The most comprehensive analysis yet of the genome of childhood acute myeloid leukemia (AML) found only a few mistakes in the genetic blueprint, suggesting the cancer arises from just a handful of missteps, according to new findings from St. Jude Children's Research Hospital. The research appears in the July 27 online edition of the Proceedings of the National Academy of Sciences.
"Our data raise the possibility that the development of AML may require fewer genetic alterations than other cancers and that a very limited number of biological processes may need to be altered in hematopoietic stem cells, multi-potential progenitors or committed myeloid progenitors to convert them from a normal cell to AML," the authors noted, referring to several types of immature and maturing cells that give rise to this cancer. James Downing, M.D., St. Jude scientific director and the paper's senior author, said the findings highlight questions about what it takes to transform a normal cell into a cancer cell. "The complement of genetic lesions varies across the different genetic subtypes of AML, but there are very few lesions in total. That is surprising. Most cancers have lots of alterations," he explained.
AML accounts for about 20 percent of childhood leukemia. This year it will be diagnosed in about 500 U.S. children. About 60 percent of young AML patients become long-term survivors.
This study reflects the push to chart the genetic changes that free cells from normal controls and allow the uncontrolled cell division that is a hallmark of cancer. Downing said the findings underscore the need to survey the entire genome of childhood AML and take a more detailed look at particular AML subtypes.
Added Ina Radtke, Ph.D., the paper's lead author: "This rigorous systemic genome-wide study was an important step to direct our future efforts to the most effective strategies to pinpoint lesions in AML." She is a postdoctoral fellow in Downin
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St. Jude Children's Research Hospital