We have a drug here
You’d find that children
might be acting out,
so you’re looking at childhood cancers.
It intercalates the DNA, making it difficult
for the DNA to properly carry its action.
So once you know it’s childhood
cancers that you’re affecting,
then you start thinking about the
childhood cancers, Wilms tumor,
the renal cell cancer in
your child, Ewing’s sarcoma.
This is your translocation that
you know about called 11;22,
and you have involvement at the diaphysis
of the bone in Ewing’s sarcoma.
especially the young type,
and you’re referring to
a.k.a. sarcoma botryoides, usually
used for childhood tumors.
are you looking for?
Here, it generates
noncovalently intercalated DNA, breaks
into DNA, and also inhibits replication.
So there are many points of
your proper DNA mechanism
or replication that
completely slows it down.
The clinical uses:
part of what’s known as ABVD,
and this is your Adriamycin,
which is part of regimen that you
probably need to know for Hodgkin.
Also, used for myelomas, solid
tumors, a lot of places.
In the process though, what you’re worried
about definitely is cardiotoxicity,
and toxic tissue because of extravasation.
It actually comes out, cause
damage to the tissue.
Doxorubicin, Adriamycin, ABVD,
Bleomycin, a G2 phase
includes a formation
of free radicals.
Again, just like we
saw with your doxy,
and it breaks your DNA strand.
Can use this in
It’s also part of your ABVD.
The B in ABVD is your bleomycin.
The A was Adriamycin, which
is part of that doxorubicin.
Well, bleomycin, it may then
cause pulmonary fibrosis,
B and B, if that helps you.
There, etoposide, or toposide, in
general; teniposide and etoposide.
teniposide and etoposide.
Well, these are the drugs that
then inhibit topoisomerase 2.
Therefore, it increases DNA degradation.
It’s used between S and G2.
It can be used for small cell lung
cancer, which is also called oat cell.
If you want, take a look
at the ETO in etoposide.
How would you pronounce OTE?
Oh, ote, if that helps you.
So etoposide, oat cell cancer.
What’s another name for small cell?
Oh, yes, oat cell
cancer of the lung.
Also, testicular and prostate,
and you’re worried about
alopecia and myelosuppression,
etoposide, topoisomerase 2, oat cell
cancer of the lung, and testicular.
You need to memorize
Bioactivation by the liver.
hemorrhagic cystitis, look
for blood in the urine,
and maybe treated
by giving mesna.
Know your couple of
You have carmustine, lomustine,
This, you need to make
sure C –, carmustine,
C – crosses the blood-brain
barrier into the CNS.
brain tumors, including GBM,
Is it always effective?
Unfortunately, it’s not.
May then, unfortunately, because of
its crossing, cause CNS toxicity.
alkylates the DNA.
CML, also used for ablating bone marrow in
hematopoeietic stem cell transplantation.
Don’t forget about that.
And here, once again, another B,
busulfan, pulmonary fibrosis.
What was the other one that start with
the B resulting in pulmonary fibrosis?
We had our bleomycin.
Here, we have our vinca alkaloids.
So, we’re in the M phase.
Vincristine and vinblastine.
Use the -cristine and the
-blastine to advantage.
You’ll see why.
Mechanism, what does it do?
Well, in the M-phase, it literally inhibits
the polymerization of your microtubule.
And therefore, the microtubules will not
properly pull your chromosomes apart.
That’s your vinca alkaloid.
It’s part of your MOPP
regimen for Hodgkin,
and this would then be oncovin,
which is your vincristine.
Also, it could be used for
the C in vincristine will
be for CNS toxicity.
Also, oncovin, also
If you’re dealing with vinblastine,
it’s going to affect the bone marrow.
B – blastine,
B – bone marrow suppression.
another method in which you
can affect the M phase.
Here, literally, the spindle
is not going to break down.
You’re going to inhibit taxing.
You can use this for, perhaps, ovarian and
breast cancers in a female, obviously.
And hypersensitivity is
what you’re looking for.
The paclitaxel and vinca alkaloids
will be affecting your M phase.
Don’t forget though, the vinca alkaloids will
behave by inhibiting the polymerization.
And then here,
it will hyperstabilize the taxols, will
hyperstabilize the polymerized microtubule.
In other words, it will
freeze the “tubules”
so that it doesn’t break down,
therefore, cannot replicate.
Make sure that you know the actual
medical pharmacologic language
when dealing with vinca
alkaloids, and also, taxols.
inhibition of polymerization.
plat-, your platinum drugs.
Acoustic, acoustic nerve damage,
eighth cranial nerve, platin.
Last time you saw hydroxyurea was
to then inhibit what’s known as --
or to help a patient
increase your hemoglobin F.
it is used and could be
used for melanoma, CML.
And the reason we have sickle disease,
even though it’s not a cancer
is the fact that it
increases hemoglobin F.
In sickle cell disease, remember your
completely deficient hemoglobin A,
you’re then going to increase
quite a bit of hemoglobin S
when you have polymerization.
This is not good.
You are then going to or wish
to increase hemoglobin F,
which will then
cause a left shift.
This is then going to also cause bone
marrow suppression and GI upset.
Here, we have prednisone.
What is a steroid doing here?
Well, it may trigger
apoptosis, as we know.
Remember, the lymphopenia stuff
that we talked about earlier.
It may even work on
Most common glucocorticoid in
cancer therapy used in CLL,
chronic lymphocytic leukemia.
May be part of that MOPP
regimen, your last P.
We have also immunosuppressed.
Meaning to say that it may be
used in autoimmune diseases,
which then require
Obviously, when utilizing prednisone,
you’re worried about Cushing-like symptom,
cataract, osteoporosis, everything
that you would expect with prednisone
or cortisol type of side effect, including
your peptic ulcer disease in the stomach.
Here, we have our
tamoxifen and raloxifene.
First and foremost, these are going to
be your estrogen receptor modulators.
These are then going to behave as antagonist
in the breast and agonist in the bone.
So therefore, these
are partial agonists.
It will block the binding of estrogen to
the estrogen receptor-positive cells.
You’re looking at your ER
positive breast cancers.
Also, osteoporosis because it is going
to be an agonist towards your bone.
We’re going to divide our
tamoxifen, raloxifene as such.
Tamoxifen may increase the risk
of endometrial cancer due to the
partial agonist type
of effective estrogen.
Whereas, raloxifene does not increase
the risk of endometrial cancer
because it is an
Raloxifene seems to be a little bit better
in terms of not having as
much of a risk as tamoxifen.
Here, we have Herceptin
Your patient is HER-2/neu
positive, which is Erb-B2.
HER-2 stands for human epidermal
receptor growth factor.
This is a metastatic breast cancer
or really, really Erb-B2 positive,
dangerous breast cancer,
Imatinib would be
used for 9 and 22.
We talked about tyrosine kinase.
It could also be used forth
on a c-kit positive,
And by c-kit, we mean that also, you’ve
heard of gastrointestinal stromal tumor,
and you could have tyrosine
kinase there as well.
And so therefore, imatinib would be
a drug to utilize in such issues.
CML and GIST, gastrointestinal
which is a smooth muscle benign
tumor found in the stomach.
Rare, but of all the benign tumors in
the stomach, GIST is the most common.
Fluid retention toxicity.