For the first time, scientists have shown conclusively how the protein that is missing or altered in the fatal childhood disease ataxia telangiectasia (A-T) acts as a key regulator of cell division after DNA damage. The finding helps researchers understand how cells in A-T patients form tumors and may lead to new understanding of other neurological and immune disorders.

Scientists have isolated the gene and identified mutations that cause the childhood disease ataxia-telangiectasia (A-T), a rare hereditary neurological disorder. Discovery of the gene paves the way for more accurate diagnosis in the short term and the potential for effective treatments in the long term. With this discovery, the investigators believe they also have identified a common genetic marker that indicates predisposition to certain cancers, and may help identify individuals who are sensitive to radiation.

For the first time, scientists have shown conclusively how the protein that is missing or altered in the fatal childhood disease ataxia telangiectasia (A-T) acts as a key regulator of cell division after DNA damage. The finding helps researchers understand how cells in A-T patients form tumors and may lead to new understanding of other neurological and immune disorders.

Scientists have isolated the gene and identified mutations that cause the childhood disease ataxia-telangiectasia (A-T), a rare hereditary neurological disorder. Discovery of the gene paves the way for more accurate diagnosis in the short term and the potential for effective treatments in the long term. With this discovery, the investigators believe they also have identified a common genetic marker that indicates predisposition to certain cancers, and may help identify individuals who are sensitive to radiation.