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Study finds missing piece of pediatric cancer puzzle
Date:7/19/2013

. Low levels of ATM allow the mTOR pathway to keep producing the microRNAs that further reduce the ATM-mediated checkpoint activity. When the microRNAs weaken the cell's damage checkpoint, the checkpoint cannot effectively prevent mutated cells from proliferating.

By making this connection, Drs. Shen and Houghton have identified a potential explanation for the early development of pediatric tumors as well as a potential target for new cancer therapies. Early tumor growth seems to be caused by cells' rapid bypass of the damage checkpoints instead of the gradual accumulation of damage at play in adult tumor growth. Future treatments that can help cells increase ATM checkpoint activity or fight the overproduction of microRNAs may slow or stop the growth of cancerous pediatric tumors.

"These results help us to not only understand the early genesis of some tumors in children, but also why many solid tumors are highly sensitive to drugs and ionizing radiation that damage DNA," Dr. Houghton said. "They also help explain why, in children not cured by these treatments, resistance to therapy arises the rapid rate of mutation due to suppression of ATM. Potentially, the rate of mutations that lead to drug or radiation resistance could be slowed by targeting mTOR."


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Contact: Gina Bericchia
gina.bericchia@nationwidechildrens.org
614-355-0495
Nationwide Children's Hospital
Source:Eurekalert

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