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My name is Gerd Pfeiffer.
The topic of my talk is DNA methylation,
inflammation, and cancer.
The talk will be divided into four parts,
in part one, a method for
DNA methylation analysis,
genome wide will be described.
In the second part,
data on the DNA methylation patterns
in B cells will be reported.
In part three, I will discuss our data
on the inner methylation in lung cancer.
And in the last part,
the relationship between inflammation,
DNA methylation and cancer and targeting
of specific genes will be discussed.
DNA methylation patterns in mammalian
cells are generally quite stable.
During DNA replication,
methylation at CpG sites is copied
by DNA methyltransferase one.
Methylation can also be introduced de
novo or methylation can be lost by DNA
demethylation processes, either active or
passive DNA demethylation.
These mechanisms can be
altered in diseased tissue.
There's many different methods to analyze
DNA methylation on a genome-wide scale.
Some are based on methylation
sensitive restriction enzymes.
They're shown here in panels A,
B and C, the information can be
detected by two dimensional gel
electrophoresis by PCR or by micro arrays.
Another method used is an antibody against
methylated cytosine is shown here in
panel D and it's called Methyl-DIP.
This method is like immunoprecipitation
and the methylated immunoprecipitated DNA
can be analyzed either by high throughput
sequencing or by microarray chip analysis.
Another way to look at methylated genes
is to use a methylation inhibitor,
5-Aza-cytidine or DAC.
Genes that become reactivated by DAC
treatment shown here in panel E and
then be scored and methylation must
then be confirmed by different,
more specific methods.
We developed a method for
genome wide DNA methylation profiling,