Hey it's professor Dave, let's talk about cancer.
Cancer. It's the ultimate expiration date for biological organisms. Any person that
were to live long enough and avoid all other health issues would eventually get
some form of cancer or another. But what is cancer, and why are there so many
varieties? Will there ever be a cure for cancer?
Now that we understand the basics of biochemistry we are ready to investigate
this topic in considerable depth. In the briefest description possible, cancer
involves cells that are dividing out of control.
We need our cells to divide at a certain rate to replace dead cells as they occur.
But this process is highly regulated so we must understand that any form of
cancer necessarily involves a genetic mutation that leads to errors in these
regulatory mechanisms. If just one of the proteins that are critical in regulating
cell division and cell death becomes incapable of doing its job even in just
a single cell,
this can result in the formation of a tumor, which is a cluster of cells that
are dividing out of control. We learned about how DNA can become mutated either
through spontaneous error during replication or by external factors like
UV radiation or carcinogens. Again, mutations that occur outside of any gene
are extremely unlikely to have an impact on the organism, but if such a mutation
occurs within a proto-oncogene, which is a gene that codes for proteins that
stimulate routine cell growth and division, it can become an oncogene,
which is a cancer-causing gene. This can occur in a few different ways. If the
gene is accidentally translocated to a new part of the chromosome where it is
adjacent to a particularly active promoter, the gene might be expressed
much more frequently than normal, leading to excessive amounts of that protein.
The gene might be amplified, resulting in many copies of the gene, which also
results in excessive amounts of that protein. Or there could be a point mutation,
a change in a single base pair either in the promoter for the gene, which could
again lead to overexpression, or within the gene itself, which may result in a
mutated form of the protein that has enhanced activity or is more resistant
to degradation, and thus operates more effectively than normal. Any of these
mutations may lead to abnormal stimulation of the cell cycle.
As it happens,
nature has evolved tumor-suppressor genes, which code for proteins that
suppress uncontrolled cell growth. If there is a mutation in one of these
genes that renders the resulting protein incapable of its function, an important
mechanism for suppressing tumor growth can be lost. Almost certainly the most
important tumor suppressor gene is called p53. The protein this gene codes
for is able to activate several other genes whose proteins are responsible for
a variety of activities that halt the cell cycle, typically by binding to
certain enzymes and disrupting their activity. The p53 protein can also turn
on genes that are involved in DNA repair, and if the DNA is damaged beyond repair
p53 can even activate suicide genes that bring about apoptosis, which is
programmed cell death.
This ensures that the faulty cell does not proliferate and become a tumor. So as
you can imagine, any mutation within the p53 gene itself that results in a
non-functioning p53 protein will be disastrous for a cell, because so many of
the safety mechanisms that guard against cancer will be knocked out. Beyond this
we learned about many of the different DNA repair enzymes that are constantly
scanning for the various types of mutations that can occur. If there is a
mutation in one of the genes that codes for these repair enzymes, a particular
type of DNA damage will suddenly become much more likely to be incorporated into
the genetic code, and with no enzyme there to fix it, so there are many types
of cancer that happen this way.
It is quite unlikely that a single mutation will result in cancer, but an
accumulation of mutations over time makes cancer more and more likely, which is why
the risk for cancer increases dramatically in old age. We know a lot
about cancer, but there is so much left to learn. Studies on cell signaling
pathways will continue, and there is hope within the naive optimist such as myself
that we will eventually eradicate all forms of cancer, as well as every other
disease, through the intimate understanding of how to combat them on
the molecular level.
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