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Two Genes Hold Cancer Prevention Clues

LONDON (Reuters) - Two genes could be the key to understanding how to protect the body from developing cancer, an American scientist said Tuesday.

Dr. Carl Anderson of the Brookhaven National Laboratory in New York told a medical conference in Glasgow, Scotland, that the genes DNA-PK and p53 are essential components of the body's repair system.

``The human genome is like a great castle. In healthy cells the castle stands strong but as cancer develops it quickly crumbles. DNA-PK and p53 are the crucial cornerstones that hold the castle up,'' he said in a statement released in London.

``When they are intact we are safe, but when either goes wrong the castle starts to collapse,'' he noted.

Cancer develops when something goes amiss in a normal cell and instead of self-destructing in a process called apoptosis, it divides and multiplies uncontrollably.

Anderson discovered DNA-PK 18 years ago while working at Cambridge University. In laboratory tests and by studying the sequence of the human genome, or genetic code, published earlier this year, he found that in many cancers there was something wrong with DNA-PK, which normally repairs damaged genes.

Cancerous cells can also harness DNA-PK's power to repair damage caused by anti-cancer treatments, making the cells resistant to the therapy.

``By understanding how DNA-PK and related enzymes work at the molecular level, we and others are learning more about how cancers arise and how they respond to radiotherapy,'' said Professor Steve Jackson of Britain's Cancer Research Campaign, Anderson's collaborator.

P53 acts as a signaling system, sending out messages that put a brake on cancer by stopping damaged cells from dividing and forming tumors. The gene, discovered by Scottish scientist David Lane, is altered in about 80% of cancers.

Understanding the mechanisms of both genes and their role in cancers could be the key to devising new ways to treat and prevent the disease, Jackson and Anderson said.

They presented their research at the 4-day Genomic Regulation and Cancer Conference in Glasgow.

Reference Source 89

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