- [Narrator] It's good to know
because chances are you,
a loved one or a friend
are going to get cancer.
It's above 25%, okay.
25% chance or above that
someone gets cancer, okay.
So it's something that is critical.
Now as I mentioned,
we spend our entire lives
writing this line of cell
growth and cell death.
Cell death is critical to
shape our organs or tissues
as well as get rid of problematic
cells, such as cancer.
But we can't give too much cell death
because then organs start failing
and organs start dying because
we can't regenerate our tissues.
So we write this line, all of our lives.
Now, as we undergo life,
we're exposed to a number
of different things
in our environment that increase
our chances of developing cancer.
We call them carcinogens.
They're essentially they're
anything from UV radiation.
Most of the time, we're not
exposed to gamma radiation,
but x-ray's x-rays can increase
your chance of getting cancer.
That's why they usually shield your body.
When you have x-rays done in your teeth
or in different parts
if you've got a broken bone or whatnot,
just to minimize the exposure
of your other cells to x-rays
because they'll mutate your DNA
and increase your
chances of having cancer.
So we're gonna talk about
what ultimately causes cancer.
This is why we talked
about the cell cycle,
because that's what cancer is.
A disease of the cell cycle.
The cell regulates its growth,
where it says oh, I need
to divide every 24 hours.
That's what your skin does.
So the stem cells in your skin are saying
oh, clock's ready, okay.
We've replicated all of
our DNA time to divide.
And it just goes through
this every 24 hours.
What controls the cell
cycle are a series of genes,
just like genes that make
your hair a certain color
and your blood type, a
certain type and whatnot.
There are also genes
that regulate how fast the cells grow.
So like any gene, it can be mutated.
You can change the nucleic acid sequence
due to some type of radiation,
due to some type of chemical
like in a Twinkie or something or.
There are some foods that have carcinogens
and then they found that a lot
of the artificial sweeteners
and other things that we
use are highly mutagenic.
Where they have a high risk
of causing your DNA to mutate.
Chemicals that you may work in gardening
there's a lot of things that
we're now beginning to understand
that when they get absorbed into our skin
and get into our blood and whatnot,
have a higher rate and chance
of causing the cells to become cancerous.
Now, there's always
just your predisposition
based upon the genetics you've
gotten from your parents.
And at the very end of this lecture,
we'll talk about how you can inherit genes
that give you a predisposition to cancer.
And they don't give you cancer,
but they make you more dispose
to developing cancer
sometime in your lifetime.
All right, now with the few exception,
most of the cells in
your body are dividing.
Some occurred very rapidly,
divide very rapidly
others not so rapidly.
And there are ways to
increase this growth rate.
For example, you cut your skin.
Well, if it only grew every 24 hours
after you cut your skin,
it would take forever to heal.
So there are usually hormones
that can be secreted by
tissues that stimulate growth.
So you can artificially
accelerate cell growth
and you can retard it or
cause it to slow down.
So there are growth factors
that your body releases,
especially with teenagers
go through growth spurts.
That's what's going on is you're exposed
to these growth hormones
and these growth factors
that are increasing your
bone growth, increasing
all of these changes
that ultimately come down
to protein stimulation.
Now, what are they actually stimulating?
They're stimulating genes
that regulate the cell cycle, okay.
So this is how our body works.
We essentially, when we need
to accelerate cell growth,
we'll usually have some type of signal.
Like you damage your skin
and the cells are like oh,
and they release a signal and say hey,
you need to grow faster to repair
the damage to the tissue so that we can
do what we're supposed to be doing,
protecting the underlying
organs and things of that sort.
So there are certain key stop points.
Now these aren't the only ones there are,
but these are just a couple of examples of
some of these stuff points.
These are checkpoints that
you have to go through.
And if you don't have the
right papers so to speak,
meaning you don't have the
ability to go past this point.
Then the cell will
usually trigger apoptosis.
Because if you don't pass
one of these checkpoints,
then there's usually some
problem with the cell.
Now a lot of times, some of
us may have got gotten cancer
never even realized it because
the default kill yourself cell mechanism
in apoptosis got triggered.
And therefore the cells
never became cancerous
because they killed themselves.
But, there becomes a problem when
they ignore these checkpoints
and just run right through them.
So what are some of these checkpoints.
For example, the first one here
is a proofreading of your DNA.
If your DNA gets damaged so
much that the cells like,
you know what, just screw it.
I can't even make all these repairs.
If it's damaged beyond repair,
this will induce apoptosis.
In fact will show that this is
exactly what radiation
therapy essentially does.
Radiation therapy is
meant to cause the cells
to induce apoptosis by
not letting them pass this checkpoint.
So there's a protein.
In fact, this is one of the
most commonly mutated protein
that's gets inherited.
And the human species that
gives you a predisposition
to cancer, right.
That gene right there
that does that checking.
Now there's other checkpoints
after let's say you're like,
you know what, DNA is good.
We don't need to repair it too much.
So it'll copy all the DNA.
Cause there's not gonna
try to copy the DNA
if it's just damaged beyond repair.
So it copies all the DNA.
Well, it won't begin mitosis
until it's sure that the DNA
has been done replicating.
There's no point in going into mitosis
unless it's all been replicated
and had been replicated correctly.
So it checks it and make sure and
readjust tiny little error.
That's why usually when you
go through this process,
there's only about three
mistakes that get overlooked
three in 3 billion.
Those are good odds.
So, it also needs to make sure
that everything's ready for mitosis.
If it's not, then it stops.
Now if it stops too long at this stage,
then it will say you know what, screw it.
Something's wrong and it'll kill itself.
So there's lots of checkpoints
in where the cell can be killed.
Now, cancer typically comes about
when the cell ignores a
lot of those checkpoints
and just grows no matter what.
It's like you know what, screw it.
I'm just gonna keep going.
I'm gonna keep replicating.
I don't care what the
cell is telling me to do.
And that's a problem obviously.
Because one of the
biggest issues with cancer
is that it ultimately robs your tissues
and your cells and your
organs of its nutrients
that it needs and causes
a stroke in your brain
or cell death and the organs
and causes organs to fail and whatnot.
Causes blood clots because it clogs up
various vessels and things of that sort.
So too many cells forming these masses
and various organs is ultimately
what causes all the problems.
Now, the first thing
I'm gonna test you on is
how we classify cancer.
Now these are not all
of the types of cancers.
This is just a small little sampling
of a few names of some well known
and not so well known cancers.
Now, generally speaking
carcinoma is essentially
a cancer of the organ,
but we usually add the
name of the organ to it.
So for example, pancreatic carcinoma
is a cancer of the pancreas,
or you could say basal cell carcinoma,
this is one of the most
common types of skin cancer.
This is the skin cancer
that usually occurs
through too much suntanning
and the like, okay.
So carcinoma by itself
really doesn't tell you
where the cancer is.
It's just cancer of the organ.
We usually quantify it by
saying pancreatic carcinoma,
basal cell carcinoma or whatnot.
Now some cancers have very specific names.
For example, if it's in the
muscles, we call it a sarcoma.
Okay so muscle cancer is sarcoma.
Leukemia, everybody's heard of leukemia.
This is cancer in the blood, okay.
So this is when you typically
have a white blood cells
that are just growing out of control.
Melanomas, this is another
type of skin cancer.
Now a lot of times the cancer
can be classified either by
the organ or by the cell type.
So let's look at this.
There is a cell, a type of cell
in your skin called melanocytes.
Now these melanocytes gonna
do a quick anatomy here.
You've got the dermis of your skin,
which is the main layer.
You've got the epidermis,
which is the top layer.
The two types of skin cancers as follows,
basal cell carcinoma has
to do with the stem cells
that regenerate the epidermis.
These are the cells that
grow once a day, okay.
These are the cells that
typically are regenerating
and renewing your skin once
a day layer by layer, okay.
When these get mutated
and start to form tumors,
they're very apparent
though that tumor mass
is very apparent on the
surface of your skin
which is why, most skin
cancers are 98% curable
because you just remove the
tumor mass and no harm, no foul.
However, melanomas are a
little more problematic
because they can go undetected
for long periods of time.
So where are the melanocytes.
Well, they sit deep in your dermis
and they cause these little projections
to go up into your epidermis.
So what do they do?
They secrete a protein called melanin.
What's melanin, well
it's the protein that is
has a very specific tertiary structure
that absorbs UV radiation.
And this is why you tan
when you suntan or are you go
into a tanning bed or whatnot.
Your body's actually
increasing the rate of melanin
production to say, stop
exposing me to UV radiation.
Because the UV radiation
will damage your DNA.
Your body has to repair the DNA
every time it's exposed to UV light.
UV light is very problematic
to genetic material.
So the more you're exposed to UV light,
the more melanin your body will produce.
Melanomas are when the melanocytes
start growing out of control.
Now these are usually seen by
having dark patches in your skin.
Sometimes they can protrude
but a lot of times they don't.
Now moles are not cancer,
but if a mole is growing
and continues to grow,
usually a doctor will
remove it because it's
it is abnormal cell
growth of the melanomas.
I'm sorry, of the melanocytes, okay.
So not all moles are cancerous,
but they can become cancerous.
Now freckles are typically
overactive melanocytes
but it has nothing to
do with cancer, okay.
So, freckles typically are high
concentration of the melanin
in spots, in your cheeks and whatnot.
And so that's kind of the relationship
between some of these things.
So usually moles you're like whatever,
they don't grow much
beyond a certain point.
But if they start growing
later on in your life,
usually the doctor will go
in and surgically remove it,
but they have to get deep into the dermis
to be able to do so, all right.
So, this is how we name them.
Now those other ones that
you're gonna see showing up later on.
I think I also bring up a brain
cancer called astrocytoma.
So an astrocytoma come from astrocytes,
which are nerve cells in the brain.
Usually these are the support cells
that support a lot of the neurons.
And those become very problematic because
not that you can't detect the cancer
is that many times you can't go in
and remove the cancer
without doing more damage
or causing too much brain
damage of the individual.
So that's a big issue
that we have to deal with
is removing the cancer
especially in organs
that tear easily or usually go unnoticed
for long periods of time.
Naming it is important to
understand this next concept
because there are two
main types of tumors.
Now a tumor is essentially
the overgrown mass of cells
that come about when
the cells lose control
of the cell cycle.
So when you get more cell
growth than cell death
and the cells ultimately
start forming this mass,
that's what we call a tumor.
Now, in the earliest
stages of most cancer,
you end up what's called
having a benign tumor.
Now it doesn't mean a benign
can't be life-threatening
because in fact, brain
tumors that are benign,
that are slow growing can
cause intracranial pressure
and stroke and death.
So just because it's benign doesn't mean
that it's not life threatening.
However, on the whole
benign tumors are typically
slow growing and not as harmful.
So that's what we mean by harmless is that
they're usually not a threat
to your body's homeostasis at first, okay.
This also is encapsulated,
benign tumors typically remain
in their site of origin.
So if they're forming in your skin,
then they stay in your skin.
If they're forming in your liver,
they stay in your liver and
your bone or your muscle, okay.
Or breast cancer or testicular cancer
or whatever the case may be.
That's where you're checking for lumps.
That's where you're checking
for abnormal growth, okay.
If the tumor progresses
because it goes unchecked
or undetected or whatever the case may be,
it can ultimately undergo a
process called metastases.
This is when you start
having big problems.
A malignant tumor is one
that has metastasized.
So what does that mean?
It means that cells have broken free
from the encapsulated tumor mass
and entered one of two main
thorough ways in your body.
Either your cardiovascular system
or your lymphatic system.
These are the two major
fluid systems in your body
that transport things all
through the rest of the body.
So if cells go through
those fluid systems,
it can see new tumors in
other parts of your body.
Where you end up having skin cancer
all of a sudden in your lungs
or you're having
any number of issues
where these cells are
showing up in other organs
causing new tumors to form.
And this is what it becomes just very,
very difficult to treat, okay.
Now, let's look at how we treat cancer.
These are many of the
tried and trued methods
that we've used.
Although there are many that
are being advanced today.
These are in no way the
best type of treatments.
In fact, we're trying to get away
from some of these because of how much
harm they cause the body.
But I'll describe what they
are, why we still use them.
And maybe some of the
new developing things
that we're coming up with.
Now most cancer research today,
it's not necessarily going into
developing drugs to kill cancer.
It's in how to understand
what's causing the cancer.
That end of itself is more
important now than ever
to know what's causing it because
the more you know about what's causing it,
the more you can target
that type of cancer.
And back in the day,
we would just kind of
use a shotgun approach
of chemotherapy and radiation therapy
and sometimes it would work
and sometimes it wouldn't.
And you have to ask the question well why?
Well, we'll answer that.
Ultimately coming down to
the reasons why two cancers,
two people could have leukemia.
Radiation works for one,
but doesn't work for the other.
Well why, so let's go over how this works.
Now, as in almost all
cases, when you have cancer,
there always has to be
some type of surgery
to remove the tumor mass of cells.
Not always in some cases
where you have something like leukemia,
where it's already going through
your cardiovascular system,
you may not necessarily have a tumor mass.
But in most cases, surgery
is one of those things
just goes hand in hand
where you try to physically remove
the mass of cells from the organ.
In some cases however,
this is not possible without
destroying the organ.
Be it a brain, be it the pancreas,
usually pancreatic cancers are so fatal
because they go unnoticed for so long.
And by the time that you
see that it's shown up,
it's almost too late.
So it's not that we can't
necessarily go in and remove it,
but a lot of times they just go undetected
for a long period of time.
Now radiation therapy.
Here's the interesting thing.
Radiation not only causes cancer
but is used to cure cancer.
So what's the trade off here.
Well, constant exposure to UV radiation,
x-rays any high level radiation over time
damages your DNA to the point where
if you damage the cells
that control the cell cycle,
then the cells will start
growing out of control.
You get cancer.
Well, what radiation therapy does
are usually high quick bursts of radiation
to the cancer cells to
damage them so badly
that they cannot replicate,
that they cannot undergo cell division
and it induces apoptosis.
Remember I told you about that checkpoint
that cells typically use right here.
That's what radiation
therapy is designed to do,
is designed so that when this
gene comes in here and says,
oh man, all the DNA is just screwed up.
It will cause the cells to die.
The problem with this is
it also kills healthy cells.
Now what are the healthy
cells that typically die,
it's usually the most rapidly
dividing cells in your body,
your hair, your immune system,
the lining of your gut and whatnot.
This is where you get sick
and you have those problems is because,
the most rapidly dividing
your cells in your body
are also triggered to undergo apoptosis.
So there's this trade
off where you have to
give enough radiation therapy
to kill the cancer in doses
and let the body recover in between
hopefully the body recovers faster
than the cancer recovers.
And ultimately after several treatments,
you eventually eradicate the cancer
without killing the individual.
That's the trade off.
That's the kind of the difficulty of this.
But not all cancers respond
to radiation therapy
because a good number of them
have a mutation in this gene
that ignores DNA damage.
And so a lot of cancers don't
respond to radiation therapy
because they've lost this ability
to trigger apoptosis
through that checkpoint.
Now chemotherapy, the name itself
kind of tells you what
it does, it's chemicals.
Now, when we say
chemicals or chemotherapy,
there is a huge spectrum.
When we say chemotherapy,
we don't just mean one type of chemical.
There are 100s of chemicals out there
that are designed to kill cancer.
So what is the target of chemotherapy?
Well, this is where we come back
to what we discussed in the last lecture.
Some chemotherapy drugs prevent the DNA
from being replicated and therefore
the cell can't divide.
Some chemotherapy drugs
prevent the mitotic spindle from forming.
So therefore they can't finish
mitosis and the cells die
and so on and so forth.
So the targets of chemotherapy
are the genes that are necessary
to initiate the cell cycle.
They're essentially
preventing DNA replication,
preventing this things
from undergoing mitosis
and the cells therefore cannot divide.
So, that's usually the target
for chemotherapy drugs.
They kill cells that have metastasized
and the distribution of
chemotherapy can vary.
But usually it's done intravenously
through the bloodstream so that
it reaches your whole body.
This is done typically when you have cells
that have metastasized
because you don't know
where they've all spread to.
And so you basically have to flood
the entire cardiovascular system
with this chemotherapy drug
to try to kill any of these loose cells
that are going all
through your fluid system.
And it's a very serious problem
when a cell has metastasized.
So chemotherapy is
typically a chemical agent
that's used to block the cell cycle
and prevent the cells from growing
and ultimately causing them to die, yeah.
- [Student] Is there a way that they
can take out the chemicals after they
or do they just put them in
and they just have to wait
until they lose their effect?
- [Narrator] Well some
therapies know that, well yeah,
usually the body will detoxify
your liver will break them down
and then you'll get rid of them
through your urinary and digestive system.
A lot of drugs in fact,
I worked at a pharmaceutical company
that was developing a
drug that was designed
to boost the immune
system after chemotherapy.
And so usually they'll do a round of chemo
and then they'll treat someone with a drug
to try to restore the healthy cells
and replenish their immune system
and get their body back to normal
before another round of chemotherapy.
So yeah, the body will naturally
eliminate the chemotherapy drugs
that are going through the liver
and going through the cycle
and then you'll go through another round.
So usually, people are given a dose
just like radiation therapy,
they're given a dose.
Now radiation therapy
there's a number of ways
in which you can distribute it as well.
But, ultimately there's only one thing
radiation therapy does.
Damages the DNA to reduce apoptosis.
Chemotherapy essentially attacks
the proteins and enzymes
that are involved in mitosis
and cell division,
even DNA replication.
So the last concept
we're gonna cover today
are just some of the
general characteristics of cancer cells.
And then when we come back on Thursday,
we'll really dive into the genetics
of how cells regulate the cell cycle.
Where they have these checks and balances,
where they, keep each other in check,
kind of how our government
was meant to be, but it's not.
You could say it's cancerous, but
that's more on a political issue.
All right, so cancer cells
are very different from
normal cells, okay.
Now doctors who specialize in cancer cells
are called what?
Oncologists now, what
do oncologist look for
when they look at tissues.
When you take a biopsy
and they take a tissue sample
and they're looking for cancer,
what is it that they're looking for?
Well in the past,
we mainly just looked at the cells,
but now we do a lot of
things to be able to test
the genetics, remember
biotechnology, microarrays,
where we look at 100s of genes.
That's another thing that's used today
to profile the cancer
cells, to look at what genes
might be going wrong.
Now, putting that aside,
let's just look at some of
the general characteristics
of cancer cells when they are,
when we would call them cancerous.
Number one, because they
devote most of their time
to growing and not doing
what they were designed to do
from their tissue of origin.
They stop behaving the
way that they should.
So they also start looking differently.
You can actually tell the
difference between that.
Now this is a very high magnification.
Doctors when they look at cancer cells,
typically don't see this
much of a difference.
But ultimately they look
through a light microscope
and they can see it different,
what we call morphology
or shape in the cells.
It's not as obvious as this picture,
if it were it'd be way
easier than it is today.
But they're specially trained
to look under the microscope
and they see that the cells
have a different morphology.
They look differently, okay.
We call that non-specialized.
So what does that mean?
Well, your skin behaves like skin
because it produces the
proteins that skin needs
to behave like skin.
When the cells start becoming cancerous,
they devote less time
to making those proteins
and more time into growth.
And therefore they become non-specialized.
They look differently,
they behave differently.
They're not skin anymore.
They're not that cell type anymore,
they're now cancerous.
Let's jump down here to
the middle, this one.
And then we'll just call it a day.
Lacking contact inhibition.
When cells become cancerous,
they lose one of the inherent abilities
that normal cells have,
which is what we call contact inhibition.
So what's contact inhibition.
Well, think about it.
When you cut your skin
and your skin starts regrowing,
there comes a point where
the tissue has been repaired
and you've packed your cells together.
Normal cells, when they
start having this contact
with other cells are
like oh, hey, we're done.
We finished the repair
we're all back together again.
And there are signals that
tell them to stop growing.
Well, when cancer cells get together,
there's like ah, make some
more room for the next guy.
They ultimately don't
care about that contact.
And this is what leads to the tumor mass,
because it doesn't stop.
There's no more repair
it just keeps growing
and growing and growing
as much as it possibly can basics.
So since cancer comes from your own cells,
many of the things
you're gonna see here are
actually normal processes that
are just taken to the extreme
that are bad when cancer uses these things
that are naturally occurring.
And in some cases they pretty
much do the opposite as well.
So you'll see both of those today.
So the first one, one that
we talked about specifically,
and that is associated with
formation of tumor masses
is the contact inhibition.
Normal cells when they repair tissue
like you get a cut in your skin
and they start regenerating your skin.
When they start typing one another
and coming in contact with one another
and filling up that gap
and forming the scar tissue and whatnot.
They essentially generate what
we call contact inhibition,
which is a way for them
to signal to each other
that the repair is done
they need to stop growing.
So it's a way to turn off
the accelerated cell growth.
Well, cancer cells pretty much
lack this contact inhibition,
which is why when they
form those tumor masses,
they just keep growing
and growing and growing
without any concern with how big
or how close they are to one another.
They don't respond to this
type of contact inhibition.
So that's a big problem
that's why tumors essentially form.
Another one is because they're devoting
most of their time to growing.
And they stop really producing
a lot of the proteins
that they were originally designed to do
before they became cancerous.
Then they look differently,
they behave differently and
we call them non-specialized.
So you have about 256 different
types of cells in your body,
each one with a specific job.
And when they're doing that job,
we call them specialized cells.
So pretty much each one of your cells
has some respective job,
which they're designed to do.
Skin behaves like skin,
liver behaves like liver and whatnot.
But cancer cells pretty
much look differently
because they behave differently
because they stop doing the things
that they're supposed to be doing.
And we call that non-specialized, okay.
Another problem is that
they can and actually reinforce each other
to increase cell growth.
So as the tumor starts growing,
the cells can say hey, we're
all having a party here.
Let's just get more in
and start causing them
to divide even more.
So it propagates itself.
It kinda starts growing exponentially.
And this is why you wanna
catch it pretty early
because of this positive feedback loop
that can be generated by the cells
as they increase in their overall mass.
Now, one of the issues with cancer
is it's not like normal cells
where they have a finite cell division.
Now, what I mean by that is
normally when cells divide,
they have a pre-established
number of cell divisions
usually about 50 before they stop.
And the reason why they stop is because
at the end of the chromosomes,
remember we talked about the
sister chromatids and whatnot.
What the ends of the chromosomes.
There are these protective
DNA regions called telomeres.
As the cells undergo cell division,
these telomeres get shorter
and shorter until the cells
once the telomeres are gone,
the cells cannot
replicate the DNA anymore.
So they can't divide.
The problem is with cancer cells
because they usually come
from our adult stem cells,
adult stem cells retain the
ability to divide indefinitely.
Because they have an enzyme
active called telomerase.
Telomerase is an enzyme
that essentially rebuilds the telomeres
every time they get shorter.
So they don't have a shelf life.
They don't have the limited
number of cell divisions.
And that's why it's so problematic
because the cancer cells having stemmed
from these adult stem cells,
have that ability to divide indefinitely
because they have this enzyme
telomerase active, okay.
So that's a problem.
You have to kill them,
they can't just wait it out and say
well, they'll eventually stop growing.
No, they won't.
Now this is not true for all cancer,
but since it is over 50%
of cancer that is diagnosed today
has this characteristic
that I make mention of it.
Over 50% of the diagnosed cancers
have lost the ability to
respond to radiation therapy,
primarily because of a mutation
in the gene that triggers
apoptosis when the DNA is damaged.
So that's one of the reasons why
a good number of cancer cells now not all,
otherwise we would never
use radiation therapy again.
But a good number of them
won't respond to DNA
damage to induce apoptosis
because of genetic mutations
that are pretty ubiquitous
in the human population.
And then here's the final thing
that is a common characteristic
of your normal cells,
but is used to,
is problematic when cancer cells do it.
Your cells automatically
regulate the flow of blood
around the tissue so that
they can get the nutrients that they need.
We call this angiogenesis.
So angiogenesis, is essential formation
of new blood vessels.
We're not talking about
arteries and veins.
We're talking about the
smallest blood vessels that
that carry nutrients to
the individual cells.
Those are capillaries.
So capillaries are only one cell thick,
meaning one red blood cell
can go through at a time.
Well a lot of times they'll get clogged.
They'll get stuck,
they'll get smashed
together and get blocked.
Kind of like if you have
a little stream or river
and it gets blocked,
it's going to redirect
around that blockage.
Well, unlike a river
where it can just kind
of navigate its new way,
you are dealing with
actual blood vessels here.
The cells, when they start
getting starved for nutrients,
secrete growth factors like VEGF
is vascular endothelial growth factor.
They secrete this hormone
and the cells essentially say okay,
let's form new capillaries
around this blockage
so that the cells can get
the nutrients that they need.
The problem with this is
as the cancer, as the tumor grows,
it's also able to stimulate angiogenesis
to increase the blood
flow to all of the cells
so that they get those
nutrients that they need.
And that becomes problematic
especially when you don't
want the cancer to grow
as fast as it possibly can.
A lot of times we use drugs called
angiostatin and endostatin
which essentially block
these signals and prevent the cancer
from forming new capillaries
that surround the tumor mass.
Sometimes when a cell gets
infected by a virus or whatnot,
you have immune cells,
cytotoxic T cells that will essentially
punch holes in your cells
and tell them to die.
There are these little
receptors on your cells
called MHC class 1 receptors that
when they get infected with the virus
or something like that,
they'll present this portion
of it to these cells.
And when the cells recognize that
it's essentially the cell saying, kill me.
So the T cell comes in
and releases certain apoptotic enzymes
that ultimately trigger cell death.
So sometimes it's not the cell itself
that trigger cell death,
but your immune system.
And this is also where it comes into play
when cells become cancerous,
they also can present these
signals to your immune system.
And as your immune system is monitoring
all of the cells in your body.
And it comes across one
of these it's like oh,
this needs to die because it's say, hey
I've got problems, kill me.
Okay, so it still is apoptosis
but it's triggered by another cell,
typically your immune cells.
So that's why a lot of times too,
people can have cancer cells,
but their immune system takes care of it.
Our immune system is
designed to take care of it.
What happens is sometimes the cancer cells
don't present this tag
on the surface of it.
So cell membrane and the
T cells just overlook it.
It doesn't bother with it.
Okay, now let's talk about
some of the genetic causes.
Now not all cancers is caused by genetics,
but that's what we're mainly
gonna talk about today.
There are many things
that can cause cancer.
In fact, they've shown that
just taking cells out of the environment
that they normally are in
and putting them into a new environment
can all of a sudden tell
them to become cancerous.
They're under a different
set of hormones or signals
or whatnot from adjacent cells.
And they can become cancerous
if they're in the wrong tissue.
So we're not gonna go
through all of the things
that can cause cancer,
but we are gonna talk about the genes.
Especially genetics mutations
that ultimately can cause cancer.
So just be aware of that
not all cancer is caused
by mutations in the genes,
but that's what we focus
on a lot of the time
because that's what's quantifiable.
But they're finding
more and more reasons of
cells becoming cancerous that are
not genetic mutations, alright.
Sometimes a viral infection
can actually cause the
cells to become cancerous.
And it's not a mutation of the genes,
but it is caused by the
virus infecting the cells
and causing all sorts of problems, so.
In fact we've used that same process
to immortalize cell lines for research,
where we actually infect
them with a particular virus
that essentially makes them a cancer cell.
Allows them to divide indefinitely.
So, we've seen what nature
can do when we study it.
And we do it for a number of
different research purposes.
Okay, now here's where we get
into the checks and balances
of the cell cycle.
Remember I told you that the
cell regulates its growth
and death by certain groups of genes.
Now we're not gonna talk about
any one gene in particular.
These are actually groups of genes,
kind of like if we look at
Congress and our judicial system
and whatnot, they're made up
of a lot of different people
all forming one large group.
And they're supposed to
have checks and balances
with one another.
And then we have our executive branch
which is screwing everything up.
They've been screwing it up for years.
So I don't have any particular beef
against one person or
the other, but anyway.
So ultimately the two groups
essentially do opposing things.
They keep each other in balance.
So the first group of genes
we call proto-oncogenes.
Now, these genes are specifically designed
to accelerate cell growth
and stop apoptosis.
When your cell needs to repair,
when your body needs to repair itself
these are the genes that ramp up mitosis.
These are the ones that be like hey,
you guys gotta repair and grow faster
because we've got a
break in the integument
and your skin and whatnot.
So the proto-oncogenes are good genes
because they're designed
to accelerate cell growth
when it's appropriate.
And when cells are damaged,
sometimes the adjacent
inflammatory response
can cause further cell death.
And so one of the things
these genes do is prevent apoptosis.
Cause you don't want cells dying
when you want cells growing.
You want to turn on one
and turn off the other.
Well, when these genes become mutated,
we don't call them
proto-oncogenes anymore.
We call them oncogenes.
And again, what are doctors who
specialize in cancer called,
oncologists that's where
they get their name from.
So oncologists study on good
genes and many other things,
but that's what we give the name for
those who study cancer and
treat cancer are oncologists.
Now oncogenes when they're mutated,
they essentially are on all the time.
And that's a problem because when
you're promoting the
cell cycle constantly,
that's what causes cancer.
Now one gene by itself is
not enough to cause cancer.
And that's why we have
these checks and balances.
So on the other end of the spectrum,
this other group of genes we have
are called tumor suppressor genes.
Well guess what?
The name tells you what they do.
They suppress the formation of tumors.
How do they do that?
They do the opposite of proto-oncogenes.
So whereas proto-oncogenes
promote the cell cycle
and stimulated proptosis,
tumor suppressor genes,
oh I'm sorry preventing apoptosis.
Tumor suppressor genes
inhibit the cell cycle
and they stimulate apoptosis.
So they essentially do the opposite.
So one gene starts going out of control
the other genes can rein it in, okay.
So no one gene really can cause cancer.
And this is the reason why
it's not as prevalent as it could be,
because yeah you can have
one thing out of control,
but everything else reins it in.
It's when the genes that
are supposed to rein it in,
when they get mutated
now you've got a synergistic problem.
Because now that these genes
are telling the cells
to grow uncontrollably
and these aren't stopping
them from doing so.
Now what's nice is that
you have two of every type of gene.
Which means that you need two mutations
in both of your genes,
to ultimately get this
combination to cause cancer.
Again, more protective
nature of our chromosomes
and of our genes.
So by having two of every gene,
the reason why we usually
focus on oncogenes with cancer
is because it only
requires one of your genes
to cause a problem for the oncogenes.
But it requires two problems
in your tumor suppressor genes
to cause a problem.
So that's the checks and balances
that's going on here, all right.
Now these are the ones
the tumor suppressor genes
are the ones that step in
once the repair is done and
shut the protocol oncogenes off.
So during normal repair,
you cut your skin.
The protocol genes ramp up the cell cycle
and then when contact
inhibition comes into play,
that's when the tumor
suppressor genes jump into play
and say hey, you're done.
And if you have too many cells,
it will stimulate apoptosis.
These are also the ones
that trigger apoptosis
through radiation therapy.
So there's a common mutation
in a very particular tumor suppressor gene
that is found in over 50% of the cancers
that are being diagnosed today
because it gets inherited.
So like I said,
one mutation is not enough.
You've gotta have the mutation
in the tumor suppressor genes
that would normally pull
rein this oncogene in.
And when you get that
combination, then you get cancer.
And this is why when you
inherit these mutated genes,
you end up having a
predisposition to cancer, okay.
So let's talk about that.
Later on we're gonna talk about
what we call dominant
Helios and recessive Helios.
Dominant Helios, you
only need one mutation
for them to cause a problem.
Recessive Helios you
typically need two mutations
for them to cause a problem.
Which is why tumor suppressor
genes are typically recessive
and oncogenes are typically dominant.
But like I said, no one
gene could cause cancer.
However, you can pass an oncogene on
and you can pass a tumor
suppressor gene on.
A mutated tumor suppressor gene on.
And that just makes you one step closer
to having those cells have those issues
because of the combination
of different genetics.
Now, what are some of these?
These are the ones that
they typically test for
when you go and get a blood sample
from say Myriad Genetics.
They specialize in
ovarian and breast cancer
and things of that sort.
One of the genes that they look at
is called the BRCA gene.
So the BRCA gene is one of those
is pretty prevalent and
inherited as an oncogene
that gets passed on.
So if you have a history of
breast cancer in your family,
from your grandmother to
your mother and whatnot,
then more than likely you
might have that oncogene
which makes you that much
closer to getting breast cancer.
Now, some genes are found in all cells.
Others are only expressed
in various tissues.
For example, RB or retinoblastoma.
This is what causes eye cancer.
This is one of the oncogenes
that can cause eye cancer.
There's other genes like the p53.
This is that tumor suppressor gene.
This is found in all cells.
So if you have this mutation,
this makes it possible that you can
get any type of cancer, really.
So it depends upon the gene
and where it's expressed
that ultimately determines
what your probability of getting cancer
in that type of cell is.
And it's very easy to do this.
In fact, this is where DNA
sequencing comes into play.
That you go in, they take a blood sample
and they'll run some
genetic tests to screen
and look at any mutations.
By sequencing your DNA in
these specific locations
where these genes are found
and they'll look for any mutations.
And they might say yeah,
you have a mutation,
but it's a silent mutation.
Basically it doesn't change
the protein, you're good.
You don't have a problem.
But in other cases they may say, yeah.
This one is one that we see a lot.
It definitely gives you a predisposition
you could get checks
more often and whatnot.
So this is where profiling your DNA
can really be important,
especially if it runs in the family.
Just some a lot of times people
come up afterwards and ask,
what was the name of that company?
It's called Myriad Genetics.
It's up in Salt Lake.
A lot of times your insurance
company will pay for it
because they'd rather prevent cancer
than pay for it after the fact.
So this is a place that
specializes in DNA sequencing
and things of that sort.
