It makes sense that understanding
the repair mechanism for oxidative damage could well be helpful in solving the
cancer problem. This work is fundamental
in nature and will surely inform further work in the field.
The flood of knowledge in
cellular biology has made conquering disease seem so much closer these last
several years. We all hope it is not an
illusion, yet I find we are also revealing an ever increasing mountain of
ignorance and even the full press attack is not making that mountain any smaller.
Yet I prefer optimism and this is
a good piece of work.
Oxidative DNA damage repair
by Staff Writers
Oxidative stress is the cause of many serious diseases such
as cancer, Alzheimer's, arteriosclerosis and diabetes. It occurs when the body
is exposed to excessive amounts of electrically charged, aggressive oxygen
compounds.
These are normally produced during breathing and other metabolic
processes, but also in the case of ongoing stress, exposure to UV light or
X-rays. If the oxidative stress is too high, it overwhelms the body's natural
defences.
The aggressive oxygen compounds destroy genetic material, resulting in
what are referred to as harmful 8-oxo-guanine base mutations in the DNA.
DNA repair mechanism decoded
Together with the University of Oxford, Enni Markkanen, a veterinarian
in the working group of Prof. Ulrich Hubscher from the Institute of Veterinary
Biochemistry and Molecular Biology at the University of Zurich has decoded
and characterized the repair mechanism for the mutated DNA bases.
This mechanism efficiently copies thousands of 8-oxo-guanines without
their harmful mutations, thus normally preventing the negative consequences of
8-oxo-guanine damage. In their study, published in "PNAS", the researchers
outline the detailed processes involved in the local and temporal coordination
of this repair mechanism.
Prof. Ulrich Hubscher hopes that this basic research can be used
therapeutically. "We expect that the DNA repair mechanism discovered
here will lead to less invasive approaches in cancer therapy and that it will
be possible to develop new clinical tests for the early detection of certain types of cancer."
In cooperation with University
Hospital Zurich
Enni Markkanen, Barbara van Loon, Elena Ferrari, Jason L. Parsons,
Grigory L. Dianov, and Ulrich Hubscher. Regulation of
oxidative DNA damage repair by DNA polymerase and MutYH by crosstalk
of phosphorylation and ubiquitination. Proceedings of the American Academy
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