Special Challenges Of Childhood Cancer

Pediatric cancer, tragic as it is, is fairly rare, because cancer is ordinarily a result of accumulated flaws and errors that accumulate as cells divide. People under around age 50 or so, whose cells simply haven’t had time to produce significant numbers of errors, only seldom have the uncontrolled cell growth that causes a cancerous tumor. In fact, this makes childhood cancer rather mysterious and difficult to understand. Now, however, researchers think they might have a better understanding than ever before of what causes cancer to develop in children.

“Our prior studies had shown that the DNA damage checkpoint protein, ATM, was very low in most pediatric solid tumors, said Dr. Peter Houghton, director of the Center for Childhood Cancer and Blood Diseases at The Research Institute at Nationwide Children’s Hospital, in a statement. In healthy cells, the protein called ATM detects these genetic errors and diverts the gene for repair. What Dr. Houghton, his colleague Changxian Shen, and their team found was that the cancer cells themselves suppress the ATM protein, creating a vicious cycle that accelerates the process by which transcription and other errors accumulate in the genetic code.

What that means for health care professionals is that it may be possible to fight childhood cancers by directly targeting this loop, which is centered around a protein system called mammalian target of rapamycin, or mTOR. The normal function of mTOR is to regulate insulin, oxygen, and other things that keep the body running, In many types of cancer, mTOR is damaged or its function interfered with. Restoring mTOR to proper functioning, then, has some potential as a way of treating cancer in children. Reversing the suppression of the ATM protein by introducing more ATM into the body may also be beneficial.

“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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