Understanding Anticancer Drugs Through the Cell Cycle

Name: Cancer Drugs/Pharmacology
Uploaded: 2026-01-16T07:21:12.046716+00:00
Channel: Dirty Medicine
Description: Understanding Anticancer Drugs Through the Cell Cycle The Cell‑Cycle Primer The cell cycle is divided into M phase (mitosis), G1, S, and G2.

Dirty Medicine

Jan 16, 2026

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3 min read

YouTube video ID: VD8h0XsEFho

Source: YouTube video by Dirty Medicine — Watch original video

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The Cell‑Cycle Primer

The cell cycle is divided into M phase (mitosis), G1, S, and G2.
M phase ends with the physical split of a cell into two daughter cells.
G1 – cellular contents are duplicated.
S phase – DNA synthesis (replication).
G2 – DNA quality‑check and preparation for mitosis.

M‑Phase (Mitosis) Inhibitors

Drug	Mechanism	Key Adverse Effect
Vincristine / Vinblastine	Bind β‑tubulin → block microtubule polymerisation → spindle cannot form	Neurotoxicity
Paclitaxel	Hyper‑stabilises microtubules → prevents their breakdown	Neuropathy
Vinorelbine	Binds high‑affinity end of microtubules → blocks function	Arthralgia

Mnemonic – Vin Christie (toxic governor) → neurotoxicity; taxi → Paclitaxel neuropathy; boo → Vinorelbine arthralgia.

G1‑Phase Inhibitors (DNA Cross‑Linkers)

Cisplatin, Busulfan, Cyclophosphamide, Carmustine (a nitrosourea).
All cross‑link DNA, preventing duplication of cellular contents in G1.
Special notes:
Cyclophosphamide – liver bio‑activation, cross‑links at guanine.
Carmustine – crosses the blood‑brain barrier, activated in the CNS.

High‑Yield Toxicities & Management - Cisplatin → ototoxicity & nephrotoxicity → prevent with amifostine + IV saline. - Busulfan → pulmonary fibrosis. - Cyclophosphamide → hemorrhagic cystitis → treat with mesna. - Carmustine → CNS toxicity (expected due to BBB penetration).

S‑Phase Inhibitors (DNA Synthesis Blockers)

Drug	Primary Target	Notable Toxicity
6‑Mercaptopurine / Azathioprine	Inhibit de‑novo purine synthesis (HGPRT activation)	Myelosuppression (treated with leucovorin for methotrexate only)
Cytarabine	Pyrimidine analog → DNA chain termination	Pancytopenia
5‑Fluorouracil (5‑FU)	Inhibits thymidylate synthase	Hand‑foot syndrome
Methotrexate	Dihydrofolate reductase inhibition	Myelosuppression – treat with leucovorin
Hydroxyurea	Ribonucleotide reductase inhibition	–

Key Mnemonics - A‑X‑O → Azathioprine metabolised by Xanthine oxidase. - Methodate → Methotrexate (DR = dihydrofolate reductase). - 5‑FU → “F‑U” (flip‑off) → hand‑foot syndrome.

G2‑Phase Inhibitors (Topoisomerase Blockers)

Topoisomerase II inhibitors: Etoposide, Teniposide (‑pide suffix).
Topoisomerase I inhibitors: Irinotecan, Topotecan (‑tan/‑can suffix).
They prevent the DNA unwinding/checking step that occurs in G2.

Anti‑Tumor Antibiotics (Do Not Fit the Cycle)

Drug	Mechanism	Toxicity
Doxorubicin (Daunorubicin)	DNA intercalation	Dilated cardiomyopathy → treat with dexrazoxane
Bleomycin	Free‑radical generation	Pulmonary fibrosis (same cue as Busulfan)

Treatable Toxicities – What to Remember for Exams

Cisplatin nephrotoxicity → amifostine + saline.
Cyclophosphamide hemorrhagic cystitis → mesna.
Methotrexate myelosuppression → leucovorin (folinic acid rescue).
Doxorubicin cardiomyopathy → dexrazoxane.
5‑FU hand‑foot syndrome – supportive care only.

Study Tips & Mnemonics Recap

Link drug names to visual or story cues (e.g., Christie → neurotoxicity).
Use suffixes: ‑pide = Topo II, ‑tan/‑can = Topo I.
Remember “B” drugs cause pulmonary fibrosis (Busulfan, Bleomycin).
Associate adverse‑effect treatments with the drug (amifostine ↔ cisplatin, mesna ↔ cyclophosphamide, dexrazoxane ↔ doxorubicin, leucovorin ↔ methotrexate).

By mastering the cell‑cycle phases, the mechanisms that each drug class targets, and the high‑yield toxicities plus their antidotes, you can answer most USMLE/COMLEX questions on anticancer pharmacology without re‑watching the video.

Linking each anticancer agent to its specific cell‑cycle phase, mechanism, and treatable toxicity provides a clear, exam‑ready framework—so you can master pharmacology without needing the original video again.

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Cancer Chemotherapy Pharmacology Textbook Recommended

Comprehensive reference that explains mechanisms, side‑effects, and clinical use of anticancer drugs, reinforcing the cell‑cycle framework discussed

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Full Transcript YouTube

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
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,
something's happening. And in mitosis,
ultimately, you get the splitting of the
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,
Pletaxel and Arubilin. So we're talking
about Mphase inhibitors or inhibitors of
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
drugs act on the Mphase is some of them
specifically are going to inhibit
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
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
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
lock it into the Mphase and not let it
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,
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
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
neuropathy and arubim will cause
arthralgia. So, how do you remember this
stuff? I think you're going to need some
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
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
neurotoxicity. I also think about this
tying into microtubules because
microtubules are all about motion within
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
off is that Vin Christine aka Chris
Christie is really toxic. So it causes
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
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
Pletaxis also involved with microtubules
because they're taking the passengers an
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
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
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
is toxic. So Vin Christine is
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
drugs, four drugs if you will, that
inhibit mitosis. Now let's move on and
talk about the drugs that inhibit the G1
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
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
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
pulmonary fibrosis. Cycloposomide will
cause both a hemorrhagic cyitis which is
very serious and
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
need to point out is that we can
actually treat some of these side
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
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
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
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
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
name, cyclloamide has hosp in 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.
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
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
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
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
cross-linking DNA for these four agents,
you'll have no problem memorizing the G1
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
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
Sphase inhibitors, and here are our
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
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
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
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
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
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.
It's five
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
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
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
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
because you're going to read this
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
because non-specific adverse drug
reactions will not be asked on USMLE or
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
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
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
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
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
it inhibits dihydropholate reductase.
So, D for dihydropholate and R for
reductase. Also again know that it
causes miloppression. Treatable with
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
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
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
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
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
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
all end in posside and topoot and
ironotic also should be considered one
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
knowing which one causes inhibits topo
isomease 2 and which one inhibits topo
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
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
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.
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
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
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
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
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,
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
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
drug? Answer would be intercolation of
DNA. C, what is going on? Answer would
be dilated cardiammyopathy. Or D, what's
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.
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
today. We talked about doc rubicon. We
talked about cyclloposomide. We talked
about cysplatin. So amifostine for
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
four adverse drug reactions and know
what you treat them with. But that's it
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
helpful to you.