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Robust DNA Repair May Lower Breast Cancer Risk
Fri Jan 21, 2005 2:15 PM ET

By Anthony J. Brown, MD

NEW YORK (Reuters Health) - The innate capacity to repair damaged DNA
seems to affect a woman's chance of developing breast cancer. Deficient
DNA repair appears to triple the risk of breast cancer, researchers
have found.

"A lot of studies have looked at the link between DNA repair capacity
and lung cancer risk, but few studies have evaluated the association
with breast cancer risk," Dr. Regina M. Santella, from Columbia
University in New York, told Reuters Health.

Santella's group used various lab techniques to compare the DNA repair
capacity of cells obtained from 158 women with breast cancer and from
their sisters who didn't have cancer.

The average percentage of damaged DNA that could be repaired was
significantly lower in the breast cancer patients than in their
unaffected siblings, the investigators report in the Journal of the
National Cancer Institute.

Moreover, as DNA repair capacity diminished, the risk of breast cancer
rose, with about a 3-fold difference between those with the highest
capacity versus those with the lowest.

Santella said these findings could have implications for breast cancer
screening. "The ultimate goal is to understand an individual's risk for
cancer development so that you can better target screening and
prevention efforts."

She noted that the assay used in the present study looked at just one
of many DNA repair mechanisms. "At this point, we're interested in
conducting a study using an assay that measures a different DNA repair
pathway. Looking at the status of several different pathways may give a
better estimate of breast cancer risk."

In a related editorial, Dr. Marianne Berwick, from the University of
New Mexico in Albuquerque, and Dr. Paolo Vineis, from Imperial College
in London, point out that measuring DNA repair capacity is complicated
at present. Once simple and rapid assays are available, it may be
possible to develop "interventions to reduce cancer incidence and
mortality."

SOURCE: Journal of the National Cancer Institute, January 19, 2005.

© Reuters 2005. All Rights Reserved.

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Ip6/double strand break repair

Cell 2000 Sep 15;102(6):721-9

Binding of inositol phosphate to DNA-PK and stimulation of
double-strand break
repair.

Hanakahi LA, Bartlet-Jones M, Chappell C, Pappin D, West SC

Imperial Cancer Research Fund, South Mimms, Hertfordshire, United
Kingdom.

In mammalian cells, double-strand breaks in DNA can be repaired by
nonhomologous end-joining (NHEJ), a process dependent upon Ku70/80,
DNA-PKcs, XRCC4, and DNA ligase IV. Starting with HeLa cell-free
extracts, which promote NHEJ in a reaction dependent upon all of
these
proteins, we have purified a novel factor that stimulates DNA
end-joining in vitro. Using a combination of phosphorus NMR, mass
spectroscopy, and strong anion exchange chromatography, we identify
this factor as inositol hexakisphosphate (IP6). Purified IP6 is bound
by DNA-PK and specifically stimulates DNA-PK-dependent end-joining in
vitro.
The involvement of inositol phosphate in DNA-PK-dependent NHEJ
is of particular interest since the catalytic domain of DNA-PKcs is
similar to that found in the phosphatidylinositol 3 (PI 3)-kinase
family.

PMID: 11030616, UI: 20483533

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