We may acquire another mutation or we may not.
In the case of tumor suppressor genes, we actually need to have
two hits, which brings us to the two hit hypothesis.
So in a tumor suppresor gene, if we came into life with one,
we are more likely to acquire another because we already have one,
then we would be if we came into life
without any copies, so we have no copies,
and we'd have to acquire two
in order for that cancer to develop.
The other cases in proto-oncogenes,
we often only need to have one copy in order for cancer to occur.
So if we have only one copy, for example,
let's say it is a growth factor, for example.
If we have a growth factor that has a mutation
that binds to the cell receptor and stays down and won't let go,
then we're going to cause promotion of cell division.
In the case for the two hit hypothesis, you need two,
if we have a recessive kind of action.
So for example if we look at p53. p53 if we have one good copy of it,
then we have the cell cycle checking,
we have checking of the DNA to make sure there's no mutations.
And it takes having two bad copies
for there to be no DNA checkpoints.
So two hit hypothesis means that you have to have
two copies of the bad gene.
And so, often a predisposition to cancer,
means you might have one copy already
and another copy could happen through mutation
from teratogens that you experienced during life.
So in summary, during this lecture,
we have explored the cell cycle.
You should be able to describe the main events
of each of the phases of the cell cycle
as well as diagram the roles of the cyclins
and cyclin dependent kinases in the various checkpoints.
And also explain the implications of broken cell cycle controls
and how those might lead to cancers.
I hope you enjoyed this lecture. Thank you so much for listening
and I'll look forward to seeing you shortly.