Given that a series of genetic mutations work together cause the disease, the researchers have named these defects ’cooperating oncogenic lesions’.

The researchers have revealed that these defects include the deletion of a gene called IKZF1, whose protein Ikaros normally helps guide the development of a blood stem cell into a lymphocyte.

They have also discovered that the loss of the same gene accompanied the transformation of chronic myelogenous leukaemias (CMLs) to a life-threatening acute stage.

"These findings provide new avenues to pursue to gain a better understanding of these disease processes and, ultimately, to develop better therapies," Nature magazine quoted Dr. James R. Downing, St. Jude scientific director and chair of the Department of Pathology, as saying.

He says that his team’s findings lend further support to the idea that malignancies frenquently require mutations in multiple genes in order to develop.

Dr. Downing says that cells contain oncogenes, which exist harmlessly until something triggers them to turn the cells malignant.

"It really takes a series of genetic lesions to lead to cancer. You may get activation of an oncogene, but you may also need activation of a tumor suppressor gene and an alteration in a cell-death pathway," he said.