Well, let's talk a little bit more about,
injury related to subsequent tumor development.
So, you can have a direct transforming effect,
many viruses will, abrogate some
of the intracellular checkpoints,
that keep the cells from constantly turning over.
When we talk about malignancy
in a subsequent talk, you and I,
I will talk about the effects
say of a herpes papillomavirus,
human papillomavirus and what it
does to p53 and the RB proteins,
that are normal regulatory checkpoints.
By causing their degradation the virus,
causes the cells to constantly proliferate,
so, you can have a direct transforming effect.
There's also an issue related
to the tumor-promoting effects,
that come from chronic inflammation.
So, in the setting of chronic inflammation,
you have, inflammatory mediators,
secreted by all the inflammatory cells,
that are there, in the setting of tissue,
that's also trying to regenerate because
of the damage induced by the virus.
G, proliferation in the setting of a
whole bunch of reactive oxygen species
and other things that can
potentially mutate the genome,
is a perfect setup, to
develop brand new mutations,
that get incorporated into
the proliferating cells.
So, in many cases chronic inflammation,
in an epithelium or in a tissue that
is turning over at the same time,
will lead to malignancy.
That's why chronic hepatitis
B or chronic hepatitis C,
makes those liver cells prone to
develop hepatocellular carcinoma.
Similarly, in the GI tract which is
being shown here with the stomach,
is that you can have chronic inflammation,
say related to a helicobacter pylori,
that epithelium is turning
over, this chronic inflammation,
helicobacter pylori is a major
driver for gastric carcinoma.
So, ongoing epithelial proliferation in
the setting of ongoing injury, means,
that we can have cellular
mutations that get locked in,
to those proliferating cells.