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The PI3K AKT mTOR pathway and cancer Part 1 with English subtitles   Complain

okay so welcome to this video in this

video what we're going to talk about is

the pi3 kinase akt mtor pathway and

cancer okay so we want to look at the

involvement of this pathway in cancer

cells okay right so what we're going to

do is we're going to start off by

talking about the basic carcinogenic

process okay so what happens in cancer

development okay then what we're going

to do is look at the pi3 kinase nkt mtor

pathway and have a look at how important

this pathway is in cellular growth and

cellular proliferation and will

understand then why it's one of the key

pathways that ends up having its

components mutated in cancer okay so

there are many components of this

pathway there's a tumor suppressor genes

and many that are proto oncogenes and

those can end up with mutations in in

cancer okay so we'll discuss which

components of the pathway are the most

commonly fabricated ok then we'll

discuss is targeting this pathway in

activating this pathway for cancer

therapy ok now it's fair to say that

with one exception which is the a drug

used to treat chronic lymphocytic

leukemia ok called Idol as it with that

one exception the initial testing of

drugs that block this pathway for the

treatment of cancer has been quite

sobering okay it's had only very modest

success and we're going to discuss

potential reasons as to why that is and

we think the key reason as to why

targeting this pathway hasn't been that

effective in

preventing the progression of cancer is

that we aren't able to give these drugs

in high enough doses again the reason is

that this pathway is actually incredibly

important in non cancerous cells as well

so blocking it can have loads of on

target side effects so remember drug

side effects can be split up into on

target side effects and off target side

effects on target side effects are the

side effects you get because even your

because the drug actually binds to the

target that we intended it to bind to

and that but that causes those of side

effects because of how important that

target is in the body okay off target

side effects refers to the fact the drug

might buy two loads of things that we

never even planned for it to bind to and

that's why I might cause those of side

effects as well but we think in the case

of these drugs that target the pi3

kinase a KTM tour before i forget the

off target side effects we can't be on

target side effects are so large that

you can't give these drugs in high

enough doses to actually have a decent

stab at the cancer basically okay and

we'll discuss potential ways that we

might be able to get around that in the

future okay alright so let's start off

with the basic cancer development

pathway okay so we want to discuss the

process of carcinogenesis how does

cancer emerge okay so we're going to

discuss the leading theory of what

happens in the development of cancer

which is the cancer occurs as a micro

evolutionary process okay where by cells

gradually accumulate mutations and these

mutations gradually build up a more and

more aggressive phenotype until we

finally get to the level where you have

cells that are cancerous okay right so

in this theory which is the leading

theory of how cancer develops you start

off with a normal somatic cell okay so

let's say here it is and it could be a

snow in all sorts of different tissues

so it could be and so of the epithelia

of the lungs

of the epithelia of the pancreas you

name a gave me any different type of

cell okay and basically this cell is

going to get a mutation that is going to

allow it to over proliferate okay now

there are two major classes of proteins

that you can get mutations in that will

then lead to a cell over proliferating

so let's introduce this concept now okay

so the two major class of proteins are

the proteins that come from

proto-oncogenes okay and these proteins

are involved in promoting cellular

growth and cellular division okay the

other types of proteins through involved

in controlling cellular growth and

cellular proliferation are what are

known as tumor suppressor genes okay and

the proteins are coded for by chima

suppressor genes these are anti growth

and anti proliferation okay so normally

in a normal cell that isn't dividing

you've got this balance between the

proto oncogenes and the tumor suppressor

genes again no one's winning basically

the proto oncogenes are all saying / 5

grow grow grow and then divide the tumor

suppressor genes are then saying no

don't stop doing that okay and their

imbalance normally so if you want to tip

this balance and cause division there

are two different ways that you can do

it either you can up the activity of the

proto-oncogene gene products or you can

down-regulate activity of the tumor

suppressor gene gene products okay so

this means that this first mutation that

is going to occur in cancer which is the

unmute ation it's generally fought in

mutation that causes over division okay

it can either be a gain-of-function

mutation which I'll breathe it down to

gof gain-of-function mutation in a

proto-oncogene that's going to cause

that proto-oncogenes activity to now go

up huge they so for instance

forcing gain-of-function mutations would

be if you amplify the number of genes

that you have for this proto-oncogene so

usually we have two copies of most

proto-oncogenes one on each of the

homologous chromosomes if somehow you

end up totally screwing up and copying a

whole new one into one of your

chromosomes then you have three copies

of the proto-oncogene and now that's

going to huge the increase the amount of

the gene product the proteins that

proto-oncogene that you produce and

therefore huge the increase its activity

okay that would be an example of a

gain-of-function mutation in the

proto-oncogene alternatively you could

have a mutation that actually affects

the structure of the protein itself and

resorts in potentially being permanently

active whereas previously it might have

been inhibited by something or just

increases its activity in some other way

maybe okay so those are all examples of

gain-of-function mutations in the

proto-oncogene that would tip the

balance because now the tumor suppressor

genes we've got wouldn't be adequate

enough to suppress the proto oncogenes

anymore okay alternatively you could

have a fool in the activity of the tumor

suppressor genes okay so you need a

loss-of-function mutation in hms

suppressor gene basically and often you

would need lots of function mutations in

both of the tumor suppressor genes that

you have because again you'll have two

copies of each tumor suppressor gene

generally warm on each of the homologous

chromosomes again generally only loss of

function in both of those genes in order

for the function of the tumor suppressor

protein to actually be lost completely

okay right so examples of loss of

function mutations would of course be

deletions of the gym and if you

completely lost the two genes then that

will completely remove the function of

that protein

within the cell okay alternatively you

could have changes in the structures of

the protein which then need them to miss

forward and be totally useless basically

okay right so those are the two main

types of genes controlling cellular

division ok so this normal cell here is

now going to get a somatic mutation okay

and this somatic mutation is going to

just so happen to either be a gain of

function in the proto-oncogene or a loss

of function in a tumor suppressor gene

again now what's going to happen ok now

cut it is so in a different color

because now it's got this mutation ok so

that's colorless in in purple now now

what's going to happen is it's going to

divide by by because it now has this

over proliferation property and

therefore what's it going to end up

producing it's going to end up producing

a whole population of styles that all

have this mutation that means that they

over proliferate basically ok so now

we're going to get a new mass of cells

which have all got this mutation that

means that they over proliferate and now

if this first mutation was powerful

enough that it causes a powerful enough

lies in proliferation that you get a

visible alone ok then we would call that

a benign tumor at this stage ok so it's

not cancer yet it's just a benign tumor

ok right so it's a new mass of cells

basically that wasn't there previously

ok right so now what is going to happen

is you're going to progress on words and

that's the first part of the progression

towards cancer now what you have to do

is to actually these cells to actually

become cancerous cells they have to

acquire a lot of other very dangerous

phenotypes ok so actually these cells

need a huge number of other mutations in

different genes in order to actually get

the phenotypes of cancerous cells ok so

now what's believed to happen

is in this population of cells that have

all got this first mutation that means

that they are over proliferate you're

now going to wait for one of them to get

a mutation in another geniune that's

going to give them another one of the

phenotypes of cancerous cells okay so in

this population these cells will be

undergoing mutations occasionally okay

many of those mutations would of course

be in things that don't progress them on

towards cancerous phenotypes some of

them might even you know be an essential

proteins such as the proteins of complex

for maybe in the respiratory chain and

therefore the star will die when it gets

that mutation okay but adventure if you

wait long enough one of them will just

so happen to get a mutation in a gene

but now gives us another one of the

phenotypes of a cancer cell and

therefore takes it towards being a

cancerous cell okay so and that's saying

that one of the cells in this population

here let's say this one here now gets

another mutations I'm going to color it

in a different color now in blue here

and this cells mutation is now going to

take it towards cancer okay so it's

going to give it a lot of one of these

phenotypes that takes you closer to

being a cancerous cell okay so

potentially it could just be another

gain-of-function mutation in the

proto-oncogene or another

loss-of-function mutation and the tumor

suppressor gene that now causes the cell

to divide even more rapidly than need

purple cells and therefore what's going

to happen is this tumor is going to

firstly get bigger and it's also going

to become dominated now by the blue

cells okay the blue clone ourselves

rather than the purple clone ourselves

so you will still have some of the

purple clone of cells but now the main

cell type that's going to dominate the

tumor is now the blue clone of cells and

this is why people describe the customer

Genesis process as a evolutionary

process as a Darwinian like process okay

because the cell population within the

tumor is evolving basically it's going

away from being

the purple sounds to now being this blue

clone of cells being the dominant clone

of cells in the shimmer population okay

so here now are the blue cells and now

we've got very few purple cells left

over okay so you can see that the

dominant clone within the tumor is

evolving basically which is why it's

compared to a Darwinian like evolution

process okay and then this will continue

in this blue clone of cells now you all

just have to wait for one of these cells

now to get a further mutation gives us

another one of the phenotypes of cancer

and takes it closer to being a cancerous

cell and this process continues this

evolutionary process continues where by

the dominant closer cells in the tumor

is going to gradually evolved basically

okay and as it does so the close of

sellers is going to become closer and

closer to having the phenotypes of

cancerous cells okay so let me just

outline some of these phenotypes that

you're going to gradually build up as

you progress towards cancer okay so the

key phenotype and everyone can name is

one of the key phenotypes of cancerous

cells is that they have over

proliferative potential okay so they

over proliferate so you're going to

gradually build up more and more

gain-of-function mutations in prose one

coaching inns and loss-of-function

mutations and shimmer suppressor genes

and that's going to lead to you over

proliferating huge thing okay another

phenotype of cancerous cells is genetic

instability and this one's very very

important okay so what do I mean by

genetic instability genetic instability

means that cancer cells undergo

mutations far more rapidly than normal

cells okay so why is this well cells are

getting damage to their DNA all the time

could that could lead to mutations

occurring okay however why does it not

lead to mutations occurring usually

in a cell and it doesn't always work but

usually they don't result in actual

permanent changes to the DNA sequence

and the reason is you have all sorts of

mechanisms for repairing the DNA when

it's been damaged okay so you have DNA

repair mechanisms okay so basically the

cancerous cells the way that they have

this property of genetic instability

this tendency to acquire mutations far

more rapidly than normal cells it's

because they have had mutations which

have resulted in loss of function in the

DNA repair mechanisms okay and if the

DNA repair mechanisms go down then your

frequency of acquiring mutation that

goes up hugely okay so at one of these

stages in the clonal evolution of the

tumor one of these cells so let's say

for instance in this next step we're

going to acquire a genetic instability

okay so we've got our blue clone of

cells here one of these cells in this

blue cone might now get a mutation in

the mechanisms for DNA repair one of the

pathways for DNA repair which

inactivates that pathway okay it will

now over proliferate because remember

it's got all of the mutations of the

purple and the blue cells okay what

about this got all the mutations are the

blue sounds which means that it over

proliferate okay so it will produce a

whole clone of cells that all have this

genetic instability now and over

proliferate okay and now in that new

clothes cells let me show this new clone

of styles up another clone of sounds

here okay in this clone ourselves the

process towards cancer will now be

hugely accelerated because you will get

mutations occurring far more rapidly in

this new clone of turquoise cells okay

so the next process the next step

towards another clonal evolution the

next step in this process will occur

much quicker than these prost

this occur okay so you had to wait ages

for one of these mutations to occur you

have to wait ages for this mutation to

occur now it's going to accelerate the

process okay accelerate this

accumulation of mutations because this

closer cells now that we're going to use

to generate the cancer now has published

genetic instability and therefore is

going to acquire mutations more rapidly

okay so that's why genetic instability

is a general phenotype of all cancer

cells because for the actual cancer

development to appear in a reasonable

time scale in the life time of a human

being it's for that you need this

accelerating step this genetic

instability which accelerates the

process after it occurred okay right so

that's one of the key phenotypes of

cancerous cells you also need to lose

senescence okay so let me explain what I

mean by this okay so lost senescence is

one of the key phenotypes of cancer

cells so normally a cells that can

divide in a human body so for instance

fibroblast dividing the human body have

parasites from dividing the human body

smooth muscle cells can find me here and

body they cannot divide forever okay if

you take them out of the human body put

them into a petra dish and let them you

know different loads of nutrients given

loads of space they will not divide

forever they will eventually stop okay

they will get to the point that they

can't stop anymore because they have

what's known as a hayflick limit okay

there is a hayflick limit as to how many

times the cell can divide and this is

because every time one of these cells

divine so let me show it here here's

this cell here every time the cell finds

the two daughter cells that it produces

have shorter telomeres ok so the

telomeres are the portions on the ends

of the chromosomes okay the telomeres

gradually get shorter every time it

divides the two daughter cells here will

now have shorter telomeres okay then the

mother cell

then these can divide again to produce

four cells and then eight cells but

every time what will be happening is the

progressive generations will have

shorter and shorter telomeres and

eventually you'll get to a generation

where they simply cannot divide again

because if they did their telomeres have

gone basically and they'd start to cut

away their actual chromosomes with the

coding DNA and then you get to the stage

where you can't divide anymore and

you've gone into the stage which is

known as senescence okay so this was a

somatic cell so it would have had a

hayflick limit it's somehow needed to

get away around this hayflick limit and

it needs to not reach senescence

basically again the usual way that sells

do this is by activating too long raise

expression which extends the telomeres

back up again and effectively means that

the cells can continue dividing as many

times as they want because they can just

re extend their telomeres back up so

that's another one of the key properties

of cancer cells okay and then that will

be one of these mutations that

progresses you on once progresses you to

a new clone that's closer to being

cancerous then okay and finally a lost

susceptibility to apoptosis i'll call

this invulnerability to apoptosis ok so

again cells in the human body which can

divide them there are cells in the human

body which can't divide so for instance

skeleton cardiomyocytes they can't

divide neurons in the brain can't divide

ok but the cells in the body which can

divide such as smooth muscle cells

fibroblasts have parasites these are

controlled basically okay if you've got

a tissue that is overcrowded okay

because too much cellular division has

occurred these sellers will commit

apoptosis okay so that we've just shown

us so let's say we've got a bit of the

liver here where it's now over crowded

because too many sales are divided what

will now occur it's some snails in

overcrowded tissue will now connect an

op ptosis okay to reduce the population

and make more space basically okay now

tumors are incredibly overcrowded okay

so why do they not commit apoptosis what

some points in this progression you must

have got some mutation that made you

invulnerable to apoptosis so that you

wouldn't have to make the apoptosis

process and you wouldn't depopulate the

tumor population and okay so again

that's a phenotype of cancer cells and

that will have occurred at some point

along this progression towards cancer

okay right now what I want to talk about

is the final mutation is believed to

occur that takes you from being what is

a length stage benign tumor to being

cancer OSU gradually go through this

clonal evolution process where the clone

is gradually getting closer and closer

to concerts acquiring more and more of

these phenotypes let's say it's now

quite all of these phenotypes okay what

is the final mutation occurs that tips

it from being a benign tumor to being a

malignant tumor or being cancer

basically well the final mutation occurs

is that it gains the ability to be

motile okay so the final mutation is the

motility and this is what takes you from

being a benign tumor to being a

malignancy and this is what tips you

into cancerous behavior okay so what now

needs to occur then is the final

mutation that's going to occur if

something that allows the cells to gain

motility so sellers are not usually

motile cells usually stay in that

position in the body and do not move

around in the body basically okay but

the cells in this malignant tumor have a

quietly a mutation that allows them to

now move around and the body basically

and this gives the

two key properties it allows them to

invade into the surrounding tissue and

set up tumors these are all extensions

of the tumor in the surrounding tissue

and it also allows them to invade into

the blood and then set up secondary

tumors at other sites dis store from the

from size of the primary tumor okay so

let me just describe this so previously

then prior to us gaining this final

mutation we had this great big tumor

here but it was contained ok it was

still benign tumor ok it was maybe

pushing on the surrounding tissues as it

expands but it was not in leading into

the healthy cells ok the cells hear was

static Oh in now what's going to happen

is warm cell in this final penultimate

clone prior to malignancy is going to

get a mutation that's going to that

allow it to a game motility ok right now

generally cancer cancers are formed from

epithelial cells ok so for instance skin

cancer that's formed from an epithelial

cell ok cancers of the gastrointestinal

tract those are formed from epithelial

cells lung cancer those are formed from

epithelial cells pancreatic cancer boza

form from epithelial cells and liver

cancer loser form from epithelial cells

renal cell cancer those are formed from

epithelial cells so generally the major

forms of cancer are formed from

epithelial cells rather than on

epithelial cells ok so what actually

happens usually for these epithelial

cells to gain the ability to move is a

process called epithelial-mesenchymal

transition again this is a process that

was used in the embryo in development

basically so in the development if you

want to move epithelial cells around the

embryo what has to first be happen is

they have to

change their phenotype to become amazing

kimmel cells but amazing kinda sounds

can then move around and then when

they've got their final location they

can then return back to being at the

fetal cells okay so if I show this

rather crude they here here's our

epithelial cell which is not motor it

can't move around okay and we're

assuming that are benign tumor at the

moment is constructed out of epithelial

cells which are not motile okay now in

embryology and development if an

epithelial cell wants to move while it

turns into is what's there is amazing

climb or cell okay which looks quite

different of a different phenotype it

was supposed to look more different than

that its first base or spindle shape

okay and this process of turning from an

epithelial cell into a nice and calm

yourself is known as EMT so I'm going to

color in the epithelial on the meeting

hymel cells in different colors to

highlight that help them they are okay

so here's an epithelial cell in blue

oops here is my knees and cry more so

even read it okay so I'll just label

this up this is a new Zhen Chi more cell

okay right so the process of emt stands

for epithelial okay meezan climb or

transition again it just means an

epithelial cell changing into a meeting

climb or SAP okay now i'm using khaimah

cells are motile these can move around

okay so now this can move around in the

embryo it can get to a new location

within the n brew and then what's going

to happen is it's going to turn back

into an epithelial cell a by process of

amazing chi more epithelial transition

net okay now this is not usually active

in the adult human okay it's something

that's reserved for development however

what we think happens is this in this

final transition where some cell

requires a mutation that then allows

it's become more time what we think is

that somehow and this isn't understood

at all or any at the moment somehow this

cell is going to acquire the ability to

return this process on it's going to

return epithelial-mesenchymal transition

on and what that now means is that this

cell here firstly it can / proliferate

because now it's you know it's got all

of those mutations that mean that it can

/ proliferate so I'll make a whole

population of cells that are all capable

of doing this and what's now going to

happen is some of these cells some of

these yellow cells here are now going to

go through the process of

epithelial-mesenchymal transition

they're going to become using Hymel

cells and then they're capable of

invading into the surrounding tissue

they're capable of moving so now here's

our knees and cry myself from moments

okay which will have him read here it's

on the move okay can go to some new

location maybe in the neighboring tissue

and then it can decide right I'll return

back with epithelial cells that will go

through the music I'm or epithelial

transition okay and now it's at this

distant site basically and now once it's

gone back to the epithelial cell type it

canal over for the throat so one else s

up its own little tumor at this site

further away from the benign tumor

basically okay so you can now set up

multiple little tumors around the major

tumor here okay so that's the property

that being invasive it's going to now

invade into the surrounding tissue and

destroy the surrounding tissue okay in

addition it gets worse than that okay

because what can happen is some of these

are easing hymel cells can end up

getting into the blood okay and then

they can get out of the blood at really

distant sites notably the most important

one here is that it can end up in the

brain okay so it can go into the brain

and then of course it will go through

meeting climb or epithelial transition

return back to being an epithelial cell

and then it will form a secondary tumor

in peripheral tissues basically in that

process of

setting up secretary tumors very far

away from the original primary tumor

here okay so this is the primary tumor

that process is known as metastasis okay

and it's generally the metastasis to the

brain that kills you okay in cancer

that's what kills most cancer patients

the metastasis that go to the brain not

the primary tumor is the Metis disease

that go to the brain that kills the

patient okay right so that's an overview

of the carcinogenic process so what we

have seen here is the utter importance

of the over proliferation of cancer

cells ok that's the utterly key

phenotype of cancerous cells in fact

it's believed to be the first driver the

first mutation that occurs to start this

whole process off is that the cell gains

the ability to over proliferate and

produces a whole population of cells

that are all capable of over

proliferating and then any further

mutations that you snack on top of that

are now going to get amplified because

you've already got be over proliferation

mutation and F we're going to produce a

whole population of cells with this new

mutation you've acquired okay so that's

the absolutely key want to set this

entire process off and indeed generally

what will happen is in this clonal

evolution process you won't just acquire

warm mutation of causing their

proliferation you'll be requiring more

to put them okay right so the pi3 kinase

a KTM tour pathway back it is extremely

important in cellular proliferation okay

so let me just explain this we're going

to give a very basic overview of what

the pi3 kinase a KTM tour pathway does

and then we'll go into it in detail okay

right so basically if a cell wants to go

from being one cell here to being two

cells okay

firstly what it has to do is it has to

grow okay so the first process in

proliferation is firstly for the cell to

grow so growth is the first thing that

needs to happen and then what can happen

is this larger selfish self as grown can

then divided into two cells it can split

okay now in order for a cell to initiate

this process you need major major

epigenetic changes okay so what do I

mean by that epigenetics is all about

what controls which genes are actually

expressed okay so you know every cell in

your body roughly has the same genome ok

it has the same collection of jeans and

it's mucus there are a few exceptions of

course red blood cells don't have a

nucleus lymphocytes have that silly old

somatic recombination to create their

own tmv cell receptors which means that

they end up with slightly slightly

different genomes okay but the hard and

fast rule that generally applies for all

sales is that they have the same genome

they all have all the same genes okay

however epigenetics is different between

different cell types okay they all

express different collections of jeans

okay now if you want a cell to start

this proliferation process start this

growth process and then proliferate into

you have to get this cell to hugely

change which genes it's going to express

okay so you need to start first be

producing the loads of new proteins okay

so that you've got enough proteins for

both cells so for instance all of the

essential enzymes of respiration are

going to have to be copied all the

cytoskeletal proteins are going to have

to make more of those because you're

going to become a bigger cell you're

going to need more cytoskeletal proteins

okay and other proteins as well so such

as the proteins involved in the

ribosomes the proteins involved in DNA

how you're going to have to cut make

more of these essential proteins so that

you've got enough for two sounds rather

than just one okay also you're going to

have to start expressing all the

proteins that are actually involved in

coordinating the division process itself

okay so who's going to have to be huge

epigenetic shift basically to make a

cell divided okay now epigenetics

involves several lines of control within

the central dogma of biology okay so the

first line of control is you need to

change which genes are actually being

transcribed okay so we can call that

transcriptional control okay so you need

to change which genes are going to

become transcribed to cause this

epigenetic shift okay the pi3 kinase a

KTM tour pathway is not going to change

transcriptional control okay there are

other pathways that you need to activate

in order to change transcriptional

control notably the rouse rat nip herb

pathway is a major one which can change

which genes are being transcribed raz

breath mech oak okay we're not going to

discuss that pathway we just need to

note that there are these other pathways

which need to occur alongside the pi3

kinase a KTM tour pathway in order for a

cell to divide oh is it's important to

note with this pathway cannot cause the

cell to divide on its own you need these

pathways as well okay the cause the

transcriptional changes okay right now

epigenetics however involves other

changes just the transcriptional control

there are other millions by which you

can control which genes are actually

going to produce proteins and therefore

be expressed okay for instance there is

also translational control you can

control which mrna knees are actually

going to be translated into protein

ok so the transcriptional control is now

said ok right transcribe all these genes

that are involved in making the cell

divided the razz Ralph Becker halfway

does that it changes which genes are

transcribed and hmm gets you ready for

the actual division process so it's made

all of the nima now that can make the

cell divided that's a-ok however there's

no point making all of that mrna if

you're not going to then translate it

okay so translational control also has a

major wet role in controlling whether a

cell goes into the proliferation process

and it's translational control that the

pi3 kinase aktn tour pathway is going to

be involved in so basically normally if

you just activated the transcriptional

control if you just made these all these

new mrna is for the proteins involved in

making the cell divided these pro

proliferation proteins then it wouldn't

actually have an effect because normally

there is a blockade on these

proliferation mrnas being translated

normally they're not allowed to be

translated ok the pi3-kinase a KTM tour

pathway is the pathway which says ok let

them go through them be translated and

therefore these two pathways the Rous

Rous neck ERG pathway and the pi3 kinase

a KTM tour pathway they control the two

major controls of epigenetics together

and they allow the initiation of the

growth and then the proliferation

pathway okies it's important to

understand that these work together okay

right and so that's an overview of what

this prof wait does and hopefully will

now appreciate how important it's going

to be for cancer cells that want to over

divide to have some over activation of

this pathway along with a bit of over

activation of this pathway okay so that

you can then divide okay

don't have over activation of this

pathway then even if you have over

activation of this pathway you can

produce as much mrna as you like but if

you're blocking it from being translated

then it's not actually going to cause

the cell to grow and then divide ok so

this pathway is extremely important in

controlling the initiation of cellular

division and therefore we can understand

that it would be a queue thing that's

going to have mutations found in it in

cancer cells and indeed it is we found a

huge number of cancer cells with

mutations of in components of this

pathway as we'll discuss later ok so in

the next video what we'll do is now

discuss this pathway in detail so we'll

start by discussing phosphoinositide

3-kinase enzymes pi3 kinase enzymes ok

then we'll discuss all of the different

ways that PR 3-kinase enzymes can be

activated because it is not repeat it is

not just by receptor tyrosine kinase

errs and then we'll move on to the next

portions of the pathway

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