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Monday, August 8, 2011

FAULTY DNA REPAIR GENE INCREASES RISK OF OVARIAN CANCER

I found this an interesting concept as to why and how we get a cerrtain type of cancer.  It's a faulty wiring system apparently.  The human body is a marvel at the best of times with it's ability to repair itself and keep us healthy but when things go wrong we want to know why.  We have repair genes in our DNA that sometimes become faulty. 
Originally they must have been pretty smart to climb out of that primordial pea soup that so many believe was the origin of the human race and  then to be able to predict that at some point in time that our DNA would have to be repaired.  Amazinging intelligent.  All that before the body was even evident.  That is so much simpler than that other 'other theory' called creation.

Women with a faulty copy of a DNA repair gene called RAD51D have a 1 in 11 risk of developing ovarian cancer compared to 1 in 70 in the general population, according to a landmark Cancer Research UK-funded study led by Professor Nazneen Rahman at The Institute of Cancer Research (ICR) published in the 7 August online issue of Nature Genetics. There is hope that personalized treatment will be available sooner than usual because a class of drugs already developed showed promise in targeting affected cells.

Rahman, who is Professor of Human Genetics and Section Chair of Cancer Genetics at ICR told the press the study represents a significant step forward in our understanding of how faulty genes contribute to the development of some cases of ovarian cancer, and there is "real hope on the horizon that drugs specifically targeted to the gene will be available".

RAD51D repairs damaged DNA. When the gene is faulty, an important repair pathway fails, leaving damaged DNA to build up in cells, which increases the risk they will become cancerous.

For their study, Rahman and colleagues examined DNA from women in 911 families with ovarian and breast cancer and compared it to the DNA from a control group of 1,060 people in the general population (the controls).
They found eight inactivating RAD51D mutations in unrelated women with cancer, compared with only one in the controls.

The association was principally with ovarian cancer, with three mutations found in 59 of the families with three or more individuals with ovarian cancer.

The researchers also found cells deficient in RAD51D were sensitive to treatment with a relatively new class of cancer drug known as a PARP inhibitor, "suggesting a possible therapeutic approach for cancers arising in RAD51D mutation carriers", they write.

PARP inhibitors are a group of drugs that inhibit the action of the enzyme Poly ADP ribose polymerase (PARP), a protein that plays a role in many cell processes that involve DNA repair and programmed cell death.

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