Cancer Drugs/Pharmacology

So, in order to understand the cancer drugs, you first have to understand the big picture of the cell cycle. Now, this

video is definitely not going to be a very in-depth uh cellular biology video.

But instead, I'll just kind of breeze through this. And if you're having any

through this. And if you're having any trouble understanding the cell cycle, I would encourage you to stop this video now and learn about the cell cycle before you attempt to learn about the drugs that act on the cell cycle. Makes

a little bit of sense that you should probably start with the basics before you learn the pharmarmacology. So, in

the cell cycle, you have mitosis, which we'll call the Mphase, and then you have the G1 phase, the Sphase, and the G2 phase. Now, in each of these phases,

phase. Now, in each of these phases, something's happening. And in mitosis,

something's happening. And in mitosis, ultimately, you get the splitting of the cell. This is stuff that's been crammed

cell. This is stuff that's been crammed into your brain uh since before medical school, well into undergraduate school, you should have a very good understanding of what mitosis is. But

ultimately, mitosis will lead to the cell splitting into two. Now, in the G1 phase, that's next. And this is where the cell contents get duplicated. This

is followed by Sphase which is where the DNA is actually synthesized. And then in the G2 phase, this is sort of like a maintenance phase where the DNA gets double checked to make sure that there are no errors. And we'll talk about this

toward the end of the video uh and talk about exactly what acts on the G2 phase and we'll make sense of all this stuff as we go through. So there the way that I want to move through this video is to talk about the drugs that affect each of

these categories one at a time and then at the end we'll talk about drugs that don't really fit into any of these four different phases and we'll talk about those at the very end of the video. So

let's get started with the anti-cancer drugs that act on mitosis. So they act on the Mphase. Now those four drugs are listed here. It's Vincine, Vinlastine,

listed here. It's Vincine, Vinlastine, Pletaxel and Arubilin. So we're talking about Mphase inhibitors or inhibitors of mitosis. Now briefly just recall that in

mitosis. Now briefly just recall that in mitosis there is a process whereby you have the formation of something called

the mitoic spindle and in that mitoic spindle you have these sister chromatids that align right across this horizontal line and they get pulled apart. What

what actually is doing this pulling are microtubules. So the way that these

microtubules. So the way that these drugs act on the Mphase is some of them specifically are going to inhibit microtubules. And by inhibiting

microtubules. And by inhibiting microtubules, they can never rip apart the sister chromatids that lay on the mitoic spindle and therefore the cell can't divide. And if you have a cancer

can't divide. And if you have a cancer cell that can't divide, these drugs prevent the spread of cancerous cells.

So that's sort of the big overview of how these drugs are working. Now the

ones that you need to be familiar with for USML and for comlex are vinchristine and vinlastine which I'll sort of talk about as one drug because they they're pretty much the same drug. Packllet and

irublin. So for the purposes of exams you should know that vin christristine and vinlastine are basically the same thing. The mechanisms throughout this

thing. The mechanisms throughout this video are going to be shown in red.

Adverse drug reactions will be shown in blue and treatment for adverse drug reactions will be shown in green. And of

course I'll summarize as we go. So the

mechanism here of these mitosis phase inhibitors is that vincine/vinlastine is going to bind to something called betatubulin and prevent

polymerization in the microtubule.

Packllet is going to hyperstabilize the Mphase. So basically it's going to just

Mphase. So basically it's going to just lock it into the Mphase and not let it get out. And it does that by acting on

get out. And it does that by acting on microtubules.

the arublin is going to bind to the high affinity end of the microtubule and prevent it from doing its job because it's sort of just like an added component sitting on the microtubule.

Now one point of distinction which I'm going to put here in parenthesis is that vin christristine and vinlastine prevent the formation of the motic spindle or the formation of microtubules because

they're preventing they're preventing polymerization but pletaxel is preventing the breakdown of it because it's hyperstabilizing it. Therefore, if

it's super stable, it can't be broken down. And if it can't be broken down,

down. And if it can't be broken down, recycled, and processed inside of the cell, then you're not going to be able to carry out the normal function that relies on the microtubule. So, if I can pause for just a second, I want you to

take away from this that vinristine/vinlastine are basically the same drug for the purposes of exams and they prevent the formation by binding to betatubulin and preventing

polymerization. Pletaxel will

polymerization. Pletaxel will hyperstabilize uh the Mphase because it's going to prevent breakdown. Irublin

is going to bind to the high ends of the microtubules, the high affinity ends of the microtubules and prevent them from doing their job. Now, some side effects that you need to know for exams. So, vincine and vinlastine are going to

cause neurotoxicity. Pletaxel will cause

neurotoxicity. Pletaxel will cause neuropathy and arubim will cause arthralgia. So, how do you remember this

arthralgia. So, how do you remember this stuff? I think you're going to need some

stuff? I think you're going to need some pneumonics. So the way that I learned

pneumonics. So the way that I learned this when I was in medical school was uh I I told a little story here. Now if

you're not familiar with US politics and you know scandals and such then this pneumonic might not work for you and I apologize but if you are familiar then maybe you remember uh a governor of New

Jersey called Chris Christie. And what

happened was years back Chris Christie was involved in something called Bridgegate where he intentionally caused a traffic jam on the George Washington Bridge going from New Jersey to New York. And this was politically

York. And this was politically motivated. And the the reason that I use

motivated. And the the reason that I use this as the beginning of the story is because Chris Christie sounds like Vin Christine and he was a very toxic governor. So I think of toxicity or

governor. So I think of toxicity or neurotoxicity. I also think about this

neurotoxicity. I also think about this tying into microtubules because microtubules are all about motion within a cell. And he was involved in

a cell. And he was involved in bridgegate which prevented motion across the GW bridge. And if you look at the GW bridge, the little spokes that go up the bridge even look like microtubules. So I

think that this story really ties nicely together. So the way that I kick this

together. So the way that I kick this off is that Vin Christine aka Chris Christie is really toxic. So it causes neurotoxicity. I can tie in that this

neurotoxicity. I can tie in that this story and Vin Christine and all of the drugs associated with this story have to do with microtubules because microtubules are responsible for motion within a cell and Chris Christie caused

Bridgegate which stopped all motion on the George Washington Bridge. Now when

motion was stopped you had to get some taxis and I tie taxis into plet taxel because taxel taxi sounds very very

similar. So I think about that in this

similar. So I think about that in this story, Pletaxel also is involved with microtubules because it ties into the story because it sounds like the taxi which had to therefore drive people

through an alternate route because of Chris Christie aka Vin Christine stopping motion on the George Washington Bridge. So you had Pletaxel or

Bridge. So you had Pletaxel or Pletaxis also involved with microtubules because they're taking the passengers an alternate route. So that's how I tie in

alternate route. So that's how I tie in Potaxel to the microtubial story. And

then when people realized what happened, they were really pissed off. They did

not like Chris Christie and he got booed. And you can see that we're going

booed. And you can see that we're going to irriain uh reminds me of booze. Booing

Chris Christie or booing Vincine and therefore acts on microtubules. So I tie all of this together and that's how I remember that these are the drugs that act on microtubules. Now the other thing

to know here is that irolin is going to cause arthralgas. And if you think about

cause arthralgas. And if you think about this when somebody's booing and they're holding up a sign that says boo, they might get some pain in their wrists.

That's an arthralgia. Um no real good way of learning that neuropathy is the side effect for pletaxel. Just memorize

it. But if but if you put all this stuff together and you're having trouble memorizing that these drugs act on microtubules, then you've got this really cool story about uh Vin Christine aka Chris Christie being a really really

bad governor of New Jersey and causing all this mess. So that's how I remember that these all have to do with microtubules. I know that Chris Christie

microtubules. I know that Chris Christie is toxic. So Vin Christine is

is toxic. So Vin Christine is neurotoxic. Uh if you hold up a sign

neurotoxic. Uh if you hold up a sign that says boo on it, arubalin will cause arthralgas in your wrist. And then I always memorize that pletaxel causes neuropathy. So those are the three

neuropathy. So those are the three drugs, four drugs if you will, that inhibit mitosis. Now let's move on and

inhibit mitosis. Now let's move on and talk about the drugs that inhibit the G1 phase. So those are going to be

phase. So those are going to be cysplatin, bulfin, cyclophosphomide and the nitro uras. So these are our G1 phase inhibitors. And you need to know

phase inhibitors. And you need to know these four drugs, right? Cysplatin,

bulfin, cyclophosphomide and carustine.

Carustine is a nitros ura. uh nitrous

ura is like the name of the category and then the specific agent is carine. So

here are the mechanisms these all cross-link DNA. So pretty easy because

cross-link DNA. So pretty easy because they all do the same thing. The only

little caveat that you need to know is with cyclophosphomide and carustine. So

cyclophosphomide will cross-link DNA specifically at guanine and it requires hpatic bioactivation.

Carustine on the other hand crosses the bloodb brain barrier and requires that its bioactivation occurs in the brain so that it can be used on CNS tumors right

so neurologic tumors tumors of the brain so carsine crosses the bloodb brain barrier and is activated in the brain cycloposphomide cross links DNA at

guanine specifically and must undergo bioactivation by the liver bulfin and cisplatin all you need to memorize is that they cross-link DNA so the the most

high yield thing about these G1 agents are actually the side effects. So what

you see here in blue cysplatin will cause ototoxicity and nephrotoxicity. Busulfin will cause

nephrotoxicity. Busulfin will cause pulmonary fibrosis. Cycloposomide will

pulmonary fibrosis. Cycloposomide will cause both a hemorrhagic cyitis which is very serious and SADH. Carine will cause central nervous

SADH. Carine will cause central nervous system toxicity which makes sense because it's used uh for tumors of the brain and it crosses the bloodb brain barrier and gets activated in the brain.

So you know it should make sense to you that the side effects will all occur in the brain. Some high yield stuff that we

the brain. Some high yield stuff that we need to point out is that we can actually treat some of these side effects. So in the case of cysplatin you

effects. So in the case of cysplatin you can prevent nephrotoxicity if you give a drug called amopostine or saline or both. So by giving amostine and saline

both. So by giving amostine and saline you prevent the nephrotoxicity associated with cysplatin. And in the case of cycloposomide if hemorrhagic cyitis occurs you treat with a drug

called mezna. I always loved this point

called mezna. I always loved this point because mezzna is such a unique sounding agent and if you're going to treat hemorrhagic cyitis you use mezna. So

there have to be some pneumonics in order to remember these high yield adverse drug reactions and I've got some awesome ones for you. So for cysplatin

it makes the kidney go splat and splat is in the name cisplatin. So you know splat cisplatin makes the kidney go splat. So it causes nephrotoxicity and

splat. So it causes nephrotoxicity and we treat that nephrotoxicity with amifine and saline. Busulopen causes

pulmonary fibrosis and this is one of two anti-cancer drugs that will cause pulmonary fibrosis and conveniently the other one also begins with the letter B.

Now in the case of this we're going to memorize pulmonary fibulfan instead of pulmonary fibrosis. So we just replace

pulmonary fibrosis. So we just replace the second part of the word with bulfan because fibrosis maybe sounds like fibrosulfan a little bit.

Cycloposphomide. Well, this has the most serious adverse drug reaction of all the G1 inhibitors. And if you look in the

G1 inhibitors. And if you look in the name, cyclloamide has hosp in the middle. So, you have to go to the

middle. So, you have to go to the hospital if you get hemorrhagic cyitis because it's the most serious adverse drug reaction acutely of any of those on

uh the G1 inhibitors. So, if you give cyclloamide, you might have to go to the hosp hospital which is in the name of the drug. if you get hemorrhagic cyitis.

the drug. if you get hemorrhagic cyitis.

So on exams if if someone has cancer and all of a sudden they're urinating blood the answer to cyclophosamide you treat it with mena that's it and for karmastine it must cross the bloodb

brain barrier and must is in the name karmastine. So these are some really

karmastine. So these are some really awesome pneumonics that you can use by looking at the name of the drug and keeping things simple. Okay so if you're wondering for one second I want to pause

and take a step back here. If you're

wondering, how am I going to remember that these four agents are in the G1 uh inhibitor section? Well, by

inhibitor section? Well, by understanding the cell cycle and knowing that in G1, all of your cellular contents get duplicated. By

cross-linking DNA, none of that can happen. So, if you understand what

happen. So, if you understand what happens at G1 and what happens at S and what happens at G2 and you can also memorize or understand or use pneumonics to know the mechanisms, then this should

all fall into place. So, by

cross-linking DNA, cellular contents will not be duplicated, which means G1 won't happen. So, if you know

won't happen. So, if you know cross-linking DNA for these four agents, you'll have no problem memorizing the G1 agents. Now, the hardest category to

agents. Now, the hardest category to memorize is our next category, and that's the Sphase. And this is where DNA synthesis occurs. The agents that you

synthesis occurs. The agents that you need to know are aoprine, cladine, citarabine, five fluoroicil, six mecapurine, hydroxyura, and methtoate.

And I'm going to do my best to simplify this for you, but this is definitely the toughest category because it's got seven drugs. So, we're talking about the

drugs. So, we're talking about the Sphase inhibitors, and here are our seven agents. Now, instead of throwing

seven agents. Now, instead of throwing up all of the mechanisms at once, I want to go through these methodically to help your brain digest this information. So

aothioprne and six mercaptopurine are basically the same thing for the purposes of exams because aothioprine actually gets metabolized into 6MPP when it's broken down. So both of these

agents are going to inhibit denovo pureine synthesis. And if you look at

pureine synthesis. And if you look at the name markeeptop pureine aothoprne that's hinting that these are going to inhibit purine synthesis because you know that they're somehow

involved with purines because of the names. Now both of these are activated

names. Now both of these are activated by HGPRT and interestingly and extremely high yieldly if that's a word these are metabolized by zanthine oxidase. We're

going to come back to this when we talk about adverse drug reactions but for now just deposit that little tidbit in the back of your brain. Aothoprne and six peraptoine are both metabolized by

zanthine oxidase. Now if you look at the

zanthine oxidase. Now if you look at the other part of the slide we'll slide we'll switch gears and talk about cladbine and citarabene. So cladrobine

is a purine analog. Look at the name ribbine. So that's you know it's hinting

ribbine. So that's you know it's hinting that it's a purine. Caiter it's hinting that it's a pyramidine right? Look at

the why. Scarabine. Okay. So so the names can tell you a lot if you're if you're stuck or you you find an exam question tricky. Methtoate is going to

question tricky. Methtoate is going to inhibit dihydroofolate reductase. We'll

come back to this because there's a very very high yield adverse drug reaction and treatment that we'll talk about.

Five floruricil is going to be a pyramidine analog. Look at the name.

pyramidine analog. Look at the name.

It's five fluoroicil. So it's an analog that's of

fluoroicil. So it's an analog that's of a perramdine and it specifically inhibits thyolate synthace. Lastly,

hydroxyiora inhibits riboucleotide reductase. So now let's talk about the

reductase. So now let's talk about the high yield adverse drug reactions. And

as a sort sort of a theme throughout the anti-cancer drug series, uh any question that you get is most likely to ask you about adverse drug reactions. Now, don't

get me wrong, they can certainly ask you about mechanisms or treatments of adverse drug reactions, but they're going to probably go after those ADRs.

So, so be sure that you know them.

Here's what here's what we got. So, for

aothoprne and six mercapurine, I told you that they were both metabolized by zanthine oxidase. So if you give a drug

zanthine oxidase. So if you give a drug such as alopurinol or fibuxostat which both have mechanisms of inhibiting zanthine oxidase then you're inhibiting

the enzyme that breaks down aothoprne and six mercaptourine. So if you give one of these cancer drugs and you give alopurinol or phoxat then aothioprne and

six mercaptopurine will not be broken down because zanthin oxidase is inhibited by the alopurinol. So on

exams, this will come up as a patient who they either hint at that has cancer or is a previous cancer patient and then all of a sudden they're given some drug

um and there's massive side effects or massive toxicity. And what they're

massive toxicity. And what they're hinting at here is that you have this cancer patient who may or may not have been or is on aothopine or six more captopurine and now they're getting alopurol and maybe the question will be

really nice to you and describe a sort of gouty arthoralic presentation and you need to figure out what these drugs are or maybe they'll ask you a question about you know like which of the following is the mechanism or the

pathophysiology by which this is occurring. So, it's it's really random

occurring. So, it's it's really random because you're going to read this question. It's going to be a question

question. It's going to be a question that's either about cellular biology or oncology and then they're going to tie it into a drug that treats gout. Your

your brain is going to be blown when you're taking the exam because you're going to be like, "What the hell are they asking me?" But if you stop for a second and understand that aothoprne and six mercaptopine are both metabolized by

zanthine oxidase, then you'll be able to tie this together on test day. For

methtoate, the high yield adverse drug reaction is miloppression. Now, let me pause for a second. If you're looking through First Aid or any other review textbook or, you know, UWorld, whatever

it is, you'll notice that every single anti-cancer drug has milo suppression as an adverse drug reaction. And what I'm going to tell you is that none of those drugs you should memorize my suppression

for. Literally erase it from your brain

for. Literally erase it from your brain because non-specific adverse drug reactions will not be asked on USMLE or COMLEX. But this is the one exception

COMLEX. But this is the one exception and that's why it's exceptionally high yield no pun intended because in the case of methtoate it does cause myoppression but this is the one example

where you can actually treat that myoppression. So if you give somebody

myoppression. So if you give somebody methtoate and induce miloppression as an adverse drug reaction you give them a drug called luccovorin and it actually

treats the myoppression. But for

literally every other anti-cancer drug which is going to inhibit some part of the cell cycle and therefore obviously suppress the myoid lineage then yeah there's you know there's nothing to

memorize there. It causes miloppression

memorize there. It causes miloppression but they can't ask you that because every drug does that. So only memorize miloppression for methtoresate and know that you treat it with luccovorin. For

cladrobine it causes nephro and neurotoxicity. First scarabine it causes

neurotoxicity. First scarabine it causes pansyenia which is easy to remember because the Y in pantopedia the Y in primdine analog and

the Y in s terabine. So it all goes together with the Y. Five fluuroil

causes hand foot syndrome which is basically just like reening of the hands and feet. Very very high yield. I I'll

and feet. Very very high yield. I I'll

give you an awesome pneumonic for this in just a second. And for hydroxyura there's no adverse drug reaction that you should memorize. It's more important to know the mechanism. So, let me give you some pneumonics for these things.

So, for aothoprne, I want you to spell it out aoth, but spell it with an exo.

And that exo will remind you that it's metabolized by zanthine oxidase. X for

zanthine, O for oxidase. For

methtoresate, I want you to write it out as methodate. And DR will tell you that

as methodate. And DR will tell you that it inhibits dihydropholate reductase.

So, D for dihydropholate and R for reductase. Also again know that it

reductase. Also again know that it causes miloppression. Treatable with

causes miloppression. Treatable with luccovorin. For citarabine again it's

luccovorin. For citarabine again it's all the y's right. Y in pancopenia y in perimeine analog and y in sitarabene.

This is the only drug where it all has y's. For hydroxyurora I want you to

y's. For hydroxyurora I want you to write it out with two Rs at the end.

Hydroxyura. R for riboucleotide reductase to help you memorize the mechanism. And then for hand foot

mechanism. And then for hand foot syndrome, well the drug is five fluoroicil and that is commonly referred to as five FU. And when you say FU to somebody, you flip them off and it

causes reening of the hands, which is known as hand foot syndrome. So flipping

somebody off or saying FU for 5 FU reminds me that it's the hand because the hand is what you use to flip somebody off. It's the hand that gets

somebody off. It's the hand that gets read as the adverse drug reaction. So

really awesome high yield adverse drug reaction and pneumonics. So know all this stuff. The S inhibitors are really

this stuff. The S inhibitors are really really high yield because there's so many of them. But I I think that I broke it down rather nicely. So know what you have here on this slide. So that's the

Sphase. Let's wrap up with uh the G2

Sphase. Let's wrap up with uh the G2 phase. So the agents that you need to

phase. So the agents that you need to know in the G2 phase, autotopicide, tenipicide, iron, and topoot. Now the G2 inhibitors are actually fairly simple because for the purposes of exams, these

are basically just two drugs. Tenipicide

and topicide are basically one drug, right? They're like the same thing. They

right? They're like the same thing. They

all end in posside and topoot and ironotic also should be considered one drug. They both end in otcan. So there's

drug. They both end in otcan. So there's

a very clear delineation here. The ones

that end in pide, right, tinipide and etopicide inhibit topo isomease 2. The

ones that end in otan or tcan inhibit topo isomease 1. So clearly if you look at the names here, you've got Topo, you got Tanipo, Etopo, IO, like they all

have O's and stuff. So it should quue you in to know that we're talking about topo isomease. The hard thing here is

topo isomease. The hard thing here is knowing which one causes inhibits topo isomease 2 and which one inhibits topo isomease 1. And the way that you can

isomease 1. And the way that you can memorize this is to think of a posi. So

a posi is like a slang term for a crew of people, right? Like, yo, where's your posi at? Like your group of friends that

posi at? Like your group of friends that are all doing the same thing. That's a

posi. And in tenipocide and etopicide, you've got the word posi, right? Tenny

posi d o eto posi d or etopicide, right?

Like I'm spelling it phonetically, but the word posi is there. So in tenipocide and etopicide because posi is in the name that inhibits topoisomease 2

because a posi of people is two or more people. So it's going to be DNA topo

people. So it's going to be DNA topo isomease 2 for the ones that have posi in the name because a posi is at least two people. That's how I memorize that.

two people. That's how I memorize that.

Really really easy. And then if you know that then by process of elimination topotan and irinocan must inhibit DNA topo isomease one. Now if you're wondering how the heck do I remember

that these inhibit the G2 phase? Well

the G2 phase is the DNA doublech check phase. And basically DNA topo isomease

phase. And basically DNA topo isomease goes through and double checks that the DNA is wound correctly because sometimes it gets wound so tightly that the DNA topo isomease has to like backtrack a

little and fix it. So because it's double-checking it in the G2 phase, you know that anything that inhibits DNA topo isomease obviously works in the G2 phase. And you should know that if you

phase. And you should know that if you studied cellular biology. Uh so you should be good to go assuming that you got the basics down. So those are all the drugs in these four categories.

There's one more category that doesn't fit onto this slide that we'll talk about now and and these are the anti-tumor antibiotics and of course um these are going to be identifiable

because the names actually sound like names of antibiotics. So we've got docar rubicon and danor rubiconin which we will consider one drug for the purpose of USML and complex and bleomy. Docar

rubicon and danor rubiconin are going to work by intercolating DNA and bleomy is going to work by generating free radicals which of course if you generate free radicals against DNA or any

substance then the cell can't divide and therefore cancerous cells can't divide.

The adverse drug reactions here um dilated cardiomyopathy for doc rubicon and pulmonary fibrosis for bleomy. So

remember that bulfan also caused pulmonary fibrosis. So the ones that

pulmonary fibrosis. So the ones that begin with B cause pulmonary cause pulmonary fibrosis and you can remember that by replacing the rest of the word fibrosis with whatever the drug is. So

for busulfan we said the pneumonic was pulmonary fibulfan and in this case the pneumonic is pulmonary fibomycin. So

fibrosis you know just remember the B in fibrosis should cue you that the drug is either bleomy which has a B or bulfan which has a B. For docar rubicon, it causes dilated cardiammyopathy. And this

is so high yield. I cannot stress this enough. On exams, the way that this will

enough. On exams, the way that this will present is you'll have a patient who they might hint at is either a cancer patient or a, you know, a cancer survivor. And then all of a sudden,

survivor. And then all of a sudden, they're going to try to hint at some type of cardiammyopathy. They might give you heart failure. They might give you like, you know, stroke volumes and afterloads and and weird graphs that

you're going to have to interpret. But

the bottom line is going to be that there's going to be a very clear cardiomyopathic process. And what

cardiomyopathic process. And what they're going to ask you is either A, what's the drug? Answer would be Dr. Rubeson. B, what's the mechanism of the

Rubeson. B, what's the mechanism of the drug? Answer would be intercolation of

drug? Answer would be intercolation of DNA. C, what is going on? Answer would

DNA. C, what is going on? Answer would

be dilated cardiammyopathy. Or D, what's the treatment? In which case, you should

the treatment? In which case, you should know that you treat dilated cardiammyopathy that's induced by DX rubicon by giving a drug called dex roxane. So this is really high yield.

roxane. So this is really high yield.

cannot stress it enough. Know the drugs that know the anti-cancer drugs that have adverse drug reactions that are treatable. So we talked about a few

treatable. So we talked about a few today. We talked about doc rubicon. We

today. We talked about doc rubicon. We

talked about cyclloposomide. We talked

about cysplatin. So amifostine for cysplatin. Mezna for cycllo phosphomide.

cysplatin. Mezna for cycllo phosphomide.

Uh dexrazoxane for docar rubicon. And we

also talked about methtoresate. Remember

myosuppression is the only one that you should memorize my suppression for is methtoresate which was treatable with luccovorin. So know those four know the

luccovorin. So know those four know the four adverse drug reactions and know what you treat them with. But that's it right? So we we are now done. We've

right? So we we are now done. We've

covered all the anti-cancer drugs that you should know. There are a couple more that I didn't include in this lecture but they're not nearly as high yield as the ones in this lecture. So if you know your cellular biology, you know the cell

cycle, you understand a little bit about what DNA topo isomease does and you know what happens in G1, G2, S, mitosis, and then you know this video, you'll be very

well suited to either dive deeper into this topic or just to superficially try to answer some questions and leave it at that. But that's it and I hope this was

that. But that's it and I hope this was helpful to you.