost.
If you had gotten your genome sequenced 10 years ago,
in 2008, it would have cost you about a million dollars.
And the cost has gone down precipitously since then,
to the point when you can now sequence a genome
for just a few thousand dollars.
So another thing you might be wondering is what we found out
when we started decoding the genome,
when we read our instruction manual.
And I can say as a person who got her degree in Genetics
before this all happened, there were a lot of surprises.
And one of them was,
we started sequencing the genome of other organisms
who were close to us.
We found out that we were way more closely related
to these other groups than we'd previously believed.
So our closest relative is a chimpanzee.
And when we looked at our genome,
we were 99% identical to the genome of a human.
So, meaning, of course, that means that only one out of 100
base pairs are different between us and chimpanzees.
With orangutans, we're about 98% the same.
Bonobos, we're also 99% the same.
And even with things like mice,
the areas, the genes themselves are very similar.
Which makes sense if you think about
that we've used some of those animals
as model organisms for us.
Another thing we found out, it was very surprising,
is when scientists were able to get DNA
from a 38,000-year-old body of a Neanderthal
that they found in a cave in Europe.
So, one of the things we found out, and this was a shock,
was that many of us in this room
have Neanderthal DNA in our genome.
So, how did that happen, why was that a surprise?
We knew that Neanderthals lived at the same time
as early humans, early homo sapiens,
but we thought that we were different species,
like a horse and a zebra.
That we couldn't mate and have children.
Well, it turns out we must've, because a lot of us
have Neanderthal DNA.
So who in the room thinks
that they might have Neanderthal DNA?
Everyone raising their hand is right,
because probably, just about, because really everyone
who isn't purely African in their ancestry
do have Neanderthal DNA.
And that's because, you know, humans,
homo sapiens started in Africa.
When we came out of Africa and moved into Europe,
that's where the Neanderthals were.
So everyone in this room who's Asian,
or European in their ancestry,
has about two or three percent Neanderthal DNA.
Another surprise came when we started looking,
when we did more and more sequences,
and did the genomes of a lot of different
humans around the world.
We found out that, it's not surprising,
that people are different from one another.
I told you that we're 99% the same as a chimp,
so maybe it's not surprising,
we're 99.9% the same as each other.
But what was a surprise was the places
where we were different.
So it used to be believed,
we used to believe when I got my Genetics degree,
that those differences would just be scattered
around the genome.
And it turns out that's not true.
Nearly everyone in the world has the same letter
in the same place almost everywhere in your genome.
So we all have a G, and we all have a T,
and we all have a G, T, G.
And then you'll get to a place
where some of us have a C and some of us have a T.
And even though that difference
is just one out of thousand base pairs,
it can make a big difference in how you turn out.
So these differences are called SNPs,
single nucleotide polymorphisms.
So SNPs, you might have heard of these.
And how it winds up, is if you look around the world,
maybe most people have an A,
but there's a significant number of people,
like 5% who have a T, or maybe, and 12% who have a G.
So looking at Americans and Europeans,
they got a feeling for these differences.
But it wasn't 'til they started to go around the world,
and sequence a genome of peoples
whose ancestors had always lived in that place,
that they started to figure out what was going on.
So it turns out, if you look around the world,
you find out that nearly everyone with a T
is from Scandinavia or Northern Europe.
And everyone with a G, let's say, is from Asia.
So how did that happen?
Professor Bard told you, that when we start off as a baby,
when a cell divides, the DNA in that cell, that genome,
also has to make an exact copy of itself,
and pass it on to the next generation.
Very, very rarely, mistakes are made.
Even more rarely, a mistake happens in a cell
that winds up becoming a sperm or an egg.
So if, a long time ago in a Norwegian village,
a man had a mutation when he was making sperm,
and now they had a T there instead of an A,
a mistake was made during the copying.
Now, they would give that to their child
and every cell in that child would then have the T.
Now, back in those days, 20,000 years ago,
you kind of tended to marry your cousin,
or at least someone in the village, right?
And so, then everyone in that village,
or many people, would wind up getting a T.
So eventually that would spread,
and so you'd see a region of the world now
that most people there have a T,
whereas other people have an A.
And by this, I would then say the same happening,
what is now China, let's say 50,000 years ago.
So people there have a G.
So now, if you just look at one of these,
you can't tell, there's enough variation.
But if you looked at hundreds,
or if you looked at thousands of them, at these SNPs,
at these places we're different,
you could tell where a person is from.
And that's exactly what those genetic tests
you've probably have seen advertised,
that's what they're doing.
They're looking at hundreds or thousands of your SNPs,
and then from that, guessing where you're from.
Has anyone in the audience had one of these done,
to determine their ancestry?
Wow, that's cool!
Any big surprises?
Don't tell me.
(audience laughing)
And that's why, when you get the data,
for those of you who've done it,
you get something like this, right?
'Cause that's what they're telling you.
They're just telling you, you have the SNPs
that are like the people who live in those places,
whose ancestors came from those places in the world.
So, Professor Bard told you earlier about genes.
So, most of these SNPs are not in genes.
She showed you there's genes along the genome,
along the DNA and the genome, and there's spaces in between.
And it turns out there's big spaces
and a lot of people,
most SNPs don't have any effect on us at all.
'Cause they're not in the part of the genome
that codes for a protein.
They're in the places in between.
We just use them as a measure to tell,
to find out information.
There's a few of them that are in genes.
One of them, in Europeans, people of European ancestry,
there's one place that codes for a protein
that determines hair development.
And if you have an A, you're gonna have straight hair.
And if you have a T, you're gonna have curly hair.
And another place they recently found out,
they knew there was one that would definitely tell
people from Europe from people from Africa.
And that's inside a gene that codes for skin color.
It's one of the major ones that codes for skin color.
So the reason that people in different parts of the world
have different skin color,
is because of variation SNPs in coding regions
for proteins that are important
in making the color of our skin.
So as I told you for the other thousand base pairs or so,
almost everyone has the exact, same genome,
sequence in their genome.
But that's almost everyone, but not everyone.
So there's many, many places in genes
where we almost all have the A,
that makes the truck with the wheels, right?
But a few of us have a T that has the blocks
on the Lego thing instead, right?
That has an incorrectly folded protein
instead of a correctly folded protein.
And those are the ones that can cause disease.
So now, we're getting to the part
about what we can do in 2018
and how this is affecting medical care.
You can go to a doctor and they can test you
for some of these genes
and find out if you have the normal protein
or the protein that would lead to disease.
And one example of how this is happening,
and I think many of you might be surprised to hear this,
in every newborn baby in America,
is tested before they leave the hospital,
for certain genetic diseases.
And here in Maryland, we're actually doing a lot of that.
Here's a pamphlet that the parents get
and when they have the newborn babies,
before they leave the hospital,
we test for mutations and it's 58 different genes.
So what they're doing is they're just getting a bit
of the baby's blood, they're looking for these changes,
and seeing if they have certain diseases.
Now, they don't test for every disease.
They're only testing for diseases
that might cause a physical impairment
or intellectual disability.
But, if you caught them early enough,
you could prevent the disease, or even at least,
make it less than it would be if you didn't know about it.
So the babies are getting tested specifically
for the presence of a disease
that they could do something about if they intervene early.
And for some of these, it's as simple as keeping a diet,
not taking a certain amino acid.
You can have a normal life
instead of being mentally disabled.
So it's a really remarkable thing we're doing now.
So that's an example of what genetics is doing now
that it wasn't doing 10 years ago.
- So I'm really curious about the treatment.
So how many of you were prescribed medication,
by a doctor, that was not effective?
You had to go back to your doctor
and get a different medication.
And that medication had, let's say, side effects.
And then you go back to your doctor
and you get prescribed yet another medication.
Raise your hands, just curious.
Okay, so what you experience is called traditional medicine.
Which is basically when we think we develop a drug
that works on a lot of people.
And for some of the people it is either not effective,
or it has horrible side effects.
But we're okay with that, because it works in some.
And so the doctors feel that eventually they will find
the drug that will work for you by trial and error.
Even though there is a wonderful thing that we,
actually in 2018, you guys have a little bit
of what is known as personalized medicine.
I experienced that when I got my glasses.
When you go to a glass doctor, eye doctor,
you get your specific prescription.
They don't give you a generic pair, right?
So we hope that very, very shortly, very soon,
you will experience what's known as personalized medicine.
Which is, basically you go to the doctor,
you get genetic tests done, and based on your SNPs,
based on your variants of your genes,
we prescribe medications.
And these medications work for you, on you,
and they work from the first time
because it's based on genetic evidence,
rather than, let us guess and hope.
So, just to give you a little bit of statistics.
So you understand about traditional medicine.
If you look on this slide, you can see that,
basically, almost more than 50% of the patients
who receive drugs for arthritis, Alzheimer's, and cancer
do not find these drugs effective.
So with traditional medicine, we give one type of drug
to all of the patients.
This drug works on some, does not work at all on others,
and causes terrible side effects on the third group.
We learned that this is partially due to one gene
that is called Cytochrome P450.
You guys don't need to remember that.
But this codes for a protein that removes drugs
and toxins from your system.
So some of us have very effective, very well-working protein
that removes drugs from the system fast.
Which makes drugs not effective,
because it's removed before it has a chance to work.
Others have a normal working protein
and so the drug has some time to work in the system.
And others have very, very slow-working protein.
So the drug stays in the system,
becomes a toxin for your system,
and causes terrible side effects.
So it would be great if we could do genetic testing,
find out what type of Cytochrome P450 you have,
and based on that, not only we could determine
what type of drug you could have, but also,
we could determine the dose.
So, for example, if you have a P450
that is slowly removing the drugs from your system,
well, doctors, tell me what you're gonna do?
Halve the dose, right, reduce the dose!
Very good!
Or, if you have a protein that works super fast,
and removes the drug before it could be effective,
what are you gonna do?
Increase the dose, yeah!
And all of that based on your genetic information.
Of course, we can apply similar approach
to many fields of medicine.
In psychiatry, for example,
we have problems with feeling anxious or depressed.
And so let me tell you why people feel depressed or anxious.
You guys probably know that the signal traveled
from one cell to the other.
And the signal, when it traveled,
for it to go from one cell to the other in your brain,
you need to release certain molecules
that we call neurotransmitters.
More specifically, serotonin.
You feel calm and happy when you have a lot
of serotonin molecules in between those two cells.
Once the signal was passed to the next cell,
serotonin molecules (whooshing)
send back to the cell that originally send them out.
If you don't have serotonin between the two cells,
you feel depressed and sad and anxious.
For some of us, the reuptake,
the taking the serotonin molecules back,
is actually too efficient.
The molecules that work really well for taking the serotonin
back into the original cell is too fast.
And so there are not enough serotonin molecules
in between the two cells.
Well, we developed drugs to fix that.
And the drug basically blocks the molecules
that send the serotonin back.
So that, like Prozac on this picture,
blocks the molecule that sends the serotonin back.
Serotonin stays between the two cells longer,
and you're no longer depressed or anxious.
We could apply the same personalized medicine approach
to doing genetic tests and finding out why exactly
we have psychiatric problems,
what neurotransmitters are missing,
what is the mechanism, and address exactly that,
rather than trying to guess which drug will work for you.
- [Kathryn] We do have these genetic tests.
Doctors, psychiatrists, and other therapists
are starting to use these.
So this whole group you know about,
these are called SSRIs, you might have heard that word.
Those are the ones like she just showed,
that block the uptake back in the cell.
So Prozac, Zoloft, they're all doing the same thing.
Well, different ones work slightly differently.
And so people are doing genetic tests
so they don't have to have the things
of trying the drug for eight weeks,
and then seeing it doesn't work, and trying another one.
So one of the other areas right now
that we are just starting,
and really holds a lot of promise,
is cancer drugs.
'Cause I'm sure there's probably not a person in this room
who doesn't know only too well,
that even if someone gets a treatment for cancer,
it often doesn't work.
And the reason for that has to do with,
because each person's cancer is a little different.
So to understand this, I just have to talk a second
about how normal cells divide and what cancer is.
So cancer is when a cell divides without stopping.
And in a normal cell,
most cells in our body aren't dividing most of the time,
if they get a certain signal, they will divide,
but then they'll stop dividing.
If they don't get the signal anymore,
they won't divide anymore.
We have about 150 different genes that control that.
And if one of 'em's wrong, you're okay.
So they control the fact that a cell is supposed,
when it stops dividing, it stops dividing,
it doesn't keep dividing.
We have about 150 different genes,
we know almost all of them now.
And those genes, if maybe you have four, or five,
or six of them that aren't functioning anymore,
because they have a mutation,
the protein isn't working correctly,
you now no longer can stop the dividing,
and you get a cell that divides without stopping.
So an example of how we're making improvements,
and we're gonna even continue into the future,
is breast cancer.
So in breast cancer 40 years ago,
if you had breast cancer, you had breast cancer.
They treated it in a way that helped the most,
the highest percentage of the patients,
which was chemotherapy and radiation.
But still, a lot of people died.
About 20 years ago, 15, 20 years ago,
doctors and scientists started looking
at individual people's breast cancer tumors,
to see if they could tell them apart.
And they learned that they could divide them
into three different groups, three different subtypes,
based on certain proteins that were on the cell surface.
So again, if you know someone who's had cancer,
you might've heard these words.
HER2-positive, ER-positive, or triple-negative.
And it turns out, in each one of those,
you have a different set of proteins
that aren't functioning correctly.
And it turns out, for each one of them,
there's a different treatment
that treats that kind of cancer the best.
Nowadays people get their breast cancers subtyped,
and they're treated specifically for the changes
that are in their tumor.
All right, so now...
We've gone to the next step.
Now that we can sequence the genome,
we're starting to look in an individual's cancer
for more genes to understand better which genes are broken.
And so you can know which ones to target
in the cancer therapy.
So in this case, this isn't sequencing your genome.
It's actually often sequencing your genome,
and then the cancer cell's genome.
It's called a cancer genome.
And you're looking for the differences.
So you can tell what it is in your cancer
that's causing it to be a cancer cell.
So you can target that better.
And one of the first people
who had this done was Steve Jobs.
When he was dying of cancer,
he actually paid to have his own genome
and his tumor sequenced,
with hope that it would help others in the future.
One of the best places in the world, I have to say,
for this is Johns Hopkins.
They've been one of the leaders,
and they're still one of the best people in the world.
And we're learning a lot from that.
So, that's just one example of personalized medicine
that's just starting now.
And I think we'll be improving
medical treatments in the future.
So up to now, when we were talking about sickle cell disease
or these cancers, we're talking about changes
that actually directly cause a disease.
And when we talked about the newborn baby screening,
it was showing that if you had a certain genetic change,
you had a defective protein
which would mean you would have the disease.
But for thousands of years,
as you can see from this Chinese text,
doctors have been trying to take it back a step.
Wouldn't it be good if we could prevent a disease,
instead of just treating diseases?
So, this is the next stage of genetics,
and something that I think most people in this room
will have tested in five or 10 years
for some of these things.
So an example is cancer.
There are cancer genes.
So you've probably heard, oh those people have,
breast cancer runs in their family.
You know, lung cancer runs in their family,
for different families.
It turns out that we now have identified
a number of the proteins that make a person
more likely to develop a cancer.
So this is just a screenshot from one of the companies
that's used, that doctors are using now.
So they don't test everyone with this,
they test people who think they have a certain cancer
in their family, to see if they have one of these genes.
Now, again, this is different
from what we talked about before.
If you have one of these genes,
it doesn't mean you will get cancer.
It means you're much more likely
to get cancer than other people.
So you can imagine though, along with your behavior,
and working with your doctor, if you knew you were gonna
be more likely than someone to get colorectal cancer,
you could do all that stuff like eat a high-fiber diet,
and eat lots of fruits and vegetables,
and the stuff you're supposed to do,
to try to reduce your chances.
You also probably wouldn't put off your colonoscopy.
And you would get it, that's what people do,
they do it like every two years or so,
and then remove polyps so that they can't become cancerous.
Same thing, if you knew you were more likely
to get lung cancer, you probably would have
a lot of motivation for quitting smoking.
Probably the most famous cancer gene,
one some of you might have heard of,
is called BRCA1.
So individuals with BRCA1, women with BRCA1,
have about a 50/50 chance of getting breast cancer
by the time they're 70.
And that's as opposed to women who have a normal gene
in BRCA1 who don't have the mutation,
where it's about 12%.
And attention to this one
has been brought by Angelina Jolie.
Because she actually has a mutation in her gene.
Her mother died when she was 50,
and at the time she had a lot of small kids.
So she decided to go get herself tested.
And when she did, she found out
that not only did she have a mutation in BRCA1,
but she had one of the worst versions,
one of the worst mutations.
So she had an 85% chance of getting breast cancer
by the time she was 70.
And so she decided to have a prophylactic double mastectomy,
which reduces your chances to almost zero,
'cause you don't have any breast cells anymore
that could become cancerous.
So she was very out about this,
she did an editorial in The New York Times.
And she's done a lot to raise awareness for BRCA1
and to encourage testing in people
who have a history of breast cancer in their family.
So that's about where we are in 2018.
But I'm pretty curious to see what's gonna happen
in the next 50 years.
Why don't you finish up?
- The future is really bright!
There certainly will be a lot of gene editing.
Gene editing is happening right now,
and it will be developing at greater pace.
A lot of the prenatal diagnosis will take place.
And genome sequencing is going to go
to the next level.
So, you probably saw this on Google News.
Well, this is very cool.
And this is called a minion.
And this is a small machine
that allows you to go to your doctor,
get a sample of your DNA,
and to test your entire genome sequence
right then and there.
By plugging it into your laptop,
you can put DNA through the little tube, a channel,
and every letter A, T, C, and G,
oh I should have asked you guys that,
(audience laughing)
goes through this test tube and it has a different current
that could be read by this machine.
And right there, at your doctor,
you could get your entire genome sequence.
Now, do not confuse that with 23andMe, okay?
That test that you can get
for however many dollars right now.
That test only segments off your DNA.
This can test your entire genome.
And it would be very nice, if by using that information,
your doctor could actually prescribe
personalized medication, right?
And figure out your treatment based on your genetic makeup.
So, of course, all of that will require
a lot of ethical discussions, political discussions,
that will happen by 2068.
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