Here we will take a look at proto-oncogenes.
Always go back and take a look at that flow chart
so that you know exactly as to where you are
located. That is your roadmap to carcinogenesis.
And at some point in time when you read a GPS you
always want to kind of want to know where you began from
and where you end up. And at this point we are looking
at proto-oncogenes and before we get into actual carcinogenesis
understand that proto-oncogenes are things that we require.
For proper normal cellular growth. For example,
as an embryo and a foetus our brain develops. We can't
do that on our own. We need the help of proto-oncogenes.
Now imagine that you have the development of cancer.
This is unregulated, not supervised growth of cells.
So what do you think happens to the proto-oncogenes.
It gets mutated and then it becomes a oncogene.
What's the name of a specialty that, maybe a clinician
such as yourself in the future will go into? An oncologist.
So here genes that actually form oncology or the practice
of cancer. So what's the mechanism of action that you want to
be familiar with. We will dive into great detail about RAS.
And before we get into that I want to make sure that you
understand a proper organization method that I will be
setting up for you. You will be looking at growth factors
and when the time is right I will talk to you about
certain growth factors that are associated with
certain cancers that you must know. Growth factors bind
to please? Receptors, good. And those receptors will then
communicate with whom? Signal transducers that are located
where? On the inside aspect of your membrane. Where are you now?
In the cytoplasm and from the cytoplasm you are then
going to communicate with and to the nucleus.
And within the nucleus you require certain transcription
factors and obviously certain oncogenes that are able to
then tell the DNA to continue replicating without stop.
I'll show you where RAS is located in that journey.
The translocations, example here will be something like
t(8;14). So now at this point I would like for us to
expand upon the translocation or specifically chromosome
14. Really important for us. Now to begin with,
take a look at the parenthesis here. There is no such thing
as an IgH, alright. There is an IgG, IgA, IgM, IgE, IgD
but there is no such thing as IgH. So what does that H
stand for. I want you to think of the anatomy of an immunoglobulin.
And in Immunology you learned about that there is a
heavy chain and light chain. Well it's the heavy chain
that you are focusing upon here, specifically
with chromosome 14. Hence, the IgH.
Now whenever you see the chromosome 14 in any type of
cancer that you are associated with including t(8;14),
t(11;14) and t(14;18), guess what they all contain an
immunoglobulin heavy chain. Versus what Dr. Raj?
Versus light chains. You have heard of multiple myeloma.
You have heard of IgG and IgA. And with multiple myeloma
you have heard of Bence-Jones proteins. Those are your
light chains and that would be kappa and lambda,
we'll obviously talk about that in WBC pathology. So what
you are looking at here is a normal chromosome on your left
8 and 14. Perfectly normal. They are not sharing
at all any particular components of the chromosome.
Then what then happens with Burkitt lymphoma is the
fact that there is a translocation of 8 upon 14.
And now at this point you have an oncogene next to IgH.
Excuse me. Better said as immunoglobulin heavy.
I want to make sure we are clear. So when you have an oncogene
next to an immunoglobulin heavy chain guess what you are going to do.
You are going to create an abundance of immunoglobulin heavy
chain. Welcome to Burkitt lymphoma. And with Burkitt lymphoma,
I want to make sure that we reinforce over and over again, you
will be responsible for two types. You'll have the endemic type
and the non-endemic type. The endemic type is the type that
you will find in Africa. Non-endemic type will be the type
that most likely will be found in North America. We'll take
a look at gene amplification. This is when you have a
messenger down in the nucleus that is able to then
cause or instruct a DNA to never stop replicating.
An example for this would be something like MYC as well.
But this one is N-myc with neuroblastoma.
I'll summarise all this for you when we get into
actual growth factors and such.