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A boy cries as he recuperates after surgery during "Operation Smile" at a hospital in Manila's Makati financial district October 26, 2009. Operation Smile aim to provide free surgery for about a hundred children inflicted with cleft lips, cleft palates, and other facial deformities over a period of five days in Makati.  REUTERS/Cheryl Ravelo

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    Study sheds light on deadly childhood cancer

    LONDON
    Mon Jan 5, 2009 1:46pm EST

    LONDON (Reuters) - A gene involved in cell division also helps fuel a deadly childhood cancer called neuroblastoma and could offer a new way to develop drugs to treat the disease, German researchers said on Monday.

    Health

    The study published in the journal Cancer Cell found that a protein produced by the AURKA gene feeds a different gene called MYCN, which scientists know plays a key role in fuelling tumor growth in children with neuroblastoma, the researchers said.

    "The MYCN gene is one that no pharmaceutical company have been able to target," Martin Eilers, a researcher at Wurzburg University in Germany, who led the study, said in a telephone interview.

    "Our finding offers hope we can make new (drugs) to attack this cancer."

    Neuroblastoma accounts for 15 percent of childhood cancer deaths, with just a 40 percent survival rate, even though it only causes about seven percent of all pediatric cancers.

    In August U.S. researchers said they had found a variation in a gene called ALK that causes most inherited forms of the disease by helping cells proliferate. Out-of-control proliferation is the hallmark of cancer.

    Eilers and his team screened 200 genes dependent on MYCN in children with neuroblastoma and found that the protein produced by AURKA was key to the wild cell growth.

    Current drugs that inhibit cell growth will not work but AURKA is a promising target for new treatments because there are already substances in the body that attack the protein. That means, in theory, newly developed drugs could do the same.

    "This is potentially a way you can get at and interrupt these tumors," Eilers said in a telephone interview.

    (Reporting by Michael Kahn; editing by Maggie Fox and Jon Boyle)



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