They came to this conclusion after carrying out a comprehensive analysis of the genome of childhood acute myeloid leukaemia (AML).
"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.
Senior author Dr. James Downing, St. Jude scientific director, says that 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 said.
Based on the study's findings, Downing stressed the need to survey the entire genome of childhood AML, and to take a more detailed look at particular AML subtypes.
Lead author Dr. Ina Radtke, a postdoctoral fellow in Downing's laboratory, said: "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."
A research article describing the study has been published in the online edition of the Proceedings of the National Academy of Sciences.