Now, before you move on, it's about organisation
first that you set up. Then you memorise.
In that way you have created containers or compartments
in which you can then fill it up with details.
Okay. But first, take a look at the skeleton of
the outline here. Important growth factors,
think about where you are. Close your eyes. Conceptualize.
These are growth factors that are going to work in excess.
And when they do, they are going to then stimulate the
receptors in excess, you are going to have increased
signal transduction down to the nucleus and obviously may
result in increased growth. The first growth that you will
be responsible for is called a FGF. A fibroblast growth
INT-2 is a FGF. Fibroblast growth factors.
Another detail. And this could be associated with many types
of cancers. And the big one that you definitely want to know,
is this one. A growth factor PDGF associated with SIS and the
type of cancer this is associated with will be gliomas.
In other words, astrocytoma. When we talk about neuropathology
under astrocytoma there will be two major astrocytomas
that you will be responsible for. One in fact will be glioblastoma
multiforme. The other one being palisidic type of neuroglioma.
Our next category would be what does a growth factor
bind to. A receptor. So these are receptors that
have now become independant autonomous of any control
whatsoever. Now these receptors are working in great excess
or in great stimulation. And now you can imagine, with autonomous
receptor activity that there will be increased signal transduction
down to the nucleus. Our big one here will be ERB-B1 and ERB-B2.
ERB-B1 and ERB-B2. ERB-B1 well, we have epidermal growth factor
receptor. And ERB-B1 is specific for squamous cell cancer of
the lung and that you have to know. Then we have ERB-B2.
How many breast do you have? Two. The other name for this
is also Her2/neu. This is the epidermal growth factor receptor
that you want to know and it's association with breast
cancer more so. You have two major epidermal growth factor
receptors. ERB-B1 and ERB-B2. Make sure you know about
lung and breast respectively. Then you have another
growth factor receptor and this is RET. Now with RET,
it's a glial neurotrophic factor receptor. Glial.
RET is associated with medullary cancer of the thyroid.
Well found often with MEN IIa and IIb. Oncogenes and now
signal transduction. We have t(9;22) being our second
major translocation in this topic. And with t(9;22)
you must know that it is a BCR-ABL fusion protein. Memorise
that. Do not get BCR confused with BCL2. Students often do that.
Do not do it anymore. With t(9;22) I told you apart from CML, chronic
myelogenous leukaemia, where the median age for this would be?
40s. ALL, acute lymphoblastic leukaemia the most common
cause of leukaemia in a child. Both associated with
Philadelphia chromosome, BCR-ABL, this then codes for? Good.
RTK, or in other words or non-receptor tyrosine kinase.
At least know the operative word TK. Tyrosine Kinase. K-RAS
really the foundation here is RAS. I have mentioned this a few times
I promise, I will go into detail. We have to. RAS is coupled
with? I asked you kindly to memorise RAS is committed to what
GTP. Once again, RAS associated with GTP. For henceforth, if
you want, you may want to pronounce or spell pancreas as
pancRAS, if that helps you. But we have pancreas and we
have the colon being two major cancers, with K-RAS.
You can have other RAS's as well including H-RAS and also
N-RAS and as we continue through our course in pathology,
I will tell you where H-RAS is associated with. And
N-RAS is already dealing with our 'N' as in Neuro.
Here we will take a look at nuclear regulators. We are down in
the nucleus. We have C-myc and this are working within the nucleus,
bringing about Burkitt lymphoma. 'L' as in L-myc would be for?
Lung. And more so with small cell lung cancer. And then 'N',
as in neuro, neuroblastoma. Take a look at what happened here.
We have N-myc and it is then being placed next to these HSR.
And this regions that N-myc might be associated next to would
then cause gene amplification. And that you have to know.
So take a look at that N-myc and next to HSR
then causes major gene amplification.
Our next topic takes us into cell cycle regulators. Within
the cell cycle regulator, I will focus upon cyclin D
as being a separate topic, I have to. But anytime that you
see cyclin D, these are within the cell and within the cell
cycle we will talk about further with tumor suppressor
genes. And I will walk you through in great detail
the exact mechanism as to how cyclin D is going to promote
a cell to be or remain within a cell cycle forever more.
And cyclin D positive to you, at least memorise mantle cell
lymphoma. And this translocation here would be t(11;14).
What's that chromosome 14 represent to you?
It represents immunoglobulin heavy chain.